Current Accepted Postmortem Lesions of Ruminant Tympany
Ecchymotic and petechial hemorrhage of the cervical musculature.
Craniad musculature congestion & hemorrhage.
Caudad musculature normal to pale in color.
Craniad lymph nodes (prescapular, submandibular, axillary, & retropharyngeal) are congested & hemorrhagic.
Caudad lymph nodes (prefemoral & popliteal are pale in color.
Rumen is greatly distended.
Intestines may appear distended with some loops containing sanguinous ingesta.
Loops may appear hyperemic due to vascular compromise.
Spleen may appear compressed and pale.
Liver & kidneys may appear pale and undergoing autolysis.
Lungs are atelectic and located cranially in the thoracic cavity.
Trachial mucosa an submucosa petechiated and ecchymotic in cervical region with clotted blood in bronchi.
Cervical esophageal congestion usually ending abruptly at the thoracic inlet (bloat line).
Cranial sinuses & meninges may be congested and cyanotic.
Pathogenesis of Accepted Lesions
INCREASED INTRARUMINAL PRESSURE (BLOAT)
Increased Intra-abdominal Pressure
Ischemia of abdominal organs.
Increased rate of autolysis.
Allows reproduction of anaerobic clostridial organisms.
Redistribution of blood from abdominal reservoirs into peripheral circulation.
Elevated PCV & hemoglobin levels.
Cranial distention of diaphram.
Prevents adequate pulmonary ventilation leading to hypoxia.
Compromised Vascular Flow
Partial occlusion of the posterior vena cava and prerenal vena cava.
Dorsal displacement of the liver into the diaphram.
Increase in total peripheral resistence due to occlusion of vena cava.
Decreased cardiac output.
Increased blood pressure.
Increase in carotid blood flow.
Peripheral resistance in carotid vascular bed constant.
Decrease in femoral blood flow.
Peripheral resistance in carotid vascular bed increases.
Decreased renal blood flow and glomerular filtration rate.
Compression of kidney and ureters.
Increase in intrarenal vascular resistance.
Hypoxia proven with AVO2 values.
Decrease GFR.
Differential Diagnoses for these Postmortem Lesions
Bloat, Lighting, Anthrax, Clostridia, Sudden death, Metabolic, Physical trauma, Plant poisoning.
Discrepancies Found in the Literature
Pale caudad musculature & lymph nodes vs. hyperemia & hemorrhage of the lymph nodes in every region of the body.
LESIONS: Postmortem or Antemortem?
Pathogenesis of Postmortem Extravasation
Pressure gradient of ~80 to 40 mmHG from abdomen to extravascular tissues of the head & neck.
Distensibility of vessel walls: veins > arteries.
Vessels have tendency to fenestrate.
Endothelial degeneration due to hypoxia.
Explains hyperemia & hemorrhage in all cranial tissues.
Poor blood clotting in sudden deaths such as bloats, and lighting.
Poor clotting allows postmortem movement of blood to cranial tissues upon rumen distension.
Personal Discrepancies
Postmortem lesions of bloat described for animals without antemortem diagnosis of bloat.
Types of gas used for ruminal insufflation studies to simulate lesions of bloat
The use & type of anesthetic agents in the study of ruminal tympahy.
Problems with periods of insufflation.
Generally not gradual distention of rumen.
Actual ruminal pressures in bloat are unknown.
Times of ruminal insufflation were inadequate to allow for physiologic compensation.
Multiple periods of distention within one study on each animal.
Evaluation of disparity contained in several articles.
Needed studies to define pathognomonic postmortem lesions of bloat
Physiologic parameters of bloat.
Multiple timed necropsies on animals diagnosed antemortem with bloat.
Conclusions
1) Evaluations of articles.
2) validity of accepted postmortem lesions.
3)pertinence personal experience.