Collapse and Sudden Death


Chapter 14

Collapse and Sudden Death



Stan W. Casteel, Consulting Editor, Joshua W. Schaeffer


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The ruminant or horse that collapses and dies within 24 hours while being observed or is found dead with no premonitory signs of illness is often a diagnostic challenge. In these situations, clients are often distressed and frequently pressure the veterinarian to declare an immediate diagnosis. Sudden death in the absence of observed clinical illness is usually the most perplexing. Obligation to clients necessitates a systematic approach to derive a specific causative diagnosis, to determine the source and extent of the problem, and to recommend corrective measures. These goals are best accomplished by delineating the characteristics of normal animals within the herd and analyzing the distribution of the disease with respect to time, place, and a variety of exposure factors and environmental influences. These factors are then correlated with necropsy results and additional diagnostic testing.



Collapse versus Sudden Death


Collapse is easily identified as a state of extreme prostration and depression. However, sudden death has a somewhat tenuous meaning, lending itself to subjective impression. The timing parameter used to define sudden death ranges from 1 to 24 hours from the onset of the fatal episode. Some veterinarians restrict the definition to a narrower time span. The 12- to 24-hour interval is sometimes selected to coincide with the frequency of owner observation of the livestock. For our purposes sudden death means clinically unexplained, rapid death (12 to 24 hours) occurring during normal activity in apparently healthy animals. Generally a condition of this nature is associated with fatal dysfunction of the cardiovascular, nervous, respiratory, or gastrointestinal (GI) system. In addition, perturbations in general cellular metabolism (cyanide or hydrogen sulfide) may result in peracute death.



Approach to Diagnosis of Sudden Death


The causes of sudden death are investigated in much the same way as for any disease. The accompanying tables of differential diagnoses include infectious, metabolic, nutritional, physical, cardiovascular, toxic, and miscellaneous causes of sudden death. Diagnostic laboratories provide an array of tests and analytic procedures on the basis of veterinarians’ needs in their service areas. Use of these facilities to support a definitive diagnosis is essential in sudden death cases. Diagnosis is rarely based on a single item of evidence and usually requires input from multiple testing procedures. Unless the cause of death is apparent, some important considerations required for effective use of a diagnostic laboratory include the following:



1. A detailed history, which consists of the herd incidence, management changes, past medical problems, vaccination records, new additions to the herd, a complete description of the environment (e.g., recent lightning?), and recognition of the frequency of animal observation. Owners and managers may not be candid for fear of being considered negligent. Inconsistencies among involved parties should be carefully evaluated. Recent changes in management practices should be scrutinized, including feeding habits and whether there have been any illnesses in commingled animals. Animals trailed or transported for long distances or introduced onto unfamiliar ranges are often poisoned by plant species normally avoided by indigenous livestock. The likelihood of foul play should be considered without creating undue alarm. Assigning blame should be left to the discretion of owners. Consideration of disgruntled former employees and equine insurance claims are particularly critical situations that may have legal implications. The precise cause of death is crucial for insured livestock (mostly horses) because of exclusion clauses in many insurance policies. Heavily insured horses should be subjected to a detailed, documented, and witnessed diagnostic evaluation. Toxicologic testing is especially critical in these cases. Evaluation of the environment before the animal is moved is necessary to eliminate questionable procedures in insurance claim cases. Evidence of struggling in the immediate area indicates a more protracted illness in contrast to collapse and death without a struggle. Suspicions should be aroused when evidence suggests the animal may have been dragged or carried to the current location.


2. The appropriate specimen is required by the diagnostic laboratory to perform the requested examination. Many cases of sudden death are attributed to central nervous system dysfunction; therefore it is necessary to remove the brain. Busy practitioners frequently do not take the time to remove this organ. There is a higher-than-normal probability of a poison being involved in sudden death cases, especially in equine insurance claims. For toxicologic examination, toxicants remaining in the GI tract must be considered, together with those in the major excretory organs, liver, and kidneys.


3. The correct amount and preservation of the sample depends on the specific test. Medicolegal cases demand that stringent photographic and written documentation, witnessing, and chain-of-custody protocol be followed during necropsy and sample collection. The amount of the sample is particularly important for chemical analysis. Sending insufficient quantities of sample may preclude multiple testing procedures. In general, 100 to 200 g of tissue or ingesta, 50 mL of urine, all fluid from both eyes, and 5 to 10 mL of blood or serum suffice for most analytic procedures. A midsagittal cut through the brain is performed to allow freezing of one half for chemical analysis and formalin preservation of the other. When poisoning is suspected, samples from possible sources such as feed, water, baits, poisonous plants, and suspect materials should be submitted. Usually 1 kg of each is adequate. Samples submitted for chemical analysis should be frozen in individual containers and labeled with date, location, and identity of the specimen. Specimens for bacteriology and virology are to be packaged separately and chilled. Dry ice should be avoided because gaseous carbon dioxide may kill some infectious agents. Tissues for histopathologic examination require fixing in 10% formalin with tissue slices 4 to 5 mm thick. Suspected poisonous plants are properly preserved by placing them in a plastic bag with wet paper towels or by drying them between sheets of paper.



Causes of Collapse and Sudden Death


Infectious Causes of Sudden Death in Horses (Box 14-1)


Foal actinobacillosis is an acute fulminant septicemia caused by Actinobacillus equuli, a gram-negative bacterium found in the upper respiratory tract, feces, and genital tract of normal adult horses. Other bacteria can also cause bacteremia/septicemia. Predisposing factors to foal septicemia with any agent include prematurity, failure of passive transfer, dam malnourishment during gestation, and environmental stress. A characteristic histologic finding is multiple bacterial emboli in renal glomerular capillaries without inflammatory infiltrate in neonatal foals. Acute anthrax may be rapidly fatal to horses after a period of excitement, depression, convulsions, and coma. Isolating the causative agent from blood confirms the diagnosis. Babesiosis is an erythrocytic parasite that may cause death within 24 hours. Identification of the organism in blood smears or complement fixation testing for parasite antibodies confirms the diagnosis.



Acute clostridial disease involving Clostridium septicum, Clostridium chauvoei, Clostridium novyi, and Clostridium perfringens has been associated with intramuscular injections of various parenterals such as ivermectin, vitamin B complex, vitamin E, prostaglandin, antihistamines, and flunixin meglumine when asepsis has been ignored. Clostridial myopathies are also associated with deep stab or puncture wounds. Botulism in foals (shaker foal syndrome) is caused by Clostridium botulinum (usually type B). Toxin may sometimes be demonstrated in feed and gut contents. The organism may be cultured from tissues or gut contents in toxico-infectious cases. Clostridium sordellii should be suspected in cases of foals having a history of colic, bloody diarrhea, and death within a few hours.1 C. perfringens type C may induce a hemorrhagic enterotoxemia and death in foals as young as 4 days.2 Severe intestinal lesions are caused by the beta-toxin produced by this species. Organisms may be demonstrated in smears of intestinal contents. C. perfringens type D also induces sudden death in the most aggressive foals in group-feeding situations. Similar enterotoxemia has also been associated with toxin-producing Clostridium difficile3 and Bacteroides fragilis.4


Equine monocytic ehrlichiosis (Potomac fever), caused by Ehrlichia risticii, is a severe colitis with diarrhea and dehydration, followed by ileus, endotoxemia, and death in adult horses. Diagnosis is based on clinical findings combined with antibody and antigen detection using immunofluorescent antibody (IFA) and enzyme-linked immunosorbent assay (ELISA) methods, respectively. Guttural pouch mycosis often results in nonfatal intermittent unilateral epistaxis. Occasionally a single episode of severe epistaxis from rupture of an aneurysm in the internal carotid artery may result in sudden death. Necropsy reveals blood in the nasal passages and guttural pouch with a diphtheritic plaque in the dorsocaudal aspect of the medial compartment. Salmonellosis is responsible for many cases of acute enterocolitis, especially when several animals are involved. The peracute syndrome may resemble colitis-X in mature horses with a course of 6 to 12 hours. Horses may die before diarrhea develops. Postmortem diagnosis is based on isolation of Salmonella spp. from bowel contents, bowel wall, and/or associated lymph nodes. Tyzzer disease is a rapidly developing fatal hepatitis of foals. The incidence is sporadic, and, because of the peracute development, clinical signs may not be observed before death. Diagnosis is based on histologic demonstration of the bacilli in bundles within hepatocytes surrounding necrotic areas.



Infectious and Parasitic Causes of Sudden Death in Ruminants


Infectious causes of sudden death range from acute septicemias and toxemias to rupture and release of abscess contents into the systemic circulation (Box 14-2). A liver abscess rupturing into the caudal vena cava; endocarditis, especially of the right atrioventricular valve, with subsequent pulmonary thromboembolism; and the rupture of a pituitary abscess are occasional causes of sudden death in individual animals. Acute anthrax and the clostridial infections, as well as ingestion of their preformed toxins, are more common causes of sudden death in ruminants. Anaplasmosis may cause sudden death in mature cattle under stress, without apparent icterus. In these cases anthrax may be mistaken for anaplasmosis because of the gross enlargement of the spleen. Anaplasma organisms may be demonstrated in blood smears, whereas newer diagnostic methods involve indirect fluorescent antibody and deoxyribonucleic acid probes. Of all domestic animals, cattle are the most susceptible to clostridial infections in which tissue invasion is present (blackleg). Because of this, vaccination status is important to ascertain. In addition, a fluorescent antibody test and isolation of the bacterium confirm the diagnosis. C. perfringens of various types is responsible for heavy losses caused by enterotoxemia in calves, lambs, kids, and feedlot cattle in apparent good health and on full feed. C. perfringens type D has been associated with focal symmetric encephalomalacia in lambs.5 Coliform mastitis may result in peracute systemic disease and rapid death if not treated early. Diagnosis is based on culture of the organism from the affected gland. Leptospira may cause an acute septicemia with hemolytic anemia and rapid death in young ruminants. Demonstration of leptospires in fresh urine or by immunohistochemical staining of tissues may assist in making the diagnosis. The course of listeriosis in sheep and goats is rapid, and death may occur in 4 to 48 hours after the appearance of clinical signs.6 Bacteriologic culture (isolation) or immunohistochemical staining of the organism in tissues is diagnostic. Acute fascioliasis (Fasciola hepatica) occurs seasonally in sheep and may cause sudden death within 6 weeks of initial infection. Anaerobic conditions induced by flukes in hepatic parenchyma predispose ruminants to the highly fatal clostridial hepatopathies such as Clostridium hemolyticum infection. Evidence of fluke infection is grossly visible. Individual animals with chronic or severe endoparasitism may present as acute collapse or sudden death if they are maintained in a herd/flock. This is especially true for South American camelids. Peracute malignant catarrhal fever (MCF) is a sporadic cause of sudden death in cattle that is usually associated with contacting ovine carriers, but most animals with MCF have diarrhea, keratitis, and other obvious clinical signs for days before death occurs. A septicemic form of mycoplasmosis has induced rapid death in kids.7 Isolation of the causative organism is diagnostic. Sudden death is the usual manifestation of septicemic pasteurellosis in lambs. Pseudorabies is a consideration in sudden death cases of ruminants having contact with infected swineherds and feral hogs in the midwestern United States. Brain for microscopic examination and virus isolation should be submitted to confirm the diagnosis. Acute septicemic salmonellosis mainly affects young ruminants and may result in death within 24 hours. Acute septic metritis usually occurs secondary to complications of parturition. Endotoxic shock and rapid death may occur in severe cases. Thromboembolic meningoencephalomyelitis caused by Histophilus somni is a peracute septicemic disease of young calves. Many cattle die without showing clinical signs. It may be associated with prior respiratory problems in the herd or feedlot. Typical lesions or isolation of the causative organism is diagnostic. Adult lymphosarcoma associated with bovine leukemia virus can be a cause of sudden cardiac death when neoplastic cells infiltrate the cardiac conduction system.




Metabolic and Nutritional Causes of Sudden Death in Horses


Hypocalcemia in horses is most common in lactating mares, but it also occurs after transit. Animals may develop tetany, synchronous diaphragmatic flutter (thumps), muscle tremors, and sweating. Low serum calcium is diagnostic. White muscle disease (nutritional myodegeneration) is associated with selenium and vitamin E deficiency. Sudden death in adult horses after severe exercise is attributed to degenerative lesions in cardiac and skeletal musculature. Death in foals may occur within hours from pulmonary edema and heart failure. Diagnosis is based on measuring whole blood and/or liver selenium and vitamin E concentrations.



Metabolic and Nutritional Causes of Sudden Death in Ruminants


Metabolic and nutritional diseases are not often considered in cases of sudden death. The primary lesion in a disorder of cattle known as “falling disease” is progressive fibrosis of the myocardium. Sudden deaths characteristic of the disease are attributed to exercise-induced heart failure.8 Rapid development of hypocalcemia is usually associated with the onset of lactation in cattle, with stressful circumstances in older lactating ewes, or with transport associated with fasting and weather stress. Hypomagnesemia may also develop under similar conditions, especially in ewes and cows in heavy lactation and on lush grass pastures. Polioencephalomalacia occurs most commonly in animals raised under intensive production techniques and can sometimes be traced to excessive sulfates in the diet and/or water. The clinical course tends to be most rapid in sheep. Severe cases of ruminal lactic acidosis, especially in animals unaccustomed to high levels of soluble carbohydrate in the diet, may induce death within 24 hours. Nutritional myodegeneration of the heart is a frequent cause of sudden death in young ruminants born to dams fed selenium-deficient diets during gestation. Diagnosis is based on histopathology and measurement of liver selenium concentration. Some cases of sudden death associated with myocardial necrosis are idiopathic.9



Cardiovascular Causes of Sudden Death in Horses


Diagnosis of sudden death caused by cardiovascular failure depends on a careful and methodic technique (Box 14-3). Usually a single animal is affected. Necropsy is necessary to identify the location and characteristics of the lesion, and further analysis may be necessary to establish the exact cause of death. Aortic ring (root) rupture in stallions is usually seen early in the breeding season, occurring immediately after servicing a mare. Rupture of the aorta may occur just distal to the aortic valve, resulting in cardiac tamponade and rapid death. Acute central nervous system embolism results from detached thrombi originating from endocarditic lesions or accidental intracarotid injection. Cerebral hematoma also can result from intracarotid injection. Endocarditis, especially of the aortic valve, may result in coronary thromboembolism and myocardial infarction. Coronary occlusion as a result of damage induced by Strongylus vulgaris larvae can be diagnosed by the presence of the larvae in the coronary thrombus. Massive abdominal or thoracic hemorrhage is found at necropsy, and the cause may be difficult to ascertain.10 Racehorses mostly die from severe hemorrhage in the thorax. Myocarditis in horses up to 4 years of age resulting from recent respiratory infection may be diagnosed with histopathologic examination. Pericardial rupture and the associated heart damage is a result of violent trauma. Splenic rupture and fatal hemorrhage rarely occur because of the protection afforded by the thoracic wall. Massive thrombi of verminous origin have been observed in young horses that die suddenly while exercising. Uterine arterial rupture involving ovarian, uteroovarian, uterine, or external iliac arteries is observed in older mares, with death ensuing in 30 minutes to 20 hours postpartum.


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Aug 11, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Collapse and Sudden Death

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