Traumatic Reticuloperitonitis by Ali Sadiek

March 23, 2018 | Author: Ali H. Sadiek أ.د. علي حسن صديق | Category: Medical Specialties, Clinical Medicine, Medicine, Diseases And Disorders, Wellness


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Traumatic Reticuloperitonitis TRP and its allied syndrome in CattleHardware Disease Foreign Body Disease by Dr. Ali H. Sadiek Prof. of Internal Veterinary Medicine and Clinical Laboratory Diagnosis Faculty of Veterinary Medicine Assiut University E-mail: [email protected] 1 Prof. dr. Ali sadiek Traumatic Reticuloperitonitis • TRP, is a common disease in adult cattle caused by the ingestion and migration of a foreign body in the reticulum. • Cattle are more likely to ingest foreign bodies than small ruminants since they do not use their lips for prehension and are more likely to eat a chopped feed. • The disease caused great economic losses among cattle (Decreased Milk yield, decreased feed conversion, and deaths) • The typical foreign body is a metallic object, such as a piece of wire or a nail, often greater than 2.5 cm in length. Or any sharp needles etc, that can cattle swallow it during grazing, hand feeding etc. 2 Prof. dr. Ali sadiek Traumatic Reticuloperitonitis • Dairy cattle older than 2 years of age more commonly affected than beef cattle since they are more likely to be fed a chopped feed, such as silage or haylage. • A large number of adult dairy cattle have metallic foreign bodies in their reticulum without signs of clinical disease. • Tenesmus or a gravid uterus, are likely predisposing factors causing migration of the foreign body into the reticular wall. 3 Prof. dr. Ali sadiek Pathogenesis of TRP • Lack of oral discrimination in cattle lead to ingestion of foreign bodies. • It may be lodged in the upper esophagus and cause obstruction. • It may be in the esophageal groove and causes vomiting. • It may remain fixed without penetration and without serious results and will gradually be voided away. • Mostly it may pass to the reticulum where the vigorous contraction, the nail penetrate it. • Rarely It may be pass toward the spleen or liver. 4 Prof. dr. Ali sadiek Common sequelle of Traumatic Perforation of reticulum 1- Acute local peritonitis Diaphragmatic hernia 2- Acute diffuse peritonitis Toxemia, Depression and Recumbency 3- Chronic Local peritonitis Vagus indigestion 4- Pericarditis Death with CHF 5- Recovery 5 Prof. dr. Ali sadiek Uncommon sequelle of Traumatic Perforation of reticulum 1- Rupture of gastroepiploic artery Internal hemorrhage & death 2- Abscess in liver, spleen, diaphragm 3- Pneumonia and pyelonephritis. 4- Endocarditis 5- Rupture of coronary artery and pericardium (Hemorrhage and Cardiac Tamponade) 6 Prof. dr. Ali sadiek Clinical signs of TRP • The classic signs of acute, localized peritonitis characterized by: Sudden anorexia, drop in milk yield, fever, ruminal stasis and local pain in the abdomen. • If the foreign body has penetrated the diaphragm and pericardium, affected cattle also can have muffled heart sounds, jugular pulses, and brisket edema secondary to congestive heart failure caused by pericarditis 7 Prof. dr. Ali sadiek I- Clinical signs of Acute Local Peritonitis 1- Sudden stop of eating. 2- Marked Depression in Milk yield to the 3rd 3- Sub acute Abd. Pain. 4-Abdominal pain, reluctant to move, often grunts when made to move 5- Stands with arched back and tense abdominal wall , stucked abdomen. 7- Urination and defecation may be assoc. with grunt. 8- Mild fever, tachypnea. 9- Absence of ruminal motility and development of mild bloat 10- Constipation 8 Prof. dr. Ali sadiek II- Signs of Acute diffuse peritonitis It is ch. by severe toxemia within 1-2 days after onset of acute local peritonitis. Complete ruminal atony. Mild fever of mild hypothermia in post-partum cases, Tachycardia > 100/min. Pain is inducible allover the entire abdomen. Finally profound depression, peripheral circulatory failure and absence of symptoms. Recumbency, coma similar to that of Milk fever, 9 Prof. dr. Ali sadiek III- Cl. signs of Chronic Local Peritonitis • A significant population of affected cattle develops chronic or subclinical TRP that is not as easily diagnosed as acute TRP. • Chronic peritonitis ch. by Anorexia and unthriftiness. Decreased milk production. Rumen hypomotility. Change in manure consistency. 10 Prof. dr. Ali sadiek Diagnosis of TRP 1. 2. 3. 4. 5. 6. 7. 8. History of Sharp fall in milk yeild and appetitie. Clinical examination. Pain test: Ferroscopy : A metal detector (Radiography of the reticulum. Laboratory tests: Abdominocentesis, hematocrit, leukocyte count, blood biochemical profiles were performed and glutaraldehyde coagulation test. Ultrasonographic examination: Exploratory laparotomy: Exploratory rumenotomy 11 Prof. dr. Ali sadiek 3-Pain test Pain test: pain accompanies reticular or ruminal contractions may be watched or induced as follow: Vigorus palpation of the abdominal wall behind the sternal xiphoid process. Exerted Pressure by the closed fist or the knee. Pinching the withers to cause depression of the back. Sharp elevation of animal under the abdomen. A positive response to any of these tests is a grunt of pain audible by the ear, but you detect it more clearly by auscultalion of the trachea. and could be watched during examination as an aid of diagnosis. 12 Prof. dr. Ali sadiek 3- pain test “pinching weather” 13 Prof. dr. Ali sadiek 3- Pain test“Sharp elevation of animal” 14 Prof. dr. Ali sadiek 3-Pain test “grunt when firmly pressed down ” 15 Prof. dr. Ali sadiek 4- Ferroscopy (a Metal detector) 16 Prof. dr. Ali sadiek 5- Laboratory tests I- Complete blood count : In general, cattle with persistent purulent inflammation have leukocytosis and neutrophilia. In acute, localized peritonitis , CBC may be normal in some cases or have a degenerative left shift (band neutrophils, outnumbering segmented neutrophils) in others. Acute diffuse peritonitis assoc. with degenerative left shift. In chronic cases, a mature neutrophilia is common. Lymphopenia: secondary to the stress (Releasing corticosteroid) causing cell redistribution; circulating lymphocytes do not reenter the lymphatics but become sequestered in lymphoid tissue and bone marrow. 17 Prof. dr. Ali sadiek 5- Laboratory tests II- Serum biochemical profile: Hyperproteinemia with a hyperglobulinemia: a total serum protein > 10 mg/dL is highly suggestive of TRP. Increased fibrinogen > 1 g/dL. Fibrinogen is an acute phase protein, and in cattle it may be the best indicator of acute inflammation because fibrinogen concentrations often increase prior to development of neutrophilia. Hypochloremia, hypokalemia, and metabolic alkalosis; may be due to sequestration of HCL in the rumen due to rumen stasis or vagal indigestion. Hypokalemia is caused primarily by anorexia, but may be potentiated slightly by ion exchange caused by the alkalosis and/or abomasal reflux into the rumen. With alkalosis, intracellular H+ ions can be exchanged for extracellular K+ ions, decreasing serum potassium concentrations. 18 Prof. dr. Ali sadiek 5- Laboratory tests 2- Peritoneal fluid of suggestive of peritonitis ch. By: Turbid or containing gross pus or fibrin are indicative of peritonitis, at least locally. Normal bovine peritoneal fluid clot upon standing. Nucl. Cell Count (NCC) > 10,000 cells,+ neutrophils > 40%. + Immature, degenerative, or toxic neutrophils is suggestive of purulent peritonitis . The presence of intracellular bacteria and/or degenerate neutrophils indicates septic peritonitis. 19 Prof. dr. Ali sadiek 5- Laboratory tests Two degenerative neutrophils with phagocytosed bacteria in abdominocentesis fluid from a cow with TRP Bacteria also in the background of the smear 20 Prof. dr. Ali sadiek 6- IV- X-ray and Sonography Hyperechoic deposits noticed adjacent to the reticular wall suggestive of fibrin deposit 21 Prof. dr. Ali sadiek 7- Exploratory Laboratomy and Rumenotomy • Refers to surgery 22 Prof. dr. Ali sadiek Differential Diagnoses of TRP TRP must be distinguished from other causes of peritonitis or abdominal pain for a definitive diagnosis. 1. Pyelonephritis: presence of pus and blood in urine. 2. LDA: presence of abomasal sounds in the left flank. 3. Hepatic leosions there is pain over the posterior ribs on the right side, Jaundice etc. 4. Rumen acidosis: Tachycardia, staggering, recumbency, blindness; hypothermia. No history of engorgement no signs of hemoconcentration. 23 Prof. dr. Ali sadiek Differential Diagnoses of TRP 5. A perforating abomasal ulcer: mild-abdominal pain. may show evidence of gastrointestinal leakage, such as plant material, on abdominocentesis,. 6. Indigestion and ketosis: Cows with indigestion or ketosis should not be painful and ketotic cows will have ketones in their urine, as detected by dipstick analysis. • Total plasma protein should not be increased in a cow with either indigestion or ketosis and are less severely increased in a cow with a perforating abomasal ulcer. 24 Prof. dr. Ali sadiek Differential Diagnoses of TRP 7. Laboratory tests can be helpful in distinguishing cases of chronic TRP from other gastrointestinal diseases and are more accessible to veterinarians than other diagnostic tests, such as survey radiology or contrast radiography of the reticulum. 25 Prof. dr. Ali sadiek Traumatic Reticuloperitonitis Metal door spring removed from a cow’s reticulum 26 A nail is embedded in the mucosa of the reticulum Prof. dr. Ali sadiek Traumatic Reticuloperitonitis A nail has penetrated the reticulum, causing traumatic reticuloperitonitis and the death of this cow. A piece of wire has penetrated the reticulum and diaphragm before lodging in the pericardium. Pericardial effusion and fibrin deposition resulted from this traumatic injury 27 Prof. dr. Ali sadiek Treatment of TRP A) Conservative treatment: • Rest, Immobilize animal by tying it to a place and front feet should be elevated about 35 cm above the floor. • Feeding and watering on the spot and reduce roughage. A Bar magnets 7.5 x 2.5 cm with rounded end should be instilled to recover or immobilize the metal foreign body Systemic antibiotic for 3-7 days (penicillin, ceftiofur, ampicillin, or tetracycline). Anti-inflammatory (phenyle-butazone, Diclofen, etc) Affected cattle should be re-evaluated in 48-72 hours. If a magnet is already in place or conservative therapy is not successful, an exploratory laparotomy/ rumenotomy is indicated for removal of the foreign body. 28 Prof. dr. Ali sadiek Prevention of TRP • Prevention of TRP is preferred to either conservative medical treatment or surgery. • Although one source does not believe magnets are an effective preventative measure, the majority of clinicians agree that all cattle over one year of age should have a prophylactic magnet placed in the reticulum. • Following oral administration, most magnets do not enter the reticulum directly, but are first deposited in the cranial sac of the rumen before entering the reticulum following ruminal contractions. 29 Prof. dr. Ali sadiek Prevention of TRP • Cattle should be kept away from construction sites and crop fields should be monitored for metal debris. • Also, processed feed can be passed over magnets to recover any magnetic foreign bodies prior to being fed to cattle. 30 Prof. dr. Ali sadiek Diaphragmatic hernia • Herniation of a portion of the reticulum through a diaphragmatic rupture caused by: 1. Weaking of the diaphragm, by 2. Lesions of T.R.P. or 3. Congenital defects causes chronic ruminal Tympany. Signs of diaphragmatic hernia • There is loss of condition, • Moderate Tympany, • Grinding of the teeth, • Pasty and scanty feces . • Cessation of Rumination and the animal may vomit when a stomach tube is passed. • No fever and pulse is slower. 31 Prof. dr. Ali sadiek Diaphragmatic hernia • A systolic murmur is usually audible on auscultation and the intensity of the heart sound; may suggest displacement of the heart usually interiorly or to the left. • More severe syndrome is recorded in cases where viscera other than a portion of the reticulum is herniated. • Peristaltic sounds may be audible in the thorax and there may be interference with respiration and signs of pain with each reticular contraction. • Death from inanition in 3-4 weeks after the onset of bloat. 32 Prof. dr. Ali sadiek
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