Tanuvas Surgery Notes 411

VSR-411 (2+2) General Veterinary Surgery, Anaesthesiology and Diagnostic Imaging. SYLLABUS GENERAL SURGERY- THEORY Introduction history classification surgical terminology and development of veterinary surgery. Asepsis antisepsis, their application in Vety.Surgery. Surgical Risk & Surgical judgement. Management of shock, haemorrhage & its management. Principle of fluid therapy in surgical patients. Differential diagnosis and surgical treatment of abscess, tumors cyst, haematoma, necrosis, gangrene burn, wound, classification, symptoms, diagnosis and treatment & complication ,their treatment and prevention. PRACTICALS- Surgical instruments and equipment. Operation theatre routines. Surgical pack: Preparation, sterilization and handling. Familiarisation with suture materials, surgical knots, suture patterns and their use. Familiarisation to live surgery haemostatsis. ANAESTHESIOLOGY- THEORY (Region specific) Preanaesthetic consideration and preanaesthetics. Aneasthesi, local analgesia / anesthesia, general anesthesia, anesthestic agents (like barbiturates, dissociative agents) inhalation anaesthesia and agents, maintenance and monitoring of general anaesthesia, aneasthestic emergencies and their management. Only awareness of neuroleptanalgesia, electro-anesthesia, acupuncture, hypothermia, muscle relaxants. Post operative pain management. General principle of chemical restraint of wild / zoo animals and aneasthesia, of lab animals. PRACTICALS- Familiarisation with aneasthetic, apparatus, endotracheal tubes. Laryngoscope, gadgets for monitoring pre aneasthetic preparation, induction of general aneasthesia, in small and large animals and endotracheal intubations in dogs. Demonstration of inhalant anaesthesia monitoring of general aneasthesia, and the management of aneasthestic emergencies. Use of artificial / assisted respiration. Various methods of local infiltration aneasthesia, and regional block, for surgical procedures of different regions of body in Large and small animals. Chemical restraint of lab animals. (Visit of a wild animals facility and audiovisual aids) DIAGNOSTIC IMAGING –THEORY Production and properties of X-rays. Factors influencing production of X-ray. Principles of viewing and interpreting X-ray films, classification of radiographic lesions, Contrast radiography: classification, materials, uses, indications and contra indications. Biological effects of radiation, radiation hazards and their prevention by adoption of safety measures. Principles of ultrasonography and its applications in veterinary practice. Awareness on principles of radiation therapy, Isotopes and their uses in diagnosis and therapy; Principles and application of CT scan, MRI, echocardiography, scintigraphy, gamma camera, xeroradiography and Doppler. PRACTICAL- Familiarization with operation of the X-ray equipment, X-ray accessories and adoption of safety measures in radiography. Dark room equipments, X-ray film and its processing. Intensifying screen and its uses. Radiographic technique-positioning of small and large animals. Handling, viewing and interpretation of X-ray films. Familiarization with film contrasts, density and detail, common defects of X-ray films. Radiographic anatomy and interpretation of radiographic lesions. Demonstration of contrast technique in small animals. Familiarization with ultrasonography of small and large animals PART- I (General Veterinary Surgery ) COURSE OVERVIEW This course is designed to teach students the general veterinary surgery, general anaesthesia and radiology. The objectives of this course are,  To assist undergraduate students in understanding o the pathophysiology, differential diagnosis and surgical treatment thorough knowledge of this subject help the student to develop the skill to diagnose and perform surgery. o the various disease conditions are enumerated system wise with etiology, clinical signs , and diagnostic methods enumerated in a sequential way. o monitoring of anaesthesia o anaesthetic emergencies and their management o production and properties of X-rays  Illustrations added will aid the student to give quick rememberence of the disease process.  View vidieo procedures by clicking on the icon.  Applied knowledge of this course information with analytical thinking will facilitate the understanding of the differential diagnosis.  Overall knowledge gained from this course will help the student to develop skill ability to approach surgical cases in a systematic manner. Horace Wells (1815-1848) though lived only a for short duration. Paracelsus administered ether to chickens. Souberian and Guthrie. Morton deserves the chief credit for the introduction of ether as anaesthetic agent. Later ether was patented as Lethon. Joseph Priestley isolated and identified depholgisticated air- oxygen and depholgisticated Nitrous oxide.  1846 William Thomas Green Morton (1819-1868) demonstrated the use of ether as anaesthetic for the removal of tumor in humans. Egyptians induced unconsciousness by compression of the carotid arteries.  1771. Ether and other vapours to surgical operations”. published valuable information through his news letter “A History of the discovery of the application of Nitrous oxide gas. Hentry Hill Hickman performed surgeries on experimental animals by inducing asphyxiation using carbon dioxide. . Chloroform was used first in animals by Flourens.  1857.  1825.  1847. Juice of mandrake plant was used during Alexandrian period.  1831.  1540. John Snow administered chloroform to Queen Victoria during the delivery of her eighth son Prince Leopold and later it became popular. Chloroform was discovered independently by Von Liebig. In following centuries various plants containing opium and atropine likecompounds were used.C.  1846. LEARNING OBJECTIVES  History of surgery  Classification  General surgery principles  Pre and post-operative considerations  History and Development of Veterinary Surgery Module-1 =  History and Development of Veterinary Surgery HISTORY OF ANAESTHESIA  300 B. Example: Castration in a male cat. Example: Tumours of lung. and “ERGON” meaning “WORK” German language it is called CHIRURGIA. Classification of surgery- DEFINITION  Surgery is a branch of Medicine. internal pudental nerve and posterior tibital nerve using cocaine in 1886. Example:Gangrenous limb. Example: removal of a benign tumour.  To make an animal sociality acceptable.  For cosmetic reasons. gum elastic catheters and metal and flexometalic tubes.  For elimination of disease process.Example: Correction of knuckling of fetlocks (Structural disorder).  For replacement of a part by an artificial one. o Removal of harmful or useless parts. Sir William Macewen (1847-1924) Pioneer of oral and nasolaryngeal intubation in diphtheria patients as an alternative to tracheotomy using rubber. Example: Rumen fistulation. Example: Suturing divided tendons and nerves. Example: Exploratory laparotomy.  To aid in diagnosis. REASONS FOR SURGERY  To save life of an animal. o Prevent spread of malignancy. . o Control of infection.  To hasten recovery from an injury.  For investigation in research work.  For correction of deformities. o Reconstruction of tissues.  The word surgery originated from a Greek word “CHEIR” meaning “HAND”.  William Stewart Halsted (1852-1922) Famous surgeon proposed the “Principles of Surgery” originated nerve block techniques like blocking brachial plexus. deformities and diseases. Later he administered chloroform and air through the tubes for induction of anaesthesia. Example: Treating a lacerated wound. in which manipulative and other modalities are used in treating injuries. FUNCTIONS OF A SURGEON  A surgeon mainly deal)s with o Repair of tissues. o Alter or correct structural and functional disorders. Example: Post pharyngeal abscess. nerves of the face. gangrenous bowel.  To prolong life of an animal. eyeball  Plastic surgery: To restore the destructive part which includes reconstructive surgery (a structure is reconstructed) e. BASED ON NATURE OF SURGERY  General surgery: Is carried out to restore the normal function of the body without substituting or discarding any part of the body.Is used when in a procedure common surgical instruments are used  Micro surgery .wounds and fractures  To make the animals to less dangerous ..castration in pigs.g.ovariohysterectomy..gangrenous tail  Removal of foreign bodies . OBJECTIVES OF SURGERY  Restoration of functions to as near normalcy as possible.to improve the live body weight  For aesthetic purposes .exploratory laparotomy ..Organ transplantation  For confirming diagnosis . .g.  Replacement surgery  Physiological surgery .debudding  For economic reasons . ear cropping etc.rumenotomy  To hasten recovery process .g. intestinal obstruction).e. skin grafting and cosmetic surgery (which improves appearance) e. docking. cattle etc.g.removal of supernumerary teat  To replace the organs .  Removal of diseased part . (Restorative Surgery)  Extirpative surgery: Involves removal of a part e.  To eliminate life threating maladies (choke..Magnification facilities are used for specialized surgical procedures.Portosystemic shunt  Diagnostic surgery  Exploratory surgery CLASSIFICATION BASED ON REGIONS/SYSTEMS INVOLVED  Specialization on particular system examples o Thoracic surgery o Cardiovascular surgery o Orthopaedic surgery o Ophthalmic surgery o Neuro surgery o Urogenital surgery CLASSIFICATION BASED ON INSTRUMENT/APPLIANCES USED  General surgery .  Cryosurgery - Involves controlled use of substances like liquid nitrogen which produces freezing temperatures to destroyed abnormal tissues.  Electro surgery - Electricity is converted into heat to incise tissue.  Laser surgery - Laser beams are used to cut or destroy diseased tissue  Ultra sonic surgery - High frequency waves are used to destroy particular tissue or a substance (lithotripsy)  Endoscopic surgery - involves use of rigid and flexible scope e.g., laparoscope, arthroscope, bronchoscope TENETS OF HALSTED HALSTED described certain essential principles for wound healing. These include:  Gentle handling of tissues to avoid unnecessary trauma  Aseptic procedures to control infection  Anatomical dissection of tissues with sharp instruments. Avoid damage to major blood vessels and nerves  Control haemorrhage with fine, non-irritating suture material in small quantities  Obliteration of dead spaces to avoid accumulation of blood and exudates which favour pus formation  Use of Minimum suture material  Avoidance of suture Tension  Immobilisation - Give rest to the operated part and to the patient  G A A C O M T I - accronymn CLASSIFICATION OF PHYSICAL STATUS  It reflects an attempt to define the condition of the animal and thereby surgeon becomes alert to problems which may occur during anesthesia and surgery.  Physical status may be of o Good o Fair o Poor o Extremely poor o Emergency good o Emergency poor o Moribund condition   The patient ->   Identification   History   Preparation of patient . IDENTIFICATION  Identification is important due to veterolegal cases  Extension of preoperative medication when owner is not available  To prepare operative site  To avoid chances of wrong animal being operated  To avoid mixing of radiographs HISTORY  Information provided by the owner may prove highly beneficial since an animal cannot describe the ailment.  A surgeon should have experience and analytical power to extract valuable information as an owner may provide misleading history.  A simple language without technical terms should be used while extracting information.  An approach of through questioning with tact and generation without irritating the owner may provide better results.  Clinical signs recorded by owner, probable duration of the disease, status of pregnancy , date of last parturition and status of milk yield should be recorded.  Information should also be gained regarding the treatment previously received by the animal  The conflicting points of history should be sorted out logically to gather reliable information.  Even though history provided by the owner may be useful it is not a substitute for careful clinical examination.  If history and clinical examination are at variance, it is better to depend upon the examination. PREPARATION OF PATIENT  Make the patient an indoor one to accustom with the environment of ward In ruminants rest for couple of hours lowers the stress(Travel of animal long distances on feet) Emergency case should be attempted immediately General physical examinations should be carried to assess prognosis.  Severe dehydration and debilitation with prominent ribs indicate poor prognosis if general anaesthesia or major surgery is indicated.  Rough and hard coat .  Sunken eyes  Prolonged lateral recumbency o Colour of the mucous membrane and capillary refill time are the o useful aids in dealing seriously ill patients  Rectal temperature, pulse and respirations should be recorded  Palpation, percussion and auscultation help to arrive diagnosis  In a febrile state surgery should be postponed  Paracentesis of swelling and cavities for differential diagnosis  Laboratory procedures – Pathological tests and their correction for treatment  Radiography  Fluid therapy particularly in case of dehydrated and worm infested animals.  With holding of feed and water  Large animals: 24 - 48 Hrs ; 12 - 24 hrs  Small animals : 12 Hrs ; 4 - 6 hrs  Administration of laxative, purgative or enema for 2-3 days before operation to evacuate the bowels and fit for general anesthesia (not recommended in Ruminants)   Preparation of operation site ->   Day before operation -   Day of operation -   Preparation of the surgeon -   Location -   Planning -   Maintenance of records . DAY BEFORE OPERATION  Clipping of long hairs by scissors or by shaving the animals. Before shaving some soapy solution should be used  Washing the area by non-irritant antiseptic lotion like Savlon liquid  Washing by plain water and rubbing gently by cotton or swab gauge  Again washing by running water  Evaporative type of antiseptic wash or lotion should be applied locally  Covering the site by sterile gauge and bandage for the next day of operation DAY OF OPERATION  Again wash with antisepti  clotion and shaving  Application of alcohol  At the time of operation the animal should be brought to the operation table PREPARATION OF THE SURGEON  Surgeon dresses should be changed in preparation room  The case sheets should be such that there can be stored for future reference and use.  Necessary assistance required for restraint of the animal should be arranged.  Records will help to identity the technical areas of difficulty  Post operative care and management - . drugs and other items required during an operation have been arranged properly.  If doubt. instruments. LOCATION  It is always preferable to do surgery in an operation theater if feasibility exists where routine professional and manual help in and equally available. owners name and address. Nails should be cut and scrubbed with nail brush or gauge. PLANNING  A surgeon must know the structure to be incised and handled in any surgical procedure and so be thoroughly familier with surgical anatomy. available literature should be consulted. MAINTENANCE OF RECORDS  A surgeon must keep records of each and every aspects of a case.  A better approach is to mentally visualize the operation to be done and make a check list of all items required.  A proper planning avoids wastage of time and energy immediately. history of the case clinical findings type of surgical and postoperative treatment and the outcome should be recorded.  Records can be analyzed to work out incidence of various diseases in an area and also to judge the efficany of the treatment measures adopted.  Getting a risk note signed from the owner even for a simple operation is essential.  Anatomical structure should be reviewed on a cadaver. before and during surgery. Hands should be immersed in cetrimide solution or rinse with surgical spirit (70% alcohol)  While putting on gloves the outer surface of the gloves should not touch with the hands . Infection from the nose and mouth should be prevented by using caps and musk  Shoes of surgical team should be changed  Hands upto elbow should be scrubbed for at least 5 minutes with soap and running water.  Description of the patient identification marks. (Major surgery)  The surgeon should also ensure that the equipments.  Antiemetics may be given to prevent vomition.  It prevents cerebral ischemia. analgesic drugs should be given to control pain which may originate from the operation site.  Liquid diet should be given at second day. enzymes should be added.  Solid food should be given after 8th day of operation. o Food must be free from fat and some vitamins. o Semisolid food should be given from forth day.  Food must be free from fat and some vitamins.  Restlessness can be controlled by the application of sedative or tranquilizer.  Routine broad or narrow spectrum antibiotic should be given. . o Solid food should be given after 8th day of operation. vomition and helps to remove tracheobronchial secretion.  Shifting of patient in the ward   Post-operative medication   Post-operative diet   Post-operative exercise   Post-operative dressing   Release from the ward   Followed by check up – SHIFTING OF PATIENT IN THE WARD  Immediately after major operation. o Liquid diet should be given at second day.  Semisolid food should be given from forth day. POST-OPERATIVE MEDICATION  According to severity of pain.  Supportive therapy with fluid and vitamins should be resorted too. enzymes should be added.  Unconscious patient should be placed in the bed of surgical ward with slightly lowered down the head except in brain surgery operation cases. the patient should be gently removed from operation table. POST-OPERATIVE DIET  Oral intake of food and fluid is restricted for 12-24 hours after major operation. o Oral intake of food and fluid is restricted for 12-24 hours after major operation. unclean. Module – 2 = ASEPSIS. RELEASE FROM THE WARD  Skin sutures should be removed between 8-10th day of post-operative days according to the condition.  Sterilize . pathogenic organisms.  Operative site should be treated with topical antibiotics and covered by light bandages.the process of destroying most. 5th and 7th post-operative days to visualize the condition of operative site. SURGERY.being free of disease-producing microorganisms. .  Microorganism . POST-OPERATIVE EXCERCISE  Exercise means walking which should be accomplished for 2-3 hours per day.the practice used to remove or destroy pathogens and to prevent their spread from one person or place to another person or place.  The time and distance of walking depend upon the severity of patient. TERMINOLOGY  Asepsis .to kill all microorganisms including spores.  The area should be washed with antiseptic lotion and rebandaged for proper healing.  Medical Asepsis . FOLLOWED BY CHECK UP  The surgeon advised the attendants that the patients must be checked by him for a certain days. POST-OPERATIVE DRESSING  Dressing should be done on 3rd. soiled with germs.a living body so small that it can only be seen with the aid of a microscope. ANTISEPSIS & THEIR APPLICATIONS IN VETY. but not all.dirty.  Disinfection . clean technique.  Contaminated .  Antibiotic: A substance derived from mould or bacteria that inhibit the growth of other micro-organisms. o Physical sterilization  Thermal  Filtration  Radiation o Chemical sterilization  Germicidal solutions Glutral dehyde. All packs should be dated.  Sterilization: Complete elimination of microbial viability including both the vegetative forms of bacteria and spores process by which an article can be rendered free from all forms of living microbes including bacteria. sterile packs should be stored in closed cabinets. STERILIZATION TECHNIQUES FOR SURGICAL MATERIALS AND INSTRUMENTS  Two general categories of sterilization methods can be grouped under. Beta propiolactone  Ethylene oxide THERMAL  Steam sterilization is the most commonly employed method of sterilization of instruments and equipment.  Haemostatic: Arresting flow of blood within a vessel. haemostatic agent used externally to stop flow of blood. .  Astringent: Causes contraction of tissues and so arrests haemorrhage. fungi and their spores and viruses.  Different types of autoclaves are o pressure steam sterilizer o steam pressure sterilizer o vacuum steam sterilizer o dressing sterilizer o gravity displacement sterilizer Points to be considered  Instrument packs are positioned vertically (on edge ) and longitudinally in autoclave  A 13 minutes sterilizing cycle (exposure to saturated stem at 1210C) is a safe minimum required  Large linen packs require 30 minutes at 1210C  Once sterilized.  Styptic: Astringent.  Antisepsis: is the destruction of micro organisms but not bacterial spores on living tissue. powders. glass surgicals etc. at 151 lbs pressure.  Hot air oven – most common method.  Sharp instruments ¾ scissors.5 hours  1600c for 60 minutes  1700c for 40 minutes  Exposure time relates to the time after specific temperature has been achieved and don’t include heating lags. paper wrapped material. CHEMICAL AGENT . Dry heat sterilization  Dry heat destroys microorganisms primarily by oxidation process.0 hours  1400c for 2. Methods  Direct exposure of instruments to flame – not reliable.  Ionizing radiations. Beta and cathode rays are used to sterilize heat sensitive prepackaged surgical materials. Petridis – 1200c for 8 hours  Stainless steel lens and glass ware – 1600c for 60 min FILTRATION  Filtration is used in air conditioning system to remove particles as small as 0. needles.g: oils. RADIATION  Ultraviolet light is used for surface sterilization.  Example: Surgical mask .to produce two fold effect.  It is used to sterilize those materials for which moist heat cannot be used either due to deleterious effects on the material or material being impermeable to steam e.  Clean gowns.3 µm in diameter and also used to filter-sterilize heat labile solutions.  Slow process and long exposure time at a high temperature is required as spores are relatively resistance to dry heat. Temperature time combinations for dry heat sterilization  1200c for 8. swabs.  An exposure to dry heat at a temperature of 1600C for 60 min will achieve sterilization equal to that of moist heat at 1210C for 15 min. surgical instruments can be sterilized by this method. carbolic acid Chemical sterilization by gases  Ethylene oxide acts by inactivating the DNA molecules in the microbial cells thus preventing cell reproduction.g. Eg: Needles.  Irritant to skin and mucous membranes. o Isoprophyl alcohol is more bacterial than ethyl alcohol  Sterilization can be done by immensities continuously. parvo cide ) Formaldehyde  Available as formalin 37% solution of formaldehyde and water. o Phenolic derivatives . Aldehyde  Formaldehyde and flutasaldehyde (cidex. non toxic o be effective in presence of organic matter o not be inactivated by other concurrently used chemicals Agents in solution form Alcohol  Ethyl alcohol (70%). PREOPERATIVE CONSIDERATIONS  A surgeon must keep certain considerations in mind before undertaking surgery. dry or stain o be stable.  An ideal chemical agent should have following properties o kill all pathogenic microorganism o work effectively in short period of time o exert residual action o not corrode. Isopropyl alcohol (90%) are commonly used  Presence of water easily denatures the protein. o Oxidizing agent e. o 70% alcohol is more qermicidal than absolute alcohol. Temperature . hypodermic needles. detergents. odorless.120 to 140F  Eg: ethylene oxide.  Used as gas for fumigation. . Halogens  Inorganic Iodine compounds  Organic Iodine compounds o Surfactants – Soaps. formal dehyde and beta propiolatone (generally used)  Sharp edged instruments – Scalpel blades.  Owner – patient – Surgeon relationship becomes very important in veterinary profession to maintain a good rapport.Ethics and centiments of the owner. patient and Surgeon.  In Eastern countries the relationship may at times be more influenced by personnel & religious sentiments of the owner. Ex. Economic aspects of the case 2. Surgical risk involved 3.  The owner must be convinced that every thing being done is in the interest of the animal patient. FACTORS INFLUENCING SURGICAL RISK  Haemorrage and shock  Fluid and electrolyte imbalances  Acidosis and alkalosis  Anemia and hypovolaemia  Malnutrition and hypoproteinemia  Pulmonary and cardiovascular complication .  After weighing each aspect carefully.  A surgeon must also consider 1.  A veterinarian is legally answerable to the owner.  It is the ethical and legal duty of the surgeon to inform the owner about surgical risk in advance. proposed surgical treatment and the possible outcome. SURGICAL RISK  The term risk is used to describe the animal’s potentiality for surviving anesthesia and surgery. Preoperative considerations may relate to the owner.  The whole approach towards the owner should be based on the logic and sound reasoning.  The owner must be well informed about the diseases.  A surgeon may be approached for surgery when it is not feasible.  Incertain instances the owner may strictly forbid the use of a knife or other cutting instrument on the animal.  To reduce the risk to minimum is of surgeons concern and alert to problems that may arise during anesthesia and surgery. THE OWNER  Owner is the custodian and provider of the animals need and therefore he has a legal right over his animal. the myths of taboos of the region. Multiple fractue of pelvis. the surgeon should make a decision and communicate the same to the owner in a confident and convincing tone. differential lecucocytic count. systemic and special examination  Essential laboratory examination including routine examination of stool. hemoglobin %. packed cell volume)  On the basis of magnitude of operation. urine and blood (clotting time. the length of time depending on the surgeon’s exposure to many and varied cases.  The decision must be based on the circumstances and the optimum condition of the patient for surgery. bleeding time.  A Surgeon who continuously makes the same errors can never develop sound judgment.complication in both very old and very young animals HOW SURGICAL RISK IS DETERMINED  Detailed history of animals  Physical status and condition of animal  Individuality  Clinical examination of the patient including general.  When examination and diagnosis favours or indication for surgical treatment then decision must be made about: o Feasibility of performing surgery in consideration to the animal’s condition. o When to under take surgery  Feasibility of performing surgery entirely depends of the evaluation of the patient but the proper timing of operation is more of a problem in clinical judgment then the decision as to performance. total count. Hepatic insufficiency  Renal and adrenal diseases  Obesity of the patient  Extreme of age . nature of aliment with foresaid findings. the risk of patient is evaluated ADJUNCTS AND SAFEGAURDS  These are o Evaluation of operative risk o Recognition and correction of preoperative deficits o Prevention of intra-operative and postoperative complication before they develop o Resuscitation and after care of surgical patient SURGICAL JUDGEMENT  Surgical judgment is something that can be developed only over a period of time. .  Such type of decision as to wheather and when to undertake surgery is applicable both for emergency and elective surgery. no single definition has been successful.  Shock can result in serious damage or even death. wherever required  Emergency surgical operations are those where there is serious injury or massive internal hemorrhage which may endanger the life of the patient. magnetic resonance imaging etc. CLASSIFICATION  There are four general categories of shock: hypovolemic. In elective surgery certain preoperative schedule should be carefully followed and evaluated.. if necessary. septic and vasogenic shock. cardiogenic. emptying of stomach.  It is never justified to omit the details of a careful recorded history and careful physical examination treatment of preoperative preparation of emergency cases. computed tomography.  Many attempts have been made to define shock.  In such cases the preoperative preparation must be limited to be rare essential. . Module -3 SHOCK & ITS MANAGEMENT – DEFINITION  A recent veterinary textbook defines shock as "the clinical state resulting from an inadequate supply of oxygen to the tissues or an inability of the tissues to properly use oxygen.  Resuscitation. empting of bladder by catheterization should be considered as general rule." This deprives the organs and tissues of oxygen (carried in the blood) and allows the buildup of waste products. but because it is such a complex disorder. o Careful recorded history o Detailed physical examination o Essential laboratory test o Radiographic study where necessary  Other diagnostic test like ultrasonography. doppler study. leading to cardiac output o Simultaneously there is increased release of ADH. fluid loss in excess of intake. the fundamental sequence of events is essentially the same in all forms of shock: o Some precipitating cause decreases cardiac output and blood pressure o Stimulation of sympathoadrenal system leads to peripheral vasoconstriction and shunting of blood away from the skin and intestinal viscera o Heart rate and myocardial contractility increases. surgical procedures. pericarditis. o Cardiogenic shock occurs from cardiac insufficiency with lowered cardiac output.Massive tissue trauma. pyometra. myocardial trauma etc.  The circulatory failure is central in origin.  · Extracardiac diseases such as cardiac tamponade. especially crushing injuries. tension pneumothorax. Direct action of toxic substance on blood vessels produces dilatation of blood vessels. osteomyelitis etc. It leads to decreased resistance and increased capacity of vascular bed. or third spacing of body fluids.  B. haemorrhagic gastroenteritis. mastitis.  A. or volvulus.Severe vomiting. Acute blood loss: .Major laceration. PATHOPHYSIOLOGY OF SHOCK  Although the nature of shock vary. intestinal strangulation. Fluid loss:. Histamine leads to increased permeability and massive vasodilatation. diarrhea. Various diseases which can cause this type of shock are peritonitis. Fluid sequestration: .  It may result from:  · Inherent heart diseases such as arrhythmias. o Vasogenic shock occurs either due to extensive vasoconstriction or extensive vasodilatation. ruptured abdominal or thoracic organs. o Septic or endotoxic shock occurs from massive infection caused by gram negative microbes. burns  C. activation of rennin-angiotensin system and release of aldosterone which .  Pain or extensive handling and traction of the viscera – massive vasoconstriction  Deep anaesthesia or spinal injury – extensive vasodilatation  Anaphylactic shock occurs due to antigen-antibody reaction and resultant histamine release. o Hypovolemic shock is the result of inadequate intravascular circulatory volume commonly resulting from haemorrhage. o Development of cellular anoxia with release of lactic acid. restlessness. urine flow. re-starting the heart. heart function). giving antibiotics to combat an infection. coma and dilation of pupils.  The end result in all forms of shock is cardiac failure ultimately leading to death. o quickly intervening to halt the underlying condition (stopping bleeding. activation of the blood clotting system). which may leads to disseminated intravascular coagulopathy (DIC). o Hypercoagulability also occurs. and depression.  Shock is dynamic and not a static process.  In microvascular level certain compensatory changes become less reversible as shock persists and provide a positive feedback. o treating the effects of shock (low oxygen.  Physical examination findings associated with hypovolemic and cardiogenic shock include: o Tachycardia o Tachypnea o Pallor of mucous membrane o Prolongation of the capillary refill time and decrease pulse quality o Heart murmurs or arrhythmias (not absolute)  Laboratory findings during shock shows lowered red blood cells. etc.). increased acid in the blood. . Click here to view the flow diagram of the Pathophysiology of shock SYMPTOMS OF SHOCK  It is easy to recognize fully established shock. and elevated blood urea nitrogen (BUN). o There is lowered oxygen delivery to tissue due to sympathetic constriction of arteriole and pre-capillary sphincters. o Permeability of cell membrane increases with release of lysozymes o Capillary stasis and decreased capillary pH triggers vascular pulling and decreased venous return to heart. TREATMENT  The most important goals in the treatment of shock include: o quickly diagnosing the patient's state of shock. but it is difficult in early or compensated shock.  Other signs include weakness. haematocrit and plasma proteins. ultimately helps to conserve water and sodium through the kidneys. reduced urine output. o and supporting vital functions (blood pressure. bandages. an antioxidant. sodium containing crystalloid replacement solution is usually the fluid of choice. and hypovolemic shock. o Carnitine may be helpful in treating cardiogenic. if any.  Vasoactive drugs are used to modify sympathetic and adrenal responses. Dopamine is most popular vasoactive drugs used in shock. septic.  Treatment with antioxidants that help rid the body of free radicals (harmful by-products of the oxidative process) may protect against some types of shock.9% NaCl. Patent airway should be ensured by intubating animal if collapsed or comatose. improved efficiency of glycolytic enzymes. stabilization of lysosomal enzymes and interference with endotoxin- induced immune reaction. plasma protein and dextran. o Coenzyme Q10 (CoQ10). tourniquet or ligation. Oxygen should be delivered via musk.  The animal should be kept in a warm and well ventilated room without exposing direct heat.  Blood and blood products: Treatment of hemorrhage Restore coagulation properties. TYPES OF INTRAVENOUS FLUIDS  Crystalloid: Dextrose or electrolyte solutions increase intravascular and interstitial fluid volume: Isotonic . prednisolone @ 30mg/kg) include: increase in cardiac output. increase in metabolism of lactic acid. . 45% NaCl). decrease in peripheral resistance.  Sodium bicarbonate is indicated to counteract metabolic acidosis caused by accumulation of lactic acid in shock state. lactated Ringers Hypotonic (5% dextrose in water.  Broad spectrum antibiotics are indicated to combat wide-ranging secondary bacterial infection and diuretics for over dehydration or poor urine output.  Haemorrhage. plasma and whole blood have obvious advantages. increase osmotic pressure: albumin.  Drugs acting on cardiovascular system are also indicated to improve blood pressure and to stimulate blood flow.  Thrombolytic therapy (drugs that dissolve clots as they form) may be considered in the case of myocardial infarction or pulmonary embolism.  Glucocorticoid: the role of glucocorticoid in shock state has remained debatable even in man and small animal. cannula or endotracheal tube.  Fluid theraphy: A multi electrolyte.  Colloids: Do not diffuse easily through capillary walls Fluids stay in vascular compartment. Beneficial effects (dexamethasone @10mg/kg. Digitalis and adrenaline are drug of choice in this case. should be controlled by direct pressure. may be beneficial in treating hypovolemic and septic shock. o Glutamine added to parenteral nutrition may protect the intestines and prevent complications from septic shock. o Example:  Haemometra .vomiting fresh blood . It may be caused by high blood pressure (by causing blood vessel rupture) or other forms of injury. When blood is collected in a newly formed cavity called as Haematoma.  Melena .  Haematuria: Blood in urine. which can cause organ rupture. MODULE-4= HAEMORRAGE & ITS MANAGEMENT HAEMORRHAGE  Haemorrhage means escape of blood from an artery. CLASSIFICATION  External haemorrhage  Internal haemorrhage  Depending on the time of occurrence  Depending on the source of haemorrhage o External haemorrhage occurs from open wounds or cut wounds that is visible on the outside of the body o Example  Epistaxis – bleeding from nose.  Haematemesis.presence of blood in faeces. o N-acetylcysteine (NAC) improved the immune system response in septic shock caused by endotoxins (toxins released from bacterial cells).  Haemoptysis – coughing up blood from the lungs .haemorrhage into peritoneal cavity . vein or capillary to extravascular space.  The complete loss of blood is referred to as exsanguination. o Vitamins B3 and B 12 -nicotinamide (a form of vitamin B3) may help protect against bacterial endotoxin that causes septic shock. especially high speed deceleration occurring during an automobile accident . o Internal haemorrhage is bleeding occurring inside the body .haemorrhage into uterus  Haemopleura .haemorrhage into pleural cavity  Haemoperitoneum . o Omega-3 fatty acids compared with omega-6 fatty acids may protect against the harmful effects of septic shock. haemorrhage in to tunica vaginalis  Haemarthrosis .g. motor vehicle accident).g.  Reactionary haemorrhage occurs within 24hours after the primary bleeding has been arrested due to mechanical disturbance of clot in vessel or due to slipping of the ligature. Venous and Capillary ETIOLOGY  Trauma .haemorrhage into spinal cord  Petechiae . o Depending on the source of haemorrhage: Arterial.  Necrosis and ulcerations of blood vessel wall  Infection and subsequent release of toxins of microorganism  Aneurysm ( weaknesses in blood vessels )  Increased blood pressure  Lack of oxygen and nutrition. vitamin K o Plant toxins (sweat Clover) SYMPTOMS  Bleeding from injured blood vessel  Skin and mucous membrane become pale. laceration. cold and moist  Patient feels thirsty  Air hunger  Thready pulse  Hypotension  Low hemoglobin and red blood cells .blunt trauma (e. or penetrating trauma (e.  Anaphylactic shock  Deficiencies of coagulation factors.  Secondary haemorrhage occurs after about a week or more due to septic disintegration of clot or due to sloughing of portion of vessel because of a septic or gangrenous lesion. fall. o Depending on the time of occurrence  Primary haemorrhage occurs immediately after injury. knife or gun).haemorrhagic spots on skin and subcutis.  Deficiency diseases o Haemophilia o Thrombocytopenia o Deficiency of vitamin C.Pinpoint haemorrhages on skin and subcutis  Ecchymosis .haemorrhage into a joint  Haematomyelia .  Haematocele . cold water etc. ice.  Administration of vitamin K (Kapillin). can be successfully used for controlling bleeding from small vessels.  Pressure haemostasis: A dressing. typically made of gauze. tail. Liq.  Topical agents like Fibrin adhesives. as it can lead to unnecessary necrosis or even loss of a limb. should be applied. penis etc. The use of a tourniquet is not advised in most cases.  Tourniquet: A cord should be tied around an extremity (limb. Vascular clips made of titanium or stainless steel is also used for ligation. calcium and other coagulation factors may have remarkable effect in controlling haemorrhage. The tissue should be gently blotted rather than wiped (Wiping causes abrasion and dislodges blood clots that have formed).  Adrenalin.  Haemostatic forceps: Crushing of tissues at the point of application leads to clot formation inside the vessel adjoining the ruptured ends of the inner coats. collodion. Methods of haemostasis  Bleeding should be addressed in calm and controlled manner. Benzoin. a vasoconstrictor agent when applied topically controls bleeding especially from a small bleeding vessel.  Ligation is the ideal method of controlling bleeding from a vessel which can be accomplished first by grasping the vessel followed by putting a ligature. Arteries less than 1mm and veins 2mm diameter causes vessel wall to shrink and lumen occlude by thrombosis. HAEMOSTASIS  Haemostasis may be defined as complex interaction between vessels. Bleeding from drilled cut or chipped edges of bone can be controlled by using bone wax plugs physically. coagulation factors. Ferri perchlor.  Diathermy: Cauterization of vessel is usually performed by Mono polar coagulation and bipolar coagulation. Gentle digital pressure on the point of haemorrhage provides an extremely effective temporary haemostasis in minor bleeding. oxidized cellulose (regenerated). Tamponing favours coagulation of blood by exerting pressure in the area. and gelatin sponge with or without thrombus are also helpful for arresting bleeding from small vessels. coagulation inhibitors and fibrinolytic proteins to maintain the blood within the vascular compartment in a fluid state. absorbable collagen fibrils. platelets.  Application of Tr.) and proximal to bleeding area to control bleeding (not more than one hour 20 to 60 minutes).  Bleeding from unidentified points of vessels in a wound cavity can be controlled by packing or plugging the cavity with sterilized gauze pieces (tampon). This can be done using artery forceps. . o Amount of donor blood needed (ml) = Recipient blood volume in ml x ((Desired PCV .  Blood transfusion is indicated in dogs whose preanaesthetic haemtocrit is less than 30 to 34% and in cats less than 25 to 29%.Patient TSP) / TSP of donar blood) FLUIDS AND THEIR USE . Lactated Ringer’s is preferred over other solutions during shock.  If the blood loss is more than 10% during surgery blood transfusion is necessary. During anaemia  If the PCV less than 20% blood transfusion is indicated and if the serum protein is less than 3 to 3. Module -5 = FLUID THERAPY IN SURGICAL PATIENT FLUID INFUSION Fluids  Routine administration of multielectrolyte containing crystalloid replacement solutions at the rate of 10 ml/kg/hr plus 2 to 3 times the volume of estimated blood loss will satisfy the requirement during surgery.  During major procedures it can be increased upto 20 ml/kg.  Blood volume is calculated as 8 to 10% of the body weight in dogs (45% cells and 55% plasma) and 6% in cats(36% cells and 64% plasma).5 g/dl further volume replacement is done using plasma or synthetic colloidal is administered.  Blood and plasma transfusion is done based on the following formula.Patient PCV) / PCV of donar blood) o Amount of donor plasma needed (ml) = Recipient plasma volume in ml x ((Desired TSP . Synthetic colloid solution  Indications o Hypoproteinemia and hypoalbuminemia o Blood loss o Hypovolemia o Sepsis o Persistent hypotension o Does not cross the capillary walls hence will have sustained effect o No risk of transmission of infectious diseases as compared with plasma and less expensive  Disadvantages o Induce pulmonary oedema in patients with permeable capillaries o May induce circulatory over load .  Disadvantages o Induce hypernatraemia. lowering the blood viscosity and reducing the size of the endothelial cells. hyperchloraemia. hypdokalaemia.Isotonic crystalloids  Indications o To maintain plasma volume in uncomplicated anaesthetized cases. o To replace deficits in dehydration o To restore interstitial fluid status o To promote diuresis  Disadvantages o Large volume of administration coupled with migration into interstitial spaces may result in oedema o Produce haemodilution in anaemic patients Hypertonic crystalloids  Indications o Expansion of plasma volume o Used in the intial treatment of shock o Administered intraoperatively during cardiac surgery o To prevent tissue oedema from the conventional therapy o These agents increase the plasma volume. cardiac output and improves the blood pressure. hypermolarity and metabolic acidosis o May induce mild cellular dehydration o Uncontrolled bleeding will become worsen due to the rapid increase in blood pressure. They increase the myocardial contractility o Improve the microcirculatory blood flow by decreasing the systemic vascular resistance. precipitation of coagulation factors. found in several species of animals in a variety of locations.  This purulent inflammation is usually caused by one of four pyogenic (pus producing) bacteria: Corynebacterium. CYST . TUMOUR. PARTS OF AN ABSCESS  Abscess consists of a wall. Module -6 DIFFERENTIAL DIAGNOSIS & SURGICAL TREATMENT OF ABSCESS. CONTENTS OF PUS AND ITS CHARACTER  Pus contains necrosed tissue. Streptococcus and Staphylococcus. DEFINITION  Abscesses are circumscribed collections of purulent material (pus) in a cavity.  Pus cells mainly consist of polymorphonuclear leukocytes along with a few mononuclear cells. increased fibrinolytic activity and decreased functional von willebrand factor. controls spread of infection. leukocytes and proteins of blood and tissues. HAEMATOMA=> ABSCESS -. dead bacteria.  The pyogenic membrane that lies between the wall and pus. o May induce coagulation disorders due to dilution of platelets. pyogenic membrane and pus (Liquor puris). and helps in phagocytosis and granulation tissue formation.  Pus is alkaline in nature and yellow in colour. Pseudomonas. .  Thus the abscess enlarges till it reaches the surface of skin or mucous membrane. and mammary glands. Streptococci. ETIOLOGY OF ABSCESS  Pyogenic organisms like Staphylococci.  Chemicals like mercuric chloride and Zinc chloride.  Chronic abscess may be:  Hard with inspissated pus. This is called Inspissated Pus. since the fibrin of exudates is digested by the proteolytic enzymes of the leukocytes.  Pus serum will not clot. . ACUTE ABSCESS  Acute abscess forms in 3 to 5 days following infection.  Dogs: Anal region.  The center of abscess becomes soft (pointing) and later ruptures.  The dead tissues and dead inflammatory cells are continuously thrown into the cavity which leads to a gradual increase in the amount of pus. discharging pus. sub-maxillary and post pharyngeal lymph nodes.  Local acute inflammatory symptoms without fever are observed in superficial abscess. o Chronic Abscess (Cold abscess): Inflammatory symptoms are less active.  Specific organisms like Corynebacterium pyogenes.or  Soft with liquid pus and thin abscess wall. udder and prominences  Horses: Shoulders. the liquid part is absorbed and the solid part is left. o Superficial or deep abscess: based on location. COMMON SEATS OF ABSCESS FORMATION  Cattle: Yoke. CLASSIFICATION OF ABSCESS  Abscess may be classified as: o Acute Abscess (Hot abscess): Inflammatory symptoms are more active. Symptoms  Acute superficial abscess appears as a local painful swelling.  In long duration abscess. Escherichia coli and Pseudomonas aeruginosa. Actinomyces bovis etc. A counter opening is made at the most ventral part (dependent Part) of the abscess. abscesses may become inactive or enclosed (sterile). fomentations and mild blisters.  Primary chronic abscess usually occurs from repeated injuries and observed on the prominences of limbs and ribs due to bed sores.  It may be painless or slightly painful. Sometimes the chronic abscess is enucleated under local infiltration analgesia. the body defenses having killed all of the causative bacteria. with predominance of necrotic events over suppurative.  Secondary chronic abscess develops in the course of various local affections. abscess must be early cleared up of pus by aspiration and subsequent washing of the purulent cavity. Deep abscess has no local symptoms.  Cellulitis or Phlegmon is diffuse. o Tincture of Iodine soaked gauge is be packed to keep the openings patent. but fever and pain on manipulation of the part are evident. will slowly become liquefied and be absorbed.  The accumulated pus.5% silver nitrate is best against most of the micro-organisms. o A chronic abscess is converted into an acute abscess by applying blisters. In cases where the pointing of abscess is not at a dependent Part. The quantity of gauze used to pack the abscess cavity has to be reduced daily as the cavity is being filled up by granulation tissue. suppurative spreading inflammation of loose connective tissue. then drainage will not be perfect. CHRONIC ABSCESS (Cold abscess)  A chronic abscess develops slowly without any inflammatory symptoms. with no route of escape. . o Further therapy is the same as that of a granulating wound. This should be changed once in 24 hours.  Chronic abscess may be hard in consistency surrounded by fibrous tissue and containing small amount of pus or it may be soft and thin walled with comparatively larger amount of pus. and then treated as acute abscess. Gauze soaked with 0. The pus should be drained and the cavity is to be irrigated with a mild antiseptic lotion.  In time. o Once mature.  Pustule is a circumscribed cavity with pus. situated in epidermis. and the skin is sutured. TREATMENT  Treatment should correspond to the stage of development of an abscess. o The abscess should be opened by syme’s abscess knife or a scalpel at the place of pointing. o Measures to accelerate maturation of abscess by using liniments. which drains to outside by multiple small openings.  Carbuncle is small boil.  Furuncle or Boil is suppurative inflammation of hair follicle or a sebaceous gland due to Staphylococcus aureus.  Acne is an abscess of sebaceous gland. empyema of joint. It is caused by Streptococci and Staphylococci. o Skin .  Tumour may be defined as “an abnormal mass of tissue. the growth of which extends uncontrolled.  Antibioma is a clinical condition resulting from improper treatment of an abscess. It appears as single or multiple pustules containing grayish white pus.Common in older dogs (often benign) but much less common in cats (malignant).” TYPES OF TUMOR Benign Malignant Grow slowly Grow rapidly Locally grow to great size Create metastases Don’t invade the neighboring tissue Invade and destroy neighboring tissues. A group of furuncles is called Furunculosis. Usually do not return after surgical removal Recurrence after surgical removal INCIDENCE  Tumors are more common in canines. . TUMORS (Neoplasm)  The term neoplasm is a Greek word used primarily for new formations or new growths. Antiseptic ointments externally and systemic penicillin gives good relief. Example: Empyema of frontal sinus.  Empyema is collection of pus in a body cavity. in comparison to the normal tissue and persists in the same excess even after cessation of the stimuli which evoked the change.  Old animals are affected more commonly than young ones.Fifty percent of all breast tumors in dogs and 85% of all breast tumors in cats are malignant. o Bone . A mass on the gums. esophagus and urogenital organs are often seen in domestic animals. o Breast . pig and goat. o Head and Neck . or difficult eating are signs to watch for. mucosa of mouth.  Horse and cattle are more often affected than sheep. The most common sites are leg bones. Fibroma is more common in horses. cattle and dogs.Testicular tumors are rare in cats and common in dogs. near joints.Cancer of the mouth is common in dogs and less common in cats. bleeding. VARIETIES OF TUMORS Tissue of origin Name of tumor Cell type Mesenchymal Fibroma Fibrous connective tumors tissue Chondroma Cartilaginous tissue Osteoma Bony tissue Odontoma Tooth substances Myoma muscular tissue Myxoma Cardiac skeleton Lipoma Adipose tissue Neuroma Nerve cells and fibers Leiomyoma Smooth muscle Rhabdomyoma Skeletal tissue Haemangioma Blood vessels Meningioma Meninges Teratoma Germ cells Epithelial tumors Papilloma Skin or mucous membrane Adenoma Glandular epithelium Basal cell tumour Basal cell of skin Hepatocellur adenoma Hepatocytes . o Fibropapillomatosis of the skin. odor. o Testicles .Bone tumors are most commonly observed in large breed dogs and rarely in cats. especially those with retained testes. despite the presence of unsolved systemic neoplastic disease. o Benign vaginal tumor – ovariotomy o Testicular tumors (Seminoma and sertole cell tumour) . Eg: sarcomas. Surgery is the treatment of choice for this type of cancer. o Mammary tumors in bitch – Spaying between 6 and 12 months of age will greatly reduce the risk of breast cancer. size and consistency  Radiography – bones and vascular organs. or relieving poor function. o Local excision: The removal of a neoplastic mass with the minimal amount of surrounding normal tissue. o Eg: Limb amputation – osteosarcoma o Spleenectomy – Bleeding haemorrhage of sarcoma .  Biopsy – exploratory cytology TREATMENT  Prophylactic treatment is undertaken either to reduce the anticipated incidence rate of a particular tumor type or the rate of recurrence of a neoplastic disease after therapy. o Radical local excision: Removes of a tumor with anatomically extensive margins of tissue extending into fasuil planes which are wndistrubed by the primary growth of the tumor us termed radical local excision or compartmental excision. Glomus tumour Melanocytes Blood cells Non-Hodgkin lymphoma and Hodgkin Lymphoid cells lymphoma Leukemia Hematopoietic cells DIAGNOSIS  Clinical examination – location. o Wide local excision: Removal of a significant predetermined margin of surrounding tissues together with the primary mass.Castration  Definitive excision refers to use of surgery as the sole treatment procedure without adjunctive radiotherapy or chemotherapy.  Palliative treatment: A procedure that remarkably improves an animal’s quality of life by providing pain relief.  The outer wall of a cyst is called as ‘capsule’. iodine to destroy the smooth lining membrane and setting up inflammation.  Use of setton to drain cyst is a good practice. Apart from surgery and chemotherapy. CYST  A cyst is a closed sac having a distinct inner lining of secreting membrane.  Cyst may contain a solid structure like tooth (dentigerous cyst) or hair (dermoid cyst) also. radiation. functional and pathological)  Renal cyst (kidneys)  Sebaceous cyst (sac below skin) DIAGNOSIS  Cysts are generally non-inflammatory in nature and develop slowly with well defined periphery. Combination therapy is commonly employed. TREATMENT  Puncture and evacuate the contents of cyst and inject an irritant solution like Tr. .  Ganglion cyst (hand/foot joints and tendons)  Glial Cyst (in the brain)  Distension cyst: (Follicular cyst of ovary. cryosurgery (freezing). or semi-solid material. hyperthermia (heating) or immunotherapy can be effectively used to treat cancers.  Most of the cysts are benign in nature. Ex: Cystecercosis)  Neoplastic (Cyst adenoma).  Dermoid (misplaced embryonic tissue).  Encapsulation cyst (around foreign bodies and parasites. cystic distension of a joint bursa).  They may contain air.  Size of a cyst may vary from a small grape to a football.  Meibomian cyst (eyelid)  Ovarian cyst (ovaries.  On palpation fluid filled cyst fluctuates uniformly while cysts with solid mass fluctuates en-masse. o Common example listed below:  Chalazion cyst (eyelid)  Retention Cyst (gland like salivary cyst)  Dentigerous Cyst (associated with the crowns of non-erupted teeth)  Exudation Cyst (Hydrocoele).  Cysts can arise anywhere in the body. but some may produce symptoms due to their size and /or location. fluids. o No pain sensation. o No pain sensation. o No pain sensation. o Doughy on palpation and forms immediately following an injury.  Necrosis is not reversible. Intact cyst is carefully dissected and removed from the surrounding tissue in possible cases. NECROSIS  Necrosis means death of tissue in the body. o No inflammatory symptoms. DIFFERENTIAL DIAGNOSIS An abscess must be differentiated from the following conditions:  Cyst o Slow in development as compared to an abscess. GANGRENE & BURNS – SCALD. o Soft and fluctuates uniformly. o Does not point like an abscess.  Hernia o History of recent injury and swelling. -------------------------------------------------------------------------------------------------------- ---- MODULE-7 NECROSIS. but not hard at periphery. o Does not point like an abscess. o Exploratory puncture with needle may reveal blood. or chemicals.  Tumour o Uniformly hard in consistency. whether from injury. radiation. o Hernial ring can be palpated. This occurs when enough blood is not supplied to the tissue.  Haematoma o Forms due to coagulation of blood or serum. CLASSIFICATION .  Surgical excision of the cyst is the preferred option. pneumonia ). a so-called "cascade of effects".  Severe damage to one essential system in the cell leads to secondary damage to other systems. infarction.g. It is marked by deposition of fibrin -like proteinaceous material in arterial walls. cancer. in testicular torsion ). ETIOLOGY  The main factors in gangrene are loss of blood supply.  Caseous necrosis is a specific form of coagulation necrosis typically caused by mycobacteria (e. compression of an artery. infarct of the spleen ). o Loss of blood supply cuts off oxygen may be due to passive hyperemia with sluggish flow of nutrients and deficient oxygenation (volvulus. aseptic necrosis. mammary tissue necrosis). o Mechanical injuries that crush or cut off blood supply. myocardial infarction . Without blood.g. strangulated hernia) and ischemia ( decreased blood supply to a part) due to thrombus or embolism. This disease also is known as osteonecrosis. and ergot poisoning GANGRENE  Gangrene is necrosis and subsequent decay of body tissues caused by infection or thrombosis or lack of blood flow.g.  Fibrinoid necrosis is caused by immune -mediated vascular damage.g. Avascular necrosis is a disease resulting from the temporary or permanent loss of the blood supply to the bones.  Gangrene may be caused by: o Direct damage to tissues which include: .  Liquefactive necrosis is usually associated with cellular destruction and pus formation (e. infection.  Necrosis can arise from lack of proper care to a wound site. and later invasion of the part by micro-organisms. toxins and inflammation . the bone tissue dies and causes the bone to collapse.  Fatty necrosis results from the action of lipases on fatty tissues (e. ETIOLOGY  There are many causes of necrosis including injury.g. and ischemic bone necrosis  Coagulative necrosis is typically seen in hypoxic environments (e. tuberculosis ). o Physical agents like excessive heat or cold. This condition is most common in the extremities . acute pancreatitis .  Haemorrhagic necrosis is due to blockage of the venous drainage of an organ or tissue (e.  It is usually the result of critically insufficient blood supply sometimes caused by injury and subsequent contamination with bacteria. frost-bite. arteriosclerosis in old age. Wet gangrene spreads swollen or blistered. improper passage of stomach tube or severe lung infection. which causes spasmodic narrowing of arterioles and leads to dry gangrene of extremities. which narrows lumen of blood vessels. favours bacterial growth.  Action of acids. arterial or nervous affections like:  Ergot intoxication. moist or blood clot.  Diabetic gangrene narrows arteries and sugar in tissues. It is mostly due to freezing or ergot poisoning. Example: bed-sores. COMMON SITES OF AFFECTION  Extremities like legs. alkali and other chemicals producing dry gangrene and moist gangrene. or due to acute. ETIOLOGY AND SIGNS OF GANGRENE Type Etiology Characteristic signs Wet Sudden interruption of blood flow  Affected tissue may gangrene.  Senile gangrene i.  Physical agents like application of heat and cold.  May also become infected. freezing. venous. It is commonly seen in feet of cattle.e.  Intestines in equines are commonly involved either with infarction due to verminous thrombosis of anterior mesenteric artery. . wattle and combs.  Involvement of lung due to wrong drenching of medicines. volvulus or intussusceptions. gangrene very quickly and can be fatal. or such as due to burns. injury appear badly bruised. CLASSIFICATION.  Impaction of intestine in the hernial ring and infestation with pathogenic microbes especially with anaerobic infection. Example: burns. sit-fast.  Mechanical compression or interference with blood and nerve supply to a part of the body or an organ while lying on a hard floor. ears.  Mammary gland: Staphylococcal mastitis produces necrosis due to toxins or thrombosis of mammary vessels. tail. local passive hyperaemia produced by intestinal torsion. o Indirect changes in tissues due to cardiac.  Offensive odour of exudates.  Application of warm antiseptic fomentations to relieve pain.  No clear line between healthy and affected tissue.  Debridement: Removal of dead.  In addition to surgery and antibiotics. hyperbaric oxygen therapy (HBOT) is used that inhibit the growth and kill the anaerobic organisms. injury or surgery. ULCER . greenish colour. penicillin is given as an adjuvant treatment to surgery.  Antibiotics alone are not effective because they do not penetrate ischemic muscles sufficiently. o Physical examination o Results of blood and other laboratory tests (presence and extent of infection). It due to exudates and typically occurs at the site of a recent gas formation. such as clostridium. Dry Insufficient blood flow through the  Affected tissue gangrene arteries such as due to atherosclerosis becomes shriveled. surgery.  Surgical excision or amputation of a limb or organ. However. or chronic disease). or blood clots. or infected tissue to improve the healing potential of the remaining healthy tissue. pale and then turns dark red or purple in color. TREATMENT Treatment should be directed to:Prevention of cause and extension of gangrene. cancer. It usually doesn't dry and blackish or involve bacterial infection. damaged.  cold to touch Gas Infection with certain types of  Swelling around skin gangrene bacteria. The bacteria rapidly  Skin initially looks destroy muscle and surrounding tissue. DIAGNOSIS  Diagnosis of gangrene will be based on a combination of o History (recent trauma.  Insufficiency of nerve and blood supply to the part. limbs.  Dog: root of tail. Traumatic ulcers including secondary stress ulcers. An ulcer is a localised defect in the continuity of an epithelial surface without any tendency to heal. but the basal layers are intact. tip of ears. CLASSIFICATION  Iatrogenic ulcers: wound breakdown post-operatively and in irritant fluid extravasating.g. tuberculosis.  Specific diseases like tuberculosis. viral. and glanders. and ulcerative lymphangitis. the slough at their base represents inadequate drainage.  Secondary infection of the site by bacteria. ulcerative lymphangitis. in diabetes ETIOLOGY  Repeated and continuous irritation of wound. Example: Traumatic ulcer.  Acutely inflamed ulcers may have an outer rim of cellulitis. glanders. elbow. COMMON SITES OF ULCERATION  Cattle: yoke  Horse: saddle place. due to drainage of deep focus.  Ischemic ulcers or Decubitus ulcers: These are due to continuous pressure which interferes with supply of nutrition to local tissues leading to pressure or bed sores.  Presence of neoplasm.  Ulcer must be differentiated from erosion which is an epithelial defect with loss of superficial layers.  It is usually associated with an inflamed base of granulation tissue with or without necrotic slough. and cornea of eye. bed sore.  Presence of necrotic tissue or foreign body in a wound.  Specific ulcers: as observed in tuberculosis. SYMPTOMS  The edge of ulcer may be raised or in level with the surrounding skin and rugged. .  The majority is chronically inflamed. fungus or virus with which the tissues cannot effectively combat. Example: Rodent ulcer.  Neuropathic ulcer e.  Non-specific ulcers: Ex.g. and secondary e.  Malignant ulcers observed in skin and gastrointestinal tract.  Infective ulcers: primary e.g. CLASSIFICATION According to the depth and severity of burn:  First Degree (Superficial): epidermis is affected and transient erythema. TREATMENT The specific treatment of an ulcer is dependent on the subtype. Healing is rapid and complete by the regeneration of epithelium unless there is involvement of secondary infection. further surgical intervention may be indicated e. coagulative necrosis of epidermal cells and vesicle formation.  Elimination of the cause adversely affecting the course of ulcerative disease and stimulation of regenerative processes at the affected site.  Exposure to ultra – violet rays to stimulate circulation and to destroy micro- organisms.  Second degree burn (partial thickness burn): Here. carbolic acid.  For large deficits or prolonged ulcers with little evidence of healing.g. Loss of epidermis is complete. copper sulphate. depth extends to the mid dermis. silver nitrate. tuberculosis. occurring due to high temperature or chemical substances. Capillaries and venules in the dermis is dilated. .g. are painful and heal rapidly.  Scald is likely to be more injurious than because of the hot liquid may penetrate into the deeper part of tissues.  Thermo-cautery with red hot iron to destroy unhealthy tissue which promotes granulation and cicatrisation.  Astringent or caustic applications for ulcers with excessive or unhealthy granulations. There is erythema.  Bier’s hyperaemic treatment. skin grafts and rotational flaps. congested and exude plasma. Epidermal burns look red.  The discharge may be serous. BURN AND SCALD  Burn is an injury of integuments and underlying tissues.  Granulations are pale or blue in colour depending upon the form.g. purulent or grayish.  The center of the lesion may be flat or concave. sometimes vesicle formation and desquamation of the epidermis occurs. E.  Burn may be defined as tissue changes that occur on excessive absorption of heat by skin. a cellulitic rim and there may be ongoing systemic infection e.  Antibiotics are only indicated for infected ulcers in which there is evidence of spread around the margin e.g.  Scald is an injury caused by hot liquids or stream. and may show necrotic spots. exudation. subcutaneous edema and little or no pain.  Fourth degree: Here. subcutaneous fascia and deeper tissue like muscles.  The degree of tissue destruction depends on the strength of the chemical and the duration of contact.  Third degree burn (Full thickness): is characterized by coagulation of epidermis and dermis. Electrical burns  No pain . black or brown. Repair is by scar formation preceded by sloughing of the necrotic tissue. desquamation and pain. The clinical features are similar to those described in third degree burn. bones etc are involved. Permanent scarring occurs due to healing by granulation.  Partial thickness. Severe edema of the sub cutis develops and dry gangrene of the damaged tissue occurs. leathery escher.  Chemical causes local coagulation of proteins and necrosis.  The chemical produces localized necrosis of skin and deeper tissues with which it comes in contact. pain. petroleum distillates and hot tars are referred to as chemical burns. The epidermis is desiccated and charred with presence of black layer in skin. CLINICAL SIGNS Thermal burns  Superficial-hyperemia. solvents. decreased sensitivity.  Full thickness.White. CAUSES The following may cause burn:  Thermal injuries o Direct heat o Flame o Scalding  Electrical burns o Electrical cord exposure o Lightning Chemical burns  Injuries caused by chemicals like strong acids and alkalis. Full thickness burn is insensitive to pain because of damage of cutaneous nerve endings. Finally soothing ointment like . citric or boric acid. o promotion of rejection of coagulated Skin and tissues. The area should be swabbed with weak vinegar (half water. Caladryl cream (Park Davis). o The treatment in chemical burns should include washing with lots of plain water and neutralization of the offending chemicals.5% Solution. Chemical burns  Line of demarcation between dead and healthy tissue  Devitalized tissues may get infected  Formation of ulcer which heals gradually TREATMENT  The therapeutic measures must be aimed at o termination of painful stimuli and improvement of the nervous system function for avoiding shock. while alkali with 2% vinegar. Several topical commercial products like Aloevera cream. o prevention of infection.1% cream. half vinegar) using cotton wool or cloth. o Topical antibacterial ointments may be applied to prevent the animal from post burn sepsis. picric acid. o Drugs like gentian violet. Soothing and protective preparations like Badional gel (Bayer). acriflavin and tannic acid should not be used as far as possible as they delay the healing process by damaging the living cells. blood less. chlorhexidine 0. Necrotic tissue should be debrided. o Analgesic should be given to reduce pain. o reduction of autointoxication. o creation of favorable conditions for regeneration of skin  Anti-shock measures are to be provided to prevent shock that may arise as burn complication.  Local treatment of burns should include: o Application of ice (3-17ºc) pack wrapped in a soft towel and cold water for 30 minutes or covers it with wet towels. Burnol (Knoll) may be used as burn dressing. pale yellow lesion.5% Solution. o Hair should be removed and gently clean from the site. povidone iodine cream can be used.  Burn may lead to renal failure and fatty infiltration of liver thus appropriate care should be extended to combat the complication. Acids can be neutralized with 2-3% solution of sodium carbonate or milk. Silver nitrate 0. gentamycin sulphate 0. This also helps to remove caustic substances (acid or alkali) if these are the cause. o Hypovolemic shock and acidosis are to be prevented by supplementation of large quantities of fluid (Dextrose 5%) including 4% sodium bicarbonate.  Well-circumscribed cold. Silver sulphadiazine cream (Indo-Pharma). FROST BITE  Frost bite is injury of tissues due to the action of a low temperature on them. and liquids. comb and wattles of birds. olive oil may be applied. CAUSES  Exposure to cold or chilling environment. penis and scrotum in horses. Besides the prepuce. . If shock occurs.  Udder and teats are commonly frozen in cows during exercise on frosty winter days. glass.  Iatrogenic freezing with cryogens like liquid nitrogen and nitrous oxide etc. keep the animal warm with heating pads or hot water bottles and a blanket of heavy coat.  The condition is rare in animals because they can withstand cold temperature due to their hairy coats and will instinctively seek shelter from inclement weather. snout of pig. tip of the ear and scrotum of dogs. A burn patient (pet) should be provided with ample warm fluids to drink and this may be given in the form of milk or glucose water. CLASSIFICATION AND PATHOPHYSIOLOGY  Various degrees of frost bite recognized are: o Mild: contraction of blood vessels (parts appear white) —> paralytic dilatation of blood vessels —> engorgement of vessels —> parts appear red and swollen —> thawing —> severe pain o Moderately severe: Below 0oC temperature for longer period than mild —> injury of Blood vessels —> inflammation of the tissues —> redness of epidermis together with certain amount of necrosis and blister formation —> desquamation o Severe: Temperature falls for lower than freezing point —> impaired circulation of blood and lymph —> parts undergoes necrosis and gangrene may ensue CLINICAL SIGNS  Loss of sensation in the affected part.  It usually occurs in a low temperature but it can also ensue in prolonged action of wet moderate above zero temperature (3-7ºc) since heat conductance of the skin is increased and heat emission is intensified by it.  Contact with cold metal. tail and distal extremities in other animals are commonly affected.  Cyanotic or pale appearance of frozen part. MODULE-8: WOUND – CLASSIFICATION.  The frozen tissue should not be massaged. Amputation of frozen part if necessary should be carried out  Diet: High protein.  In neglected cases. TREATMENT  Withdrawal from cold  Warming of frost bitten extremities. high caloric diet and vitamins should be instituted. DIAGNOSIS AND TREATMENT Learning objectives This module deals with  Wound and its classification  Symptoms of wound  Phases of wound healing  Factors affecting wound healing . DRUGS  Prevention of infection with systemic antibiotics  Fluid therapy with dextrose should be considered.  Analgesics may be provided to prevent self-trauma.  Necrosed tissue if there should be removed. and restoration of blood and lymph circulation: Frozen animals must be immediately put in a warm housing to restore body core temperature. frozen parts should be bathed in increasingly warm water until pink colour is restored.  Moderate edemas. necrosis and sloughing of skin. SYMPTOMS.  Artificial respiration should be provided to frozen animals. pain and very cold to touch.  Shivering. Hot water bag or hot pad may be used for warming. only deeper tissues. and joints etc. one of entrance and other of exit.  Perforating wound is having two opening. nerves are damaged to a varying degree.g. surgery or noxious physical agents. Wounds have irregular jagged borders and loss of tissue is limited to skin and subcutaneous tissue e. It is caused by blunt objects and the subcutaneous tissues.: barbed wire.  In closed or interstitial wound. bleeds freely and painful. edges are regular. CLASSIFICATION OF WOUND Open or external wound  There is discontinuity in the skin and other covering tissues to a varying depth. scalpels.  According to the severity and extent of tissue damage it may be of: o First degree with rupture of capillary vessels of the skin and subcutaneous tissue. There might be presence of infection/ . Open wounds  Incised wounds are caused by sharp cutting instruments such as knives.  Penetrating wounds are types of deep wounds communicating with cavities like abdomen. INTRODUCTION  A wound is a separation or discontinuity of soft tissues caused by trauma. barring the skin or mucous membrane are damaged.  Punctured wound are caused by sharp pointed objects like nails relatively with a small opening.: stab wounds. o Third degree with major damage of tissues leading to gangrene formation. o Second degree with rupture of larger vessels leading to haematoma formation. Closed wound/ internal wound  Contusion is injury to the skin without any break in the continuity of tissue surface. muscles.  Lacerated wounds are caused by tearing of tissues with torn and uneven edges. fragments of glass etc with minimum loss to tissue.g. e. thorax.  Neuritis extending along the course of the nerve involved in the wound. injuries caused by bullet. Explosions. Ex: Stab wounds. inflammation.  Before the advent of modern veterinary practice.  Each phase of wound healing is distinct.g. SYMPTOMS OF WOUND  Localized pain and bleeding.: FMD. and remodeling. foreign particles deep into the wound with inadequate opening for drainage.  Virulent wounds are caused by bacteria or virus leading to formation of pustules or vesicles e.  The difference that the modern veterinary practice has made is that the more severe injuries that would have killed the animal are now . PHASES OF WOUND HEALING  Wound healing involves a complex series of interactions between different cell types. gunshots.  Aseptic wound is surgical wound made under aseptic conditions where chances of bacterial contamination are negligible.g. many soft tissue injuries healed with time.  Granulating wound is one in which there is a tendency to heal within expected time. paralysis or a loss of function in a dependent portion. and the extracellular matrix.  Bite wounds are caused by snake.  Avulsion occurs when an entire structure or part of it is forcibly pulled away.  The phases of normal wound healing include hemostasis. with each phase overlapping the next. proliferation. and animal bites may cause avulsions.  Infected/ septic wound: A contaminated wound may become infected after a period of 6 -8 hours where bacterial multiplication may occur and liberation of their toxin. dog or wild animals bite with significant degree of tissue damage. although the wound healing process is continuous. cytokine mediators. generally not deeper than the epidermis.  Weakness. anthrax.  Abrasions are superficial damage to the skin.  Contaminated wound is one where there is presence of micro organisms.  Gaping of the lips of wound.  Febrile disturbances in severe septic wound.  Gunshot wound is produced by various forms of firearms e. setting the stage for subsequent tissue healing and regeneration. or other factors related to the patient’s .  A 5-10 minute period of intense vasoconstriction is followed by active vasodilatation accompanied by an increase in capillary permeability. manageable. the deformity and infection that often accompanies natural unaided tissue healing can be avoided or minimized. infection. the inflammatory phase lasts for 1-3 days in uninfected wounds.  The initial vascular response involves a brief and transient period of vasoconstriction and hemostasis. Neutrophil migration ceases after the first few days post-injury if the wound is not contaminated. The neutrophils engulf debris and microorganisms. o Classic signs include the following:  Redness (rubor)  Swelling (tumor)  Pain ( dolor)  Heat (calor)  Loss of function (function laesa) o Process  The inflammatory response increases vascular permeability.e. providing the first line of defense against infection. nutritional deficiencies. medication use. INFLAMMATORY PHASE  The second phase of wound healing i.  The Four phases of wound healing are o Haemostasis o Inflammatory phase o Proliferative phase o Wound remodeling HAEMOSTASIS  Tissue injury initiates a response that first clears the wound of devitalized tissue and foreign material. If this acute inflammatory phase persists. resulting in migration of neutrophils and monocytes into the surrounding tissue. due to wound hypoxia.  Platelets aggregated within a fibrin clot secrete a variety of growth factors and cytokines that set the stage for an orderly series of events leading to tissue repair. dermatan sulfate. o Early in the proliferation phase fibroblast activity is limited to cellular replication and migration. o These form an amorphous. gel-like connective tissue matrix necessary for cell migration. scavenge tissue debris and destroy remaining neutrophils. Macrophages begin the transition from wound inflammation to wound repair by secreting a variety of chemotactic and growth factors that stimulate cell migration. . immune response. chondroitin-4-sulfate.  In the late inflammatory phase. PROLIFERATIVE PHASE  The subsequent proliferative phase is dominated by the formation of granulation tissue and epithelialization. o Collagen synthesis and cross-linkage is responsible for vascular integrity and strength of new capillary beds. o The amount of collagen secreted during this period determines the tensile strength of the wound. o Improper cross-linkage of collagen fibers has been responsible for nonspecific post-operative bleeding in patients with normal coagulation parameters. o Chemotactic and growth factors released from platelets and macrophages stimulate the migration and activation of wound fibroblasts that produce a variety of substances essential to wound repair. o Collagen levels rise continually for approximately three weeks. and heparan sulfate) and collagen. monocytes converted in the tissue to macrophages. including glycosaminoglycans (mainly hyaluronic acid. and formation of the tissue matrix. o Its duration is dependent on the size of the wound. which digest and kill bacterial pathogens. it can interfere with the late inflammatory phase. o Around the third day after wounding the growing mass of fibroblast cells begin to synthesize and secrete measurable amounts of collagen.  New capillary growth must accompany the advancing fibroblasts into the wound to provide metabolic needs. proliferation. The characteristics features include incisional swelling. Primary traumatic neuralgia persist for prolong period whereas secondary one appear during cicatrisation. WOUND REMODELING  The final phase of wound healing i. redness.  This phase is characterized by reorganization of new collagen fibers. forming a more organized lattice structure that progressively continues to increase wound tensile strength.  Fistula (abnormal passage between two internal organs) may develop due to paucity of drainage from a purulent cavity. pain and heat often with hardness.e. preventing epithelial cells from growing across the wound.  Septicemia and pyemia are the common complications of wound healing cause by the bacterial toxins due to massive infection and may lead to endotoxic shock. Evisceration is protrusion of viscera through the wound.  Traumatic neuralgia is the pain perceived at or around the vicinity of wound. achieving 40-70 percent of the strength of undamaged tissue at four weeks.  Exuberant granulation tissue (proud flesh) is granulation tissue which grows above the level of the surrounding skin (overgranulation).  Traumatic fever is the resultant of pyrogen release from neutrophils and injured body tissue. Eventration is protrusion of the bowels from the abdomen.  Haematoma (accumulation of blood in the Subcutis) or seroma (accumulation of serum in the dead space) may occur due to rupture of blood vessels following injury. COMPLICATIONS OF WOUND HEALING  Wound dehiscence is the splitting and separation of previously closed wound layers. The main causes responsible for these conditions include improper surgical technique and the local and systemic factors described below.  Sinus (draining tract from a suppurative cavity to the surface) may develop due to presence of necrotic tissue debris and foreign bodies.  Cellulitis is inflammation of the connective tissues presenting as oedema. Dehiscence usually occurs 3-5 days after surgery before collagen deposition. remodeling develops 3 weeks following injury and continues up to two years. necrosis and unusual exudation. . discolouration.  Haemorrhage due to rupture of blood vessels can lead to development of hemorrhagic shock and ultimately death.  The strength of scar tissue formed in this phase is less than the surrounding normal tissue. equine and camalidae are more susceptible to tetanus. The principles include: o Gentle handling of tissue. o Close tissue approximation and obliteration of dead space o Removal of necrotic and devitalized tissue. certain antimicrobial agents and local anesthetics delay the healing process by destroying cellular elements of wound.  Adhesions are the major post-operative complication following abdominal surgery due to rough handling of viscera.  Topical medications promote wound healing by minimizing bacterial infection. promotes disordered leukocyte function and ultimately prevents the development of new blood vessels and formation of granulation tissue. epithelialization and resistance to infection.  Gas gangrene may develop. Tetanus may develop due to Clostridium tetani infection particularly in deep penetrating and punctured wound.  Tissue vascularity ensures oxygenation and nutrients which is essential for wound healing. However. FACTORS AFFECTING WOUND HEALING  Local factors  Systemic factors  Medication  Systemic diseases LOCAL FACTORS  Good surgical technique is warranted for proper wound healing if Halsted’s principles are followed.  Traumatic emphysema arises due to punctured wounds of the respiratory or gastrointestinal tract where gas or air accumulate in and around the wound area.  Venous thrombosis and embolism may occur when fat tissue accidentally entered in the circulation. Oxygen influences angiogenesis. moist dressing triggers .  Infection is one of the major factors which retard the wound healing significantly as it prolongs the inflammatory phase. Nonadherent. Lavage with sterile isotonic solutions like normal saline decreases the concentration of the microorganisms mechanically and aids in healing process. disrupts the normal clotting mechanisms.  Lavage and dressings accelerate wound healing by protecting healing tissue. o Aseptic surgical technique o Perfect hemostasis and preservation of blood supply to the wound area. Caprine. neovascularisation and formation of early ground substances of the wound. . particularly important for collagen synthesis.  Carbohydrates and fats: These provide the energy required for cell function. the body breaks down protein to meet the energy needs. It is also important for the inflammatory phase of wound healing. Zinc deficiency contributes to delay epithelisation and disruption in granulation tissue formation by inhibiting fibroblastic cellular proliferation. or nonabsorbable braided suture materials delay the healing process by exacerbating the inflammatory response and inciting infection. delaying fibroplasia and producing edema.  Ionizing radiation retards wound healing by decreasing fibroblast formation. Fatty acids are essential for wound healing.  Vitamins A and B complex are responsible for supporting epithelialization and collagen formation. copper are important for enzyme systems and immune systems.  Glucose balance is essential for wound healing. collagen synthesis and neovascularisation within fortnight of surgery. which affect their circulation and oxygenation to the wound bed as compared to young.  Movement of the wound site prolongs the healing process as movement can disrupt cell migration. epithelisation whereas adherent gauge dressing mechanically debride the contaminated wound. When the patient does not have enough.  Mutilation of the wound not only disturbs the healing but also complicate by creating evisceration like condition.  Presence of foreign bodies such as tissue debris. SYSTEMIC FACTORS  Advanced age retards healing because of reduced skin elasticity and collagen replacement.  Protein is required for all the phases of wound healing.  Nutrition plays a pivotal role in wound healing process. dirt. Hypoproteinemia slows healing by decreasing wound tensile strength. soil.  Vitamin C is essential for formation of intercellular cementing substances as it is needed for hydroxylation of the lysine and proline moieties of collagen.  Iron is required to transport oxygen.  Minerals like zinc. Hyperglycemia delay wound healing.  Obliteration of dead space and prevention of fluid accumulation promote migration of reparative cells and minimizing the risk of infection during wound healing. Older animals are also susceptible to other chronic diseases. sequestrum. The immune system also declines with age making patients more susceptible to infection. MEDICATION  Anti-inflammatory. epithelial proliferation and subsequently strength of healing wund. collagen synthesis and neovascularisation. granulocytes cell functions and ultimately leading to wound dehiscence. o Most NSAIDs lower resistance to infection and ultimately delay healing. cytotoxic. immunosuppressive and anticoagulant drugs all reduce healing rates. o Chemotherapeutic agents like methotrexate. uncontrolled diabetes. decrease fibroplasia. producing chachexia. healing process is adversely affected by depressing immune function. neovascularisation. CLINICAL SIGNS OF INFECTION  Local pain/tenderness  Local swelling/oedema  Increased exudate  Frank pus  Wound breakdown  Pyrexia  Delayed healing  Change in appearance of granulation tissue .  In patients with uncontrolled diabetes. In addition.  Uremia delays fibroblastic proliferation. doxorubicin and cyclophosphamide delay the wound healing process by inhibiting cell division or collagen synthesis. there is delayed healing as hyperglycemia impairs collagen formation. renal and hepatic disturbances delay healing process. granulation tissue formation. o Anti-inflammatory drugs like corticosteroids if used in long term and at higher doses impair the inflammatory phase. epithelialization and contraction. o Anticoagulant drugs retard the healing by interrupting clotting mechanism and thus making a wound more prone to infection due to presence of blood clots. and minimizing inflammatory cell division.  A malignancy in the body retards wound healing by altering metabolism. SYSTEMIC DISEASES  Systemic diseases like malignancy. Contaminated wound  A fresh wound gets contaminated when it is more than 4 -5 days old.  Dependent drainage should be provided if haemotoma or seroma formation is expected. contaminated and septic wound or infected wounds. o Contusions: are treated with cold and astringent applications to minimize extravasation. excessive trauma and haemorrhage – lower the wound infection.  Surgeon should avoid drying of the tissue. o Haematomas: when small get absorbed other wise they may have to be opened and treated. Thirty years ago physicians believed pus in a wound was laudable and anxiously awaited its arrival. . surgeons today attempt every conceivable means to prevent its presence. Surgical or aseptic wounds  A surgical wound made with all aseptic precautions in a non infected tissue is an aseptic wound. o Open wounds: surgical or aseptic wound.  Local application of Fly repellents – hot summer months.  The principal therapeutic strategies of the open and contaminated wound are to convert it into a clean closed wound.  Prophylaxis against tetanus.  The patient and the affected injured part should be kept at rest.  Suture should be supported upto healing time 8 -14 days  Systemic use of specific antibiotics as a therapeutic or prophylactic measure.  Bridging of epithelial tissue  Abnormal smell MANAGEMENT OF WOUNDS  Humans have always been faced with the dilemma of how to treat wounds.  Many diverse and interesting approaches to wound management have been applied throughout medical history.  Warm tap water is required otherwise cold water may reduce the temperature of the wound surface to a degree where cell mitosis will not recommence for up to 4 hours. where possible.g.  Gauze / soft wash cloth: Contaminated wound. nonviable and heavily contaminated tissues should be removed. the soaked wash cloth must be squeezed over it allowing the water to wash over it.basin for this purpose must be washed with soapy water. is painful and causes trauma to healing cells  Disposable gloves (clean but not sterile) o The following procedures should be meticulously adhered:  A sterile gauze pad should be placed over the wound followed by shaving the surrounding skin and finally. residue from hydrocolloid dressings o Purulent exudate i. immerse and clean.not sterile – procedure. Reasons to clean a wound  Presence of: o Foreign bodies o Debris e.  Again the wound area should be exposed by gentle traction and carefully irrigated.  The surrounding area should be draped with a sterile one. .  Devitalized and ragged skin edges. WOUND CLEANSING PROTOCOL  Wound cleansing is a clean . infection EQUIPMENT  Clean basin . This is not a routine practice as it redistributes bacteria. cleaning the edges of wound with a detergent soap and water. Non-fiber shedding gauze should be used where foreign bodies remain. slough. Not all wounds require cleaning.  The wound area should be prepared for surgical debridement by gentle irrigation with lukewarm isotonic saline solution. rinsed and dried before use.e. Otherwise. dead space.  Lavage: after removal of the necrotic debris. dry surrounding skin but not the wound itself. o The incision for drainage should be placed in the most direct route possible and away from anastomotic sites.  The operative field should be again prepared by placing sterile gauze over the wound and redraping the surrounding area.  Wound drainage can be achieved by using Penrose drains. plastic or rubber tubes or open drainage with bandage support. hematoma and seroma. SEPTIC WOUND OR INFECTED WOUND Basic principles of infected wound treatment strategies  Debridement: Thorough debridement is most essential to manage septic wounds which will provide easy access to the wound depth. the wound and its periphery should be copiously irrigated with warm normal saline or water and soap or 2% hydrogen per oxide.  Capillary and venous oozing should be controlled by gentle pressure and ligating blood vessels if necessary. They may cause pressure necrosis. . o Addition of antibiotics or antiseptics is not required when large volume of fluid is used as improper concentrations of such drugs may have deleterious effect to the wound healing process. The following guidelines should be observed: o Dependent drainage of wound exudate should be provided if possible so that gravity will aid drainage of the exudate. o Volume and nature of lavage fluid depends on the degree of gross contamination and size of the wound. o Infected wound should not be plugged or closed unless infection is well controlled for primary healing but should be left to heal by secondary healing.  After cleansing. The aim is to reduce fluid accumulation. o All necrotic tissue debris and foreign materials should be removed until clean.  Wound closure should be done either by suture without drainage or placing a small rubber drain into the depths of the wound and other end in the skin margin. healthy tissue margin of the wound are achieved. tendon and major vessels.  The wound may be loosely packed with petrolatum- impregnated gauze and sutured at a later date (delayed primary closure). The drain exit site should be prepared in an aseptic manner and should be covered with sterile bandages to prevent premature removal or loss of the drain and to access the nature of the exudate. o Usually drain should be removed after 24-48 hrs. breeds. o Through and through drainage should not be used. In most cases.  Antimicrobial therapy: Selection of the antimicrobial agent should be based on culture and antibiotic sensitivity test. age and disease status.  To reduce salivary secretion and airway secretion. colonization of the wound by opportunistic organisms and to prevent environmental contamination with the infective agent. o Soft. intra and post operative analgesia.  To provide smooth induction.  To produce pre. PART – II ANAESTHESIOLOGY --------------------------------------------- Module – 9 PREANAESTHETIC CONSIDERATION & PREANESTHETICS- PREMEDICATION  Premedication and selection of premedicants are important components of safe anaesthetic protocol in tailoring anaesthetic regimen suitable for species. o Incision to place the drain should be made within the zone of reaction. Antimicrobial therapy should be continued for 10-14 days. empirical antimicrobial agents should be advocated in life–threatening infections that exists or develops while awaiting culture and sensitivity results (48- 72 hrs).  Sterile protective bandaging is a good practice to avoid hospital infection. ( insert picture).  To reduce distress during restraining and minor manipulations like placement of catheters.  To reduce the delecterious side effects of the major anaesthetic drug. petrolatum based antiseptic gauze should be used to keep the wound edges apart. Aims of premedication  To reduce fear and calm the patient. avoid cutting into non-infected areas. However.  To reduce intra operative complications like vomiting and regurgitation and . animals with existing wound infection are treated initially with loading dose of intravenous medication.  To decrease the total quantity or amount of the major anaesthetic drug. S. Acepromazine. Meperidine . Detomidine. Premedicaments Examples 1 Anticholinergics Atropine sulphate. Azaperone Benzodiazepines Diazepam. Glycopyrrolate 2 Transquilizers or neuroleptics Chlorpromazine.Meditomedine Alpha 2 adrenergic agonist Ranifidiae Chloral hydrate 4 Opioid agents Morphine. CLASSIFICATION OF PREMEDICAMENTS  The premedicants used in veterinary anaesthesia are classified as follows based on their properties. Zaazepur clamazolam 3 Sedatives Xylazine. Medazolam.No. Phenothiazine derivatives trith promaziae promethorine Butyrophenones Droperidol.  To provide safe and smooth recovery.  Anticholinergic premedication is contraindicated in ruminants as the salivary and bronchial secretions will become more viscid and block the airway. Atropine sulphate is a natural product widely available invarious plants like Atropa belladonna.  Though the routine use of these drugs has decreased in anaesthetic protocols. Scopolamine is not used in veterinary practice.  It is also found in Jimson weed. They also induce ruminal atony.  Decrease salivary secretion.  They increase the heart rate by blocking vagal tone on S. .A node. But their use is justified and recommended along with anaesthetics and adjuncts.  Herbivores are more resistant to anticholinergics. Xylazine). heart failure and cardomyopathies. CLINICAL PROPERTIES AND USES  These agents are administered to o suppress the vagal tone o reduce salivary and bronchial secretions. scopolamine and glycopyrrolate. The increase in heart rate is associated with increased myocardial oxygen consumption.  Glylcopyrrolate is a synthetic quaternary ammonium compound. their use is still recommended in patients with preexciting bradycardia or in combination with drugs anticipated to cause bradycardia. hence contraindicated in animals with pre exciting tachycardia. Butorphenol Partial Agonists/Antagonists ANTICHOLINERGICS  Anticholinergic premedicants are atropine sulphate. which cause excessive salivation and bradycardia (eg.  These agents are competitive of acetylcholine (Ach) hence attenuate the physiological responses of parasympathetic nerve impules. gastric acid secretion and gastrointestinal motility. In animals with preexciting bradycardia they increase the cardiac out put. Agonists Pentazocaine.  Large dose of atropine may cause dilatation of cutaneous vessels due to the effect on the cholinergic receptors of the vascular smooth muscles (Atropine flush).  Decrease bronchial secretion.  may induce sulphate  Tachycardia is not extreme variety of cardia as in glycopyrrolate arrythmias if  Indicated in animals myocardial requiring immediate oxygen demand is treatment for bradycardia not satisfied. excitement and seizures.  Induce mydriasis due to the cholinergic blockade of iris and ciliary body and paralyze accommodation reflex (cycloplegia) resulting in photophobia and blurred vision.  Iduces bradycardia initially if administered through intravenous route due to the stimulation of vagal nuclei in the medulla: hence intravenous administration is contraindicated for caesarian . And this central stimulation is not noticed after administration of glycopyrrolate.  Indicated in eye surgeries whether performed under local or general anaesthesia to prevent oculo-cardiac reflex. ADVANTAGE AND DISADVANTAGES OF ATROPINE AND GLYCOPYRROLATE- Drug Advantages Disadvantages Atropine  Less expensive. dilate bronchi and increase the pulmonary dead space. as it does not cross the blood- brain barrier.  The undesirable effects of atropine and glycopyrrolate can be reversed with neostigmine or physostigmine.  Excessive dose of atropine and scopolamine may induce hallucination.  Relax the urinary tract smooth muscles and tend to cause urinary retention. due to its quick action. Due to this property glycopyrrolate is considered as a usefulo premedicant in equine anaesthesia. 20 mg/kg I.M Pigs 0.C/I. section in bitches. Glycopyrrolate  Less dose (0.M/I.02 mg/kg S.M 0.11 mg of glycopyrrolate in intravenous route).02 mg/kg I.  Causes less intestinal stasis hence indicated in equine anaesthetic regimen to reduce the incidences of post anaesthetic colic due to ileus.02—0.44 mg of Not completely effective atropine is equivalent to in preventing sialorrhea 0.8 mg total dose 0.M 0.C/IM Goats 0.01 mg/kg I.05 mg/kg S. CLINICAL DOSES Species Atropine Glycopyrrolate Horses 0.  Controls bradycardia effectively.M 0.3—1.01—0.  Effectively controls gastric acidic pH and avoids aspiration of gastric acidic secretion.02 mg/kg S.V .05 mg/kg S.02 – 0.C/I.V Dogs 0.C/I.  Indicated in caesarian section as it does not cross the placental barrier and causes excessive increase in the heart rate of neonates.02 – 0.  These agents are weak anticholinergics and have extrapyramidal stimulating properties. spinal or segmental anaesthesia./I.  Acepromazine maleate. promazine. promethazine and methotrimeprazine are the commonly used phenothiazines.  Tranquilization with phenothiazines is contraindicated in animals undergoing epidural.02 – 0.C/I. norepinephrine and dopamine. o With the previous history of epilepsy.M.  At high doses and some times in clinical doses induce extrapyramidal signs such as rigidity. o Undergoing myelographic procedures o With the history of recent intake of organophophorus drugs or toxicity  Pulmonary functions are maintained following the administration of phenothiazines except slight depression in respiratory rate  Induce urine production due to the suppression of antidiuretic hormone  Animals undergoing intradermal allergic tests should not be administered with phenothiazines as they are potent antihistaninics  Depletes catecholamines of the thermoregulatory center and render the animal’s body temperature susceptible to the changes in the environmental temperature.  The steriochemical model of phenothiazine derivatives is similar to epinephrine.V Cats 0.02 mg/kg S. 0. Among these agents acepromazine. Following . 9 October 2010. triflupromazine and chlorpromazine are used in veterinary anaesthesia. CLINICAL PROPERTIES AND USES  Produce sedation.01 – 0.  These agents increase the dopamine and norepinephrine turn over in the brain and block the peripheral actions of catecholamines at alpha 1 receptors.V Last modified: Saturday.02—0. chlorpromazine.1 mg/kg S. Hence contraindicated in patients.V 0.C/I.  They act on the central nervous system by depressing the brain stem and connections of the cerebral cortex. 06:32 AM PHENOTHIAZINE DERIVATIVES  Phenothiazine derivatives are basically three ring structures in which two benzene rings are linked by a sulphur and nitrogen atom. triflupromazine hydrochloride.02 mg/kg I. general calming and reduction in motor activity  Antagonize dopamine excitatory chemoceptors and suppress vomiting. tremors and catalepsy. Promazine Horses = 0.04 – 0.1 mg/kg I.55 – 4. This response is abolished by the generalized vasodilationinduced by phenothiazines. Goats = 0.03 – 0.4 mg/kg I.02 – 0. 1. Chlorpromazine Dogs = 0. Cattle = 0.05 mg/kg I. Pigs = 0.M.V.V.M.05 mg/kg I.V.V.1 – 6.M.2 – 6.M.2 – 6.M.2 mg/kg I.4 mg/kg I.05 mg/kg I.M.6 mg/kg I.4 mg/kg I. 0. Horses = 0.0 – 2.09 mg/kg I. CLINICAL DOSES Drug Dose Acepromazine Dogs = 0.M.2 mg/kg I.M.04 – 0. Sheep = 0. 2.M. Cattle = 0.V.M. 2.M.M.09 mg/kg I. .2 – 1.1 mg/kg I. Cats = 0. 0.05 mg/kg I.1 mg/kg I.05 mg/kg i.2 – 6. Cats = 0.55 – 4.1 – 2.6 mg/kg I.V.V/I.0 mg/kg I.V.M Horses = 1. 0. Cattle = 0. 0.M.4 mg/kg I.V.02 – 0.1 mg/kg I.44 – 1. Pigs = 1.03 – 0.V.6 mg/kg I.03 – 0. 0.55 – 4.1 mg/kg I.induction of regional anaesthesia there will be vasodilation in the anaesthestised part of the body and this effect is compensated by the vasoconstriction in the unanaesthetized parts of the body to maintain cardiac out put.6 mg/kg I. 2.44 – 1.03 – 0.55 – 4.V/I.2 – 2. 04 mg/kg mixed with 4.  They induce minimal changes in respiratory parameters.  They are potent antiemetics and even prevent drug induced vomiting produced by opioid analgesics by acting on the chemoemetic trigger zone. DRUGS AND DOSES  Droperidol o It is available in combination with an opioid analgesic.5 mg/kg intravenously reverse the side effects of droperidol-fentanyl combination. Hence used as neuroleptic analgesics in anaesthetic regimen.V/I. Triflupromazine Dogs = 1.0 mg/kg I.V. 0.M  Azaperone o It is widely used in pigs for control and transportation.44 – 4.4 mg of fentanyl citrate and 20 mg of droperidol per ml = Innovar vet) This combination produces profound analgesia for 30 minutes and sedation for a considerable time in dogs.C  Pigs 0.M  Cats 0. aggression upto 48 hours after recovery.1 mg/kg I. (0.M. rigidity and catalepsy in clinical doses hence not popular.44 – 1. Goats = 0. Sheep = 0. Naloxone .10 – 0. fentanyl citrate.00 mg/kg BUTYROPHENONES  Butyrophenones have similar properties like phenothiazines.  They are more likely to produce extrapyramidal signs like tremors.1 mg/kg I.1 mg/kg I.  Droperidol.4 mg/kg I.M. azaperone and lenperone are the butyrophenones used in anaesthesia.aminopyridine .0.  Butyrophenones have less cardiac depressive effects and the hypotension produced by the agents can easily be reversed with phenylephrine. o In cats it may induce undesirable central nervous system stimulation.M.44 – 1.1 mg/kg I.11 mg/kg S.05 – 0. In pigs it is administered prior to metomidate. defecation and salivation. Azaperone sometimes produce .10 – 0. o Other effects noticed after administration are panting. o Clinical dose  Dogs 0. Pigs = 0.  They block the central actions of dopamine and norepinephrine.0.V/I. fluanisone.44 – 1. M (high dose)  Fluanisone o It is available in combination with fentanyl citrate.  They do not have analgesic property.  These agents produce muscle relaxation.M.V. 4.1 mg/kg of fentanyl citrate (neuroleptanalgesia).315 mg of fentanyl and 10 mg of fluanisone = Hypnorm). BENZODIAZEPINES  Benzodiazepines exerts their effects by binding to a specific binding site on aminobutyric acid (GABA) receptor. o Cats 0.  In human it causes congenital anomalies if administered during the first trimester of pregnancy.M (low dose).05 – 0.Dogs = 5 mg/kg along with 0. infusion bags and infusion tubes are not advisable.2.  It can not be used as a sole sedative agent in dogs and cats. climazolam and zolazepam are the commonly used benzodiazepines.  These agents are good anxiolytics.3 – 0.4 mg/kg I.2 mg/kg I.Pigs = 0.  They have minimal respiratory and cardiovascular depression.M.1 – 0.5 mg/kg I.3 – 1. sweating and excitement in horses hence it is unsuitable for equine anaesthesia.V. And the significance of this is not clear in veterinary practice.  Diazepam.  It is used as an effective appetite stimulant in dogs and cats at the dose of 0. (0. midazolam.  It decreases the release of catecholamines and act as antidysrhythmic agent.0 mg/kg I.  Rapid intravenous injection may cause thrombosis.05 – 0.  It is absorbed by plastic materials hence storage in plastic syringes. o This combination is contraindicated in patients with respiratory. renal and hepatic diseases. 0. 0. o Horses 0.04 mg/kg I. o Clinical dose .M. o Clinical dose . Naloxone is the reversal agent for this combination.0 mg/kg I.02 – 0. cats and human.0 mg/kg I.40 mg/kg Oral/I.5 mg/kg I.M (medium dose). DIAZEPAM  Diazepam is used to treat status epilepticus in dogs.  In horses it produces excitation if used as a sole sedative premedicant hence combined with xylazine.4 – 1.V .  These agents are combined with opioid analgesics and dissociative anaesthetics. muscle tremors.  Dose o Dogs 0. hypnotics and anticovulsants. 2 mg/kg I.5 – 1.6 .I.1 mg/kg I.07 – 0.M  Sheep & goats 0.9.0 mg/kg I. o Dose . For dose calculation the two drugs are considered as one product (500 mg).M  Pigs 0. o It is metabolized in the liver rapidly hence less cumulative can be stored in aquane solution in plastic container upto 100 hours without loss of potency.  Flumazenil .M ZOLAZEPAM AND FLUMAZENIL  Zolazepam o It is marketed in combination with dissociative drugs like tiletamine (250 mgs of tiletamine and250 mgs of zolazepam in lyophilized form).0 mg/kg I. o Can be administered as premedicant to thiopentone.0 mg/kg I.V MIDAZOLAM AND CLIMAZOLAM  Midazolam o It is twice as potent as diazepam. o Dose  Dogs 6.1 – 0.M.V o Cattle 0.1 mg/kg I.1 mg/kg I.5 mg/kg in combination with 5. sheep.22 mg/kg I.V  Horses 0.0 .M/I.2 mg/kg I. o Foals 0.43 mg/kg I.V o Goat 0.M.1 – 0. o In horses the drug is combined with other premedicants and anaesthetics as it may produce excitement and muscle weakness.V o Pigs 1.0 .5 – 1. horses and dogs.M  Chicken 5.9 mg/kg I.Dogs & cats = 0.05 – 0.5 – 1.V  Climazolam o It is a potent benzodiazepine.5 – 11. 2.1 mg/kg I. o Dose  Dogs = 1.V  Cats 6.9 mg/kg. has variety of use in cattle. ketamine and propofol anaesthesia.0 – 1.15 mg/kg of fentanyl I.V  Cattle 0.11.  Produces muscle relaxation.  Emesis is common in dogs and cats after xylazine injection due to the stimulation of central emetic center.  In horses it is a reliable sedative and the horse will be in standing position in clinical doses. meditomidine and romifidine.1 mg/kg. Administration of anticholinergies as premedicants reduce the incidence of bradycardia and even the bradycardia that occurs after administration of xylazine can be reversed with atropine (0.045 mg/kg initially and followed by 0. But it must be used with caution as it may mask the clinical signs and may aggravate ileus.V block.  It is contraindicated in branchycephalic breeds.  It produces dose-related depression of the central nervous system. older dogs and in intestinal obstruction. XYLAZINE HYDROCHLORIDE  Xylazine is a sedative analgestic having alpha 2 adrenergic agonist activity.  Xylazine induce profound depression of cardiovascular system. decreased cardiac out put. ALPHA 2 ADRENERGIC AGONIST  Alpha 2 adrenergic agonists are referred as sedative analgesics. detomidine. Further increase in the dose will not increase the intensity of sedation. hypotension and and increase in central venous pressure are noticed.01 mg/kg intravenously). Drooping of head and buckling of hind limbs are commonly noticed in horses. Bradycardia. which is attributed to decrease in intraneural and synaptic transmission in the central nervous system.  The popular agents are xylazine hydrochloride.1 mg/kg I.  The duration of analgesic activity is 15 – 30 minutes and the sedation is for 1-2 hours. One tenth of the dose used in horses and dogs induce sedation and recumbency in cattle. It also often produces A.V.  Ruminants are more sensitive to xylazine. only the duration will be increased. Intravenous administration causes a transient increase in blood pressure. o The actions of all benzodiazepines can be reversed or antagonized with flumazenil at the dose of 0. . The clinical dose through intravenous route is 1.  Xylazine is used in the treatment of equine colic for pain relief. 17 mg/kg in 5.V  Upto 4. o Epidural 0.1.0 ml of saline OTHER AGENTS Detomidine  Detomidine is a potent alpha 2-adrenaergic agonist mainly used in horses and cattle.M.C o Cattle.05 – 0.  It increases the sensitivity of myocardium to the circulating catecholamines.08 mg/kg I.0 mg/kg I.2 --. standing restraint  0.  Advantages of these drugs o Does not stimulate pituitary adrenocortical adrenocortical axis hence stress is less. o Provides standing restrain in cattle at the dose of 10 to 20 µg/kg I.  In ruminants it reduces the gastrointestinal and ruminal motility with relaxation of cardia oesophageal sphincter.1 – 0.V .V/IM o Dogs & cats 0.0 – 2.2 mg/kg I.  Other effects o Excessive urine production because of the suppression of antidiuretic hormone o Salivation o Hyperglycemia  Dose o Horse 1. Increase in intrauterine pressure may cause embryo/ovum ejection if administered in embryo/ovum transplantation.1 – 0. recumbency and prolonged  0.  Xylazine is used as epidural anaesthetic because of the presence of alpha receptors in the spinal cord and its structural similarity with lidocaine. Cardiac dysrhythmias may occur if used along with halothane.V recumbency o Pigs  1.07 – 0.3 mg/kg I. This favors ruminal tympany and regurgitation.V/I.M.  Xylazine has oxytocic property and increase the intrauterine pressure hence it may induce abortion in pregnant animals.M/.0 mg/kg I. o Can be administered in pregnant animals o Can be administered in animals which are not fasted o It is very effective in relieving pain from colic in horses.1 mg/kg I.  Thermoregulation is depressed following xylazine administration and the animal may become hypothermic or hyperthermic depending on the ambient temperature.M.1 mg/kg I. sheep & goats  0.0 to 10.S. o It is an alpha 2 adrenergic blocking agent used at the dose of 0.M/S.C o Cats 0.40 µg/kg I. CHLORAL HYDRATE  Chloral hydrate is used as a reliable sedative hypnotic in cattle and horses.04 mg/kg) for better results. Used in horses and maximum sedation is achieved at the dose of 80 µg/kg I.02 mg/kg I.04 .0.  The central nervous system depression is due to its metabolic product namely 2.V SPECIFIC REVERSAL AGENTS Alpha 2 antagonists -  Yohimbine hydrochloride o It is a specific reversal agent for xylazine and detomidine.  It has deeply penetrating aromatic odour and is bitter in taste.V Meditomidine  It is a potent alpha 2 adrenergic agonist used in small animal anaesthesia. o Yohimbine is used in the treatment of equine colic due to ileus. hence the sedative effect is prolonged even after cessation of administration. o It is often combined with 4-aminopyridine (0.01 .2.M/S.1 mg/kg I.08 mg/kg I.  Doxapram o It is not a specific reversal agent to alpha 2 adrenergic agonists but offer certain beneficial effects due to its central nervous system stimulation and respiratory stimulation. o It reverses the gastrointestinal stasis produced by xylazine.0.V/I.V/I.2 trichloro ethanol. Cattle. Sheep & Goats 10 .V Romifidine (Sedivet)  It is developed from clonidine and has alpha 2 adrenergic agonistic action.V. The other properties are similar to xylazine.5 mg/kg I.  Atipamezole o It is used to reverse the effects of meditomidine at the dose of 0.04 – 0.C o Cattle 0.  It is less expensive and still perfectly acceptable sedative agent.01 . o Dose (not recommended in dogs cats and wild felines): Horse.0. .04 mg/kg I.V.  Dose o Dogs 0.  Trichloro ethanol conjucates with glucuronic acid to urochloralic acid and excreted.8 mg/kg. 50 to 75 mg/kg for profound sedation and hypnosis and 150 to 250 mg/kg for anaesthesia. at the dose of 30 to 120 grams dissolved as 1 in 20 solution in water.5 to 2 mg/kg o Chloral hydrate 100 mg/kg and ketamine 1.4 to 0.08 mg/kg. 7% chloral hydrate 20 to 40 mg/kg and thiamylal 1 to 2 mg/kg.  Bullls that are uncontrollable and free in the yard can be controlled by water deprivation for brief period and allowing them to drink chloral hydrate dissolved water (90 to 120 grams in 12 litres of water).6 mg/kg.6 to 0.meperidine and oxymorphone -  Fentanyl citrate and etorphine - . swelling and necrosis o Induces abortion in mares  Opioids Derivatives -  Pure agonists-  Morphine  Pathadine.  It does not have analgesic property.  Intravenous dose of chloral hydrate in horses o Chloral hydrate alone 5 to 10 mg/kg for mild sedation and hypnosis. o Chloral hydrate 100 mg/kg and thiopentone 1.  Chloral hydrate is combined with magnesium sulphate at 2:1 or 3:1 ratio (weight) and administered in cattle. 7% chloral hydrate 20 to 40 mg/kg and thiopentone 5 to 7 mg/kg o Acepromazine 0. 20 to 40 mg/kg for moderate sedation and hypnosis.  Disadvantages of chloral hydrate o Prolonged hangover with ataxia and stupor o Perivascular administration causes pain. 7% chloral hydrate 20 to 40 mg/kg and thiamylal 2 to 4 mg/kg.5 to 2 mg/kg o Promazine 0.  Chloral hydrate depresses the motor and sensory responses at sedative dose and produces cerebral and medullary center depression at anaesthetic dose resulting in muscle relaxation and depression of cardiac and respiratory system. o Xylazine 0.  It is combined with magnesium sulphate and pentobarbital and administered to horses (Equithesin mixture).  In cattle it can be drenched preferably through stomach tube.  Chloral hydrate is administered as 10% solution intravenously in cattle at the dose of 80 to 90 mg/kg.04 to 0. Initial use may cause defecation and chronic use will result in constipation.6 mg/kg I.  Morphine is used as a postoperative analgesic for pain relief in veterinary practice.  Preservative free morphine can be administered epidurally to relieve pain. The laboratory synthetic agents are codeine. MORPHINE  Morphine o Morphine is derived from the dried milky exudates of the unripe seed capsules of the opium poppy (Papaver somniferum). pigs.  Dose o Horses Morphine gives good results in horses if administered after xylazine sedation.  It is used in the treatment of congestive heart failure to relieve pain and decrease after load.M/I.V o Cats 0. Hence must be used with suitable tranquilizer.5 mg/kg ( total dose not exceeding 10 mg ) I. horses.  Morphine decreases motility of stomach with increase of antral portion. .2 – 0. but produce increase in vagal tone and slowing of heart.V and morphine 0. must be administered with caution because it may induce CNS stimulation. 5% noscapine and 0. o Morphine acts and produces  Analgesia  Drowsiness  Produce nausea and vomiting by stimulating chemoceptor trigger zone for vomiting. o The laboratory synthesis of morphine is different hence still it is derived from opium poppy.M. Xylazine 1.  It is absorbed from the gut and oral mucosa.05 – 0.  Induce respiratory depression  Depress cough  The effects on myocardium are not significant. Partial agonists -  Partial agonists (agonists/antagonistics)  Pure Antagonist PURE AGONISTS . It induces dopaminergic excitement in cats.8% papaverine. heroin (dimorphine = diacetylmorphine) and oxymorphine.1 mg/kg S.V o Dogs 0.0 mg/kg I.C/I. o The exudates contains 3-25% of morphine. dogs and cattle. 05 .  Its analgesic property is 80 times greater than morphine. o It is used popularly in small animal anaesthesia due to its analgesic and lack of release of histamine.6. o It reduces salivation and respiratory secretion without inducing vomiting and defecation. less potent (one tenth of morphine) and used in dogs and cats.V/I.M/S.5 mg)  Cats 0.M.0.4. PATHADINE.0.M  Oxymorphone o Oxymorphone is a synthetic derivative having 10 times greater potency than morphine.V/I.5 mg/kg S.C (total dose not exceeding 4.V/I. o Dose  Dogs = 2 . o Intravenous administration causes release of histamine hence most often used along with acepromazine. o It is also administered epiduraly to control pain in the hindquarters (0.M  Meperidine o It is a synthetic product. o Dose  Dogs 0. o It is widely used in dogs and cats for its analgesic property.05 mg/kg). . Acepromazine 0.2 mg/kg I. o Morphine is administered after administration of Acepromazine.C/I. and Morphine 0.C/I.M.6 mg/kg I.M.4 mg/kg S.0.1 mg/kg I.M  Catls = 2 . FENTANYL CITRATE AND ETORPHINE Fentanyl citrate  Fentanyl is a synthetic opioid product related to phenylpiperidines. (Phenothiazines are potent antihistaminics) o Dose: Dogs and Cats 2-5 mg/kg I.025 . o It does not cause histamine release as meperidine. o Pathadine induces histamine release if administered through intravenous route.C  Horses 0.05 .0.4 mg/kg I.M/S. Analgesia lasts for 4 hours.02 .03 mg/kg I. o The only limitation with drug is stimulation of vagus leading to bradyarrhythmias and it can be reduced or prevented with the use of antichlinergic agents in the protocol. MEPERIDINE AND OXYMORPHONE  Pathadine o Pathadine is a vagolytic and negative inotropic drug at clinical doses. V.074 mg/ml and Methotrimeprazine 18 mg/ml  Revivon L A contains Diprenorphine 3.01 . PENTAZOCAINE. Each pack of the marketed drug will be having two components. sufentanil.  The other synthetic pure agonists are afentanil.45 mg/ml and acepromazine 10 mg/ml  Immobilon S A contains Etorphine 0. lofentanil and carfentanil.Dogs 0.  Preparation  Immobilon L A contains Etorphine 2.0.315 mg of fentanyl and 10 mg of fluanisone per milliliter) Fentanyl combinations provides good intra operative analgesia.  The dose of etorphine is 0.272 mg/ml  This mixture is popularly used to capture elephants and giraffes  Not recommended for domesticated and wild felines  Etorphine is extremely potent in human and any accidental injection may cause death if not treated with naloxone or diprenorphine. Its general properties are similar to morphine. (Hypnorm contains 0. heart rate.  In clinical dose etorphine along may produce initial excitement hence it is marketed in combination with phenothiazine derivatives. Separate combinations are available for large and small animals. Etorphine  Etorphine is a potent synthetic morphine derivative. BUTORPHENOL TARTRATE AND BUPRENORPHINE Pentazocaine  It is used as an analgesic.  Fentanyl citrate is available alone.  Dose . respiratory rate and arterial oxygen tension (PaO2) are reduced following administration of fentanyl.  In clinical doses it produces pulmonary vascular resistance.  In human it causes dysphoria and hallucination and pentazocaine is developed to prevent drug abuse.  In dogs and primates it produces sedation and myosis whereas in horses it produces excitement and mydriasis. (see butyrophenones for other doses).0 mg/ml  Revivon S A contains Diprenorphine 0. 1-Immobilon and 2-Revivon.W  Etorphine is an extremely long acting agent whose effects are maintained by enterohepatic recycling.M/I. .5 mg/500 g B.  Cardiac out put.  The action of this drug can only be terminated by the administration of the specific antagonist Diprenorphine.4 mg of fentanyl and 20 mg of droperidol per milliliter) or fluanisone. or in combination with droperidol (Innovar vet contains 0.02 mg/kg I. It is not recommended in cats. V o Dogs = 0.V Module.005 .02 .M PURE ANTAGONISTS  Naloxone hydrochloride.2 mg/kg I.0.C/I.04 .  Penlog -Duration of analgesia 3-4 hour .0.1 mg/kg I. LOCAL ANAESTHETICS . rapid Buprenorphine  Respiratory depression is more and often treated with intermittent positive pressure ventilation. analgesia and increase in pulmonary vascular resistance. temperament of the animal.C/I.V.V  Diprenorphin-Dogs & Cats = 0.4 mg/kg I.V  Horse = 0.33 mg/kg I.01 .2 – 0. health status of the animal and magnitude of the procedures.M/S.  Dose o Horse = 0.V o Cats = 0.02 mg/kg S. depending on the species.  Dose -3 mg/kg for 1 to 3 hours of analgesia.02 mg/kg S.  Dose o Horses = 6 . cats and dogs.2 – 0.  It produces sedation.10 µg/kg o Dogs = 0.10 => LOCAL ANAESTHESIA (Introduction)  Varieties of minor and major surgical procedures canbe accomplished in domestic animals under local and regional anaesthesia. breed.M/I.0.  In horses it is used in the treatment of colic and administered at the rate of 0.V/I.8 mg/kg I.0. nalorphine hydrochloride and diprenoorphine are the opioid pure antagonists used for the reversal of the effects of pure agonists and partial agonists.M/S.M/S.C o Cats = 0.V/I.C  Horses 0.V.C o Onset 1 mint – 15 mint I.005 = 0. o Dose  Naloxone  Dogs and cats = 0.0272 mg/kg I.1 mg/kg I.03 mg/kg I.  In horses naloxone is used in the control of crib biting.  Onset 1 min – one hour Butorphenol tartrate  Butorphenol is used in horses.  It is often combined with thiopentone due to its dysrhythmic property and protective action on myocardium.  The maximum dose is 780 mg in horses. respiratory depression. 120mg in large dogs.Cocaine  It is an extract from the leaves of Erythroxylon coca.  It is an irritant and toxic in small doses. which does not posses convulsive properties as an ajunct (See injectable anaesthetics). cardiac arrest and death. opisthotonus. Lidocaine hydrochloride  It is a fast acting amide local anaesthetic detoxified in the liver.25 mg/kg in cats and 2 mg/kg in dogs to control cardiac arrhythmia due to myocardial ischemia. loss of consciousness and paralysis of medullary centres.  In clinical practice adrenaline free lignocaine is administered intravenously at the rate of 0.  The lethal dose is 15 mg/kg.5% and 5% viscous ointments.  Only topical preparations are available for eye(4% solution) and nasal and laryngeal areas (10 to 20% solutions). Bupivacaine hydrochloride . The duration of action is two hours.  The convulsive dose is 15 mg/kg in cats. Procaine hydrochloride  It is a short acting local anaesthetic derived from ester. tonic clonic convulsions.  It is also used as adjunct to thiopentone sodium to maintain anaesthesia.  In clinical practice it is administered intravenously to relieve pain in fire injured patients.  The local anaesthetic preparationis marketed in combination with adrenaline 1 in 200000.  Goats are extremely sensitive to lignocaine.  Cocaine was used as a doping agent in horses.  Cocaine is withdrawn from the injectable forms due to its toxicity.  The margin of safety is high in terms of convulsive dose (35 mg/kg in cats).  Lignocaine is combined with general anaesthetics. The toxic manifestations in goats are excitation. It is also available as 2% jelly and 2. The total dose should never be exceeded 10 mg/kg in any route.  Procaine is combined with adrenaline 1 in 100000 to potentiate its anaesthetic action.  The toxic manifestations include clonic convulsions.  It is detoxified in the blood and liver rapidly. 45 mg in small dogs and 15 mg in cats.  Bupivacaine is a fast and long acting amide derivative.  Its margin of safety is less.  The convulsive dose in cats is 3.4 to 5 mg/kg.  Intravenous administration induces mdyocardial depression.  Bupivacaine associated ventricular dysrhythmia are due to prolonged inhibition of sedum conductance in the cardiac muscles.  It is not combined with general anaesthetics.  High molecular weight substance like dextran is added to prolong the duration of action in obstetrical anaesthesia. POTENTIATION OF LOCAL ANAESTHETICS  Epinephrine/Adrenaline - 1 in 1000000 or 1 in 200000 is added to increase the intensity and duration of action.  Hyaluronidase - It increases the diffusion of local anaesthetics and favours quick onset of action. It is added at the rate of 150 TRU (Turbidity reducing unit) Addition of hyaluronidase will reduce the duration of action.  Dextran - High molecular weight substance is added to reduce the rate of absorption and increase the duration of action. TYPE OF NERVE BLOCKS SURFACE ANALGESIA  Surface anaesthesia includes topical analgesia of skin, eye and mucous membrane of nose, mouth, penis,vulva, urethra and rectum and intra – synovial analgesia. TOPICAL ANALGESIA  Ice, ethyl chloride spray, ether spray and carbonic acid snow are used to achieve superficial analgesia of the skin.  Absorbent cotton or gauze soaked in 4% procaine or 2% lignocaine is often used on superficial aberrations of the skin and eczematous lesions to alleviate pain.  Lignocaine 4% and proxymetacaine 5% (Ophthaine) are used as topical anaesthetics for eye.  Analgesia of mucous membrane is induced for examination, catheterization or intubation.  The commercial preparation containing lignocaine with carboxymethyl cellulose is applied on mucous membrane.  This preparation is also used to lubricate catheters and endotracheal tubes. Lignocaine 4% is sprayed on nasal or oral mucous membrane to achieve analgesia.  In horses 60 ml of lignocaine 1% can be administered intra rectally to reduce the discomfort during examination. INTRA-SYNOVIAL ANALGESIA  Intra-synovial analgesia is induced to relieve pain arising from the joint and tendon sheath.  Often it is used in the diagnosis of lameness in horses.  Strict aseptic precautions muse bt adopted prior to injection.  Inadvertent introduction of infection will be disastrous.  If the needle is placed into the synovial cavity one can notice synovial fluid at the hub of the needle.  Some quantity of synovial fluid is aspirated before injection into a distended synovial cavity.  The intra-synovial injection techniques in horses are Distal interphalangeal (coffin) joint  Site - in the midline approximately one centimeter proximal to the coronary band with the needle angled slightly steeply than at right angles to the skin.  Needle and volume 19 G x1”, 5 - 8 ml. Proximal interphalangeal (pastern) joint  Site - Pastern joint is situated approximately 1 cm below an imaginary line through the attachment of the collateral ligaments to the first phalanx.  The joint is entered near the midpoint on the dorsal midline approximately 3 cm proximal to the coronary band with the needle pointing obliquely downwards and inwards.  Needle and volume 20 Gx 1”, 5 - 8 ml Metacarpophalangeal (fetlock) joint  Site - The fetlock joint is entered in the triangular space formed by the third metacarpal bone, the proximal sesamoid bone and the suspensory ligament. Can be performed with the limb weight bearing.  Needle and volume 20 G x 1”, 10 ml Digital flexor tendor sheath  Site - Usually performed onlyd in the presence of synovival distension. The site of injection is the most prominent distended part of the sheath on the lateral aspect of the digital flex or tendons just proximal to the fetlock.  Needle and volume 20G x 1”, 10ml Carpal joints  Site - The two carpal joints into which inje3ction can be performed. (mid carpal joint and antebranchiocarpal joint). The mid carpal joint opens with the proximal (antebrachiocarpal joint) between the third and and fourth carpal bones hence does not require separate injection. The joints can be entered on the dorsal aspect of the flexed limb just lateral to the extensor carpiradialis tendon.  Needle and volume 20G x 1”, 10 ml. Elbow joint  Site - The elbow joint can be entered either in front or behind its lateral ligament. To enter in front of the ligament the needle is inserted just under themargin of the lateral condyle of the humerus.  Needle and volume 19G x 2”, 15 ml. Shoulder joint  Site - The shoulder joint is entered horizontally between the anterior and posterior part of lateral tuberosity of the humerous.  Needle and volume 19G x 3.5”, 20 ml Tarsometatarsal joint  Site - Over the head of the fourth metactarsal bone and fourth tarsal bone  Needle and volume 20G x 1”, 5 ml Stifle joint  Site -This joint has three synovial sacs, one in the femoropatellararticulation and two, one medial and one lateral in the femoro-tibial artibulation.  Femoro-patellar sac can be entered on either side of the middle patellar ligament.  Medial sac of the femoro-tibial articulation can be entered between the patellar ligament and the medial femoro-tibhial ligament.  Lateral sac of the femoro-tibial articulation can be entered behind the lateral patellar ligament. Another route is between the lateral femoro-tibial ligament and the common tendon of the long digital extensor and the peroneus tertius.  Needle and volume 18G x 2”, 20 ml each sac. Hip joint  Site - Can be performed in standing horse. The needle is inserted between the anterior and posterior parts of the trochantger major.  Needle and volume 2 mm x 15 cm extirpation of superficial tumors.  This form of analgesia is useful in the treatment of wound. skin incision.  Following disinfection of the skin 0. INFILTRATION ANAESTHESIA  In this procedure the nerve ending is desensitized at the actual site of operation. Production of a cup  A cup of desensitized area is produced by making fan wise injection.5 to 1 ml of local anaesthetic is injected intradermally before injecting into deeper tissues.  There are two types of infilteration anaesthesia o Line block o Field block LINE BLOCK  The needle is inserted parallel to the skin incision and for every 1 cm area of incision 1 ml of the local anaesthetic solution is deposited.  A linear continuous wheal can be produced by the use of a longer needle with single prick and it reduces the number of pricks in case of paravertibral nerve block.  Depending on the duration one can use procaine. Inveted “L” block  Two lenior infiltration at right angle in the form of an inverted “L” desensitizes the flank region in cattle.  If the length of the incision is longer than the length of the needle the needle can be inserted at the mid point of incision to preent multiple pricks.  The needle is withdrawn gently as the solution is deposited. lignocaine or bupivacaine. Ring block . This called as an intradermal skin wheal.  Small circular wheals are created for catheterization of vessesl. FIELD BLOCK Field block  Making walls of desensitized areas enclosing the operation or incisional site.  Bupivaccaine is not normally used in this technique due to its myocardial effects. Inverted “V” block  This is an another alternative method for ring block normally done in teat for the repair of teat fistula.  A tight tourniquet or blood pressure measuring cuff is placed proximal to the site of operation to block venous drainage.  It supplies sensory nerve to the first and second molar (PM 1 & 2). cheek.  Procaine or lignocaine is injected into the engorged superficial vein so as to facilitiate the retrograde flow of blood and deposition and infiltration of local anaesthetic into the tissues. nostrils and lower part of the face. canine and incisors as it passes the canal.  After emerging from the canal it supplies sensory fibres to the upper lip. REGIONAL INTRAVENOUS ANAESTHESIA  This technique is used for amputation of limbs and digits. .  In dogs the infra orbital foramen is situated in front of the anterior margin of the PM 4 where it can be palpated.  Analgesia lasts as long as the cuff or tourniquet is in place and maintains the pressure above the systolic blood pressure.  Used in the extremities like limb for amputation of digit in cattle or in teat for teat surgery. INFRA ORBITAL NERVE BLOCK Nerve  Infra orbital nerve is the division of trigeminal nerve.  The infra orbital foramen is located about one half the distance and 2. Infiltration is done proximal to the site of operation. Site and technique  The nerve can be blocked either as it passes the canal or after emerging from the canal using a 19 G x 5 cm needle. Local anaesthesia of fracture  Lignocaine is directly injected into the haematoma of fracture site with through aseptic precautions to relieve pain and favours closed method of reduction.5 cm dorsal to a line connecting the nasomaxillary notch and the rostral end of the facial crest in horse. Site and technique  The nerve can be blocked as it enters the mandibular foramen or as it emerges out from the mental foramen. If it is blocked in side the canal in addition to the above structures PM 1 & 2. Then it passes through the mandibular canal and supplies sensory dental and alveolar branches to the side.  Its better to have the tip of the needle slightly curved to enter into the canal. Area desensitized  The skin of the lip. canine. It emerges from the orbit through the foramen accompanied with the artery.  Site and technique . 0. and incisors with their alveoli and gum and the skin upto the inner canthus of the eye. 4 to 6 ml of the solution is deposited using along spinal needle. The site is selected medially 3 cm below the temperomandibular articulation on the posterior boarder of the mandible.  Mandibular block: The mandibular foramen is located opposite to the point of intersection of a line passing vertically downwards from the lateral canthus of the eye and another line extending backward from the tables of the mandibular teeth. face of the side upto the level of the foramen is desensitized if blocked at the level of the foramen. MANDIBULAR NERVE BLOCK Nerve  Mandibular nerve is the alveolar branch of mandibular division of the 5th cranial nerve. It supplies sensory fibres to the upper lip andpartof the skin on the forehead.5 to 2 ml may be required in dogs and 10 ml in large animals. After emerging out it is called as mental nerve and it supplies to the lower lip. SUPRA ORBITAL NERVE BLOCK Nerve  Supra orbital nerve (frontal nerve) is a sensory terminal branch of the ophthalmic division of 5th cranial nerve.  Mental block: Mental foramen is easily located on the lateral aspect of the jaw below the angle of the lip (in the middle of the interdental space) 3 to 5 ml of the solution is deposited. It enters the mandibular foramen at the medial aspect of the vertical ramus of the mandible.  In cattle with large horn a second injection is given about 1 cm behind the first to block the posterior division of the nerve.5 cm needle.  The infratrochlear nerve emerges from the orbit dorsomedially. Goats  In goats the horn is supplied by the corneal branch of lacrimal (zygomaticotemporal) nerve and corneal branch of infratrochlear nerve.  It supplies sensory fibres to the horn corium and the skin around the base of the horn.  The block is done more easily 2 to 3 cm below the base of the horn with 5 to 10 ml of 2% lignocaine.  The infratrochlear branch can be blocked half way between the medial canthus and the medial base of the horn. Dogs do not have supra orbital foramen.  The frontal nerve leaves the orbit medial to the ligament. SITE AND TECHNIQUE Cattle  As the nerve run from the orbit to the base of the horn it becomes more and more superficial. . as this block will not desensitize the perostium and sinus mucous membrane.  The foramen is palpated as a pit like depression midway between the upper and lower borders of the supra orbital process close to the frontal bone (about 6-cm dorsal to the medial canthus) 5 ml of the solution is injected with 19G x 2. Goats  The lacrimal branch can be blocked half way between the lateral canthus and the lateral base of the horn. CORNUAL NERVE BLOCK Cattle  Cornual nerve is a branch of lacrimal (zygomaticotemporal) division of ophthalmic division of trigeminal nerve.  Successful block desensitizes the upper eyelid and the frontal region.  The nerve passes through the periorbital tissues dorsally and then runs along the frontal crest to the base of the horn.  To amputate the horn at the base it is better to provide sedation. SITE AND TECHNIQUE  All these nerves except the optic nerve pass through foramen orbital.  The notch formed by the supraorbital process.  If analgesia of caudal paralumbar area is required additionally the third lumbar (L3) is blocked which result in weakness of the hind limb. third eyelid.sensory innervation to lower eyelid. . medial canthus. zygomatic arch and the coronoid process of the mandible is located and a 18G x 7 to 11 cm needle is inserted directed towards the opposite side last upper premolar until it reaches the pterygopalatine fossa. cornea and sclera and the frontal sinus  Optic nerve (II)  For enucleation of eyeball all these nerves are blocked to achieve analgesia of the eye and orbit and immobilization of the globe. PARAVERTIBRAL NERVE BLOCK  This regional anaesthesia is very important for bovine laparotomy. soft palate. maxilla maxillary sinus and adjoining bones and the region supplied by the infraorbital nerve.  The last thoracic nerve is blocked half way between the last rib and the transverse process of the first lumbar vertebra about 5 cm from mid line.  Deposit 15 ml of the solution.  The dorsal and ventral nerve roots of last thoracic (T13) and first and second lumbar (L 1 & 2) spinal nerves are blocked as they emerge from the intervertibral foramen. RETROBULBAR NERVE BLOCK  Auriculopalpebral branch of the facial nerve .  Ophthalmic branch of the trigeminal nerve . caudal part of nasal septum.sensory innervation to the upper eye lid. SITE AND TECHNIQUE  Each nerve is blocked immediately in front of the cranial border of the transverse process of the succeeding lumbar vertebra.  Anaesthetic solution is deposited anterior to the foramen.  This block does not provide desensitization of eyelids. and abducens (VI) nerves – motor innervation to the ocular muscles  Maxillary branch of the trigeminal nerve (V) .motor nerve (VII)  Oculomotor (III). An additional 10 to 15 ml can be deposited slightly caudodorsally as the needle is withdrawn. trochlear (IV). hence for extirpation of eye ball in addition to this the auriculopalpebral nerve block and infiltration of eyelids mut be carried out. the nasal cavity. and analgesia of perineum rectum.  Successful block shows analgesia of flank.Between I & II coccygeal vertebrae o Canine .  The first and second lumbar nerves can be blocked at the posterior edge of the transverse process of the corresponding vertebrae about 5 cm from the mid line. TECHNIQUE Cattle and horse  The exact position of the sacrococcygeal junction or the space between the first and second coccygeal vertebrae cn be located by palpating the borders with simultaneous pumping of the tail.  In horses the block is performed on T 18. increase in the temperature of flank.Sacrococcygeal junction between I & II coccygeal vertebrae o Equine . paralysis of flank muscles.  The anterior epidural is achieved by increasing the volume of local anaesthetic injected.  The needle pricks are made through the subcutaneous wheals. L1 and L2. to penetrate the intertransverse ligaments and 15 ml of local anaesthetic is deposited below the ligament and another 5 ml above the ligament.  This space is filled with extradural fat.Lumbosacral space  The terms high (anterior) and low (posterior) are often used to describe the level of block.  In high epidural or anterior epidural the animal will be recumbent and the motor functions will be lost. internal vertebral plexus of veins and the spinal nerves.  Injection of local anaesthetics will desensitize the nerves.  If the block extends the segment from where the sciatic nerves arises (second sacral and more cranial segments) the block is termed as anterior epidural.Lumbosacral space o Sheep and Goats . . and scoliosis towards the desensitized side. EPIDURAL ANALGESIA  Epidural space is that compartment between the duramater and the bony and ligamentous wall of the spinal canal.  3 ml of 2% lignocaine with epinephrine is injected in cows for low epidural which will induce paralysis of tail.  Normally the site is preferred after the end of cona medularis of the spinal cord. and the inner aspect of the thigh.Lumbosacral space o Swine . SITE OF INJECTION IN DIFFERENT SPECIES o Bovine .  The internal pudental nerve is found a finger width dorsal to the pulsating pudental artery. posterior medial thigh and urethral opening are achieved. pareses or paralyses due to infection and fistula formation.  A 20G x 8 cm needle is inserted caudal to this line at an angle of 20 caudal to the perpendicular. bladder. ANALGESIA FOR CASTRATION . distal colon. clonic spasms.  Local anaesthetic is injected at the rate of 1 dml for every 10 kg.  Penile relaxation and cutaneous analgesia over the anus.  Higher dose upto 120 ml of 2% lignocaine is administered in adult cow to achieve high epidural in which the cow will be recumbent for more than 4 hours.  The ischorectal fossa is prepared aseptically and an 18G x 8 to 10 cm needle is inserted and directed towards the nerve under rectal guidance 20 to 25 ml of local anaesthetic is deposited and the process is repeated on the other side. Hypotension and death are more common in pigs following epidural analgesia.  The compliation of epidural anaesthesia includes hypotension. convulsions (goats are more sensitive). respiratory collapse due to the block on higher levels.  In horses low epidural is induced using 5 to 7 ml of 2% lignocaine. INTERNAL PUDENTAL NERVE BLOCK  This block is commonly done to induce relaxation and analgesia of penis to aid in examination and treatment in cattle. just caudal to the transverse line between the cranial prominences of the wing of the ilium on either side. Swine  The site of needle placement is on the midline.  The lesser sciatic foramen is located by rectal palpation as a circumscribed depression in the sciatic ligament.  Some time the local anaesthetic is administered between sacrococcygeal or I and II coccygeal vertebrae for docking.  The block is done bilaterally on both the sides.  Sympathetic blockade and hypotension are common in high epidural.  Analgesia of rectum tail. perineum. and reproductive organs are produced. Dogs  The site of injection is lumbosacral space which is located in the middle just behind the line joining the highest points of these crests.  Skin desensitization occurs on the dorsal aspect of the proximal metacarpus.  Median nerve is blocked at the caudomedial borner of the radius just distal to the superficial pectoral muscle. 10 cm proximal to the lateral malleolus. then aspirated to ascertain that no blood vessel is punctured.  Peroneal nerve is blocked between the long and lateral digital extensor tendons on the lateral aspect of the crust.  Needle and volume 20G x 1”.  Ulnar nerve is blocked in the groove on the palmar aspect of the antebrachium between the ulnaris lateralis and the flexor carpi ulnaris muscles. 20 ml on each site.  After reaching the costochondral junction the needle is withdrawn 0.  If the leg is held.  1 to 10 ml of 2%lignocaine is injected depending on the size of the dog.5 to 1 cm. Skin desensitization involves only the medial aspect of the pasern.  The brachial plexus in the dog is best blocked on its lateral recumbancy.  An 8 to 10 cm long needle is inserted towards the costochondral junction.  The peroneal nerve has deep and superficial branches. . as in the normal positionthe correct site of needle insertion will be medial to the shoulder joint directed parallel to the vertebral column.  First the costochondral junction of the first rib is located by moving the upper limb. BRANCHIAL PLEXUS BLOCK  This block is mainly induced in dogs. Analgesia can be provided by injecting local anaesthetic into the spermatic cord or directly into the testicle.  Tibial nerve is blocked just caudal to the deep digital flexor tendon and cranial to the Achilles tendon about 10 cm proximal to the top of the tuber calcis on the medial aspect of the limb beneath the fascia. The incisional site must be infiltrated subcutaneously on the scrotum. 10 to 15 ml on each site.  Successful analgesia will show all the symptoms of radial paralysis.  Needle and volume 19G x 2”.  Skin sensation is usually lost between the bulb of the heel. MEDIAN AND ULNAR NERVE BLOCK  Median and ulnar nerve block will desensitize the carpus and structure distal to it. TIBIAL AND PERONEAL NERVE BLOCK  Tibial and peroneal nerve block will eliminate deep sensation from the hock and structures distal to it. 10 cm proximal to the accessory carpal bone at a depth of 1 to 2 cm.  The nerve lies cranial to the median artery and vein.  10-ml of 2% lignocaine is injected around the deep branch and 5 ml around the superficial branch as the needle is withdrawn.  Palmar nerve is formed by the fusion of the terminal branch of ulnar nerve and the terminal branch of median nerve  Plantar nerve is the result of bifurcation of the tibial nerve.  Two types of intravenous catheters are available.  The area of desensitization includes pastern and one third of the hoof with portions of navicular area. they are  Through the needle catheters . MODULE-11: GENERAL ANAESTHESIA .  Needle and volume 20 to 25 G x 2. PALMAR/PLANTAR DIGITAL NERVE BLOCK  The palmar/plantar nerve is desensitized in the palmar region of the pastern joint medially and laterally.  Following are the commonly used equipments o Syringes o Needles o Butterfly needles o Intravenous catheters. 2 ml on each site.  The equipment required for administration of injectable anaesthetics is minimal.5 cm.INJECTABLE AGENTS Learning objectives This module deals with  Introduction to injectable anaesthetics  Routes of administration  Advantages and disadvantages of injectable anaesthetics  Classification of injectable anaesthetics INTRODUCTION  Injectable anaesthetics can be administered through various routes. droperidol – fentanyl in cats ADVANTAGE AND DISADVANTAGE Advantages  Simple to administer  Have rapid onset of action  Useful as induction agents  Does not irritate the airways  Non explosive and inflammable  Does not pollute the theatre  Controls convulsions  Disadvantages  May induce tissue damage if not injected through appropriate route (thiopentone if administered perivascularly induce severe tissue reaction and accidental administration of xylazine through carotid artery may cause fatal). thiopentone in horses  Intramuscular e.g. intermittent positive pressure ventilation and other life saving supports.g.  Excess dose administered without calculating the dose or patient evaluation may cause toxicity.g. pentobarbitone in pigs for castration  Subcutaneous e. 12 to 16 gauge 5¼ inch catheters are used in large animals and 18 to 22 gauge catheters are used in small animals.g. It may not be possible to recover the patient without the use of specific reversal/antagonistic agents. CLASSIFICATION OF INJECTABLE ANAESTHETICS Main category Examples . ketamine in dogs  Intraperitonial e. thiopentone in cats  Intratesticular e.g. oxygen supplementation. Through the needle catheters are long and used for long term administration of fluids. thiopentone in cats  Intrathoracic e. (Refer Anaesthetic equipment) o Infusion controllers and Syringe devises (refer Anaesthetic Equipment).g.  Over the needle catheters. ROUTES OF ADMINISTRATION  Intravenous e. The narcotic and anaesthetic action is induced by the unbound fraction. Saffan.Barbiturates  Thiobarbiturate e.oxybarbiturate. Althesin Imidazole derivatives  Etomidate  Metomidate Alkylphenols  Propofol Opioid synthetic analgesics  Fentanyl citrate  Alfentanil  Sufentanil  Lofentanil  Etorphine Neuroleptanaesthetic mixture  Droperidol and Fentanyl  Fluanisone and Fentanyl  Etorphine combinations Centrally acting muscle  Glyceryl Quaiacolate relaxants Chloral hydrate -   ULTRA SHORT ACTING— BARBITURATE= >  The commonly used ultra short acting barbiturates are thiopentone sodium .  These agents are strong alkalies (11 -12 pH) and the alkalinity is due to the addition of sodium carbonate. These agents produce dose dependent action varyhing from hypnosis to general anaesthesia. . o Binding with protein depends on the drug concentration and the ptotein level. Hence care must be taken in calculating the dose of thiopentone.thiobarbiturates o Methohexitone . thiopentone sodium. thiamylol sodium and methohexitone sodium. Thiopental and thiamylal are converted into acid form.g.g. thiamylal sodium  Methylated oxybarbiturate e. o Thiopentone and thiamylal . the blood buffers neutralize the sodium carbonate. which bind with the plasma protein particularly with albumin fraction. Following administration. phentobarbital sodium Dissociative anaesthetics  Ketamine hydrochloride  Titatamine  Phencylidine Steroid anaesthetics  Combination of Alphaxalone and alphadolone e. methohexitone sodium  Oxybarbiturate e.g.g. The duration of anaesthesia varies from 5 to 15 minutes. The distribution depends on the speed and quantity injected. Thiopentone and thiamylal are administered as 1 to 5% solutions in dogs and cats and 5 to 10% solutions in horses and cattle. Separate syringes must be used for administration to prevent the formation of precipitation. bigeminy.  Respiratory effects o Ultrashort acting barbiturates induce severe respiratory depression even at clinical doses. o The recovery from anaesthesia is not due to the detoxification. premature ventricular contraction and depression/elevation/slurring of S- T segment. o It prevents and corrects ventricular arrhythmia and reduce the requirement of barbiturates. . o The amount of thiopentone and thiamylal required to produce anaesthesia vary from 10 to 18 mg/kg in small animals and 6 to 10 mg/kg in large animals. o Rapid administration results in apnea during induction. Anaesthesia is induced by administering half of the calculated as a bolus followed by slow incremental doses to abolish pedal reflex. o Lidocaine can be administered to control ventricular arrhythmia and it can act as a useful adjunct if incorporated in the anaesthetic regimen. If fluids are administered during recovery the redistributed fractions may be mobilized into the circulation resulting in further deepening of anaesthesia. it is due to distribution. biotransformation and elimination. thiamylal and methohexitone for hypoprotinemic animals. o These agents produce unconsciousness in 30 to 90 seconds as they cross the blood-brain barrier in one arm-brain circulation. o These actions are due to the reflex action secondary to the stimulation of baroreceptors and chemoreceptors and myocardial hypoxia. The dose is 3 to 5 mg/kg intravenously. Unbound fractions will be more and may cause profound depression. o Administration of oxygen will prevent further manifestations. o They increase the heart rate and peripheral resistance with reduction in cardiac out put and increasein central venous pressure. o Myocardial hypoxia may result in cardiac arrhythmia. o Methohexitone is administered as 1% solution in small animals and as 6% in large animals. From the blood it moves to the highly vascularised tissues and from there slowly redistributed to less vascularised tissues. CARDIOVASCULAR AND RESPIRATORY EFFECTS  Cardiovascular effects o Barbiturates are potent cardiovascular depressants. A small quantity injected rapidly as a bolus will produce high plasma and brain concentration resulting in narcosis and the recovery will be faster. Initially the concentration in the fat will be more. 1 .011 mg/kg I.06 - 0.04 mg/kg I.  Tranquilizers o Tranquilizers are administered to reduce the anxiety and the dose of the anaesthetic drugs o Triflupromazine .1.55—2.V (combine anticholinergics) o Diazepam .  Horses = 0. o Artificial respiration by compressing the chest and stimulation of respiratory reflex may help to over come apnea but may not be as effective as oxygen supplementation. tidal and minute volume.1.M.5 .V  Cattle 0. o Thiopentone protects the ischemic brain hence used in patients with brain injury and in cardiopulmonary bypass anaesthesia. 0. phenols and carboxylic acids through urine. hypotension and cardiac arrest.Dogs & Cats = 0.M.Dogs & Cats = 0.0 mg/kg I.V  Neuraleptanalgesics o Not safe to combine with barbiturates as the combined effects will be extreme bradycardia.C/I. ketones. o These agents do not cause prolonged decrease in gastrointestinal motility.M.Dogs & Cats = 1. 0.022 mg/kg I.V o Glycopyrorolate . o Barbiturates readily cross the placental barrier and depress fetus.M.2 mg/kg I.V o Acepromazine .2 mg/kg I. brain and in other tissues.1.M. Horses = 0.Dogs & Cats = 0.5 .1 mg/kg I.1 mg/kg I. If respiratory arrest is noticed it must be managed with oxygen supplementation and mechnical ventilation.1 mg/kg I.  Cats = 0.0 mg/kg I.2 mg/kg I. o The changes are reduction in respiratory volume.0. CONCURRENT USE OF OTHER DRUGS AND BENEFITS  Antichlolinergics o Anticholinergics are administered to reduce salivation and prevent bradycardia.V.22 .M.V/I. They are eliminated as alcohols.Dogs & Cats 0. Thiopentone is used as an induction agent in patients suffering from epilepsy. o Atropine sulphate .2. Microsomal enzymes of the liver get elevated following administration of barbiturates.2 mg/kg I.M.1 – 0. o Xylazine  Dogs = 0. However the amount of thiopentone transferred is not large enough to be detrimental to the neonate at birth. They produce sufficient muscle relaxation required for minor surgery.1 .  Narcotics .. o These agents are metabolized in the liver and to a less extend in kidney.V/I. In horses anticholinergics can be administered if they are fasted for 6 to 8 hours. o Chlorpromazine .044 mg/kg S.Dogs & Cats = 1. For continuous infusion an initial loading dose of 2 .Dogs 0.11 – 0. They should not be mixed in the same syringe because the local anaesthetics are acidic and barbiturates are alkaline.66 mg/kg S.M. .Dogs 1 ml/7 to 9 kg I.Dogs 0.3.C o Pentozocaine . o Advantages  Analgesia.30 mg/kg without premedication 10 . Anaesthesia can be induced by the intravenous administration of the solution at the rate of 1 to 2 ml/kg in horses./S. gallamine and other products can be combined with barbiturates.3 mg total dose I.Dogs & Cats 2. o In dogs . The testicles must be disposed carefully otherwise dogs may get access and die due to poisoning.55 mg/kg I. This solution is often used to castrate large boars. Use of pentobarbital is restricted to small animal and swine anaeshesia.C o Innovar vet . Cats not recommended o Methadone . . Cats not recommended o Oxymorphine .  Dose .M/S.succinyl choline. Oxygen administration and intermittent positive pressure ventilation are essential to maintain respiratory and cardiovascular functions.88 --.Dogs & cats 20 .2 mg/kg/hr. Castration is performed immediately after reaching light stage of anaesthesia by ligation of the cord and emasculation. Reduce the dose of barbiturates to 50% .3 mg/kg I.  Procaine and lidocaine o Procaine hydrochloride and lidocaine hydrochloride can be combined with thiopentone and thiamylol. Protects the myocardium and brain from ischemic changes.M/S.11 – 0.V/I.C. pancuronium.C.V.5 mg/kg is given followed by 1 . Act as antidysrhythmic agents and Provide good muscle relaxation.V/I. The standard solution is diluted and given intravenously.20 mg/kg with premedication. o Morphine .Dogs 0. LONG ACTING BARBITURATES  Pentobarbital sodium is the long acting barbiturate used in anaesthesia and is marketed in vials containing 50 mg/ml and 65 mg/ml.22 mg/kg I. Every time the needle or the catheter must be flushed with normal saline before administration of each agent.  A special preparation containing 240 mg/ml of pentobarbital is available and is used for euthanasia of animals. The solution is administered deep into both the testicles at a dose not exceeding 24 mg/kg.M. For euthanasia it is administered at the rate of 48 mg/kg (1 ml/5kg). Cats 0. 2 to 3 grams of thiopentone is added to 50 grams of glyceryl guaiacolate and 5% solution of glyceryl quaiacolate is prepared using 5% dextrose solution. Cats not recommended  Muscle relaxants o In large animals centrally acting muscle relaxant glyceryl quaiacolate (Guaifenisin) is combined with barbiturates.2 – 3. o Narcotics markedly reduce the dose of barbiturates.M/I. . systemic and pulmonary blood pressure. DISSOCIATIVE ANAESTHETICS  Ketamine hydrochloride and tilatamine are the commonly used dissociative anesthetics in veterinary field.  It can cause seizures even in patients not known to be epileptic and may occur even after 24 hours administrations. superficial analgesia and catalepsy o Involuntary spontaneous movements o Persistence of reflexes like swallowing. Salivation can be controlled by the prior administration of anticholinergics.  The depression effects of ketamine are determined in the central nucleus of thalamus.  Phencyclidine is another cyclohexamine product withdrawn from use because of drug abuse.  It induces copious salivation and lacrimation. neocorticothalamic axis and nociceptive cells in the medial medullary reticular formation.  It was first synthezied in 1963 and introduced in human anaesthesia in 1965 and in veterinary anaesthesia in 1970.Ketamine increases heart rate.  It allows the impulses to reach the cortical receiving areas but not perceived because of the depression and dissociation of limbic system and other cortical association areas. cardiac out put.  Cardiovascular effects . The cardiovascular stimulation is attributed to o Stimulation of sympathetic discharge o Vagolytic activity and o Negative inotropic effects on heart. cardiac contractility and myocardial oxygen consumption. Also the partial arterial carbon dioxide level (PaO2) will increase with reduction in partial arterial oxygen level (PaCo2).  The dissociative anaesthesia is characterized by o Profound amnesia.  Ketamine alters the central nervous system activity to sensory impulses without blocking it at spinal cord or brain stem levels.  Muscle relaxation will be poor hence must be used with other drugs which produce muscle relaxation. pharyngeal palpebral and corneal o Large dose may induce convulsions o Lack of muscle relaxation KETAMINE  Ketamine is a popular anaestheic used in veterinary and human anaesthesia due to its wide margin of safety and compatibility with other agents. peripheral vascular resistance.  Respiratory effects .The effect of ketamine on respiratory functions are increase in respiratory rate with or without decrease in tidal volume. 15 minutes later.5 mg/kg I.V and Ketamine 5 mg/kg I.  Midazolam 0.M.V. and Ketamine 20 --.M.M.1 mg/kg I.1 mg/kg I.  Acepromazine 0.0 mg/kg I. o Butorphenol 0. tranquilizers or sedatives the dose can be reduced to 5 .M.M.  Butorphenol 0.25 mg/kg I. and Ketamine 10 mg/kg I. Meditomidine 40 µg/kg I.  Ketamine maintains the uterine blood flow hence can be a useful alternative for thiopentone in cardio vascular surgery.5 mg/kg I.V o Meditomidine 40 µg/kg I.  The aims of combining ketamine with other agents are to achieve o Muscle relaxation o Eliminate side effects like salivation and recovery delirium. If it is combined with narcotics.  Meditomidine 40 µg/kg I. Meditomidine 25 µg/kg I. and Ketamine 5.M (lower dose in larger dogs) and Ketamine 10 mg/kg IM/IV o Diazepam 0.7.V  Meditomidine 80 µg/kg I.M  Midazolam 0.V  Dogs o Xylazine 1 .30 mg/kg I. and 2.M.1 mg/kg I.V  Butorphenol 0.V and Ketamine 1.2 mg/kg I.4 mg/kg I.2 . and Ketamine 20 --. and Ketamine 2.25 mg/kg I.M.V.2 mg/kg I.15 mg/kg I. o Improve visceral analgesia and o Prolong the period of anaesthesia DOSE RATE OF KETAMINE  Cats o In cats the dose of ketamine is 10 .5 mg/kg I. .  Decreases total RBC counts due to the sequestration of RBCs in the spleen  Classical stress leukogram. Meditomidine 40 µg/kg I.M.25 mg/kg I. and Ketamine 5 mg/kg I.  Not recommended for intraocular surgery as it increases the blood pressure and intraocular pressure.M.  Induces hyperglycaemia  Contraindicated in patients with increased intracranial pressure or in patients who are undergoing brain or spinal cord surgery as it increases the cerebrospinal fluid flow and pressure.M.25 mg/kg I. and Ketamine 5 mg/kg I.M. Ketamine is metabolized in the liver and certain amount is excreted as unchanged through urine.M. and Ketamine 1.M.M.V and Ketamine 5 mg/kg I.5 – 7. o The standard protocols are  Xylazine 1.5 mg/kg I.M.M.M.M. leukocytosis with lymphopenia and neutrophilia can be observed following ketamine administration.2 mg/kg I. 10 mg/kg I.V o Acepromazine 0.2mg/kg and Ketamine 1230 mg/kg I. Salivation is more marked and can be controlled by the use of anticholinergic premedication.4.V  Sheep and Goats o Xylazine 0.4.  Detomidine 20 µg/kg I.05 – 09.075 mg/kg and Ketamine 2 mg/kg I. Anticolinergic premedicationis very important while using this combination  Dossage o Cat @ 7 .M.2 . Premedication with xylazine minimizes the adverse reactions in horses.V o Detomidine 40 µg/kg and Ketamine 2.V can be combined to reduce muscle fasciculation.V  Acepromazine 0. 5 .V  Pigs o Xylazine 2 mg/kg.M.15 mg/kg I.V  Promazine 1.22 mg/kg I. Xylazine 2.5 mg/kg I.7 mg/kg I.M o (Further maintenance is done with a mixture containing 0.1 mg/kg I. To prolong the anaesthesia half of the initial dose of both the drugs must be repeated at every 10 to 20 minutes.  It induces muscle rigidity and tonic-clonic convulsions if administered alone hence it is marketed in combination with a benzodiazepine Zolazepam. Its use in horses may result in potential severe reactions. Diazepam at the rate of 0.0 mg/kg and Ketamine 1.5 mg/kg I.44mg/kg.V o Horses o Xylazine 0.15mg/kg I.2 mg/kg I.10 mg/kg and Ketamine 2.V  Cattle o Xylazine 0.V. laryngeal.4 mg/hg I.1.  Animals anaesthetized with telozol – zolazepam will respond to palpebral.0 mg/kg I.  (Telozol in USA and Zoletil in Australia) It contains 250 mgs of tilatamine and 250 mgs of zolazepam. pedal and pinnal reflexes. 5 .04 .V and Ketamine 2.V o Detomidine 20 µg/kg and Ketamine 2 .5 .V o Dog @ 10 . This combination provides muscle relaxation and a dissociative state of anaesthesia in dogs.0. Often glyceryl quaiacolate is combined with xylazine and ketamine at the rate of 50 mg/kg I. o Acepromazine 0.2 . Oxymorphone 0.4 mg/kg I. pharyngeal.5 – 2.1 mg/kg and Ketamine 2 . TILATAMINE  Tilatamine is closely related to ketamine and is two to three times potent than ketamine.V and even administered as mixture to maintain anaesthesia and this mixture gives good muscle relaxation. cats and wild animals.4 mg/kg and after 30 minutes Ketamine 15 mg/kg I.M. Horses o Xylazine 1.2 mg/kg I.V and 4 to 5 minutes after Ketamine 2.06 mg/kg and Ketamine 2.2 mg/kg I.5 to 1 ml of xylazine (100mg/ml) and 1 ml of ketamine (100mg/ml).0 mg/kg .  It selectively decreases cerebral oxygen consumption to a greater extend by reducing the blood flow. vomiting and twitching of facial muscles may occur during induction. twitching and violent kicking.3 mg/kg I. Some trials have been conducted on dogs for caesarian section.  It induces respiratory depression.  It can be used in cats for caesarian section because the neonates are less depressed at the dose of 4.0 mg/kg. Indicated in cats with head injuries.V STEROID ANAESTHETIC  Combination of alphaxalone and alphadolone is marketed as Saffan (in veterinary) and Althesin (in human).V o Pigs 4 .kg I.5 .  It may cause oedema of ear pinnae and paws in cats due to histamine release.V o Pig neonates 2 .  It poduces good muscle relaxation. All the dogs were given prior anti histaminic medication and premedicated with phenothiazines.  Dose o Cats 4 .V o Sheep 1.  Each milliliter of Saffan contains 9 mgs of alphaxalone and 3 mgs of alphadolone.  Saffan is used in cats.  Low solubility of these steroids in water made them less popular.M/I.6 mg/kg I. o Tilatamine zolazepam 0.1.3 mg/kg I.  Saffan froths in syringes due to the presence of cremophor EL and is miscible with water.  In cats it does not induce significant change in cardiac index and systemic vascular resistance.  Retching.65 . This preparation is viscid and the pH is around 7.V .  Alphadolone is another steroid which has hypnotic property and increase the solubility of alphaxalone in cremophor.6 mg/kg I.  Alphaxalone is insoluble in water and can be dissolved in Cremophor EL (polyoxyethylated caster oil).0 mg/. It is not recommended in horses.  In dogs it induces histamine release and causes severe hypotension hence not recommended in dogs.  It has got week antioestrogenic effect  It may induce laryngeal oedema  In horses it produce excitement for upto 30 minutes during induction and recovery is associated with marked tactile and hyperaesthesia. 5 .0 mg/kg I.  Dose  Birds 3 . but does not have analgesic property hence oftencombined with fentanyl or azaperone premedication.  In room temperaturethedissolved solution is stable only 24 hours. Hence it is used in dogs for caesarian section at the dose of 1. involuntary muscle tremors and hypertonus. It is not recommended in horses.2 mg/kg I.8 mg/kg) at the rate of 3.  Etomidate is recommended in high risk allergic patients who had exhibited or are expected to exhibit severe anaphylactic responses.5 mg/kg I. ALKYLPHENOLS  Propofol is a lipophilic alkylphenol (2-6 diisoprophylphenol) becoming popular in human and veterinary anaesthesia.20 mg/kg I.  Metomidate has hypnotic and central muscle relaxant property.3.  It is an oil at room temperature and can not be injected hence was formulated with Cremaphor EL (polyoxyethylated casteroil) as vehicle.2 – 0. IMIDAZOLE DERIVATIVES Metomidate  Metomidate is a non-barbiturate crystalline power belonging to imidazole group.  Etomidate like thiobarbiturates decrease the circulating cortisol concentration in hyperadrenocortism. hence can be used as safe induction agent in these patients.Cremaphor EL as .V.  In horses it was used with azaperone (0.  It is mainly used in pigs and birds.M Etomidate  Etomidate is a white crystalline power available as 20 mg dissolved in 10 ml of a mixture containing 35% propylene glycol and 65% water (v/v).V along with diazepam (0. Recovery was violent.  Premedication with fentanyl or diazepam reduces the side effects.  Intravenous injection is associatred with high incidence of spontaneous movements.V total dose not exceeding 5 mg).  It induces less cardiovascular depression and does not release histamine. 6 mg/kg/minute) o Cats  8 mg/kg I.0 mg/kg with xylazine 0. The vehicle added favors bacterial growth hence the open ampule after 6 to 12 hours must be discarded.  Recovery periods are shorter without any undesirable side effects in propofol anaesthesia half of the calculated dose in infused as a bolus and the remaining half is administered in a slow phase.  Propofol induce rapid loss of unconsciousness in 20 to 40 seconds after I.  5 .Propofol induce 20 to 40% reduction in arterial blood pressure due to reduction in cardiac output and systemic vascular resistance.V.  It is conjugated in the liver and metabolized as glucuronide and sulphate and excreted in urine.  It reduces the intraocular pressure hence can be used in patients undergoing intraocular procedures  Propofol is a good induction agent for caesarian section in dogs and cats.V.V.  Cardiovascular effects . Now the vehicle is changed and reformulated with a parental nutritional agent called as Intralipid which contains soybean oil.  Propofol can be administered in continuous infusion to maintain anaesthesia. administration due to its lipophilic nature.  Propofol does not affect hepatic and renal functions  It can be used for long term sedation and anaesthesia in intensive care patients.Propofol induce apnea and greater respiratory depression.  It is a safe anaesthetic in branchycephalic breeds of dogs.V o Rabbit = 7.V o Reptiles = 10 mg/kg .5 . with other agents induced histamine release in human and animals. in Unpremedicated (continuous infusion 0. It reported that the puppies were bright and the mother was alert enough to care the puppies immediately following recovery.  It crosses the blood-brain barrier in one arm-brain circulation and further redistributed from plasma.  Respiratory effects .15 mg/kg I. as it does not alter adrenocortical function.  The new formulation is milky in colour.V. brain and well-perfused tissues to less perfused tissues as thiopentone.V.V o Birds = 1-15 mg/kg I.(continuous infusion 0.4 mg/kg I.5 mg/kg I. glycerol and purified egg phosphatide.V o Mouse = 26 mg/kg I.4 – 0.4 mg/kg I. in premedicated.2 mg/kg/minute) o Sheep and goats = 3 . Its use is cautioned in dogs with serious volume depletion.  Dose - o Dogs  3 . inunpremedicated (continuous infusion 0.5 mg/kg I.6.51 mg/kg/minute) o Horses  2. Acepromazine 0. o Morphine is used as a postoperative analgesic for pain relief in veterinary practice.05 – 0. PURE AGONISTS . Xylazine 1.M. MEPERIDINE AND OXYMORPHONE  Pathadine o Pathadine is a vagolytic and negative inotropic drug at clinical doses. o Preservative free morphine can be administered epidurally to relieve pain. heroin (dimorphine = diacetylmorphine) and oxymorphine.5 mg/kg (total dose not exceeding 10 mg) I. . and Morphine 0.0 mg/kg I. o It is used in the treatment of congestive heart failure to relieve pain and decrease after load. pigs. Hence must be used with suitable tranquilizer.6 mg/kg I. o It is absorbed from the gut and oral mucosa.8% papaverine.V and morphine 0.  The laboratory synthesis of morphine is different hence still it is derived from opium poppy.M/I.V o Cats 0.  Dose o Horses Morphine gives good results in horses if administered after xylazine sedation. o It reduces salivation and respiratory secretion without inducing vomiting and defecation. o Morphine decreases motility of stomach with increase of antral portion.M.2 – 0. o Induce respiratory depression o Depress cough o The effects on myocardium are not significant. but produce increase in vagal tone and slowing of heart. The laboratory synthetic agents are codeine.  The exudates contains 3-25% of morphine.MORPHINE  Morphine is derived from the dried milky exudates of the unripe seed capsules of the opium poppy (Papaver somniferum). o Morphine is administered after administration of Acepromazine.C/I. must be administered with caution because it may induce CNS stimulation. horses. dogs and cattle. Initial use may cause defecation and chronic use will result in constipation. 5% noscapine and 0.1 mg/kg S.6 mg/kg I.V o Dogs 0.  Morphine acts and produces o Analgesia o Drowsiness o Produce nausea and vomiting by stimulating chemoceptor trigger zone for vomiting.1 mg/kg I.M. It induces dopaminergic excitement in cats. PATHADINE. 0. (Phenothiazines are potent antihistaminics) o Dose: Dogs and Cats 2-5 mg/kg I. o Pathadine induces histamine release if administered through intravenous route. less potent (one tenth of morphine) and used in dogs and cats.C (total dose not exceeding 4. . o It is widely used in dogs and cats for its analgesic property.  Fentanyl citrate is available alone.M  Meperidine o It is a synthetic product.4. It is not recommended in cats.0.M  Catls = 2 . (Hypnorm contains 0. o Intravenous administration causes release of histamine hence most often used along with acepromazine.4 mg of fentanyl and 20 mg of droperidol per milliliter) or fluanisone.5 mg/kg S. o Dose  Dogs = 2 .315 mg of fentanyl and 10 mg of fluanisone per milliliter) Fentanyl combinations provides good intra operative analgesia.M.  Its analgesic property is 80 times greater than morphine.4 mg/kg I.  Cardiac out put. or in combination with droperidol (Innovar vet contains 0. o It is also administered epiduraly to control pain in the hindquarters (0.V/I. o Dose  Dogs 0.03 mg/kg I.C/I.6. o The only limitation with drug is stimulation of vagus leading to bradyarrhythmias and it can be reduced or prevented with the use of antichlinergic agents in the protocol.M  Oxymorphone o Oxymorphone is a synthetic derivative having 10 times greater potency than morphine. o It does not cause histamine release as meperidine.05 mg/kg).V/I.02 .V/I.M/S.C  Horses 0.5 mg)  Cats 0. heart rate. respiratory rate and arterial oxygen tension (PaO2) are reduced following administration of fentanyl.0.0. o It is used popularly in small animal anaesthesia due to its analgesic and lack of release of histamine.05 .C/I. FENTANYL CITRATE AND ETORPHINE Fentanyl citrate  Fentanyl is a synthetic opioid product related to phenylpiperidines.  In dogs and primates it produces sedation and myosis whereas in horses it produces excitement and mydriasis.025 .4 mg/kg S.2 mg/kg I.M/S. Analgesia lasts for 4 hours.05 . Each pack of the marketed drug will be having two components. 1-Immobilon and 2-Revivon.M/I.02 mg/kg I. Preparation  Immobilon L A contains Etorphine 2. BUTORPHENOL TARTRATE AND BUPRENORPHINE  Pentazocaine o It is used as an analgesic.5 mg/500 g B.  The action of this drug can only be terminated by the administration of the specific antagonist Diprenorphine. o Penlog -Duration of analgesia 3-4 hour .V. Its general properties are similar to morphine. o Dose . o In horses it is used in the treatment of colic and administered at the rate of 0.V.Onset 1 min – one hour  Butorphenol tartrate o Butorphenol is used in horses. lofentanil and carfentanil. o In human it causes dysphoria and hallucination and pentazocaine is developed to prevent drug abuse.33 mg/kg I.  The other synthetic pure agonists are afentanil. cats and dogs. Etorphine  Etorphine is a potent synthetic morphine derivative. o Dose -3 mg/kg for 1 to 3 hours of analgesia. Separate combinations are available for large and small animals. analgesia and increase in pulmonary vascular resistance. PENTAZOCAINE.45 mg/ml and acepromazine 10 mg/ml  Immobilon S A contains Etorphine 0.0 mg/ml  Revivon S A contains Diprenorphine 0.W  Etorphine is an extremely long acting agent whose effects are maintained by enterohepatic recycling.  Dose . sufentanil. o In clinical doses it produces pulmonary vascular resistance. (see butyrophenones for other doses).  In clinical dose etorphine along may produce initial excitement hence it is marketed in combination with phenothiazine derivatives.074 mg/ml and Methotrimeprazine 18 mg/ml  Revivon L A contains Diprenorphine 3. o It produces sedation.0.  The dose of etorphine is 0.272 mg/ml  This mixture is popularly used to capture elephants and giraffes  Not recommended for domesticated and wild felines  Etorphine is extremely potent in human and any accidental injection may cause death if not treated with naloxone or diprenorphine.Dogs 0.01 . Diaphragmatic muscle is composed of mainly striated titanic fibers and not striated tonic fibers. hypertonicity of muscles and cardiac arrest. In practice.4 mg/kg I.  Concentration greater than 10% is irritant to body tissues and can induce haemolysis.02 mg/kg S.V. it is administered as 5% (50 mg/ml) solution in 5% dextrose.M.  The maximum dose of GGE is 90 to 100 mg/kg and if this dose is exceeded it will cause spasm.  It affects the polysynaptic reflexes more than monosynaptic reflexes hence it has got little action on the diaphragm.2 – 0. These mixtures are administered after routine premedication.1 mg/kg I.C  Onset 1 mint – 15 mint I.01 .  Horse = 0.0.8 mg/kg I.M/S.02 mg/kg S.V  Cats = 0. GGE dissolves readily in 5% dextrose if warmed slightly.M/I. CENTRALLY ACTING MUSCLE RELAXANTS (guaifenisin)  Glyceryl quaiacolate ether (Guaifenisin) is the centrally acting muscle relaxant and it acts on the internuncial neurons of the spinal cord.005 .  It also induces sedation and hypnosis due to its action on the reticular formation of the brain stem. Horses .0.2 – 0.  GGE is used in combination with other agents in 5% dextrose solution as induction and maintenance agent.V/I. hence GGE does not affect the diaphragm. rapid  Buprenorphine o Respiratory depression is more and often treated with intermittent positive pressure ventilation.  GGE does not cross the placental barrier due to its high molecular weight.  It does not influence the respiratory canters in brain.C/I.V  Dogs = 0.M/S.  It has got bactericidal action.C  Cats = 0.C/I.10 µg/kg  Dogs = 0. o Dose  Horses = 6 . V is administered for induction and further maintenance can be done with this mixture.V  Horse = 0. at the dose of 30 to 120 grams dissolved as 1 in 20 solution in water.0 mg/ml is the mixture used in cattle.04 .V CHLORAL HYDRATE  Chloral hydrate is used as a reliable sedative hypnotic in cattle and horses.V/I.  Chloral hydrate depresses the motor and sensory responses at sedative dose and produces cerebral and medullary center depression at anaesthetic dose resulting in muscle relaxation and depression of cardiac and respiratory system.  Dose—Naloxone-.C Horses -. hence the sedative effect is prolonged even after cessation of administration.M/S.  Induction is achieved at the dose rate of 1.0 ml/kg I.  The central nervous system depression is due to its metabolic product namely 2.02 .  Trichloro ethanol conjucates with glucuronic acid to urochloralic acid and excreted.1 mg/kg I.  It does not have analgesic property. 1. .0.75 ml/kg/hour.  GGE 50 mg/ml (5% solution) in 5% dextrose mixed with xylazine 0.0 mg/ml is the routinely used mixture in horses.  In horses naloxone is used in the control of crib biting.2 mg/kg I.2 mg/kgIV) andfurther maintenance can be done with this mixture.  GGE can be combined with thiopentone or thiamylal (1-3 grams) and administered in horses (See barbiturates) Cattle  GGE 50 mg/ml (5% solution) in 5% dextrose mixed with xylazine 0.1 mg/kg I.0.Dogs & Cats = 0.5 mg/ml and ketamine 1.V Diprenorphine.005 = 0. nalorphine hydrochloride and diprenoorphine are the opioid pure antagonists used for the reversal of the effects of pure agonists and partial agonists.  It is less expensive and still perfectly acceptable sedative agent.V) and ketamine (2.0272 mg/kg I.2 trichloro ethanol.03 mg/kg I.1 ml/kg and further maintenance is done with this mixture at the rate of 2. PURE ANTAGONISTS  Naloxone hydrochloride.  In cattle it can be drenched preferably through stomach tube.05 mg/ml and ketamine 1. Alternatively induction can be done using xylazine (1.0.2.  It has deeply penetrating aromatic odour and is bitter in taste.Dogs and cats = 0. o Xylazine 0.  Bullls that are uncontrollable and free in the yard can be controlled by water deprivation for brief period and allowing them to drink chloral hydrate dissolved water (90 to 120 grams in 12 litres of water). swelling and necrosis o Induces abortion in mares MODULE-12: GENERAL ANAESTHESIA .  Disadvantages of chloral hydrate o Prolonged hangover with ataxia and stupor o Perivascular administration causes pain.04 to 0. desflurane.5 to 2 mg/kg o Promazine 0.5 to 2 mg/kg o Chloral hydrate 100 mg/kg and ketamine 1.  It is combined with magnesium sulphate and pentobarbital and administered to horses (Equithesin mixture). cyclopropane. isoflurane and sevaflurane.At any given temperature the mass of a gas dissolved in a solution (i.e.  Chloral hydrate is administered as 10% solution intravenously in cattle at the dose of 80 to 90 mg/kg.  Their uptake and distribution determine the anaesthetic action of these inhalant agents. 7% chloral hydrate 20 to 40 mg/kg and thiamylal 1 to 2 mg/kg.  Intravenous dose of chloral hydrate in horses o Chloral hydrate alone 5 to 10 mg/kg for mild sedation and hypnosis. 20 to 40 mg/kg for moderate sedation and hypnosis.6 to 0.  The uptake and distribution depends on  Solubility coefficient .INHALANT ANAESTHETIC AGENTS AND MAINTENANCE Learning objectives This module deals with  Inhalant Anaesthetic Agents and  Its Maintenance INTRODUCTION  The inhalant anaesthetics are chloroform.  Chloral hydrate is combined with magnesium sulphate at 2:1 or 3:1 ratio (weight) and administered in cattle. halothane. 50 to 75 mg/kg for profound sedation and hypnosis and 150 to 250 mg/kg for anaesthesia.6 mg/kg. o Chloral hydrate 100 mg/kg and thiopentone 1. its concentration in the solution) varies directly with its tension .4 to 0. trilene. 7% chloral hydrate 20 to 40 mg/kg and thiopentone 5 to 7 mg/kg o Acepromazine 0. enflurane.8 mg/kg. ether. 7% chloral hydrate 20 to 40 mg/kg and thiamylal 2 to 4 mg/kg.08 mg/kg. That means the tissue – blood partition coefficient will be almost the same.  Its MAC is more than 100% in animals (Dogs 188%. Whereas halothane is almost 60 times more soluble in fat than other tissues.  Solubility of inhalant anaesthetic is defined as a concentration distribution ratio between alveolar concentration and the tissue concentration. Brain – lipid (fat) coefficient will be almost equal (2. For example the blood gas partition coefficient of nitrous oxide is 0.The inhaled anaesthetic gas is diluted in the residual air when it enters pulmonary ventilation and then distributed to alveolar membrane. potentiates the analgesia. Cats 255%). The MAC of each inhalant anaesthetic varies in each species.  Blood flow . From alveolar membrane two types of diffusion take place. The second process occurs across the capillary membrane of the lung into the interstitial fluid.47. . hence the blood partial coefficient will be lesser than the fat. and is governed by the solubility of the gas in the particular solvent. then to the cells through the cell membrane and finally into the venous blood leaving the lung (bronchial circulation).  Mininimum alveolar concentration (MAC) . This term is used to mention the potency of the anaesthetic.6) because of the lipid nature of brain. The solubility of most of the inhalant agents in brain and other tissues except fat are almost common as that of blood. In thismanner the arterial and venous tension of the anaesthetic slowly increases towards the ventual equilibrium with the inspired air. which interact selectively with opiate receptor endorphin system. The major diffusion process takes place into the pulmonary blood (pulmonary circulation) and it reaches equilibrium with alveolar tension immediately.MAC is the concentration of the inhalant anaesthetic in the alveoli to produce lack of response in 50% of the subjects to a standard stimulus. This means that there will be 47 parts of nitrous oxide inblood for every 100 parts of nitrous oxide per unit volume (litre) of alveolar air. The solubility of inhalant anaesthetics influences the induction and recovery time.  The other factors are o Physical and chemical properties of the agent o Absorption o Pulmoanry blood flow o Cardia output perfusion o Lipid content of tissues o Final elimiantion NITROUS OXIDE  Nitrous oxide is the oldest anaesthetic gas available as liquid at room temperature in cylinders (See anaesthetic equipment). Methoxyflurane is highly soluble than isoflurane in the body tissues hence the induction and recovery will be slow.  It has got good analgesic property and combining narcotics. METHOXYFLURANE . it is combined with other injectable and inhalant agents.  Nitrous oxide moves rapidly through tissues faster than carbon dioxide and diffuses into the closed cavities filled with gas such as pneumothorax and distended intestinal loops due to obstruction or strangulation and induces detrimental effects by inducing further distension.  It is eliminated rapidly from the body because of low partition coefficient and relatively insoluble nature. The ignition temperature is 304 C.92%. as it will diffuse into the rumen and results in distension and increase in transdiaphragmatic pressure.  Prolonged exposure to nitrous oxide causes bone marrow depression due to depletion of Vit.  It is used as fresh gas source or carrier gas.  It induces tachypnoea at higher concentration due to direct central stimulation. In older animals and animals maintained for a longer duration with nitrous oxide must be supplemented with oxygen.  It gives an irritating vapour and may cause salivation if not premedicated with anticholinergics. The theatre environment must have less than 25 ppm of nitrous oxide.  Nitrous oxide is administered at 66 to 70% of the total inspired air. highly volatile and inflammable liquid with a boiling point 35oC. Nitrous oxide is used as the principle anaesthetic at a level of 80% in combination with 20% oxygen for dental extraction in human.  The use of ether is decreased due to its explosive and inflammable nature.B12.  One pound of ether mixed in air can given 277 cubic feet of flammable mixture.  Health hazards are more in human exposed to ether for a prolonged period.  It is not used in ruminants. In horses prolonged administration induce distension of bowels and increase in transdiaphragmatic pressure. DIETHYL ETHER  It is a colourless.  During recovery it may induce diffusion hypoxia following prolonged administration.  Catecholamine level increases following ether administration. In veterinary anaesthesia.  The MAC is 1. Oxygen is given at 30% concentration. It helps in additional uptake of the inhalant agent and potentiate the desirable effects at a minimal concentration of the inhalant agent (Second gas effect). Hence it can cause occupational hazards to humans.  In low concentration the vagal activity is decreased and at higher concentration it induce arrhythmia. The outward movement of nitrous oxide from the alveoli reduce the alveolar partial pressure of oxygen. The expired air may contain more than 10% of nitrous oxde. which is associated with reduction in cardiac contractility.  Methoxyflurane reduce the minute volume and induces respiratory acidosis.  Concurrent use of epinephrine and adrenaline are contraindicated as methoxyflurane sensitizes the myocardium to the actions of catecholamines.  It does not alter the cardiac function much except slight hypotension.25%  The MAC is reduced when combined with agents like morphine (reduced 84%).  Halothane reacts with metal and soda lime and decomposes if exposed to ultra violet light.  Biotransformation of methoxyflurane results in fluoride ions. which are potent toxic agents to kidneys and is further aggravated by the concurrent use of tetracycline. alfentanil (48%). .9 and the specific gravity is 1. o Cats 0.  It is highly soluble in fat hence recovery will be prolonged in obese patients. xylazine and nitrous oxide.1 mmHg at 20oC.87%.  It is marketed in amphor coloured bottles with thymol. and cardiac out put.  Methoxyflurane induce dose dependent central nervous system depression. rubber and soda lime.23.  This antioxidant may accumulate in the vaporizer wick hence methoxyflurane vaporizer must be often cleaned and rinsed with diethyl ether.41 at 25oC.4 and specific gravity 1. o Dogs 0.  It has fruity odour and an antioxidant butylated hydroxyflurane is added for stability.  Halothane is a potent anaesthetic with a molecular weight of 197.  It reacts with metal.  In veterinary practice its use is restricted to small animals. its better to induce with injectable anaesthetics.  Compared to halothane the sensitization and cardiac arrhythmia are less. Though it can be used to mask induction.2-dichloro-1.1 difluoro ethyl methyl ether).9% o Pigs 1. Its molecular weight is 165.  It is non-flammable and nonexplosive.  The MAC is 0.  It can be used in most of the breathing circuits with oxygen and nitrous oxide. o Horses 0.2oC and the vapour pressure is 244. Methoxyflurane is contraindicated in patients with renal disease.  The MAC varies in various species. Methoxyflurane is a halogen-substituted ethyl ether (O2.  Its boiling point is 104oC and is non-flammable and nonexplosive.86 at 25oC. and decomposes if exposed to ultraviolet light. HALOTHANE  Halothane is colourless volatile liquid with aboiling point of 50.75%. The incidencesof hepatic necrosis are higher in goats following halothane anaesthesia. In human the rate of successful deliveries following embryo transfer or gamete intra fallopian transfer were less as compared with isoflurane. Halothane reduces cerebrospinal fluid production and pressure hence can be used in patients undergoing brain and spinal cord surgeries and in patients with increased intracranial pressure.  It is relatively insoluble hence induction and recovery are quick. . 16% reduction in plasma bilirubin and 46% reduction in biliary bile acid concentration was noticed. (21 to 22%) thus resulting in ventilation perfusion mismatch. Following binding the genes will alter the coding and non-self protein will be synthesized which may result in allergy.  Its vapour pressure is almost equal to halothane hence halothane vaporizers can be used after cleaning thymol. thus favouring higher incidences of post anaesthetic infection. The metabolic products or the intermediary products induce allergic and toxic responses similar to autoimmune diseases. It has got pungent odour. Initial conception rate was high followed by higher incidence of aborption.  It induces AV shunts (arterio-venous shunts) and is further aggrevated by hypoxia. It’s better to revaccinate horses with tetanus toxoid following halothane exposure. Centrilobular necrosis is the toxic manifestation induced by halothane in liver.  It is non-inflammable and does not react with metal.mean arterial pressure and coronary blood flow.  Halothane decreases arrhythmogenic thresholds and sensitizes the myocardium for the actions of catecholamines. Oxygen exchange is further reduced in patients with pulmonary diseases. Exogenous administration of epinephrine or adrenaline induces cardiac arrhythmia and ventricular stand still.  It does not decomposed if exposed to ultra violet light. In ponics following halothane anaesthesia 138% increase in plasma bilirubin excretion.  It suppress adrenal cortical hormone release by 50% due to its action and inhibition on the carrier .  Halothane undergoes biotransformation in the liver.mediated transport system of choline.  Halothane induces hepatic hypoxia.  Halothane suppress the number and activity of natural killer cells (NK cells) and produce immune suppression. This property is taken as an advantage in patients undergoing tissue transplantation.  Experimental studies revealed that halothane has got teratogenic and mutogenic properties.  The minute volume decreases during halothane anaesthesia due to the decreased contractility of inspiratory muscles. rubber or soda lime. ISOFLURANE  Isoflurane is the new inhalant anaesthetic widely used in human anaesthesia. anaphylaxis or autoimmune like diseases.  Halothane depress cardiac out put. The metabolic intermediary products bind with the bivalent genes responsible for self-protein synthesis in the liver. CFH2-O- CF2H (CF3)2 Type Halogenated Ether Ether Molecular weight 197.86 1.2 48. not due to myocardial depression as in halothane.5 187. It increase the myocardial perfusion by reducing the coronary vascular resistance. Hence it is recommended in patients with cardiac diseases.gr. Still trials are conducted in veterinary anaesthesia. SEOFLURANE  It is the newest inhalant anaesthetic used in humans. It has little or no action on sensitizing the myocardium for the actions of catecholamines.0 Sp.4 184. 32% 239.  It induces more respiratory depression than halothane and results in hypoventilation. 1.  It has better muscle relaxation property than halothane and does not promote convulsions.50 Preservative Thymal Not required Not required Reaction Soda lime Yes No Yes U.  It does not interfere with of central autoregulation of blood pressure. Light Yes No Metal Yes No No Boiling point C@ 760 mm 50. 31% . PROPERTIES OF INHALANT ANAESTHETICS Property Halothane Isoflurane Sevoflurane Formula CBrCIH-CF3 CF3-CHCl-O. hence indicated in patients with head injures. Reduction in blood pressure is noticed during isoflurane anaesthesia due to the reduction in peripheral vascular resistance.V.  Only 2% are metabolized in the liver due to its relative insolubility.  It provides cardiac stability.5 Hg -Vaplour pressure (mm hg) 243. hence recommended in patients with liver diseases. Pulmonary during anaesthesia monitoring INTRODUCTION  Pre.2 for parameters). pulmonary and CNS and body temperature.0 255. cardiovascular.23 - Nitrous oxide 188.2 2. TABLE 1  Normal physiological.37 2. respiratory and hematobiochemical parameters of domestic animals (Dog. fluid and electrolyte balances.86 0.  The monitoring procedures are aimed to assess the functions of cardiovalscular.63 1.31 Methoxyflurane 0.  Intraoperative monitoring must be carefully done because during this stage the anaesthetic drug will act on various compensatory mechanisms and surgery will be having its effects on physiology and anatomy of the patient (See Table - 1 and Table .12 Isoflurane 1.0 - MODULE-13: MONITORING ANAESTHESIA Learning objectives This module deals with  Pre operative patient monitoring  History  Physical and Clinical Examination  Functions of CNS. Cardio vascular. intra and post operative monitoring are most important for the final out come of anaesthesia and surgery. MAC OF COMMONLY USED INHALANTS Agent Dogs Cats Horses Halothane 0.88 Enflurane 2.98 0.28 1. horse and cattle) .23 0. cat. 39.17.60 50 .12 2-4 T.600 PaO2 mm Hg >100 >100 85 .350 200 .90 47 .5 .42 8 .15 11 .20 15 .140 90 .40 .5 Globulin g/L 26.2 37 .130 120 .8.5 6.70 60 .7.200 120 30 .S.19 8 .45 HCO3 mmol/lit 20 .7.22 24 .120 90 .7 .mm 9 .110 100 .110 115 .35.ml/kg 75 .40 30 . Parameters Dogs Cats Horses Cattle Rect.45 32 .150 Diastolic 80 .100 80 .66 65 .7.4 30 .100 Mean 100 .350 150 . Temp 0C 37.12.2 37.7.100 Blood pressure mm of Hg Systolic 120 .700 .7. rate/min 10 .55 25 .32 20 .28 Hb g/dl 14 .46 ESR mm/hr 1-5 7 .16 RBC x 10 cu.35 30 .85 75 .46 7. Protein g/dl 6 .30 24 .5 7 .140 120 .7.10 N% 65 .30 L% 20 .7.8 Fibrinogen mg/ml 200 .50 pH 7.35 Tidal volume ml/kg Minute volume ml/dkg/min 170 .120 Resp.37 30 .40 60 .49 35 .43 7.8 6 .240 Blood vol.100 65 .4 .5 Albumin g/L 26 .60 25 .34 .25 .90 80 .40.45 80 .110 PaCO2 mm Hg 28 .45 7.49 38 .27 .70 55 .34.120 Cardiac output ml/kg 100 .5 6 .5 .25 17 .110 85 .8 .39.27 2 .5 8 .39 Heart rate/min 70 .15 5.52 24 .60 70 .mm 10 7 WBC x 10 cu.65 E% 2-5 2-5 2-5 2-5 M% 5 5 5-6 5 B% <1 <1 <1 <1 PCV % 40 .400 50 .13 10 .30 400 300 .38 38 .200 35 .25 30 . 37 1.160 60 .46 .75 BUN mg/ml 10 .120 Diastolic 60 .57 .120 80 .850 97 .55 2.3.110 75 .102 6 .3 Icterus index.7 .8.30 10 .120 80 .44 .3 .71 .1.40 Heart rate/min 70 .412 692 .5 2.81 17 +/-2 TABLE 2  Normal physiological.132 Lactate dehydrogenase IU/L 45 .77 Total cholesterol mmol/l 3.118 70 .28 20 .Blood glucose mg/ml 65 .37 .230 66 .84 .120 75 .99 2.2 0.8 Calcium mg/L 10.1.4.23 14 .07 .233 63 . goat and pig) Parameters sheep goat pig Rec.184 Blood vol.5.80 60 .273 100 .71 36 .70 55 .450 Sorbitol dehydrogenase IU/L 4 .35 4 .55 7.80 Bilirubin mmol/L (total) 1.55 Cortisol nmol/L 27 .89 2. respiratory and haematobiochemical parameters of domestic animals (Sheep.1 3.20 6 .130 60 .188 150 .17 .13.100 .8.5.460 100 .80 Mean 80 . ml/kg 55 .200 Cardiac output ml/kg 110 .109 Potassium mmol/L 4.90 50 .143 Chloride mEq/L 98 .2.445 Creatinine kinase IU/L 14 .30 Creatinine mg/ml 0.unit 2-5 2-5 5 .4.11 ALT (GPT) IU/L 21 .8.115 45 .0 . temperature 37 .5 .80 60 .1 .6.1.43 226 .3.110 90 .59 1.40 38 .25 25 .32 0.30 AST (GOT) IU/L 23 .34.28 20 .66 26 .2 .94 .9 .3.30 Sodium mEq/L 130 . cardiovascular.188 9 .130 70 .366 78 .15 Bile acids umol/L 0-5 0-5 5 .20 5 .40 38 .100 Blood pressure mm Hg Systolic 80 .83 3 .4 0. 38 30 .rate/min 15 .4 3.84 Lactate dehydrogenase IU/L 238 .ml/kg 7-8 7-8 11 Minute vol.7.64 Fibrinogen mg/ml 100 .71 .07 .53 7.58 AST (GOT) IU/L 167 .122 N% 25 .7.9 .40 33 .27 Hb g/dl 8 .884 .71 .1.10 8 .5 .50 T.S.57 27 .39 79 .41 .440 123 .37 0.95 75 .49 52 .55 55 .7 Icterus index (unit) 2-5 2-5 2-5 Total Bilirubin mmol/I 1.83 31 .mm 7 .68 0.7 .97 2.6.5 Albumin g/L 24 .80 50 .8.7.16 8 .16 RBC x / cumm 11 7 WBC x /cu.71 0 .50 T.65 50 .392 380 .75 85 .500 Blood glucose mg/dl 50 .14 10 .30 Creatinine mg/ml 1.5 .100 85 .42 .48 7.38 32 .634 Potassium mmol/L 3.1.7.30 35 .59 1.25 10 .1.89 Globulin g/L 35 .3.1. Protein g/dl 6-8 6.20 10 ..6.35 L% 60 .Resp.80 PaCO2 mm Hg 30 .46 20 .12 15 .133 300 .20 10 .7 4.400 PaO2 mm Hg 75 .6 .28 24 .40 ALT (GPT) IU/L 24 .93 .7.500 100 .150 BUN mg/dl 8 .1.40 30 .30 27 .5 6.5.cholesterol mg/dl 1.60 M% 5 5 5-6 E% 2-5 2-5 2-5 B% <1 <1 <1 PCV % 30 .513 32 .ml/kg/min 100 .4 .40 Ph 7.45 Tidal vol.40 15 .38 .43 .55 0 .1.35 .50 Bicarboante mmol/L 21 .400 100 . rectal temperature. examination of lymph nodes. History of the present illness  Details of the duration of illness. clinical signs and severity of illness are collected. application of cetoparasiticide etc. poisoning. pulmonary. In diabetic patients half of the insulin dose is administered after stabilization).. anaesthetics administered. breed.g thiopentone is used as induction agent in patients with the history of epilepsy. (e. . reflex status. age and other identification marks. horse that suffered from myocarditis will be an anaesthetic risk patient. hepatic. HISTORY Identification  Identification includes the details of species. PHYSICAL AND CLINICAL EXAMINATION  Physically examination includes general body condition. auscultation. medication.Cortisol nmol/L 62+/-10 65+/-8 82+/-3 PRE OPERATIVE PATIENT MONITORING--  Preoperative assessment of the patient is done for the safe administration and maintenance of anaesthesia. Previous medical history  This includes the collection of detils regarding the previous illness. sex.  It will help in tailoring a suitable anaesthetic regimen suitable for the patient. location of the lesion and weight of the animal. renal functions and haemato biochemical and electrolyte balances (eg. integument. Main complaint  The main complaint is detected to find out whether the disease condition will interfere with the normal anaesthetic practice and to tailor suitable anaesthetic regimen. deworming. pulse and respiratory rates. vaccination. percussion. appearance of the mucous membrane. measurement of heart.  The importance of preoperative assessment o To prepare the patient for safe administration of anaesthesia o To assess the cardiovascular. palpatin.  This relfex is abolished in stage III anaesthesia. X-rays and other special examinations. PALPEBRAL REFLEX .  Weight calculation o Horse = (Heart girth cm. where as with halogenated inhalants it disappears even in the light plane of anaesthesia.  The following reflexes are assessed o Pedal reflex o Palpebral reflex o Corneal reflex o Lacrimation o Yawning o Swallowing reflex o Laryngeal reflex o Anal reflex o Pupillary reflex o Eyeball position o Hearing sense PEDAL REFLEX  This reflex is elicited by applying firm pressure on the interdigital skin in dogs and cats. renal gastrointestinal. squeezing the claws to gather in cattle and swains and firm pressure on the pastern on horses. drugs used and cerebral blood flow.  Pedal reflex is reliable in barbiturate anaesthesia to assess the depth of anaesthesia. INDIRECT MONITORING  Indirect monitoring of CNS function is assessed by the reflex status. Further tests-. Presurgical laboratory examination  It includes the determination of a complete blood count and total plasma protein. hepatic. central nervous system.63. pulmonary.Includes ECG. endocrine and musculoskeletal functions.7)/0. Systemic examination  Systemic examination includes the assessment of cardiovascular. The reflex status is modified by the stages of anaesthesia.38 = body weight in Kg. SWALLOWING AND LARYNGEAL REFLEX Swallowing reflex  This reflex disappears at the light plane of anaesthesia with exception of young foals. Sterile mineral oil or plain eye ointment must be instilled to prevent corneal ulcer.  Corneal reflex is not abolished during ketamine anaesthesia.  In horses absence of corneal reflex indicates deep plane of anaesthesia.  Palpebral reflex is not abolished during ketamine anaesthesia CORNEAL REFLEX  This reflex is stimulated by gentle palpation of the cornes on the lateral aspect. Yawning  Dogs under light plane of anaesthesia yawn when the mouth is opened.  It is abolished in the light plane of anaesthesia in dogs where as in horses sluggish response can be noticed even at surgical plane of anaesthesia when inhalants are used.  Tapping the skin at the medial canthus or running the finger along the eyelashes stimulates this reflex. It may result in keratitis and ulceration. in dogs its not reliable and in cattleit may be abolished by repeated stimulation. LACRIMATION AND YAWNING Lacrimation  In horses and cattle lacrimation is reduced during deep plane of anaesthesia. ANAL REFLEX . leading to drying of cornea. In cats local anaesthetic is sprayed on the larynx to prevent laryngeal spasm before intubation. Laryngeal reflex  This reflex is abolished in the light plane anaesthesia except with ketamine induction.  The response is observed by the closure of eyelids. This reflex is protected in ketamine anaesthesia.  E.  In horses it is abolished soon after induction with ketamine.g. Atropine induces pupillary dialatation and narcotics induce constriction in dogs. Hearing sense  It is the last sense to disappear during induction and the first sense to reappear during recovery.  This reflex is abolished in the middle of III stage of anaesthesia in dogs and cats. PUPILLARY REFLEX  In general the pupil in unpremedicated animals will dialate during early excitement phase and then constricts progressively upto surgical anaesthesia. then gradually rotates dorsally and finally fix to the central position.  In small animals the eyeball rotates medially and ventrally in the early stages and then centrally placed at plane I surgical anaesthesia when inhalants like halothane or isoflurance is used.  Premedicants alter the papillary reflex.  In ruminants the eyeball rotates ventrally in light plane of anaesthesia. OTHER REFLEXES Muscle relaxation  It will be modified with the use of anaesthetics and muscle relaxants. EYEBALL POSITION  The position of eyeball depends on the species and the anaesthetic used. ELECTROENCEPHALOGRAPH .  In small animals the jaw tone is used as the criteria of muscle relaxation and anaesthetic dept.  Again the pulil will dialate as the animal enters into the IV stage of anaesthesia (progressive medullary paralysis) followed by respiratory and cardiac arrest.  This reflex is elicited by sudden gentle manipulation of the anus and the response will be sphincter contraction.  In horses under halothane anaesthesia nystagmus is common during light plane of anaesthesia and it is centrally placed at the surgical plane of anaesthesia. TACHYCARDIA . hyponatremia and at excessive depth of anaesthesia it becomes high voltage and low frequency. duration 15 to 30 minutes o Ephedrine 0. oesophageal stethoscope.  The normal EEG pattern is low voltage high frequency activity in the activated state of brain.5 mg/kg I.  The alteration in heart rate must be simultaneously compared with cardiac output and blood pressure. electronic heart rate meters.4 ti 1. hypoglycemia. 75 bpm in horses and ruminants are considered as high heart rate.  Then it become isoelectric (burst suppression) as the condition worsened and finally becomes complete inactive. o Dopamine 2. duration 15 to 30 minutes. BRADYCARDIA  Bradycardia may arise due to o Excessive depth of anaesthesia o Excessive vagal tone (often increased by intubation vasovagal reflex and traction of abdominal organs) o Terminal hypoxia o Endogenous and exogenous toxaemias o Conduction disturbances in myocardium o Hyperkalaemia o Hypothyroidism Treatment o Administration of atropine or glycopyrrolate. electronic stethoscope.  Heart rate above 250bpm in dogs.5 to 20 ug/kg/min (20 to 200 mg in 250 to 500 ml of 5% dextrose or saline)I. o Isoproterenol 5 to 10 ug/kg/min (0. o Mephenteramine 0.  Intracranial pressure also provides valuable information regarding the cardiovascular and pulmonary system and underlying disease. elecrocardiography and Doppler blood flow detector.V.  Heart rates below 50 to 60 bpm in dogs and cats. HEART RATE  Heart rate can be monitored by using stethoscope.05 to 0.V. hypothermia.V.5 to 20ug/kg/min (40 to 200 mg in 250 to 500 ml of 5% dextrose or saline )I.V.V.75 mg/kg I. Cardiovascular Functions. 25 bpm in horses and ruminants is considered to be low heart rate. 300 bpm in cats. o Dobutamine 2.0 mg in 250 to 500 ml of 5% dextrose or saline )I.1 to 0.  During cerebral hypoxia.  Other forms of arrhythmia o Premature atrial contraction o Premature ventricular contraction o Pacemaker actrivity o Bundle branch blocks  Premature ventricular contraction may progressively lead to ventricular tachycardia and fibrillation. tachycardia and atrioventricular conduction block and all these conditions may response to the treatment suggested for bradycadia. o Variable diastolic ventricular filling o Electromechanical dissociation of heart. The other arrhythmia are sinus bradycardia. Tachycardia m ay arise due to o Light level of anaesthesia o Hypovolaemia o Hypoxia o Hypercarbia o Hyperthyroidism  Normally pulse rate may either be equal or slightly deficit of heart rate because all the contraction may not produce palpable effective wave and waves may overlap.  The abnormal conditions which causes deficit of pulse rates are o Premature contraction. HEART RHYTHM  Supraventricular and ventricular ectopic pacemaker activities are common during general anaesthesia.  The atrial and ventricular premature contraction may be caused by o Too light level of anaesthesia (due to the release of catecholamines) or due to deep plane or anaesthesia (due to hypoxia and hypercapnia) o Hypoxia and hypercapnia o Hypovolaemia and hypotension o Exogenous catecholamine therapy o Digitalis toxicity potentiated by hypokalemia o Hypokalemia potentiated by respiratory or metablic alkalosis or insulin therapy o Hypercalcemia potentiated by respiratory acidosis o Anaesthetics sensitizing the myocardium for the actions of catecholamine activity (halothane and xylazine) o Endocarditis and myocarditis o Endocardial stimulation by the catheters or epicardial stimulation by the tubes or surgery . 05 to 0. o Check the oxygen supply and maximize the inspired oxygen level.  Lignocaine 1 to 5 mg/kg I.3 mg/kg I.  Procainamide 1 to 5 mg/kg I.05 to 0.V  Verapamil 0.V  Propranolon 0.V  The other ECTG abnormalities are o Change in the rhythm o Change in the configuration of PQRST o Absence of P wave or shortened P – R interval (Right ventricular hypertrophy.V. Bundle branch block and ventricular premature contraction all will show bizarre – locking ORS o Abnormal T wave (tent shaped) due to hyperkalemia and hypoxia o Depressedor elevatedor slurred S – T segment due to myocardial hypoxia. ECG lead placement in anaesthetized animal (LEAD II) Small animals RA Right arm or any where on the body rostral to the heart LL Left hind leg or any where on the body caudal to the heart LA Left arm or any where on the body (ground) Large animals RA Right arm or low on the chest towards the sternum (negative pole) LL Left hind leg or on the chest above the spine of scapula (Positive pole) LA Left arm or on the neck (ground) VENTRICULAR PERFORMANCE .15 mg/kg I. o High preload or afterload o Severe hypothermia o End stages of visceral organs function o Increased intracranial pressure and intracranial diseases  If the premature ventricular contraction is persistent with heart rate exceeding 180 to 200 the following treatments must immediately be adopted. o Administer anyone of the following. (10 ml/kg/min in circle system and 200 ml/kg/min in nonbreathing system) o Institute intermittent positive pressure ventilation o Start fluid aministration o Discontinue the agents which results or lower the threshold for the onset of arrhythmia. anaesthetics. PERIPHERAL PERFUSION  It is assessed by the colour of the mucous membrane and the capillary refill time.5 to 20 ug/kg/min (40 to 200 mg in 250 to 500 ml of 5% dexotrose or saline) o Dobutamine 2. myocardial weakness.5 to 20 ug/kg/min (40 to 250 to 500 ml of 5% dextrose or saline) o Mephenteramine 0. o Digitalis o Amrinone (new inotropic agent ) 0. execessive or insufficient end-diastolic filling volume.  Indocyanian green a dye is injected into the right atrium at a known concentration.  The normal capillary refill time is less than 2 seconds. and can be assessed by the loudness on auscultation using ordinary stethoscope or oesophageal stethoscope or heart sound amplifier. pericardial tamponade or pericardial fibrosis) o Decreased contractility o Excessive bradycardiaand arrhythmis o Regurgitation and retrograde flow o Stnosis o Positive inotropic drugs are administered to correct the cardiac output.  The thermodilution catheter is inserted into the right atrium through jugular vein using fluoroscopy or blindly (flow directional balloon catheters are used for blind methods).V. severe metabolic disturbances. .  Ventricular performance can be improved by o Dopamine 2. Ventricular performance is the contractile force of the heart.1 to 0. endo and exogenous foxins.  In thermodilution technique iced saline or saline in room temperature is administered in the right atrium and change in the temperature is assesses at downstream using thermodilution catheter located in the pulmonary artery.  Diminished heart sound is due to hyproventilation.  The causes for reduced cardiac output o Insufficient venous return o Ventricular restrictive diseases (hypertrophy.  The change in the concentration at the down stream (pulmonary artery or aorta) is measured and the cardiac output is calculated.V o Calcium chloride 10% 0.V (peak effect in 10 minutes and the duration is 30 to 120 minutes) CARDIAC OUTPUT  Cardiac output can be measured by dye dilution technique or thermodilution technique.75 to 3 mg/kg I. hypoxia.75 mg/kg/I.1 mg/kg. I. common digital artery  Cattle Middle coccygeal artery.  Indirect technique o In indirect technique a cuff is placed snugly around the limb or tail and inflacted until the blood flow is occluded. metatarsal artery. o The extraluminal pressure just to occlude the blow is considered as the pressure. electromagnetic flow probes. dorso metatarsal artery.l lingual artery  Horses Facial artery. BLOOD PRESSURE  Blood pressure is one of the important parameter to be monitored during anaesthesia because adequate blood pressure is needed to perfuse the brain and heart.  The other methods to assess the peripheral perfusion is by the use of ultrasonic Doppler. nuclear magnetic resonance and position emission tomography. o A transducer is placed in machines to record both diastolic and systolic pressure. which is above the systolic pressure.  The reasons for reduced peripheral perfusion o Stress induced increase in sympathetic tone o Hypovolemia o Low cardiac output o Fear and pain o Exogenous alpha – Receptor agonist catecholamine therapy.  A minimum 50 to 60 mm of Hg mean arterial blood pressure (MAP) is to be maintained for coronary and cerebral perfusion. o The first sound represents systolic pressure and the muffing or disappearance of the sound represents the diastolic pressure. o Cuff Placement  Dogs above the elbow  Horses Coceygeal artery  Sheep and goats above the elbow or around the tibia  Direct technique o direct method of blood pressure measurement is done by catheterization of a suitable artery and connecting it to an aneroid manometer to assess the mean arterial pressure. o Pediatric cuffs are well suited for veterinary use. o The flow can be assessed by direct palpation of the artery (only for systolic pressure) or by auscultation for Korotkoff sounds. As the cuff pressure is reduced the flow will restore. o Catheterization of artery  Dogs femoral artery. radionuclide imagery. median auricular artery .  Arterial blood pressure can be measured by o Direct and Indirect techniques in animals. Pale mucous membrane and prolonged refill time are due to reduction in perfusion. The MAP is always close to the diastolic pressure.5 g/dl further volume replacementis done only by plasma or dextran.  (See Anaesthetic emergenices) CENTRAL VENOUS PRESSURE  Central venous pressure (CVP) is the luminal pressure of the intra thoracic anterior vena cava or right atrium. o The normal systolic. 25 to 35 cm of H2O in anaesthetized recumbent horses and 5 to 10 cm ofH2O in cattle.  Lactated Ringer’s 10 to 40 ml/kg is administered over a period of 10 to 30 minutes. TREATMENT OF HYPOTENSION  Discontinue the anaesthetics and adjuncts. Systolic pressure below 80 and mean arterial pressure below 60 mm of Hg are considered as hypotension and will result in poor cerebral and coronary perfusion. sheep and goats. 60 to 100 and 80 to 120 mm of Hg respectively.  The nomal CVP is 0 to 10 cm of H2O in small animals. which induces hypotension and use the agents like diazepam and ketamine.  During anemia and hypoproteinemia crystalloid solutions are not administered. diastolic and mean arterial pressure is 100 to 160. During major procedures like thoracotomy. If the PCV is less than 20% blood is indicated and if the total serum protein is less than 3 to 3. . o The mean arterial pressure can be calculated from systolic and diastolic pressure using the formula: o MAP in mm of Hg + Diastolic + ((Systolic – diastolic)/3) o The mean blood pressure is not the half of the total of systolic and diastolic pressure.  Increase in CVP could be noticed in reduced cardiac output vascconstriction and hypervolemia. t to 15 cm of H2O in awake horses.  Sheep & goat Auricular artery  Cat Superficial musculocutaneous branch of femoral artery.  The central venous catheters are positioned through percutaneous catheterization of jugular vein.  The zero level of the manometer is maintained at the heart level. fracture repair and laparotomy it can be increasedupto 20 ml/kg.  Multielectrolyte sodium containing crystalloid replacement solutions can be administered routinely at the rate of 10 ml/kg/hr plus 2 to 3 times the volume of estimated blood loss.  Sympathomimetic drugs are used in extreme hypotension with caution and continuous monitoring as they may induce cardiac arrhythmia. The difference between the systolic and diastolic pressure is called as pulse pressure.  Hypocapnia in anaesthetized patients may resulting apnea. right ventricle to reach the pulmonary artery bifurcation. PULMONARY ARTERY PRESSURE AND WEDGE PRESSURE  Pulmonary artery and wedge pressures indicate the functional capacity of the left side of the heart.  In anaesthetized patients each respiration must be long and large to satisfy the ventilatory requirement and oxygen demand. o Biot’s breathing: characterized by cyclic hypoventilation and apnea and this pattern is also a sign of serous medullary disturbance.  Pulmonary wedge pressure is recorded when the balloon is in inflated condition and pulmonary artery pressure isrecorded when the balloon is in deflated condition.  Fluid therapy is indicated when increase in CVP is noticed with heart failure.  During spontaneous ventilation the pulmonary artery and wedge pressure will decrease. CVP decreases during vasodilatation.  The pulmonary wedge pressure is 3 to 8 mm Hg.  Increase in pulmonary artery and wedge pressure is observed during positive pressure ventilation.  Anaesthetic depression and hypoxia  Medullary dysfunction  The altered breathing patterns are o Apnea due to medullary dysfunction o Diaphargmatic breathing: during respiration the diaphragmatic component precedes and thoracic component. hypovolemia and obstruction to venous return. BRADYPNEA  The reasons for bradypnea are  Cerebral oedema. Pulmonary artery diastolic pressure will almost be equal to wedge pressure.  A flow directional balloon catheter is inserted into the jugular vein to pass the right atrium. neoplasia or haematoma. o Cheyne – Stokes breathing: It is characterized by cyclic hyperventilation and hypoventilation due to the delay in medullary response to changing carbon dioxide tension. mitral insufficiency and excess pulmonary venous pressure.  Normal pulmonary artery systolic and diastolic pressures are 20 to 40 mm Hg and 5 to 10 mm Hg respectively. . Pulmonary Functions-----RESPIRATORY RATE  Carbon dioxide is the primary chemical stimulant of respiratory centers to maintain normal respiratory pattern. indicative of fluid bubbling sound .  During surgical procedures apnea may develop due to o Spinal cord oedema secondary to CSF tapping o Injection of contrast agents for myelography o Due to neuromuscular blocking agents o Deep anaesthesia.  The abnormal ventilatory efforts are o Exaggerated breathing effort. o Agnoal gasps: Characterized by periodic retraction of the hyoid apparatus and gasping through the mouth may or may not associate with diaphragmatic contraction.indicative of upper airway obstruction o Wheezing. o Stertorous.indicative of respiratory stimulation. gravid uterus and pyometra o Atelectasis and airway collapse o Anesthetic drugs like ketamine.  Reasons for tachypnea o Hypercapnia o Hypoxia o Hypotension o Hyperthermia o Too light level of anaesthesia inducestachypnea and hyperventilation o Too deep anaesthesia induces tachypnea and hypoventilation o Airway obstruction resultsiln tachypnea and hypoventilation o Pneumothorax. diazepam and certain narcotics.indicative of lower airway narrowing o Crepitation. easy. haemothorax and diaphragmatic hernia o Space occupying abdominal lesions such as gastric/intestinal tympany. Treatment o Proper intubation o Articifial ventilation oncein 30 seconds in case of apnea o Institution of intermittent positive pressure ventilation o Sighing of the patient once every minute (squeezing the rebreathing bag) NATURE OF VENTILATORY EFFORT  The normal respiratory effort is smooth. TACHYPNEA  Elevated respiratory rate (tachypnea) may be associated with normoventilation or hypoventilation. neoplastic mass. ascitis. oApneustic breathing: This pattern is associatedwithbrain stem disease and is commonly seen in ketamine anaesthesia. regular and comprised of thoracic and diaphragmatic movements. chylothorax. hydrothorax. cardiac arrest and intrathoracic lesions.  If cyanosisis noticed during anaesthesia immediately the oxygen supply must be checked for the correct delivery.  The syringe is kept in ice and sends for analysis using blood gas analyzer. COLOR OF MUCOUS MEMBRANE  Cyanosis indicates severe hypoxemia. Minute volume below 100 ml.indicative of upper airway obstruction o Predominance of diaphragmatic component during inspiration-indicative of deep anaesthesia.  PaCO2 above 45 mm Hg indicates hypoventilation.  PaCO2 above 60 mm Hg indicates severe respiratory acidosis  PaCO2 less than 20mm Hg indicates severe respiratory alkalosis and decreased cerebral blood flow  PvCO2 (venous) will be 2 to 5 mm Hg greater than PaCO2.  The other reasons for cyanosis are shock.kg/min is considered as hypoventilation and above 300 ml/kg/min as hyperventilation.  The normal ventilation is 150 to 250 ml/kg/min. Partial pressure of carbon dioxide (PaCO2)  The normal PaCO2 is 35 to 45 mm Hg.  The oxygen is supplied at the rate of 10 ml/kg/min in circle system and 20 ml/kg/min in nonrebreathing system.  PaCO2 indicates the ventilatory status of the patient  PaCO2 level can be used to calculate the alveolar partial pressure of oxygen (PAO2) using the formula o PAO2 = FiO2 x ( P B – P H20 ) – PaCO2 / R . PaCO. o Intercostal retraction during inspiration. VENTILOMETRY  Measurement of ventilation volume is ventilometry. hypothermia.  Drugs like acetaminophen induces cyanosis in cats and benzocaine induces cyanosis in dogs and cats.  Visual observation suggests the volume roughly.  Ventilometers are fitted on the expiratory side of the breathing circuit will indicate the tidal and minute volume. BLOOD GAS  Arterial blood is collected in 2 ml heparinized syringe with 22 to 25 gauge needle and the needle is corked or the needle guard is replaced immediately.  PaCO2 less than 35 mm Hg indicates hyperventilation.  During anaesthesia drop in temperature could be noticed due to the reduction in metabolic rate. .  FI02 – Fractional concentration of inspired oxygen (normal air contains 21% oxygen hence it is 0.  Premedicants like acepromazine deplete the catecholamine in the thermoregulatory center and render the animal to pick up the environmental temperlature. TEMPERATURE  Recording body temperature is important in anaesthetized patients as it indicates the systemic function. not for all acidotic conditions.(See hypothermia and hyperthermia in Anaesthetic complication) URINE OUTPUT  It is an indirect assessment of visceral perfusion. decreased ionized calcium.Respiratory quotient. nausea. Urinary catheters are placed aseptically and the urine is collected.  Pa02 less than 60 mm Hg indicates hypoxia and hypoventilation  Animals breathing enriched oxygen mixture will be having higher Pa02  Pa02 indicates the oxygenating capability of the lung METABOLIC ACIDOSIS  The pH will indicate the metabolic acidosis and is attributed to the lactic acidosis secondary to inadequate tissue perfusion due to vasoconstriction.  The amount of bicarbonate in mEq to be administered is calculated as base or bicarbonate deficit x 0.  The temperature can be recorded at deep rectum.3 x body weight in kg (approximately 1 to 5 mEg/kg). vomiting. hyperthermia or infusion of acidotic fluids. hypokalemia.8 (ratio of carbon dioxide production to oxygen consumption) Partial pressure of oxygen (PaO2)  The normal PaO2 is 90 to 100 mm Hg. cervical oesphagus.  R .21.  The commercially available bicarbonate powder is equal to 12 mEq per grams. it is a constant.  Bicarbonate is administered only for the patients having bicarbonate deficit.  PH20 – Water vapour pressure (47 mm Hg when the air is fully saturated at 37oC) given in the blood gas report. hypotension. hypotension. collapse and even cardiac arrest.  Bicarbonate solution must be administered slowly because rapid administration may cause alkalemia. which is equal to 0. pharynx and under the tongue.  PB – Barometric pressure (normally 760 mm Hg at sea level) given in the blood gas report. misconnected gas lines and kinked or plugged endotracheal tubes. tachycardia and shock. Mannitol (0. MODULE-14- Anaesthetic Emmergencies & its management - REASONS FOR ANAESTHETIC EMERGENCIES  Human error o Not familiar with the equipment and anaesthetic drug and its action. incorrect route of administration and wrong medications. hyperventilation due to inadequate anaesthesia and ventilatory depression.  The other agents administered to induce diuresis are o Furosemide 5 mg/kg diuresis occurs in 5 to 10 minutes o Glucose.  Ventilatory problems o Hypoventilation due to anaesthetic over dose.  Circulatory problems o Hypotension. bradycardia.5 g/kg over 20 to 30 minutes) as infusion o Dopamine 1 to 5 µg/kg/min. empty cylinders. miscalculation of dose.  Equipment problems o Failure to deliver oxygen. BRADYCARDIA .  If the urine output is reduced lactated Ringer’s is administered at the rate of 20 to 40 ml/kg rapidly to induce diuresis. The normal expected urine output in anaesthetized animals is 1 to 2 ml/kg/hr. Reasons for intraoperative bradycardia  Due to increase in vagal tone o Difficulty in intubation o Deep abdominal surgery o Intraocular surgery o Neck and thoracic surgery o Effect of anaesthetics o Premedication with atropine or glycopyrrolate will control this o condition.  Non vagal bradycardia o Excessive depth of anaesthesia o Hypoxia o Hypothermia o Hyperkalemia TACHYCARDIA  Tachycardia may arise due to o Light level of anaesthesia o Hypovolaemia o Hypoxia o Hypercapnia o Hyperthyroidism .  Bradycardia may arise due to o Excessive depth of anaesthesia o Excessive vagal tone (often increased by intubation vasovagal reflex and traction of abdominal organs) o Terminal hypoxia o Endogenous and exogenous toxaemias o Conduction disturbances in myocardium o Hyperkalaemia o Hypothyroidism Treatment o Administration of atropine or glycopyrrolate. o Mephenteramine 0.V.0 mg in 250 to 500 ml of 5% dextrose or saline )I.V.5 to 20ug/kg/min (40 to 200 mg in 250 to 500 ml of 5% dextrose or saline )I.5 to 20 ug/kg/min (20 to 200 mg in 250 to 500 ml of 5% dextrose or saline)I.05 to 0. o Dobutamine 2.1 to 0.V.V.75 mg/kg I. duration 15 to 30 minutes o Ephedrine 0.5 mg/kg I. o Isoproterenol 5 to 10 ug/kg/min (0.V.4 ti 1. o Dopamine 2. duration 15 to 30 minutes.  Normally pulse rate may either be equal or slightly deficit of heart rate because all the contraction may not produce palpable effective wave and waves may overlap.  The abnormal conditions which causes deficit of pulse rates are o Premature contraction, o Variable diastolic ventricular filling o Electromechanical dissociation of heart.  Heart rate above 180 per minute in dogs and above 200 per minute in cats are considered as tachycardia. SHOCK  Shock is defined as inadequate blood flow to the vital organs or the inability of the body cells to metabolize nutrients normally.  The tissue perfusion depends on the cardiac function, circulatory volume and integrity of vascular function.  Shock can be classified as o Hypovolemic shock o Cardiogenic shock o Vasculogenic shock o Hyperdynamic shock o Hypodynamic shock HYPOVOLEMIC SHOCK Causes  Due to inadequate volume of fluids or blood due to the loss of whole blood, plasma or loss of water and electrolytes  Loss of blood in accident  Loss of polasma protein into inflamed body cavities  Loss of fluid and electrolytes in diarrhea Symptoms  Depressed, dull and lack luster/lusterless eyes  Pale or white or blue mucous membrane  Reduced capillary refill time  Cold extremities  Tachycardia  Fast and weak pulse  Elevated respiratory rate  Reduced body temperature CARDIOGENIC SHOCK Causes  Occurs when the heart fails to pump adequate blood to maintain perfusion. Failure could be due to reduced venous filling and reduced cardiac output. This condition is common in small animals.  Cardiac tamponade  Rupture of chordae tendinae  Toxic myocardial depression  Cardiac arrhythmia  Severe prolonged systemic vascular resistance Symptoms  Depressed, dull and lack luster/lusterless eyes  Pale or white or blue mucous membrane  Reduced capillary refill time  Cold extremities  Tachycardia  Fast and weak pulse  Elevated respiratory rate  Reduced body temperature  Distended pulsating peripheral veins  Hepatomagaly  Peripheral oedema  Cardiac dysrhythmia  Heart murmurs VASCULOGENIC SHOCK Causes  The vessels supplying the blood to the tissues are affected and the perfusion is reduced  Arteriolar constriction  Prolonged sympathetic stimulation  Vasomotor paralysis due to head injuries  Endotoxic and septic shock can also be categorized under vasculogenic shock as the toxins produce vasodilation due to the release of histamine, bradykinin and prostoglandins. HYPERDYNAMIC SHOCK Causes  An early stage of septic shock is an example of hyperdynamic shock. Signs Stage I  Increase in cardiac output  Decrease in arteriovenous oxygen difference  Decrease in systemic vascular resistance  Blood pressure may be normal or reduced  Oxygen utilization at cellular level is reduced Stage 2  Cardiac output may be normal  Hypotension  Respiratory acidosis with metabolic alkalosis  Elevated heart rate Stage 3  Reduction in cardiac out put  Elevated heart rate  Increased difference in arteriovenous oxygen level  Increase in systemic vascular resistance  Hypotension  Brick red mucous membrane due to peripheral vasodilation  Pyrexia due to toxins and damaged leukocytes Otherwise called as ABC of CPR. E.V. which is to be treated immediately within a period of 2 to 3 minutes.  Hypodynamic shock is common in large animal practice. TREATMENT OF CPR . Breathing(B) and circulation(C). Signs  Myocardial depression  Maldistribution of blood volume  High peripheral resistance  Endothelial damage  Infarcts in vital organs  Acute respiratory failure and hypoxaemia SIGNS OF CPR  No ausculatatable heart sound  No palpable pulse  Cyanotic mucous membrane  Dilated pupil  No ventilatory attempts or agonal gasps  Unconsciousness  It is really a true emergency condition.  Examine for the possible obstruction of the airway with food materials or kinked endotracheal tube  In emergency perform tracheostomy to maintain airway patent  In case of bronchospasm treat the animal with aminophylline 5 mg/kg I.g. HYPODYNAMIC SHOCK  It occurs at the terminal stage of sepsis or during the absorption of toxins. terminal stage of horses with colic and cow with coliform mastitis. This can be otherwise called as fourth stage of septic shock. intubate the animal immediately.  The basic life support in cardio pulmonary resuscitation(CPR) is the optimal management of airway(A). AIRWAY  The head must be immediately extended  If not intubated. Calcium gluconate 10% solution at the rate of 0.V. DRUGS USED IN CPR Calcium solutions  Administered as inotropic agent or in hypocalemic agent. The power setting depends on the weight of the animals. Dose Calcium chloride 10% solution at the rate of 0. Circulation  External cardiac massage by chest compression at the rate of 90 to 120 per minute. In cats the forefinger and the thumb is used.V. If surgery is performed in the thorax its easy to provide open chest massage. In dogs the chest compression can be attempted by placing the hands on either side of the chest.  The other agents are specific alpha 2 antagonist (yohimbine) and opioid pure antagonists (naloxone) (See premedication). In small animals the heart is defibrillated at the rate of 1 to 10 J/kg using external paddles and 0.  Supply 100% oxygen  Or use Ambu type resuscitation bag (using room air 21% oxygen) or mouth to endotracheal or mouth to muzzle procedures to maintain breathing  Analeptic agents like doxapram can be administered at the rate of 1 mg/kg I.  It strengthens the myocardial contraction.1 mg/kg I.V. (halothane decreases calcium availability in heart muscles.  Examine for the possible obstruction of the airway with food materials or kinked endotracheal tube  In emergency perform tracheostomy to maintain airway patent  In case of bronchospasm treat the animal with aminophylline 5 mg/kg I.V. Dobutamine .Airway  The head must be immediately extended  If not intubated intubate the animal immediately.The defibrillation is done using external or internal paddles of cardiac defibrillators.1 to 1 J/kg using internal paddles. Breathing  Institute artificial respiration using rebreathing bag or mechanical ventilators at the rate of 12 to 20 breaths per minute. During abdominal procedures if emergency occurs the thoracic cavity can be entered through the diaphragm.  Defibrillation .  Open cardiac massage is done at the rare of 60 to 100 per minute.5 mg/kg I. Sodium bicarbonate . whichstimulates beta 1 and beta 2 adrenergic receptors and to a lesser extend alpha 1 receptor. 0.  The systolic. bronchialsmooth muscles.  It can cause dysrhythmia if administered during halothane anaesthesia. to reverse the effect of xylazine it is administered at the rate of 1. mucosal and renal vasculature. blood pressure and tissue perfusion.  In extreme condition it is administered through intracardiac route.05 to 0.66 mg/kg I.55 mg/kg I.V.V in small animals and 0.  Dose 0.  It is indicated in mild to moderate hypotension.V in large animals as a bolus. beta 2 and adrenergic receptors located in the heart.25 to 20 µg/kg/min in small animals and 0.5 mg/kg I. Dose. MAP andpulmonary blood pressures are increased following administration.  Dose 0. 2 and beta 2 adrenergic receptors. Epinephrine  It is a sympathomimetic amine that stimulates alpha 1. Doxapram (Dopram)  It is a nonspecific analeptic agent used to act on the peripheral chemoreceptors.  Rapid intravenous administration may cause cardiac dysrhythmias. Ephedrine  It stimulates beta 1.  It dilates the vasculature of muscles and constricts cutaneous. diastolic blood pressure and mean arterial pressure and increases cardiac output and systolic blood pressure. skeletal muscle vasculature and alimentary tract.0 mg/kg I. which stimulates beta 1. Isoproternol  It is a sympathomimetic amine.5 to 2.  It decreases peripheral vascular resistance and increases cardiac output.  It is administered at a dose of 5 ml of a 1 in 1000 solution for a 454 kg horse.0 µg/kg/min in large animals (40 to 200 mg in 250 to 500 ml of 5% dextrose or saline).V.  It decreases peripheral vascular resistance.022 to 0.  It is a sympathomimetic amine. beta 2 and alpha 1 receptors.  The cardiac output and blood pressure are increased.  Indicated in shock and malignant hyperthermia.V. Module -15 = Neuroleptanalgesia PHENOTHIAZINE DERIVATIVES Phenothiazine derivatives  Phenothiazine derivatives are basically three ring structures in which two benzene rings are linked by a sulphur and nitrogen atom.5 to 2 mg/kg in large animals and 1 to 5 mg/kg in small animals followed by 40 to 60 µg/kg/min I.  They have inotropic effect on the heart and maintain vasomotor response and suppress the adrenal gland.3 x base deficit (mEq/L) x Body weight. It is contraindicated in slow ventricular rate combined with sinus arrest. . Coricosteroids  These group of agents increases the glucose production.  The steriochemical model of phenothiazine derivatives is similar to epinephrine.  It is a buffer aids in reversing metabolic acidonin.  Dose 0. sinoatrial block or atrioventricular block.  Only the epinephrine free preparation is used.  They act on the central nervous system by depressing the brain stem and connections of the cerebral cortex. induce hypdokalemia by sodium retention. Lignocaine  Indicated in premature ventricular contraction.  These agents increase the dopamine and norepinephrine turn over in the brain and block the peripheral actions of catecholamines at alpha 1 receptors. Dose mEq of HCO3 = 0. norepinephrine and dopamine. promethazine and methotrimeprazine are the commonly used phenothiazines.V.  These agents are weak anticholinergics and have extrapyramidal stimulating properties. promazine.05 mg/kg I. Following induction of regional anaesthesia there will be vasodilation in the anaesthestised part of the body and this effect is compensated by the vasoconstriction in the unanaesthetized parts of the body to maintain cardiac out put. o With the previous history of epilepsy.03 – 0.  Cats = 0.  Tranquilization with phenothiazines is contraindicated in animals undergoing epidural. 0.M. triflupromazine and chlorpromazine are used in veterinary anaesthesia.05 mg/kg I.03 – 0.  At high doses and some times in clinical doses induce extrapyramidal signs such as rigidity.02 – 0. Hence contraindicated in patients.V.03 – 0. 0. o Undergoing myelographic procedures o With the history of recent intake of organophophorus drugs or toxicity  Pulmonary functions are maintained following the administration of phenothiazines except slight depression in respiratory rate  Induce urine production due to the suppression of antidiuretic hormone  Animals undergoing intradermal allergic tests should not be administered with phenothiazines as they are potent antihistaninics  Depletes catecholamines of the thermoregulatory center and render the animal’s body temperature susceptible to the changes in the environmental temperature.05 mg/kg I.03 – 0.1 mg/kg I. Clinical properties and uses  Produce sedation.V. . triflupromazine hydrochloride.09 mg/kg I.04 – 0. tremors and catalepsy.M. chlorpromazine.05 mg/kg I. This response is abolished by the generalized vasodilationinduced by phenothiazines.  Acepromazine maleate. general calming and reduction in motor activity  Antagonize dopamine excitatory chemoceptors and suppress vomiting.  Horses = 0. 0.M. Clinical doses of phenothiazine derivatives CLINICAL DOSES OF PHENOTHIAZINE DERIVATIVES Drug Dose Acepromazine  Dogs = 0. Among these agents acepromazine. spinal or segmental anaesthesia. 1 – 2.  Pigs = 0. Promazine  Horses = 0.M.M.1 mg/kg I. 0.1 mg/kg I.4 mg/kg I.6 mg/kg I.M.55 – 4.0 – 2.1 – 6.44 – 1.05 mg/kg i.  Goats = 0.4 mg/kg I.V.4 mg/kg I. 2.  Goats = 0. 2. INTRODUCTION .V.44 – 4. 0.2 mg/kg I.V/I.16-Acupuncture.M  Horses = 1.44 – 1. Electro-anaesthesia.V/I.1 mg/kg I.2 – 6.1 mg/kg I.0 mg/kg I.1 mg/kg I.2 mg/kg I.M.V.M.V/I.M.V.6 mg/kg I.00 mg/kg Module.6 mg/kg I.M.  Pigs = 0.44 – 1.M.2 – 1.  Cattle = 0.  Cattle = 0. 1.M.04 – 0.6 mg/kg I. 0.1 mg/kg I.M.44 – 1.0 mg/kg I.09 mg/kg I.V. Cats = 0.2 – 6.  Sheep = 0.V.  Pigs = 1. 2.4 mg/kg I.V/I. Chlorpromazine  Dogs = 0.1 mg/kg I.M.M.55 – 4. Hypothermic anaesthesia  ACUPUNCTURE .  Sheep = 0.  Cattle = 0.55 – 4.2 – 2.02 – 0. Triflupromazine  Dogs = 1.M.2 – 6.V.44 – 1.55 – 4. All other sensations (touch. if applied carefully. Acupuncture (AP) can be used to obtain pain relief in clinical disorders or as an  alternative or complementary method of inducing pain control during surgical procedures. In vet surgery. the animal) patient can feel the knife. AP analgesia (AA) is a misnomer. with some positive results. usually involving the entire body. They reach the midbrain via the ascending spino-thalamic tracts. Direct ES of human thalamic or spinal areas can abolish clinical pain. This method may have application in time of war or national disasters. found that various types of stimuli applied indirectly or directly to the nervous system can reduce or abolish clinical and operative pain. It is a pain inhibition phenomenon caused by stimulation of peripheral nerves via certain AP points. AA also can be induced by other stimuli.  In emergencies a slight degree of hypo-algesia can be obtained in humans and animals by heavy digital pressure over the correct AP/nerve points. In this case the technique is called Electro-APanalgesia (EAA). thalamus and possibly other areas. research on uses of low-power (cold) Laser as an AA stimulus is ongoing. Consciousness is retained throughout the operation but many animals become slightly drowsy (as if slightly sedated) during and for a short time after AA stimulation. AA can be induced by simple AP (manual twirling of the needles) but it is more common to use electrical stimulation (ES) via the needles.  The degree of pain inhibition may be complete or partial. traction etc) are intact. Since the late 1980s. Thus. tickle etc) and reflexes (to sight or sound stimuli. fear. It should really be called AP hypoalgesia.  Stimuli via the AA points are carried in the peripheral sensory nerves to the spinal cord. Transcutaneous Electro-Stimulation Analgesia (TESA) has been used in childbirth in the human female and is somewhat comparable to EAA. Dorsal Column Stimulation (DCS) of the spinal cord has been used in intractable pain in humans. such as injection or electro-static fields applied to the points. traction. presumably. However.  Stimulation-Produced-Analgesia (SPA): Since the 1970s. In the midbrain the ascending signals cause release of endorphin. ES via electrodes implanted in specific sites in human or animal brain can induce a high degree of analgesia. it is too early to attempt to assess that method. Vaginal stimulation (electrical or mechanical) can cause potent whole-body analgesia in rats. pressure. AA can be said to "close" various "pain gates" in the nervous system. The result is that the human (and. serotonin and other neurotransmitters which activate a "descending inhibition mechanism" and prevent the "pain signals" from the surgical area from reaching the cerebral cortex. TYPES OF OPERATIONS UNDER AA . when anaesthetists and anaesthetics may not be available. western researchers. the AA technique. These gates are thought to be located in the spinal cord. often is sufficient to allow surgery without the use of other anaesthetics. the touch and traction etc but does not "feel pain". working independently of the Chinese. inguinal hernia. dogs. It should have outputs for at least 8 electrodes. o castration. cattle. The animal species involved include horses. Newer models for human use would be adequate for EAA in animals. Canada. limbs and teats. It is safer to use models which deliver a bipolar waveform. frontal sinuses. orchidopexy. trachea. USA. USA. cavies. . goats. Some are made in China. o rumen. ovario-hysterectomy. monkeys. Canada and Australia. o nephrectomy. o gastric and intestinal surgery. o navel hernia repair. dense- disperse waveform). as has AP therapy for the relief of dystocia. anal and vaginal region. EQUIPMENT AND METHODS OF RESTRAINT FOR AA Equipment  Most AA is done using electrostimulation (ES) through needles in the correct points (Electro-AP analgesia = EAA). as in prolonged surgery. There is little standardization of equipment. Austria. Japan. Europe and Australia etc. portable and battery-operated. o surgery of the eye. Needles were inserted 12-20 mm in the points. donkeys. o removal of parotid and submaxillary glands. o surgery on the bladder and urethra. Germany. Occasionally adjustable waveform at 5-10 Hz was used. o removal of mammary and skin tumours.  The equipment should be strong.  Workers in Eastern countries such as China.  Types of surgery successfully done in animals include: o caesarean section. mules. Taiwan etc have used the method for many years. o orthopaedic surgery (bones. pigs. This prevents the development of serious electrolytic lesions which could arise if a monopolar waveform was used for long periods. major surgery has been done in animals under AA as the sole analgesic agent in many countries in the West.  The late Dr. rats.  Since the mid 1970s. I had 8 teeth extracted and 8 teeth filled under EAA with the Model 71-3. sheep. oesophagus. at each electrode. others in Japan. guinea pigs and mice. (+) and (-). o surgery on the lip. Westermayer's method for reposition of the prolapsed uterus has been mentioned already. Belgium. Many different types of electrostimulator are on the market. I used mainly ChiaChe (ST06) plus Earlobe "Dental Analgesia Point" on the affected side. joints).  The Model 71-3 General Purpose Electro-AP Apparatus is suitable for AA as well as AP therapy. These include France. Voltage was increased slowly to maximum tolerance (anaesthesia mode. The choice of points will be discussed later. ear. cats. or ropes may be used through rings in the wall to keep the animal in one position. depending on the type of operation and whether or not the animal is quiet. movement and fuss should be kept to a minimum. Kicking may be prevented by the usual methods as applied in operations under local anaesthesia. Cats are difficult animals to handle and some vets who have tried AA in cats have ceased to use the technique in this species. It helps if the owner or an attendant talks to the dog and comforts the animal from time to time during surgery. turning up the voltage usually controlled it. Horses and nervous cattle should be knocked by ropes or a short-acting knock-down anaesthetic.  After 30 minutes of induction. lateral or ventral recumbency. Sweden. An impacted wisdom-tooth required 10 minutes of very strong rocking to remove it from its socket. An attendant may hold the nose and the animal should be restrained in a suitable cattle crate. When heavy needle-probing of the gum caused no pain. available from Dan Sjo Elektronik AB.  In human patients. Unnecessary noise.  The standing position may be used for surgery in quiet cattle.  Recumbent animals should be roped securely and an attendant should ensure that the head is kept down. A blindfold over the animal's eyes helps to avoid fright by visual stimuli. operations under AA may be performed with the animal in the standing position or in dorsal. Caesarean section has been done in Japan using electro- static or electromagnetic fields around the hands and feet. If a special operation-harness is not available they are restrained by tying bandages from the hocks and elbows to suitable anchor-points on the operating table. Dental fillings under EAA were uneventful except in deep root fillings. TESA does not appear to have been tested in animals. Childbirth has been helped in 60-80% of women treated by transcutaneous ES analgesia (TESA) of the thoraco-lumbo-sacral region.  Small animals are normally operated on in lateral. The apparatus used was the Travisens. Box 144-17224. dorsal or ventral recumbency. In large animals. There was rather severe pressure-pain with that attempt but I was able to tolerate it without asking for another anaesthetic. the output was usually at a setting of 4-5 on a 10 point scale. If "nerve pain" arose. Restraint for AA in animals  Surgery under AA requires adequate restraint because consciousness and all sensations and reflexes (except those of pain) are retained. dentistry could begin. . My dentist told me that most patients could not have had the tooth removed unless they had general anaesthesia. The apparatus used does not appear to have been tested in Europe or America. Sundbyberg. Dogs are excellent subjects for AA but it is advisable to tie a tape bandage around the jaws to prevent biting.  Extraction was painless or caused minimal pain in 5/8 cases but 3/8 extractions caused moderate to severe pain but were completed without the use of drug analgesia. Nervous animals may be given a tranquilliser i/v. AP needles are placed to the correct depth in the AA points related to the operation site. As long as one of a pair is twitching. on rare occasions. after switch-on. struggling. During these stages of the operation the frequency or output voltage should be increased. This is normally sufficient to counteract the pain. especially during incision and suturing of the skin. In this case the correct connection would be as in the diagram on the next page. This is especially advisable if the instrument uses (+) and (-) electrodes. Note: A needle can not twitch unless it is embedded in reactive muscle.  When the needles are in position. full sensitivity to pain is present. the paired needle is also receiving a similar stimulus. Do not connect the leads from one output across the thoracic or posterior cervical region. Needles may not twitch in points such as GV26. the operation site is tested for analgesia using rat-tooth forceps. serosa (peritoneum. reduce the output to the tolerance of the patient. Tape or suture the needles firmly in position. vocalisation etc). When the animal is properly restrained.  After 5-10 minutes. The output leads are then connected to the needles. the response to pain stimulus decreases. In that case. In the first few minutes after stimulation begins it is usual for the animal to show a mild stress reaction (dilated pupils.  Pain stimuli may exceed the hypoalgesia (thereby inducing pain response by the animal) at certain stages of the operation. Reduce the output to a "strong but acceptable level" (that which can be tolerated without obvious discomfort). Excessive stimulation reduces the EAA effect and to weak a stimulus may induce little or no analgesia. Attach the leads and turn on the power switch. AA TECHNIQUES IN LARGE AND SMALL ANIMALS  Electro-AP analgesia (EAA) is the most common method used. the animal indicates a degree of discomfort or pain (restlessness. increased blood pressure. the output controls are checked to ensure they are set at zero. After 20-40 minutes.  Occasionally (in those animals which respond poorly to AA) it may be necessary to use small volumes of local anaesthetic injection or spray at these stages. they are liable to become dislodged by muscle twitches induced by the stimulation. in successful cases. as indicated by local muscle twitch or guarding. towel clip.  Turn up the output controls slowly until the needles begin to twitch in time with the frequency of the stimulator. Every 5 minutes or so. the animal will indicate discomfort.  An output circuit placed across the thorax may interfere with cardiac function and may. The operation may then commence.  If output voltage is too high at such points. Otherwise. Increase the output voltage from each control to the maximum tolerance of the patient. cause cardiac arrest. At that point. Initially. or by struggling in nervous animals.  The stimulator is checked to ensure that the power switch is off. vocalisation or defence reactions/struggling. pleura etc) and incision of periosteum and nerves. the animal makes no response to strong pain stimuli in and around the operation site. defensive reaction. faster . clamp or pin prick. the pulse rate was irregular.  The corneal reflex remained positive in all animals. Because sight and hearing are unaffected (pupil reflex is also intact).  The results suggest that the apparatus did not cause electroanaesthesia or electrosleep but had mainly an electroimmobilising effect on the experimental animals. These quickly return to normal or near normal levels. and the reaction to painful stimuli was positive in 15 out of 29 experimental animals.e. In one pig the heart activity stopped some minutes after the onset of the current. However. the animals are still conscious and can eat or drink and (in dogs) wag the tail if petted by someone they know. to check the analgesic and other practical effects of the apparatus. Before and after administration of the current the electroencephalogram recordings were similar. the use of such an apparatus cannot be recommended. unnecessary noise should be avoided and a blindfold may be desirable. and plasma cortisol level remained constant in the control animals. ELECTRO NARCOSIS  Since the end of the last century many investigations with electroanaesthesia have been performed in animals and man. this usually indicates that excessive traction on mesentery/internal organs is the cause. similar to those of drowsiness or light sleep. Three animals of each species were used as control animals. and should remain at this level during the operation. and 9 pigs. which were equipped with EEG and ECG electrodes. If salivation is excessive or retching/vomiting occurs. The body temperature. The body temperature. pulse rate..  Studies of EEG patterns in animals under AA indicate that brain waves are in the alpha range (8-13 cycle per second) i. The interest in this method of anaesthesia has emerged because anaesthesia is achieved immediately after the onset of the current and the recovery is very rapid after cutting off of the current. Changes in the electroencephalogram and electrocardiogram were not observed in the control animals during their treatment. Moreover. Because of the dubious effects on the animals' welfare. except in one calf and one sheep. respiration and heart rate). the breathing movements appeared to be somewhat impaired.  Pupillary dilation and salivation occurs in some animals. Recently a battery operated appuratus became available (Feenix Stockstill) for application of electroanaesthesia and electroimmobilisation under field conditions.  In all animals. 10 sheep. during administration of the current. and the pulse rate were raised durring the current administration. This may be partly counteracted by increase in frequency or output of the AA stimuli. HYPOTHERMIA . the plasma cortisol level. The duration of current administration was 20 minutes. both of which showed patterns suggesting a decreased consciousness.  The electrocardiogram recordings showed pronounced changes in cardiac activity. and an experiment was conducted with 10 calves. Increased postoperative protein catabolism MODULE-17: MUSCLE RELAXANTS Learning objectives This module deals with  Physiology of neuromuscular transmission  Reversal of Neuromuscular Blockade  Ventilation INTRODUCTION . 2.and also maintaining low flow rate and attachment of humidifier to endotracheal tube. should be warm. A decrease in temperature of 1-3ºC below normal has been demonstrated to provide substantial protection against cerebral ischemia and hypoxaemia in anaesthetized dogs. Life threatening cardiovascular depression may develop when the temperature decreases below 32. during protracted total intravenous anesthesia and during recovery from anesthesia. Decreased resistance to infection 6. Impaired cardiovascular function.8ºC. Fluids to be administered i.  Rectal or esophageal temperature should be monitored at regular intervals during inhalation anesthesia . Decreased metabolism and detoxification of anesthetic drugs 4. Hypoventilation 3. Weakness during recovery 5.  It is very difficult to influence production of heat but care should be taken not to wet the animal excessively to reduce evaporative heat losses. Increased incidence of surgical wound infection 7.  Hypothermia may develop in animals anesthetized in a cool environment.v. placing the animal on a warm surface and covering with blankets . Basically . The adverse effects of perianaesthetic hypothermia are 1.the causes consists of a reduction in heat production by the animal . drapes . usually coupled with an increased heat loss. such losses are reduced by the use of rebreathing circuits.  Respiratory heat losses are increased when animal breathes cold dry gas from non-rebreathing system. wrapping of extremities with towel and blanket and plastic insulation or hot air circulating devices. The small gap between the nerve fibre terminal and the muscle membrane is 60 nm wide and is called as junctional cleft. Interaction between the receptor and acetylcholine triggers an end plate potential. Anaesthesia is comprised of narcosis.  Muscle relaxation is best achieved by the administration of neuromuscular blocking agents. The area where the nerve ending lies close to the proximity of the muscle fibre is called neuromuscular junction.  Use of neuromuscular blocking agents  To provide the muscle relaxant component of anaesthesia  To minimize the dose of general anaesthetics  To provide easy access to the deep structures in the abdomen  To aid in intubation without laryngeal spasm  To prevent fighting the ventilator during controlled ventilation  To help removal of foreign bodies from the proximal portion of oesophagus as it is composed of striated muscles.  To aid in reducing the luxated joints  To ensure immobility of the patient during delicate surgery  To stabilize the eyeball in central position during ophthalmic surgery PHYSIOLOGY OF NEUROMUSCULAR TRANSMISSION  The large myelinated nerve from the ventral horn of the spinal cord carries impulses to the muscles. analgesia and muscle relaxation. which crosses the junctional cleft to stimulate nicotinic-cholinoceptors of the post synaptic muscle membrane. The areas of secondary cleft are rich in mitochondira.  The action potential traveling along the motor fibre produces depolarization of the nerve terminal and triggers the release of acetylcholine.  Acetylcholine is synthesized from choline and acetate in the presence of an enzyme acetyltransferase.  The muscle fibre membrane forms the groove and the grooves are deeply corrugatede and called as secondary clefts.  As the nerve approaches the muscle cell its branches lose their myelin sheaths and the terminal ends lie in grooves on the surface of the muscle fibre and are covered by Schwann cell. The acetylcholine molecules are present as uniform sized vesicles near the presynaptic membrane and these areas are called as active zones. It carries stimuli to several muscle fibres that must be activated for contraction. After activating the receptor the .  When acetylcholine is released it travels a minimum distance across the junctional cleft to reach the receptors. which is converted into muscle action potential leading tocontraction. However prolonged administration results in decrease in serum potassium level. hypothermia and magnesium ions potentiate the effect of suxamethonium.  In dogs 0. Organophosphorous compounds (use as ectoparasiti-cides) decrease the action of pseudocholinesterase. Their effects can be reversed using anticholinesterase. respiratory alkalosis. Hence liver damage. Repeat dose may result in dual block (nondepolarizing) which can be reversed with anticholinesterase drugs. magnesium slats and volatile anaesthetics potentiate the action of these agents.  Its administration is associated with the release of potassium into the blood from the muscles.  During partial paralysis monitoring it shows fade andpost titanic facilitation followed by exhaustion and depression of muscle twitch. acidosis and nondepolarizing drugs.  Isoflurane. Cholinesterase is synthesized in the liver. hence not recommended in patients recently exposed to such agents. The drugs used for neuromuscular blockade are classified into o depolarizing muscle relaxants o nondepolarizing muscle relaxants. It is hydrolysed by cholinesterase and pseudocholineesterase into choline and succinic acid. Depolarized muscles are unresponsive to other stimuli such as electrical stimulation.  The following are nondepolarising muscle relaxing agents o Tubocurarine chloride o Gallamine triethiodide o Pancuronium bromide o Vecuronium bromide o Atracurium besylate . Their action is not reversed by anticholinesterases. DEPOLARIZING MUSCLE RELAXANTS  Depolarizing drugs produce intial muscle fasciculations and their action is rapid.  Acidosis. In partial paralysis neuromuscular monitoring slow depression of muscle twitch.  Nondepolarizing drugs are either quaternary ammonium or steroid compounds. which may result in cardiac irregularities.3 mg/kg intravenously produces muscle relaxation and it extends upto 25 to 30 minutes. acetylcholine is rapidly hydrolysed to choline and acetate. The only drug used in this group is suxamethonium chloride (Succinyl choline).  The relaxed muscles will response to other stimuli such as electrical stimuli. no fade and no post titanic facilitation are noticed. Its effects are antagonized by halothane. NONDEPOALRIZING MUSCLE RELAXANTS  These drugs do not produce muscle fasciculations and are slow in action. cachexia and malnutrition may prolong the action of suxamethonium. .V.  It has minimal effects on cardiovascular system and some times produces rise in heart rate. VECURONIUM BROMIDE  It is a steroidal agent supplied in lyophilized form and soluble in water (stable for 24 hour only). GALLAMINE TRIETHIODIDE  It has atropine like action on the heart. It is a safer drug for cardiac and renal patients. .  The drug is primarily excreted through bile in an unchanged form hence can not be used in patients with hepatic diseases and recommended in patients with renal disorders. Duration: around 29 minutes. TUBOCURARINE CHLORIDE  Tubocurarine is derived from Chondrodendron tomentosum tree.V.  Dose 0.  This drug is excreted through kidney hence not indicated in patients with renal diseases. Duration around 31 minutes.  It has got minimal cardiovascular effects and does not release histamine. Not recommended in dogs due to its profound cardiac defects/effects.V.  It is administered with caution inpatients with the history of anaphylaxis as it may release histamine.  Only 30% is metabolises and the rest is excreted unchanged through bile (10%) and the reaming through the kidney. ATRACURIUM BESYLATE  It is a novel muscle relaxant.  Dose 0.1 mg/kg I.  It also blocks the muscarinic effects of acetylcholine and acts directly on the B receptors resulting in tachycardia and rise in blood pressure which may lead to greater blood loss during surgery.  Its duration of action is less than pancuronium. which does not depend on body system tometabolize. Duration 18 to 25 minutes.06 mg/kg I.1 mg/kg I.  Dose .  It is broken down by a self-destruction process known as Hofmann elimination. PANCURONIUM BROMIDE  It is an amino-steroid having no steroidal effects.  It is contraindicated in patients having renal and hepatic diseases. and is eliminated by Hofmann effects.V or Edrophoniumj 1.2 mg/kg) or by continuous infusion (0.  It is achieved by the administration of certain drugs.  The other nondepolarizing drugs are mivacurium. VENTILATION  There following are the different types of ventilation o Spontaneous ventilation o Assisted ventilation o Controlled ventilation o Intermittent positive pressure ventilation . lincomycin and metronidazole.01 mg/kg) administered intravenously atleast one minute prior to the administration of reversal agent to block the muscarinic effects of acetylcholine.  No clinical literature is available on its use in veterinary anaesthesia.g.  Neostigmine 0.V. and tobramycin by decreasing the release of acetylcholine. which will inhibit cholinesterase.  Intermittent positive pressure is discontinued only after achieving train of four responses (all must be of equal force).5 mg/kg I.0 mg/kg I. rocuronium and doxacurium.  In clinical condition reversal is attempted when at least two twitches are present. The other antibiotics include polypeptide antibiotics like tetracycline.04 mg/kg) or glycopyrrolate (0.1 mg/kg I. Calcium can be given prophylactically in these patients. edrophonium and neostigmine. has no cardiovascular effects. REVERSAL OF NEUROMUSCULAR BLOCKADE  Reversal of nondepolarizing drugs is achieved by establishing high concentration of acetylcholine at the binding site.V.  Atropine (0. duration around 40 minutes further maintenance can be done with incrementaldose (0. gentamicin.5 mg/kg/hr). streptomycin. and the drugs are pyridostigmine.  The action of neuromuscular blocking agents are potentiated and prolonged by aminoglycoside antibiotics e. Dose: 0. CISATRACURIUM BESYLATE  This drug is 5 times potent than atracurium. does not release histamine. cats and in horses during open thorax as their mediastinum is incomplete. cerebral ischemia. Assisted ventilation  The patient initiates the respiration but the tidal volume is increased or assistedby the ventilator or by squeezing the rebreathing bag. But still use of intermittent positive pressure in these animals also helps in maintaining cardiopulmonary parameters. In cattle.  Used in patients whose respiratory centre is depressed by drugs. TYPES OF VENTILATION Spontaneous ventilation  It refers to breathing without any assistance from mechanical ventilator or the anaesthetist squeezing the rebreathing bag. (fenestrated mediastinum). Intermittent positive pressure ventilation  This is a technique used in controlled ventilation or assisted ventilation to force air into the lung during inspiration and lower it to atmospheric pressure or slightly below during expiration. .  Spontaneous ventilation can be abolished by hyperventilation. Intermittent positive pressure ventilation is essential to maintain pulmonary function in dogs.  To provide controlled respiration during thoracotomy.  To maintain near normal acid base status and oxygenation during long surgical procedures. and cardiac or respiratory arrest. Controlled ventilation  The total breathing function of the patient is done entirely by a mechanical ventilator or by the squeezing of rebreathing bag.  To reduce ventilation-perfusion mismatch during prolonged periods of anaesthesia. sheep and goats the mediastinumis complete (unfenestrated mediastinum) hence thoracotomy can be performed in one side with out the need of ventilator. USES  To provide ventilation during neuromuscular blockade and respiratory muscle paralysis due to toxins. increased intracranial pressure.  Guidelines o Volume.  Used in thoracic diseases. MODULE-18: GENERAL PRINCIPLES OF CHEMICAL RESTRAINT OF WILD AND ZOO ANIMALS Learning objectives This module deals with  Chemical Immobilization of Wild Animals CHEMICAL IMMOBILIZATION OF WILD ANIMALS  Wild animals are chemically restrained for the following reasons o Animal translocation and transportation o To study the ecology and population estimate o For veterinary studies o To relieve wild animals in distress .12 o Pigs 8 --.  Volume o Small animals 10 to 20 ml/kg o Large animals 10 to 15 ml/kg (maximum limit is for open thorax)  Pressure o 15 to 30 cm of H20  Rate per minute o Dogs 8--.14 o Cats 10---14 o Horses 6 --. rate and inspiratory: expiratory ratio must be properly set in the ventilators. pressure. pleural effusion.10 o Sheep & goats 8 --. Diaphragmatic hernia.10 o Cow 6 --. pneumothorax.  Used in patients having inadequate respiratory exchange due to obstruction or pulmonary oedema. (-5 cm of H2O during expiration and -12 cm of H2O during inspiration) eg. which affect the negative pressure of the thorax.12  Inspiratory: Expiratory ratio o It should be 1:2 or 1:3 to minimize the interference with venous return the inspiratory time is kept shorter than expiratory time. 5-9mg/kg (Combination) Bison  Chloral hydrate 250mg/kg body weight Elephant  Asian elephant 100-175 mg Xylazine (total dose) . long range.89-8.51 mg/kg intramuscular Bears  Xylazine 2-4 mg/kg and Ketamine 4.54 mg/kg body weight combination Deer  Xylazine 0. projectile syringes (short range.27-0. Primates  Ketamine – 5-20 mg /kg intramuscular  Xylazine 2 mg/kg intramuscular Chimpanzee  Ketamine 10-15 mg/kg body weight  Xylazine 2 mg/kg Kangaroo  Xylazine 8 mg/kg body weight and Ketamine 3 mg/kg combination  Thiopentone less than 20 mg/kg body weight Antelope  Xylazine 0. blow pipe. blow gun rifle. and stick syringe.23 mg /kg and Ketamine 11.0 mg/kg body weight  Ketamine 10-20 mg/kg body weight Camels  Xylazine 0. and extra long range). o Control of animals causing distress to the public  Various devices used for injecting the drug from a distance are drug darts. Monitoring and Maintenance of normal physiology INJECTABLE ANESTHESIA .4 mg/ml-Etorphine and 10mg/ml of Acepromazine per ml) Dose 1 ml/4 feet of shoulder height Reptiles  Ketamine 20 mg/kg intramuscular  Xylazine 1 mg/kg Snakes  Ketamine 50-130 mg/kg intramuscular  Tiletamine 10-20 mg/kg intramuscular MODULE-19: ANAESTHESIA OF LABORATORY ANIMALS Learning objectives This module deals with  Injectable Anesthesia  Inhalant Anesthesia  Gas Delivery Systems  Anesthetic Machine  Preparation.  Etorphine-Acepromazine combination (2. Supportive care may be needed.Insert the needle into a large muscle mass.small veins are hard to access (i. Bolus dosing is simpler. the saphenous. the caudal thigh muscles. 1/2 of the original dose is given for repeat doses. it is necessary to put pressure on the vessel to prevent bleeding. intramuscular and intravenous. the tail veins are best. Less frequently used routes. When the needle is placed correctly. Once the needle is withdrawn.  Injectable anesthetics can be administered by various routes depending upon the specific compound.  Advantages . technique is simple .rapid delivery of drug. If blood appears in the hub of the needle. The most frequently used routes of administration in laboratory animals are intraperitoneal. For larger animals. The vessel may be stroked with a finger to stimulate blood flow into it. will improve your chances for success.e. Using a new. oral and rectal.  Advantages . are intrathoracic. For rodents. For rabbits and swine. This will help avoid injecting into the sciatic nerve. Draw back. Then the needle is lowered to align with the longitudinal axis of the vessel and advanced slightly. even if it is the same animal. Contact RAR at 624-9100 for training materials on handling animals and administering injections. or if from the caudal aspect. irritating substances may be given IV  Disadvantages . inject from the lateral aspect. Infusion rates are calculated based on the clearance time of the drug. developing skill in venipuncture takes experience Intramuscular(IM)  Method . The best muscle masses to use are for small animals. Techniques are described below. the lateral dorsal spinal muscles or the cranial or caudal thigh muscles may be used. among others. The needle is inserted at a 30-45° angle to the vessel. Draw back slightly. The vein is held off proximal to the venipuncture site. ability to titrate dose. try redirecting the needle (before you pull it out of the skin) and repeat. ear veins may be used.An appropriate vein must be selected. Intravenous(IV)  Method . cephalic or jugular veins are best. When administering into thigh muscles. direct the needle slightly lateral. sharp needle for each stick. Typically. you are in a blood vessel. You may need to try several times while learning. the drug may be injected. inject the drug. restraint is critical. If blood is aspirated. It involves admininsistration of the drug and monitoring the depth of anesthesia. If not. Maintenance of injectable anesthesia can be through repeated bolus doses of the drug or through a constant infusion. For large animals. small animals).Fairly rapid absorption. Redirect the needle.  Anesthetic induction using injectable anesthetics is fairly simple. )  Disadvantages .2 MAC to an animal via a mask or nose cone. .Irritating substances cannot be given this way. you have likely hit the viscera. For this reason induction using a mask or nose cone held over the animal's nose can only be performed on smaller or non-fractious animals.  Advantages .5 ml in mice. Inject into the center of the "tent" created by pinching.relatively large volumes may be injected (0. large volumes may be given (basically as much as the tent of skin will hold that doesn't cause discomfort to the animal)  Disadvantages .  Maintenance of inhalation anesthesia is normally accomplished by delivering approximately 1.The animal is usually restrained in dorsal recumbency. draw back.Pinch an area of loose skin. If the needle is placed correctly the drug may be injected. Anesthetic gases are irritating to eyes and nasal passages. absorption is slow INHALANT ANESTHESIA  Induction of inhalation anesthesia can be difficult. In smaller animals gas can be delivered into an induction chamber large enough to contain the entire animal.IM injections are painful.  Disadvantages . Induction via a nose cone or chamber requires delivery of the anesthetic gas at 2-3x MAC. If anything is aspirated. Subcutaneous (SQ)  Method . drug may be administered into the viscera resulting in no effect or in a complication.  Advantages . The drug may be injected anywhere in the caudal 2/3 of the abdomen. it is best to try to avoid the left side in rodents and rabbits because of the presence of the cecum. the animal may try to bite or escape Intraperitoneal (IP)  Method . 2 ml in rats.Technique is the simplest of any. Frequently an injectable anesthetic is used to induce anesthesia and the inhalation agent is used for maintenance. small volumes are necessary.technique is more difficult than IM injections. etc. However. After the needle is inserted. Withdraw and get a new needle before trying again. Animals may resist as they begin to lose consciousness or they may stop breathing temporarily. o Re-breathing circuits include typical circle systems used in large animals. In older machines with metal valves a non- rebreathing circuit may be necessary for rabbits and cats as well.  Anesthesia circuits can be re-breathing or non-rebreathing. Endotracheal access is essential to provide ventilation support. GAS DELIVERY SYSTEMS  The most complicated aspect of using inhalant anesthesia is the delivery system.  It must also ensure that animals receive adequate oxygen. The gas/oxygen mixture is delivered to the animal via a one-way valve.  Anesthetic concentration is accomplished by sets of mixing valves or a precision vaporizer. Intubation is recommended whevever possible. When the animal breathes out the gas passes out another valve attached to a y-piece. Machines can vary in construction and design. particularly when a procedure will be prolonged. Anesthetic machines typically require more training to learn to operate. Vaporizers are easier to use but are very expensive. These machines precisely mix the gas with air or oxygen and can be easily adjusted. The CO2 absorbent must be replaced regularly. A Bain system is the most common non-rebreathing circuit available. ANESTHETIC MACHINE  The best method of delivering an inhalant anesthetic is with an anesthetic machine. o Re-breathing circuits conserve anesthetic gas and the animal's body heat. . With newer machines non-rebreathing circuits are normally only necessary for rodents and birds. Vaporizers are calibrated for the specific anesthetic gas to be used. There are several types of delivery systems typically used in laboratory animals. A delivery system must provide the anesthetic gas to the animal at a known and constant rate. This is passed over a carbon dioxide absorbent and then back into the system. o Non-rebreathing circuits are primarily used for smaller animals that cannot cycle the valves in a re-breathing system. Additional gas and oxygen are continuously delivered to replace that lost. or directly into the lungs via an endotracheal tube. o The non-rebreathing circuit is attached to the same anesthetic supply as used for a re-breathing system. an intra- operative anesthesia record must be kept and included with the . Other scavenging systems can be used. Apparatus for rodent anesthesia  Left: a non-re-breathing nose cone that can be used with a large animal anesthetic machine.  Normal physiologic functions such as body temperature. Once animals are under anesthesia they must be monitored closely while they are anesthetized to ensure that they do not become too deep and die. and to ensure that they do not become too light and experience pain from the surgical procedure.  Anesthesia machines must have a waste gas scavenging system. However. respiration and cardiovascular function must also be monitored and supported while the animal is anesthetized. MONITORING AND MAINTENANCE OF NORMAL PHYSIOLOGY  A variety of things must be done to prepare for anesthesia. This tends to increase anesthetic usage and can increase body heat loss in the patient. Right: a gas scavenging system that can be used with a drop system. the exhaust line is connected directly to the waste gas scavenging system. Middle: a typical drop system closed anesthetic chamber. Normally the exhaust line on a non-rebreating system or the pop-off valve on a re-breathing system is connected to a vacuum line or to the building exhaust. PREPARATION. contact RAR at 624-9100 or Environmental Health & Safety at 626-5804 for further information on anesthetic delivery systems.  For all major surgical procedures on non-rodent mammals. o Non-rebreathing circuits depend on gas and oxygen being delivered at a higher pressure than is present in the exhaust line. Please consult RAR's policy for fasting requests. It is not necessary to withhold food and water from rodents prior to anesthesia. The anesthetist must be prepared to handle emergencies if they occur. animals in dorsal recumbency may experience compression of the diaphragm by abdominal viscera. mechanical ventilation is rarely needed . PREPARATION  Withhold food and water from large animals for 12 h prior to anesthesia and from small animals for 2 h to prevent regurgitation and aspiration. even if injectable anesthetics are being used. surgeon's reports as part of the animal's record.  Premedication with atropine or glycopyrrolate (anticholinergics) may reduce the respiratory tract secretions in some animals  Protect the eyes from drying out using an ophthalmic ointment and protect them from being contaminated with surgical scrub solutions. RESPIRATION  Most anesthetics cause direct depression of the respiratory center in the brain and reduce ventilation. Intubation can be achieved on animals as small as a rat. There are several ways to monitor and support the ventilation of an anesthetized animal. Also protect pressure points. Contact RAR at 624-9100 for training materials. This will prevent aspiration pneumonia and allow you to assist respiration if the animal stops breathing.  Assist respiration during the procedure. You may not have time to look for things once the animal is under.  Intubate the trachea whenever possible. from pressure necrosis or peripheral nerve damage by providing padding between the animal and the table. These reflexes are lost during anesthesia. However.  The airway may be compromised by regurgitated food or pharyngeal and tracheal secretions that normally would be removed by reflex swallowing or coughing.  Have an assistant: Anesthesia takes time to perform and monitor. When an animal is in lateral recumbency the lung that is down is being compressed by the rest of the body. This can be done with a mechanical ventilator. such as bony protrusions. Prolonged food or water deprivation are distressful to animals and are rarely necessary. Likewise. A person should be available to assist so the surgeon does not have to break sterility to monitor the animal or administer medications. This is complicated by other factors that may interfere with respiration.  Have all drugs and equipment ready before the animal is anesthetized. o Monitor the color of the mucous membranes (gums.  Monitor respiratory function throughout the procedure and recovery. A diuretic like furosemide can be administered. underhydration results in sticky mucous . many anesthetics are metabolized in the kidney (creating a slight diuresis minimizes renal toxicity). (unless a thoracotomy or diaphragmectomy is being performed) and can be detrimental to the animal if over-done.  To minimize the effects of surgery and anesthesia on hydration: o Place an intravenous catheter whenever possible to provide access for fluids and medications o Supplement fluids. o Monitor respiratory rate and depth (compare to normal for your species. You can expect them to be slightly decreased). or expired oxygen and carbon dioxide concentration or by use of a pulse oximeter. Observe chest movement. Attaching an AMBU bag to the endotracheal tube or using an anesthetic machine's rebreathing bag will allow you to administer a deep breath every 2-5 min during the procedure. This can result from overventilation or overhydration. vulvar mucosa). This is further complicated by increased fluid requirements during anesthesia and surgery that may result in hypovolemia. but prognosis is poor. or use a stethoscope or esophageal stethoscope. decreasing cardiac output and blood pressure. A bluish color means the animal is not getting enough oxygen.ventilate! o Red-tinged foam present in the airway along with dyspnea (difficulty breathing) may indicate pulmonary edema. the animal has not received its normal fluid intake since it was fasted. FLUID THERAPY  Many anesthetics have direct effects on the heart or vasculature.Overhydration results in frequent urination and pulmonary edema. This will inflate all areas of the lungs and improve gas exchange. ventilation can be performed using a nose cone or face mask. cold oxygen (if inhalant anesthesia is used) increases respiratory fluid loss. otherwise intraperitoneally or subcutaneously  Fluid should be supplemented at the rate of 5-10 ml/kg/hour during anesthesia  Monitor hydration status. fluid may be lost through hemorrhage or exposure of moist viscera to room air. o Sophisticated respiratory monitoring can be achieved by measuring blood gasses. conjunctiva.  Fluid requirements are increased because: breathing dry. If the animal is not intubated. intravenously if possible. administer 3X the volume of blood lost by slow IV drip. decrease in blood pressure and increase in heart rate  To replace blood loss with saline or lactated ringers. and loss of normal thermoregulatory mechanisms and behaviors.  All of these can contribute to anesthetic death. or if the other cardiovascular parameters are out of normal range (determine normal for the species you are using!) you may have a cardiovascular emergency. hot surgery lights or malignant hyperthermia in genetically pre-disposed animals.using your fingers o Blood pressure .  Hypothermia depresses all physiologic functions. whole blood replacement may be necessary. slows the metabolism of anesthetics and results in prolonged recoveries. Monitor the hematocrit. membranes. loss of skin elasticity. but may occur because of excessive application of heat. Consult with an RAR veterinarian for more information on anesthetic emergencies. Increasing the rate of intravenous fluid administration will improve cardiac output temporarily. the capillary refill time is greater than 2 seconds. However the depth of anesthesia will need to be reduced and if there is a primary cardiac problem it will require specific treatment. the eyes sinking into the orbit. THERMOREGULATION  Animals frequently become hypothermic during anesthesia because of inhalation of cold gases. If it drops below 20%.stethescope or esophageal stethoscope o Pulse rate and pressure .  Monitor cardiovascular function by monitoring one or more of the following: o Mucous membrane color and capillary refill time (the time it takes for the mucous membranes to regain their normal color after pressure is applied) o Heart rate and rhythm .arterial catheter or Doppler cuff required o ECG . including respiration and cardiac function. exposure of body cavities to the room air.If the animal has pale mucous membranes. Hyperthermia is less common. To thermoregulate your patient: . animals on gas anesthesia can be turned down. If an animal is too light the anesthesia should be supplemented. While animal normals vary from species. Instead respiratory and cardiovascular support must be administered until the anesthetic is metabolized and the animal begins to lighten on its own. an animal is considered hypothermic. when body temperature drops below 99° F. Animals that are too deep run the risk of experiencing cardiopulmonary arrest. o Prevent heat loss by insulating cold surfaces with a blanket o Prevent heat loss during gas anesthesia by utilizing low flow techniques that conserve heat o Supplement heat with a thermal blanket (keep blanket temperature below 40 C to prevent burns!) or with pre-warmed fluids o Treat hyperthermia by administering intravenous fluids or applying water to foot pads or exposed skin. if too deep. Only use an ice bath as a last resort.to-species.  To monitor the depth of anesthesia.  Animals given injectable anesthetics can not be lightened directly. Animals that are too light will experience pain and may move during the procedure. as it may cause cardiovascular shock. Below 95-96° F an animal cannot regain normal body temperature without supplementation. in general. MONITORING ANESTHESIA Monitoring anesthesia  The depth of anesthesia must be monitored carefully. o Monitor the body temperature frequently using a thermometer during the procedure and during anesthetic recovery. perform the following: . IV.04 IV For bradycardia Epinephrine 0. resulting in poor blood oxygenation and tissue perfusion and decreased blood pressure and temperature. o Reflexes . Test muscle tone by pulling on the lower jaw or a limb.  Corneal reflex.these reflexes disappear as the animal becomes deeper in the following order:  Palpebral reflex .04 IV For reversal of narcotic sedation or respiratory depression Yohimbine 0.02-0. For cardiac arrest only. it is not sensing pain. o Muscle tone increases as the depth of anesthesia decreases. IM For pulmonary edema.touching the eyelids causes blinking. respiration and cardiac output decrease.1 ml/kg IV. Rigid tone indicates inadequate depth of anesthesia. Anesthetic Dose Indications Emergency (mg/kg) Drugs Doxopram 1-5 IV (10x in Respiratory stimulant. The animal is light if it is blinking. for complete (Dopram) farm animals) respiratory arrest only. If the animal withdraws the toe it is not deep enough. elevations in heart rate and blood pressure may be indications that an animal may be feeling pain and is anesthetized too lightly. . Monitor as previously described. use with CPR Furosemide (Lasix) 2.  Toe pinch reflex . Likewise. it is too deep. Administer IV.touching the cornea of the eye with a tuft of cotton results in a blink. Once the animal has lost its corneal reflex.1-0.15 IV Reversal of xylazine or detomidine sedation Atropine 0.pinching the toe or foot web will cause a pain response. Monitor cardiopulmonary function and body temperature  As an animal becomes too deeply anesthetized. Administer as needed Naloxone (Narcan) 0. unless the animal is receiving a cataleptic drug like ketamine in the absence of a sedative. If it doesn't. Administer to effect and monitor Recovery  Monotoring and support must continue until the animal is completely recovered from anesthesia. Complete recovery means the animal is able to hold itself in a normal upright position. IV (0.5 For diagnosed ventricular tachycardia mg/kg in cats) only. IM intratracheal or intracardiac and perform cardiac massage Lidocaine 2. IC. has returned to normal body temperature and all physiological indices are within normal limits. --------------------------------------------------------------------5556666--------------------------------- --------------------- PART – III DIAGNOSTIC IMAGING SECTION MODULE-20: .  Anesthetic recovery can be rapid for gas agents and short anesthetic episodes.(1:1000) IT. Recovery time can be prolonged if animals were under for a long time or if injectable agents were used. It is the major radiation hazzard y fluorspar examinations. the k shell electron is .  Some are deviated from their course as scatter radiation which decreases the quality of a radiograph by causing fog on the film. the photon travel in a new direction as scatter radiation. Thus the x-ray beam emitted by the machine traverse through the part to be examined to reach the film.  Some x-rays are differentially transmitted through the patient carrying information. carrying useful information that is recorded as a image on the film. It occurs more with low energy incident photons and high atomic numbers element. o Coherent scattering o Photoelectric effect o Compton effect o Pair production o Photo disfiguration Photoelectric effect  The effect is mostly produced when x-ray photos interact with inner shell electrons of a atom (KLM). PRODUCTION AND PROPERTIES OF X – RAYS Learning objectives This module deals with  Types of X-ray apparatus  Parts of X-ray machine  Production of X-rays  Properties of X-rays BASIC INTERACTION OF X-RAY WITH MATTER  For an x-ray examination. the part to be examined is kept between the x-ray source and an x-ray film.When an incident photon with energy slightly greater than the binding energy of a k shell electron encounter the scatter. While passing through the patient. provided that the photons have sufficient energy to over come electron building energy with atom.Compton effect produce almost all the surface radiation encountered is diagnostic radiology.Some photons are absorbed and least to exist. Compton effect  As an incident photon encountered a free electron of the outer shall of the atom.  Photon defected at a narrow angle is electron to reach the film being exposed to cause fog.X ray photon can interact with matter in five ways of which the Photoelectric effect and Compton effect are important in diagnostic radiology. 1000mA . Uses in diagnostic radiology  Contrast of the image is enhanced. o They need little maintanence. o They can be operated from any 15 A electrical point . o They are light and easily manoeuvered . neck. The output ranges from 300 . o They can be easily transported.  The disadvantages is their low milliamperage necessitates longer exposure time and it predisposes to movement blur. The photon disappears as most of its energy is utilized to over come the binding energy of k shell electron. Mobile x-ray apparatus  In machines of this type the transformer are larger to permit higher output and hence cannot be transported easily. it gives off energy is the form of characteristicradiation.  The advantages are o They are less than other types of machines.  Uses o Suitable for x-raying of limbs below stifle and elbow of large animals and abdomen and skeletal system of small animals. (the maximum of 125 kv and 300mA)  Uses o Can be used for large animal for radiographing head . Another electron from an adjacent or outer shell of another atom immediately fills in to the void created by an ejected electron. As this electron drops in to the created void. They are mounted on wheels .90 Kv and 15-30 mA.  The free electron flies off as photoelectron. affected from its shell. and are cumbersome to use for restive animals. Maximum output is 70 . TYPES OF X-RAY APPARATUS Portable apparatus  Portable x-ray machines are widely used in veterinary practise. and limbs and this machine is quite useful for small animal practices Fixed x-ray apparatus  This machine requires transformer which have to be built in the room and special electric connection (3 phase).  No scatter radiation – Excellent quality of radiology  Increases radiation ion of patient. The output varies from 40-60 mA and 90Kv. x-rays ionises the atoms & bring about disturbances in the cells by chemical activity which may cause either destruction or activation or mutation. Suitable for both large animal and small animal radiography. . o Tube stand and o Control panel. So the X-ray machine incorporate some mean to collimate or restrict the beam. o Transformers. density. the cathode (-) and the anode (+). PARTS OF X-RAY MACHINE  It consists of four main parts o X-ray tube. o To minimize genetrical distortion. X-ray tube  An X-ray tube consists of a large thermionic diode glass tube which has been evacuated to produce a high vaccum and in to which are sealed two electrodes.  This is done by using cones or light beam diaphragm in a semi-darkened room. The purpose is three fold & they are o To prevent unnecessary radiations of the patients or persons restraining the animals o To reduce the scattered radiations. thickness of the material  Photographic effect .  Biological effect . This effect is utilised to intensify the x-ray effect by using intensifying screen in the x-ray cassetes. Collimation of X-ray beam  The x-rays because of diverting property is capable of extending to a considerable width. calcium tungstate etc fluoresce when exposed to x-rays & emit green or blue light. This type of mahcines are suitable only for big institutions because of high expenses involved.on photographic emulsions x-rays ionises silver halides on the photo film  Fluoroscent effect . and 120-200kv.certain chemicals such as zinc sulphide. Properties of x-ray beam  X-rays are invisible to eye & travel at high speed & at straight lines  They can penetrate objects depending on atomic no. The oil in the tube helps to dissipate heat apart from acting as a electrical insulator.  Stationary or rotating is placed 1 .stationary and rotating. o Modern machines have two filaments made of tungsten -rhenium alloy to increase the thermionic emission efficiency and hence the tube life. o It is important that the x ray beam should arise from the smallest practical portion of the anode.3 cm apart. The anode angle differs according to individual tube design and may vary between 10 deg and 20 deg and the size of the focal spot may vary from 0. Transformers .3mm to 2 mm. As 99 % of it is converted in to heat. o The stationary one is used in dental x ray machines. o Immediately prior to making an x ray exposure the filament is heated to create an electron cloud by a low voltage current (average about 10 volts and amperege about 3-5.  The vacuum in the tube creates a free flow for the electron beam and also prevents oxidation of cathode filament. This area is often termed as target or focal spot.  The passage of a high kilo voltage electric current across the electrodes results in the production of X-rays. the heat produced at the target is rapidly transferred to the copper block and hence to the oil. Tungsten is preferred because of its high melting point ( 3370 c) and high atomic number.  This also increases tube life. Focussing cup is a concave cup made of nickel or molybdenum and its function is to restrict the electron cloud to a small beam.)The tube current decides the quantity or intensity of the x rays produced and also can be altered in the control panel.  The glass tube isfitted in to an oil filled casing and the whole assembly is housed in a metal encased with lead covering with a small opening for the useful X-rays to exit after filtration. o There are two types of anode . The glass tube is made of borosilicate to with stand high temperature generated inside.The tube current is measured in milliampereage and decides the number of electrons flowing per second from the filament to the target.  Anode o Anode is the target made up of thin sheet of tungsten embedded in a copper block serves to obstruct the electrons to make them give up their energy.  Cathode o The negative electrode consists of tungsten filament and a focussing cup and it serves as the source of electrons. o Larger x ray tubes possess rotating anode to with stand the heat generated due to large exposure. or by bombarding a tungsten target with an electron beam it gives up some of electron of its energy . milli amperage selector the timer. kilovoltage selector. Tube stand  This is to support the x ray tube during the exposure. the reminder of the energy will be converted into x-rays. This results in transient electron vacancy in the K shell into which an electron from the outer shell or from another atom falls and this process continues till the atom becomes stable.  The atom resembles a tiny planetary system with the nucleus as the sun and the electrons as the orbiting planets.  This consists of an auto transformer. and exposure button.  A auto transformer corrects the fluctuations in input voltage. Control panel  This contains the meters switches.  As x-ray beam passes thriough the patient differential absorption takes place depending on the tissue density and shadowgraph is obtained. Electron orbits and energy level  Electrons are negatively charged particles revolving round the nucleus. on and off voltameter. Characteristic radiation or Line radiation  When the projectile electron interacts with the electron in the K shell of the traget atom rather than the electron in the outer shell it results in the ejection of electron in the K shell if the energy of the projectile electron exceeds the binding energy of the ejected electron.  Most of the energy (over 99A) will be transformed into heat. a step down or filament transformer and a high tension transformer. PRODUCTION OF X-RAYS  X rays are produced by energy conversion when a fast moving streams of electrons is suddenly decelerated in the target anode of the x-ray tube.  X rays are generated by two different processes when high speed electrons lose energy in the target of the x ray tube due to radiative interaction. it must contain an equal number of protons and electrons. step down transformer permits the suitably reduced current to the cathode. and the high tension transformer produces a high voltage current for the production of x rays. This .Since an atom is electrically neutral in its normal state. electro magnetic energy etc. heat energy. This makes use of X-rays for its wide application amd so also its potential harmful effects. chemical energy. energy or charge remain unchanged Like matter. energy may exist is many forms eg: Kinetic energy. electric energy. converting all its kinetic energy to a single X-ray photon. potential energy. it slows down. and this loss of kinetic energy is emitted as X-ray photon. Hence physics of X-ray production and priciples involved must be explained. During this the incident electron loses its kinetic energy. due to its slow down. due to the opposite charges.  Matter in the universe is a substance made up of mass and occupies space. energy of one form can easily be converted into another form. TYPES OF X-RAY APPARATUS  X-rays remain the main domain in diagnosis although various other imaging specialities were later explored and being practiced. Hence the X-ray photon energy is characterisitic of the shells involved in an element and so called as characteristic radiation. shifting of electrons results in emission of X-ray photon which possoses an energy equal to the difference between the binding energies of the electrons involved. The incident electron may also collide with the nucleus at times. and gets difflected from its original course. MODULE-21: FACTORS INFLUENCING PRODUCTION OF X.RAYS Learning objectives This module deals with  Factors affecting radiographic quality FACTORS AFFECTING RADIOGRAPHIC QUALITY .  The X-ray produced by this type is called bremstrahlung or breaking radiation. Einstein law of conversion of energy states matter and energy can neither created nor destroyed as its mass. Bremstrahlung radiation or Breaking radiation  When the projectile electron approaches the nucleus of the atom avoiding the orbital electrons.  The main reason behind this is the cost of the equipment involved in the latest imaging techiniques. nuclear energy. For example X-rays are produced in X-ray machine from electrical energy. The lower the kv produces a radiograph with a “short scale of contrast”. provided all other factors remains constant. Secondary radiation and scattered radiations causes lack of contrast. There can be long scale contrast and short scale contrast. (FFD) o Closeness of the object to the film. Contrast  Contrast is the difference between blacks. mA Time and FFD are employed. The factors affecting the detail are: o Shorter Focal Spot film distance.To get good radiograph in veterinary patients the following technique should be followed o Fastest exposure time possible (To prevent movement blur) o Higher kvp. Detail  Detail is the degree of definitions of an object on a radiograph. Density  Radiographic density is determined by the amount of light absorbed by an exposed x-ray film and is a measure of the degree of blackness of the film. o Over exposure or under exposure.  Higher milliamperage produces more x-rays and thus more density and lower milliamperage results is less density. correct density and the proper scale of contrast.  The density of the radiograph varies directly with milliamperage. . Improper development of film and use of warm developer cause lack of contrast. o Use of intensifying screen.  Radiographic density is affected by te subject density which the weight per unit volume of different body constituents. The proper use of various radiographic exposure factors KVP. o Screens.  An good diagnostic radiograph is one is which there excellent details. Good detail is the true reproductions of an object. Radiographic density varies directly with exposure time. o Focal spot size. grays and whites. o Movement of either the patient. cassette on movement of the machine. film contrast. o Any condition fogging the film will bring out loss of detail. Radiographic contrast varies inversely with the kilovoltage.Radiographic contrast is the difference in density between the image of parts or structures on the radiograph. before giving final diagnosis. . in a semi darkened room. Always follow the same conventions. o Constant distance o Constant milliamperage Viewing of the radiograph  Radiograph should be viewed on a good. MODULE-22: PRINCIPLES OF VIEWING AND INTERPRETING X .RAY FILMS Learning objectives ------.  Handling of X-rays  Viewing of X-rays  Interpretation of X-rays HANDLING.  To give radiological interpretation the viewer must have a comprehensive data of clinical and physical examinations and also have a knowledge of the range of radiological animal anatomy and for this a library of normal films taken in the standard position is an asset. Though provisional diagnosis can be given on a wet film. The film is loaded in a suitable size cassette and stored in lead lined boxes. it is advisable to wait till the film is dry. VIEWING AND INTERPRETATION OF X-RAYS Handling  Cassettes with exposed film should be opened in a dark room and the film is removed by holding the corners. the left side of the film should be facing the viewers right side and when viewing the lateral views it would be better that the anterior aspect should be directed towards the left side of the viewers.  When viewing radiographs of the dorsoventral or ventrodorsal or skull.  Over exposed film should be viewed against bright light.This module deals with. evenly lit viewing box. Classification of Lesion---The lesions in the radiograph are classified as developmental. traumatic.RADIOLOGICAL PATHOLOGY OF THORAX Cardiomegaly  Outline of the heart becomes more rounded. Radiographic diagnosis  Radiographic diagnosis consists of two parts namely location of the lesion and classification of the lesion. density.  Trachea and major blood vessels are seen displaced. and degenerative. Viewing  Radiography should be viewed on a good evenly lit viewing box in a semi darkened room.  Lateral view radiographs are viewed by placing it facing left. neoplastic. Radiographs of extremities are viewed with lateral aspect on left side of the viewer.  The loaded cassettes and the exposed film cassettes are kept with radiopaque surface upwards. Unexposed film boxes are always kept in lead lined boxes. Location of the lesion requires knowledge of normal radiographic anatomy. metabolic. architecture. contour.  Occupies a much larger area of the thorax. basic radiographic signs in terms of changes such as size. o Physical examination and o Correct radiographic technique. A systematic and methodical examination of each radiograph will prevent overlooking unexpected lesion. ventrodorsal abdomen or skulls are viewed with a right side of the film facing the viewer’s left side. Module 23 . Interpretation  The three important factors to be considered before interpreting a radiograph are o Case history. .  Posterior border of heart becomes straighter. position and function.  Dorsoventral chest. infectious.  Typical leafy appearance Diaphragmatic Hernia  Disappearance of the normal diaphragm line.  Presence of air in the pleural cavity  Floating heart shadow Fluid in the pleural cavity  Fluid shadow will be masking the structures in the thorax. Tuberculosis  Areas of opacity in lung parenchyma  Recognition of cavitations and calcified nodules in the lung parenchyma or pleura.  Areas of consolidation can be visualized Pneumothorax  Collapse of the lungs. Module-24 = RADIOLOGICAL PATHOLOGY OF ABDOMEN Gastric torsion .  Displacement of lungs and visualization of part of GI tract in thoracic cavity. Bronchitis  Slight increase in the radio-density of the bronchial tree Pneumonia  Areas of increased density of lung substance.  Fluid level appears as area of increased density.  Cardiac silhouette in contact with sternum and diaphragm. Prostate enlargement  Relatively dense mass just anterior and ventral to the pelvic brim in the position normally occupied by the bladder. which is displaced anteriorly. with appearance of homogenous density Kidney calculi  Small irregular dense areas roughly central to the kidney outline Cystic calculi  Radiopaque cystic calculi easily visualized slightly radiopaque calculi can be demonstrated by using penumo cystography. Intussusceptions  Sausage shaped mass with increased density  Thin layer of gas outlining the layers of intussusceptions  Barium enema.  Greatly distended gas filled organ occupying the major portion of the anterior abdomen. Metritis and pyometra .‘coiled watch spring’ pattern. Oesophageal achalasia  Distended organ occupying the upper half of the chest in the lateral view  Dorsoventral view-distended organ projecting beyond the shadow of the spine Oesophageal foreign body  Thickening of the oesophageal wall  Increased density from that of the surrounding tissues. Compartmentalization of stomach. Hydronephrosis  Large mass with a smooth outline in the anterior abdomen filled with fluids. Pyloric Obstruction  Enlargement of the stomach  Accumulation of fluids/material (accumulation of barium) in pyloric area. new bone formation involving acetabulum. Module-25 = RADIOLOGICAL PATHOLGY OF Limb (BONES AND JOINTS ) Radiographic signs of bone diseases  Altered contour of the bone  Altered size of the bone  Decreased one density  Change in trabecular pattern Radiographic signs of joint diseases  Widening or narrowing of the joint space  Cystic changes  Swollen joint capsule-soft tissue swelling Osteoporosis  Diminished density of the bone.  Long bone fractures o Disruption of the continuity of a bone .  Slight thickening and enlargement of uterus.  Hip dislocation o Abnormal width of intra articular space.thickened disorganized appearance of the femoral neck-remodeling and flattening of the femoral head.may be uniformly tubular or sacculated.  Displacement of the colon. Small animals  Hip dysplasia o Bony exostosis. Density  Barium . the absorption of x-ray by the tissues of the body. fat and gas form the basis of plain film radiography. Bone is clearer because of surrounding soft tissues.  In other words. o2 and N20 or atmospheric air.4 (Average)  Fat .  But the kidney pelvic is not visible or the mucous pattern of bladder or stomach are not seen normally due to lack of contrast. Module-26 = CONTRAST RADIOGRAPHY . Ex: Kidney is seen clearly in a plain radiography if there is perirenal fat around the organ. muscles. Examples of positive contrast media re Barium sulphate.  Artificial methods of delineating such organs are required and so a suitable contrast medium is employed.3  Gas (Air) . Radiodense objects absorb larger percentage of the x-rays than radiolucent objects resulting in less film exposure and the recording of white object image. Comparison of equal volumes of different tissues/with their densities. That means absorption capacity of an organ or object is directly proportional to the number of orbital electrons in the atom of the molecule of the absorbing material (atomic number). organic iodine compounds. Organ. The contrast medium may have either high atomic weight and provide positive contrast or a low atomic weight and provide negative contrast. and thus their radidensity. .  Agents used for the demonstration of Alimentary tract. Positive contrast agents  Positive contrast agents can be precisely classified and may be divided into five main groups.1 to 2  The differences in density (radiographic contrast) between bones. depends upon the atomic weight of the principal substances of which the tissues are composed.CLASSIFICATIONS  Radiography is founded upon the principle that an object when exposed to an incident x-ray beam will absorb a part of the x-ray beam and a part willpenetrate the object and interact with the film.6. fluid  Soft tissue 7.14 (Average)  Muscle.56  Bone . Examples of negative contrast media area co2. The substance used routinely for this purpose is barium sulphate. Contrast property. (6) of low viscosity for injecting quickly through a small catheter and (7) of low toxicity and irritancy so that large quantities can be employed. Iopamidol metrizamide (non-ionic)  Agents excreated selectively through biliary system to study the gall bladder. Viscous solution are used to demonstrate bronchial tree and the uterus. Urografin (Ionic agent). The ideal criteria for the contrast media included in this group are that they should be (1) opaque to x- rays and they all contain iodine (2) pharmacologically inert (3) very water soluble so that they can be injected at high concentrations (4) chemically stable so that the iodine is not released in the body (5) rapidly excreted by the kidneys. Ex: Conray.  The substance used for this purpose should be insoluble and non absorbable and inert.  The conventional water soluble contrast media are ionic and are therefore hypertonic and their osmolality ranges from 4 to 7 of that of blood. They are cheap easy to administer and are comparatively safer. Viscous and oily agents  These agents are developed to overcome immediate climination which occure with the water soluble preparation. INTRAVASCULAR CONTRAST AGENTS AND CONTRAST RADIOGRAPY CONVENTIONAL IONIC MEDIA Generic name Proprietary name Meglumine iothalamate Conray-280 Sodium iothalamate Conray-420 Meglumine diatrizoate Urografin-150 Sodium diatrizoate Urografin-370 NEW LOW OSMOLAR NON-IONIC MEDIA Metrizamide Amipaque .  Oily solutions are used in those situation in which it is essential to avoid even the slightest local irritation once introduced they are slowly climinated. The newer low osmolar non-ionic contrast agents have ratio 3 contrast as compared to the conventional high osmolar ionic contrast agents which have only ratio 16. Water soluble agents  These form the largest single group of contrast agents. Radiographic quality  Gaseous agents: Are those most frequently employed. Ex: Biligrafin and Ipodate calcium powder (solu-Biloptin) (Scheringe). after absorption from alimentary system or intravascular injection. Iohexol. Radiographs are taken immediately on completion of the injection.  To reveallesions in the wall of the alimentary tract.27 :-CONTRAST RADIOGRAPHY OF THORAX & ABDOMEN => THORACIC CAVITY Angiography  The radiographic demonstration of the vascular system by the injection of a water soluble organic iodide compound into a suitable vessel. Procedure  Oesophaqus o No preparation is required. o Normal oesophequs should not retain bacium. Ex: Dilatation of stomach or oesophagus. Ex: Hernia. o Technique-  Contrast agents are injected rapidly by means of a syringe of an appropriate volume connected to a hypodermic needle or cannula or catheter which is inserted into a suitable blood vessel. Ex: Neoplasms – Ulcer. Ex: Tumour or stenosis.  To find out distorsion of the wall of alimentary tract such as enlargement. Orally (Braium Swallow) and taken with lateral and ventrodorsal projections immediately after administration.Iopamidol Niopam Iohexol Omnipaque MODULE.  To find out displacement of the alimentary tract. Specialized techniques o Arteriography-Arteries o Venography-Veins o Aortography-aorta o Portal venography–Portal vein o Angiocardiography-Heart and vessels o Cerebral angiography–Cerebral vessels. Only a thin streak of barium indicating the position of the oesophegus and outlining the . ALIMENTARY TRACT Indications  To reveal obstruction of the alimentary tract. Take plain radiography and administer Barium sulphate paste about 50 to 100 Gms. 1 hr. Space occupying lesions or obstructive lesions can be easily demonstrated. o The stomach should be empty by starving overnight or by administering laxative or enema if necessary. mucous surface is seen as normal oesophagus is a collapsed tubular structure.  Contrast agents used o Oily fluid containing 40% iodine (Ex. right lateral.  Stomach o 50 to 100% suspension of about 15 to 100 ml. ventro dorsal and oblique if necessary to demonstratethe different areas of stomach and mucosal surface. and 4 hrs.  Small Intestine o To promote easy passage of the contrast agent 25% suspension is preferred. Technique  Cysterna puncture  Lumbar puncture  Under general anaesthesia the contrast agent is injected into the sub-arachnoid space. In the first method cisterna magna is punctured and in the second .CONTRAST RADIOGRAPHY OF SPINAL CORD & URINARY SYSTEM = MYELOGRAPHY Indication  To outline the neural canal  To demonstrate disc lesions and other space occupying lesions. Double contrast gastrography or colonography can be obtained by combining air (negative contrast agent)  The functional and anatomical abnormalities could be better assessed by means of flucroscopy apparatus. Is given orally observed under fluoroscopy or x-rays are taken at regular intervals 10 minutes. Iohexol. o Water soluble: Metrizamide soluble. MODULE. at different angles like left lateral. o Normal stomach start emptying the barium within minutes after the administration. Iopamidol solution.28 :. Myodil). etc. 30 mts.  Large Intestine o To demonstrate large intestine barium is best given by enema. Intestinal motility can be assessed. Repeated x-rays at interals could demonstrate lesions inside or outside the intestine easily. if available. 10 mts. Of normal saline and given by drip taking about 20 to 40 mt. Pictures are taken at 5 mts.3 ml.  The animal may be positioned in an inclined plane for easy flow caudally. Sodium diatrizoed (Hypoque). Cystography  Indications . Meglumine Iothelamate (conray-280). method sub-arachnoid puncture is made using a spinal needle between 4th and 5th Lumbar vertebral space in lateral recumbent position. And 10 mts. Is injected into the subarachnoid space and x-rays are taken immediately. 5 mts. Time to give more accurate evidence of kidney function and is a safer method.body wt. And 20 mts.  Preparation: With hold food for 24 hrs. To 0. Per animal.  To show the presence or absence of lesions in the renal pelvis. Empty the bowels with enemata. Interval under lateral and ventrodorsal projection. With ventrodorsal and lateral projections.5 ml/kg. In the case of oily agents the contrast material will tend to globulate and remain in the canal for longer period causing at times undesirable side effects. UROGRAPHY: (PYELOGRAPHY AND CYSTOGRAPHY) Intravenous urography (Intravenous pyelography. IVP)  Pyelography is used to demonstrate kidney shadow when it cannot be demonstrated in a straight radiography. Iopamidol (Niopem) Metrizamide have also been used. Body weight may be administered I/V usually 1 to 2 ml/kg. Use of a compression bandge over the abdomen will enhance the clarity of renal pelvis and ureter. Anaesthesis as optional  Technique o Inject the dyeasa single bolus I/V by taking about 1 minute.  Contrast agents used o Ionic contrast agents such as sodium Iothalamate (conray-420). If Metrizamide or any other water soluble agent is used.  Dosage: To give better demonstration upto 600 mg to 1200 mg/kg. Body weight. and water for 12 hrs. o This technique is popularly known as intravenous pyelography or excretory urography.  To get a rough indications about renal function..If myodil is used the quantity is 0. Another method to carry out this procedure is to mix the contrast agent about 1200 mg/kg. Non-ionic contrast agents such as Iohexol (Omnipaque-300). Straight firms may be taken before injection and subsequent to injection at 1 mt. With 150 to 250 ml.  The advantage of the new water soluble non-ionic solution is that it gives better visualization of the spinal canal and the agent gets eliminated within few hours.5 to 2 ml. 0. Sodium and Meglumine diatrizoate (Uregrafin 60% or 76%).  Preparation: The G. To recogrise radiolucent small calculi 2. the gonads.  Certain tissues especially those which contains many multiplying cells. tract should be empty.29 =RADIATION HAZARDS AND ADOPTION OF SAFETY INCREASERS Dangers of radiations  Ionising radiation used in diagnostic radiography is potentially harmful and if proper protective measure are taken the risk is small compared with the benefit to the patient. 1.  X-rays have long term effect of producing Cancer. long after irradiation injury has healed. To demonstrate space occupying lesions in the bladder. Are employed after catheterizing the bladder. 3. lymphoid tissue. spleen). such as blood forming organs (bone marrow. inject the contrast agent either iodine solution or air (100 to 300 ml). For double contrast small quantity of iodine solution followed by air may be used for better visualization of the interior of bladder.  Procedure: After evacuating the bladder. Radiography is taken (lateral & ventrodorsal projections). Iodine compund 10 to 20% about 40 to 100 ml. To demonstrate abnormal prostate gland. embryos and cetain tumours are radiosensitive. .I. Module. 20. A transducer is a device that converts one form of energy to another.e greater than 20. In 1957 – Ian Donald invented – scanner or diagnostic ultrasound. The piezoelectrical crystal in an ultrasound transducer generates a pulse. Mechanical transducers are devices where the movement of crystals suspended in a coupling medium generates ultrasound.PRINCIPLES AND ITS APPLICATION IN VETERINARY PRACTICE Learning objectives This module deals with  Principles of ultrasonography  Properties of ultrasound waves  Different modes of echo display PRINCIPLES OF ULTRA SONOGRAPHY Introduction Medical sonography is the only diagnostic imaging modality that does not use electromagnetic radiation. A basic understanding of the physics of ultrasound. When this crystal is stimulated electrically it changes its shape and produces sound waves of a particular frequency.000 Hz. What is ultrasound?  Sound waves of frequencies greater than audible to the human ear i. MODULE-30: ULTRASONOGRAPHY . Diagnostic ultrasound uses frequencies between 1 to 10 MHz  A sound wave travels in a pulse or a wave and when it is reflected back it becomes an Echo and this pulse-echo principle. is called Ultrasound waves.where as . its interactions with tissue and the functions of the controls are important while using the machines. Modern ultrasound instruments are highly sophisticated pieces of equipment. is used for ultrasound imaging.  As the transducer is placed in close contact with the body surface through a coupling medium it undergoes continuous modification. lower in liquids and lowest in gases. wavelength and velocity are parameters used to describe the sound waves.  When this crystal is stimulated electrically it changes its shape and produces sound waves of a particular frequency. which is used for ultrasound imaging.  Diagnostic ultrasound frequency ranges between 2 mega Hertz and 13 mega Hertz. PROPERTIES OF ULTRASOUND WAVES  Frequency.  It is this pulse-echo principle. Interaction of ultrasound with matter . which occurs through three processes those are absorption.Medically sound waves travel fastest in bone and slowest in gas filled structures.  Wave length is the distance travelled by the sound in one cycle and is expressed in millimeters and is important for image resolution. A pulse is generated by one or more piezoelectrical crystal in an ultrasound transducer. because they use the average velocity of sound in soft tissue 1540m/s. reflection and scattering. electronic transducers also called array transducers do not have intrernal coupling medium and are fired electronically. an image can be produced on the display of the scanner which relates to the acaustic independence of tissues encountered by the ultrasound beam and the depth / distance of tissue interfaces. How is ultrasound generated?  When a high voltage electrical current is applied crystals in the transducer are vibrated and this is called piezo electric effect.  A sound wave travels in a pulse and when it is reflected back it becomes an Echo.  This causes a problem for diagnostic ultrasound machines.  Velocity is the rate at which sound travels through an acoustic medium. As a rule it is greatest in solids.  By means of the echo principle.  Absorption: It occurs when the tissues absorb heat energy in the sound beam. Absorption process forms the basis of therapeutic ultrasound.  Reflection: The reflection gives rise to an echo and forms the basis for ultrasound scanning. Interfaces between tissues of different acoustic impedence give rise to different echoes. These echoes are converted by piezoelectric effect into electrical signals and displayed onto a oscilloscope screen.  Scattering: It occurs when the beam encounters an interface that is irregular and smaller than the sound beam. The portion of the beam than interacts with this interface is scattered in all directions. Since the scattering interfaces are small, only a small portion of the beam is involved. Once the echoes are converted into electrical signals, these are processed and transformed into a visual display of the measure of the amplitude of the echo. This is known as echo quantification. Generation of images on the display  Two basic shapes of ultrasound images are encountered: images made in sector fashion are pie shaped and linear fashion are rectangular  Images are usually generated from the systemic scanner converter or frame store which processes the reflected ultrasound in to a form required for screen presentation.  Information is displayed regarding distance and amplitude. Each echo position is represented as a dot on the screen. Thus a two dimensional image is generated.  The brightness of each dot is related to the amplitude of the reflection and is referred as a grey scale display.  Resolution is the ability of the ultrasound machines to distinguish echoes on the basis of time, space and strength. o Axial resolution: Ability to differentiate two objects lying closely together in the direction of the beam. o Lateral resolution: Ability to different the two objects lying side by side. The ultrasound beam is refracted when it enters a tissue of different acoustical density.  The image of refraction depends on the relative velocity of sound in the two tissues.  Depth of sound wave penetration varies inversely with frequency. DIFFERENT MODES OF ECHO DISPLAY Different modes of echo display  Different modes of echo display are Brightness mode, B – mode B scan or grey scale used commonly for abdominal scanning and cardiac imaging.  Static B mode: Transducer is moved in the scanning plane by hand.  Real time B mode: Sound beam automatically and rapidly moves in the scan plane. In this method the image is continuously updated to allow movement.  Motion mode: M–mode mainly used for echocardiography.  A MODE or amplitude mode is simplest form of display. It displays two parameters of the echoes in the form of spikes, ie., distance from the transducer and the amplitude. The horizontal line shows the distance and the amplitude is depicted on the vertical line. It is used for ocular biometry. Different types of basic probes  Linear curvilinear and sector probes  Transducers are classified based on the location of crystals on the scan head. When elements are located at the end of the probe they are called end fire transducers and they are used in abdominal and cardiac scanning. Side fire trasducers are used for intracavity scanning like large animal reproductive scanning. Doppler ultrasonography  The pitch of a siren in a train changes with the proximity of the train movement, due to difference in the sound wave frequency, called Doppler shift, the principle used in imaging the direction and velocity of blood flow. It was first proposed by Johann Christian Andreas Doppler in 1842.  Four Doppler modes are used in medical ultra sonography. They are Continous wave Doppler, pulsed wave Doppler colour Doppler and power Doppler. MODULE-31:- RADIATION THERAPY - PRINCIPLES, ISOTOPES AND THEIR USES IN DIAGNOSIS AND THERAPY Learning objectives This module deals with  Radiation therapy and its methods  Complications 0f radiation therapy RADIATION THERAPY - INTRODUCTION  Radiation therapy for the treatment of neoplasm of domestic animals has been used since the discovery of X-ray. Dr. R. Eberlin was the first to report on the use of radiotherapy in veterinary practice.  Radiotherapy is usually indicated for localised solid neoplasm’s that cannot be excised completely. It is not indicated if neoplasm has the potential of high incidence of metastasis.  The other indication are : 1. When surgery is expected to or has already failed. 2. When the regional or distant metastasis not occurred. 3. When radical surgery is unable to remove whole of the neoplasm. 4. When bulk of the neoplasm needs reduction in size so that it can subsequently be removed surgically.  Radiotherapy is not done by a single dose, rather multiple treatments are given over a period of time, termed fractioned therapy. In animals, it is usually in 10-12 fractions of a radiation dose of 4-5 Gy each time, usually three times per week. METHODS OF RADIOTHERAPY Teletherapy  The radiation source is kept at a distance from the lesion. It is of four types o Superficial X-ray therapy: Given through X-ray machine with energy range of 60-100 keV. o Deep X-ray therapy: Given through X-ray machine with energy range of 100- 200 keV. o Super voltage therapy: Provided through (i) X-ray machine having linear accelerator or betatron or cyclotron, (ii) isotropic X- ray machine with cobalt or cesium. It is used in deep and substantial lesions o Particulate beam therapy: Electron, neutron or proton beam can also be used as a mode of teletherapy. Brachytherapy  It is the therapeutic use of radioisotope either within the interstitium or on the surface of a neoplasm. The isotopes used are 198 Au , 60 Co, 125 K. Specific methods of brachytherapy are o Interstitial brachytherapy: Sources of radiation are within the interstitium of the neoplasm. o Pliesotherapy: It is surface brachytherapy for superficial lesions. o Systemic brachytherapy: 132 I and 32 P can be used systemically. It is used in extensive lesions and specific malignant conditions. life span shortening .PRINCIPLES AND THEIR APPLICATION Learning objectives This module deals with  Digital Radiography (DR)  Computed Tomography (CT)  Magnetic Resonance Imaging (MRI)  Nuclear Medicine DIGITAL RADIOGRAPHY (DR) Basic principles  DR involves translating x-ray energy into an electric signal that is in turn converted to digital data (numbers). In direct DR. In indirect DR. and the x-ray image is available for viewing almost immediately after exposure. MODULE-32: SCAN AND MRI . COMPLICATIONS OF RADIOTHERAPY  Complications of radiotherapy are o Immediate (minute to days): epilation. or hybrid. cancer. which is connected to a computer. the light is then converted to an electrical pulse. erythema . the x-ray energy is first converted to light by using a phosphorescent plate. lethal gene expression etc. indirect. hematological depression and GI disturbances and chromosomal aberration. the x-ray energy is converted directly into an electrical signal. The process may be direct.  The data are recorded on a plate. Hybrid radiographic processes record the output of the phosphorescent plate with a system . It can then be stored or printed out. o Latent (months to years): leukemia . CT . This image represents a slice of the body at the level under examination. inverting the image. However. CR and DR systems have a number of advantages compared with film screen systems. such as brain white and gray matter or liver and gallbladder.  The pattern of x-rays that reaches the detectors is recorded—a projection. A fan- shaped beam of x-rays passes through the body at a predetermined level. The entire gantry assembly is then rotated slightly.  A computer uses complex mathematical formulas to create an image from the series of projections.  The advantage of CT is its ability to distinguish different types of soft tissue. The tube and the detectors rotate in unison around the subject under examination.  The images may be quite large files. applying sharpening filters. DR and CR images are stored on a computer hard drive and should be saved as DICOM (Digital Imaging and Communication in Medicine) files.  The linear response of digital systems to the x-ray exposure means that these systems are relatively forgiving of errors in radiographic technique. Some form of backup device is recommended. These images may be manipulated in multiple ways. including adjusting brightness and contrast. A series of such projections is obtained. generating a new projection. and the procedure is repeated. The tube is mounted on a gantry opposite a series of detectors. COMPUTED TOMOGRAPHY (CT) Basic principles  CT is an imaging method that uses the principles of tomography. completely encompassing the body under examination. ideally at another location. but they can be easily transmitted to a remote location for review by a radiologist or other specialist. Tomography is the demonstration of a slice through the body displayed without interference from structures lying above or below the level under examination. and magnifying part or all of the image. the quality of DR images depends on software processing to produce a degree of contrast that is familiar to the reader. similar to that found in a digital camera.  CT uses x-rays generated by a high-output x-ray tube. Superimposed structures are eliminated. and ears. If the tissue attenuates or stops the x-rays less than the reference tissue or less than expected. and the reference tissue or structure is usually stated. Therefore the gray scale of the image is adjusted to assign useful grays to tissues with varying levels of attenuation. principally in water molecules. tissues and structures are described in terms of attenuation. MRI uses hydrogen atoms to generate an image. A soft tissue window shows good contrast and detail within soft tissue structures such as the liver. In CT imaging.  The term hyperattenuating is used to describe tissues with more attenuation than expected.  CT images are digital. referred to as the window. The appearance of a tissue is defined in relation to some reference tissue or its expected normal appearance. Attenuation is equivalent to radiopacity in radiography. brain. it is described as hypoattenuating and is portrayed as a darker shade of gray. Thus isoattenuating means having the same attenuation and would be displayed as the same shade of gray. sinuses. achieves this degree of contrast by being able to measure very fine differences in the ability of tissues to stop x-rays passing through them. These terms are relative rather than absolute. Iodinated contrast agents such as those used for myelography or excretory urography may be used by intravenous injection. whereas bone appears white and lungs dark. The gray scale can be adjusted to highlight specific features such as bone or soft tissue (windowing). which is a measure of the capacity of a tissue to stop x-rays. whereas soft tissues appear gray with little detail and lungs appear quite black. It may also be used to evaluate the spine. joints. and abdominal masses MAGNETIC RESONANCE IMAGING (MRI) Basic principles  Unlike CT. pleural cavity. but almost all other structures appear white with little detail. CT may be used to image almost any body part. brightness and contrast are adjusted to highlight specific structures. Hydrogen is universally distributed in the body. In viewing CT images. A bone window will display detail of skeletal structures such as cortex and trabeculae. no ionizing radiation is used in magnetic resonance imaging (MRI). and a computer is used for viewing. .  Hepatic veins can be distinguished from the gallbladder and other soft tissues. mediastinum.  Lesions with abnormal circulation may show marked contrast enhancement after such injections.  A lung window will show detail within the lungs. CT can resolve far greater contrast than can be displayed on a monitor or appreciated by the human eye. Among the more common applications are diseases of the nasal cavity. lungs.  MRI uses relatively strong magnetic fields. which can resolve objects of 0. Signal intensity is used to describe the appearance of tissues in MRI. However. This is similar to CT but compares poorly to radiographic systems. a small majority of the protons will be forced to point in the direction of the field while spinning at a specific rate. in the case of MRI. they release energy in the form of a radio signal.  Bones. Under normal circumstances.  A radio signal pulse at the same frequency as the spin of the protons will knock them out of their equilibrium state. it has the same appearance as some reference tissue—for example. whereas hyperintense means more signal and a brighter appearance. This signal is collected by a scanner.  Lesions that accumulate gadolinium appear bright (hyperintense) with some sequences.1 mm in size.  Smaller gradient magnetic fields are used to localize signals from specific blocks of tissue. MRI can provide useful data about these structures. or appearance before the use of contrast. . In a strong magnetic field. Nonetheless. As in CT. As the protons return to their original state. which is termed spatial resolution. MRI uses contrast agents that enhance lesion visibility. MRI is capable of distinguishing or resolving objects of approximately 1 mm in size. Whereas CT offers good soft tissue detail.  It is a relative measure of the radio signal generated by tissues in response to the stimulating radio energy pulse. a mass might be isointense to the gray matter of the brain. which creates the impression of much finer detail. just as attenuation is in CT imaging. Each atom acts as a tiny bar magnet.0 tesla in clinical use. and displayed. MRI has excellent contrast. the contrast seen with MRI is superb.  Hypointense means less signal and appears darker. Different sequences of radiopulses can be used to emphasize different tissue characteristics. Hydrogen atoms are essentially spinning protons and have an electrical charge. effectively an echo of the original pulse used to disturb the protons.  MRI has superb contrast resolution in soft tissues and is very sensitive to changes such as edema and hemorrhage. showing different soft tissues as distinct shades of gray. Manipulation of the parameters such as the timing and duration of the radiopulse and the interval before an echo is recorded is used to highlight tissue features. ligaments. reference tissue. processed. these terms are relative and must be defined in relation to the expected normal appearance. If something is termed isointense.05 to 3. these tiny magnets are arranged randomly. ranging from 0.  Like CT. which alters the local magnetic field and changes signal intensity. the agents are based on gadolinium. and tendons appear quite dark on all image sequences because they have very little water content and therefore very little hydrogen to generate a signal. It is an imaging technique in which radionuclides (radioactive elements emitting gamma rays) are administered to a subject. Nuclear medicine images are described in terms of uptake of the radiopharmaceutical. MRI applications include imaging disease of the central nervous system. while in others quantitative analysis is performed. so slices can be varied infinitely to highlight lesions. which is limited to images in the plane of the gantry. and their concentration. MODULE . joints.  The radionuclides are attached to chemicals to form radiopharmaceuticals that accumulate in the tissue of interest. images can be obtained in any plane.PRINCIPLES AND ITS APPLICATION Learning objectives This module deals with  Doppler Ultrasound  Types of Doppler Ultrasound  Applications of Doppler Ultrasound DOPPLER ULTRASOUND . Mostradiopharmaceuticals are analogues of physiologic substances or biologic organic molecules.  The degree of uptake is subjectively assessed in some techniques. can be detected by gamma-ray detection equipment—usually a gamma ray camera.  The gamma rays are converted by the camera into signals from which a computer produces a digital format that is used to construct an image of the area under examination. In this way normal and abnormal tissues can be identified by the selective accumulation of the radioactive substances within them. and the abdomen. NUCLEAR MEDICINE (SCINTIGRAPHY) Basic principles  Scintigraphy is a branch of nuclear medicine. nasal cavity and sinuses.  Unlike CT.33 :- ECOCARDIOGRAPHY . Their presence. Power Doppler is most commonly used to evaluate blood flow through vessels within solid organs. the pitch does not change.  It can show blocked or reduced blood flow through narrowing in the major arteries of the neck that could cause a stroke.  Duplex Doppler: Duplex Doppler ultrasound uses standard ultrasound methods to produce a picture of a blood vessel and the surrounding organs.  During pregnancy.  Color Doppler: Color Doppler uses standard ultrasound methods to produce a picture of a blood vessel. including blood cells. It helps to evaluate blood flow through major arteries and veins. Power Doppler can get some images that are hard or impossible to get using standard color Doppler. or DVT) that could break loose and block blood flow to the lungs (pulmonary embolism).  Information from the reflected sound waves can be processed by a computer to provide graphs or pictures that represent the flow of blood through the blood vessels. See a picture of a Doppler ultrasound. such as those of the legs and neck. Doppler ultrasound may be used to look at blood flow in an unborn baby (fetus) to check the health of the fetus. It also can reveal blood clots in leg veins (deep vein thrombosis. Also. a computer converts the Doppler sounds into colors that are overlaid on the image of the blood vessel and that represent the speed and direction of blood flow through the vessel. These graphs or pictures can be saved for future review or evaluation. This type of ultrasound can be done at the bedside in the hospital with a portable machine to provide a fast estimate of the extent of blood vessel damage or disease.  During Doppler ultrasound. a computer converts the Doppler sounds into a graph that gives information about the speed and direction of blood flow through the blood vessel being evaluated. The veterinarian listens to the sounds produced by the transducer to evaluate the blood flow through an area that may be blocked or narrowed. TYPES OF DOPPLER ULTRASOUND The basic types of Doppler ultrasound are  "Bedside" or continuous wave Doppler: This type uses the change in pitch of the sound waves to provide information about blood flow through a blood vessel.  The movement of blood cells causes a change in pitch of the reflected sound waves (called the Doppler effect). . The sound waves bounce off solid objects. If there is no blood flow. Also. The transducer sends and receives sound waves that are amplified through a microphone. Power Doppler is a special type of color Doppler. a handheld instrument (transducer) is passed lightly over the skin above a blood vessel.  A Doppler ultrasound test uses reflected sound waves to see how blood flows through a blood vessel. coronary arteries and limbs  Can show if you have any blood clots in the veins in limbs  Can show the amount and speed of blood flow in your veins and arteries  Can be used instead of some more invasive procedures further reading. . arms.Nuclear Scintigraphy NUCLEAR SCINTIGRAPHY  Scintigraphy ("scint. and the emitted radiation is captured by external detectors (gamma cameras) to form two- dimensional images. spark) is a form of diagnostic test used in nuclear medicine. wherein radioisotopes (here called radiopharmaceuticals ) are taken internally. APPLICATIONS OF DOPPLER ULTRASOUND  Non-invasive  Generally painless  Does not use radiation  Can show if you have any blocked arteries in neck." Latin scintilla. abdomen. GAMMA CAMERA. XERORADIOGRAPHY AND DOPPLER Learning objectives-This module deals with. MODULE-34: PRINCIPLES AND APPLICATIONS OF SCINTIGRAPHY. In both the case sodium iodide crystalis used which absorbs gamma rays emitted by the radioisotope from the patient and converts it to light flashes. 3. Thus the localisation of radioisotope can be detected by using camera due to emission of gamma rays. ------------------------------------#@#----------------------------------------------------- --------- THE END . images of vertebral column and detecting the neoplasms. GI tract. The interpretation is based on the appearance of increased (hot spots) or decreased (cold spots) radioactivity region. cardiac. Any inflammatory or pathological process that causes increased bone activity can be diagnosed by scintigraphy. This impulse is shown on a oscilloscope or converted to an image. Usefull in diagnosing occult lameness. in addition. lung functions .  Problems associated with scintigraphy are 1. It has also been used to study renal. Non specificity to the aetiology and difficulty encountered some times in interpreting the scan especially skeletal system. radiation exposure is minimum.  A scan appears as a image formed of dots. Active process produces hot spots where as cold spots observed in case of abscess. The light is converted to an electrical impulse. lungs thyroid glands etc. Precise and strict safety precautions required.  The distribution of the labelled isotope can be detected by a gamma camera or a hand held detector. Using this technique it is easier to detect localised increase or decrease in bone turn over as a result of trauma or disease. liver . The principle is based on the use of pharmaceutical labelled with radioisotope which after entry into the blood stream get localised in particular tissue or organ. Image can be produced in colours or in a grey colour. Most widely used radioisotope is Technetium-99m. This isotope has the advantage of a short half life of 6hrs and thus animal can be discharged next day after the scan .  It is mainly used to detect functional disorders of kidney. Cost of the gamma camera 2.