Snake bite: pit vipers

Pit vipers are the largest group of venomous snakes in the United States and are involved in an estimated 150,000 bites annually of dogs and cats. The severity of any pit viper bite is related to the volume and toxicity of the venom injected as well as the location of the bite, which may influence the rate of venom uptake. The toxicity of rattlesnake venom varies widely. It is possible for pit vipers' venom to be strictly neurotoxic with virtually no local signs of envenomation. Venom consists of 90% water and has a minimum of 10 enzymes and 3 to 12 nonenzymatic proteins and peptides in any individual snake. The onset of clinical signs after envenomation may be delayed for several hours. The presence of fang marks does not indicate that envenomation has occurred, only that a bite has taken place. Systemic clinical manifestations encompass a wide variety of problems including pain, weakness, dizziness, nausea, severe hypotension, and thrombocytopenia. The victim's clotting abnormalities largely depend upon the species of snake involved. Venom induced thrombocytopenia occurs in approximately 30% of envenomations. Many first aid measures have been advocated for pit viper bite victims, none has been shown to prevent morbidity or mortality. Current recommendations for first aid in the field are to keep the victim calm, keep the bite site below heart level if possible, and transport the victim to a veterinary medical facility for primary medical intervention. The patient should be hospitalized and monitored closely for a minimum of 8 hours for the onset of signs of envenomation. The only proven specific therapy against pit viper envenomation is the administration of antivenin. The dosage of antivenin needed is calculated relative to the amount of venom injected, the body mass of the victim, and the bite site. The average dosage in dogs and cats is 1 to 2 vials of antivenin.     

Brown spider envenomation

The venom from spiders of the genus Loxosceles, the most famous being Loxosceles recluse (the most brown recluse spider) can cause serious poisoning. These spiders inhabit the south and south central states from Georgia through Texas and north to southern Wisconsin. They are commonly called violin spiders because of the violin-shaped marking on the dorsum of the cephalothorax. Many dermonecrotic lesions are incorrectly diagnosed as Brown recluse bites, as up to 50% of the diagnoses are in geographic regions of the country which do not have Loxosceles spiders. Sphingomyelinase D is the primary venom dermonecrotic factor. The toxin depletes serum hemolytic complement, prolongs the activated partial thromboplastin time and depletes clotting factors VIII, IX, XI, and XII. The venom induces rapid coagulation and occlusion of small capillaries, causing subsequent tissue necrosis. A classic "bulls eye" lesion develops, an erythematous area inside of which is a pale ischemic region that develops a dark necrotic center as the lesion matures. Healing is slow, and these ulcers may persist for months leaving a deep scar. Systemic signs occur less commonly but can be life threatening. The most prevalent sign is a hemolytic anemia with significant hemoglobinuria. There is no specific antidote. Dapsone a leukocyte inhibitor has been shown to be effective in treating dermal lesions in animal models. Conservative therapy includes several cleanings daily with Burrow's solution and hydrogen peroxide. Systemic signs of Loxosceles envenomation are potentially fatal and should be aggressively addressed. Hospitalization and intravenous fluid therapy may be needed to maintain adequate hydration and to protect renal function.     

Snake envenomation in dogs in New South Wales

OBJECTIVE: To obtain baseline data on the prevalence of elapid snake envenomation in dogs presented to veterinary practices in New South Wales and to assess attitudes of veterinarians to this clinical entity. PROCEDURE: A mailed questionnaire, sent to all veterinary clinics within New South Wales, was utilised to collect epidemiological information regarding elapid snake envenomation in dogs. RESULTS: A response rate of 68% was obtained and a yearly prevalence of snake envenomation in dogs across New South Wales veterinary clinics was estimated as 0.31%. The most common species reported to be responsible for envenomation within NSW was the Red Bellied Black snake (Pseudechis porphyriacus) followed by the Brown snake (Pseudonaja textilis) and then Tiger snake (Notechis scutatus). The reported envenomation syndromes caused by these common snake species were perceived to be similar for Brown and Tiger snakes but differed for Red Bellied Black snakes. Diagnosis of snake envenomation was based predominantly on the recognition of clinical signs. Specific diagnostic tests, such as venom detection kits, were used infrequently. The most common treatment was reported to be a combination of intravenous fluid therapy and antivenom, and monitoring of response to this treatment was usually through assessment of clinical signs. Survival after antivenom administration was reported to be highest for Red Bellied Black snake species. Survival was perceived to be associated with time between envenomation and presentation to the veterinary clinic and with antivenom administration. CONCLUSIONS: Current attitudes and perceptions of veterinarians have been defined. Diagnosis of species-specific snake envenomation is shown to be made on the basis of clinical signs which are, however, reported as similar for each species. Clearer definition of these envenomation syndromes and identification of accessible diagnostic testing procedures are needed.     

Snake bite: coral snakes

North American coral snakes are distinctively colored beginning with a black snout and an alternating pattern of black, yellow, and red. They have fixed front fangs and a poorly developed system for venom delivery, requiring a chewing action to inject the venom. The severity of a coral snake bite is related to the volume of venom injected and the size of the victim. The length of the snake correlates positively with the snakes venom yield. Coral snake venom is primarily neurotoxic with little local tissue reaction or pain at the bite site. The net effect of the neurotoxins is a curare like syndrome. In canine victims there have been reports of marked hemolysis with severe anemia and hemoglobinuria. The onset of clinical signs may be delayed for as much as 10 to 18 hours. The victim begins to have alterations in mental status and develops generalized weakness and muscle fasciculations. Progression to paralysis of the limbs and respiratory muscles then follows. The best flied response to coral snake envenomation is rapid transport to a veterinary medical facility capable of 24 hour critical care and assisted ventilation. First aid treatment advocated in Australia for Elapid bites is the immediate use of a compression bandage. The victim should be hospitalized for a minimum of 48 hours for continuous monitoring. The only definitive treatment for coral snake envenomation is the administration of antivenin (M. fulvius). Once clinical signs of coral snake envenomation become manifest they progress with alarming rapidity and are difficult to reverse. If antivenin is not available or if its administration is delayed, supportive care includes respiratory support. Assisted mechanical ventilation can be used but may have to be employed for up to 48 to 72 hours.     

Elapid snake envenomation in dogs in New South Wales: a review

Elapid snake envenomation in dogs is a commonly occurring yet poorly described clinical entity. Twelve species of dangerously venomous elapid snakes are found in New South Wales that are capable of causing disease in dogs. Geographical distribution of these species varies, as does their venom composition and systemic envenomation syndromes produced in target species. Elapid venom may be divided into the components of prothrombin activating enzymes, lipases and peptidic neurotoxins. Each species of elapid snake may possess venom components that fit any or all of these classifications. The action of these venom components may result in neurotoxic (pre-synaptic and post-synaptic), haemotoxic (red-cell destruction and coagulation disturbance), cardiovascular, myotoxic and secondary nephrotoxic effects. Marked variability may occur in venom composition between and within snake species, resulting in varying toxicity between species and also potentially unreliable clinical syndromes following envenomation. The existence of certain components consistently within the venom of each snake species allows the broad definition of basic pathological processes and clinicopathological changes resulting from snake species-specific envenomation and these are discussed. Diagnosis of snake envenomation is unreliable if based on clinical signs alone and the use of these signs in conjunction with history, physical examination and laboratory investigation, including snake venom detection kits, is recommended. Treatment of systemic envenomation should be undertaken with initial effective first aid and subsequent administration of snake species-specific antivenom.     

Snake envenomation in cats and its detection by rapid immunoassay

Objective To determine the usefulness of a snake venom detection kit (SVDK) in the management of envenomed cats.
Design A clinical study.  

Animals

Twenty-two cats were investigated.
Procedure Cats injected subcutaneously with approximately 0.25 or 1.0 lethal dose (LD) of tiger snake venom or 1 or 4 LD of brown snake venom were observed for clinical symptoms of envenomation at intervals over the ensuring 24 to 48 hours(h). Blood and urine samples were taken at regular intervals and assayed in a quantitative laboratory assay for snake venoms. Selected samples were assayed in parallel in a rapid, semi-quantitative SVDK.
Results The studies showed that it was important to estimate the elapsed time from envenomation to presentation. If this time was less than 8 h, blood was the most appropriate sample and a negative result should exclude serious envenomation. If the elapsed time exceeded 8 h, it was essential that urine be sampled. Venom levels in urine were high at 8 h and approached the level of test sensitivity over 24 to 48 h; however by this time clinical signs were obvious in endangered cats.  

Conclusions

Careful use of the SVDK is a valuable aid in the management of a potentially envenomed cat.     

Prospective determination of the specificity of a commercial snake venom detection kit in urine samples from dogs and cats

Objective To determine the specificity of a snake venom detection kit in urine samples from dogs and cats presenting to a referral centre for diseases unrelated to snake envenomation. Design Urine was collected from 50 dog and 25 cats presented for investigation and treatment of diseases unrelated to snake envenomation. Urine was collected as a voided sample, by cystocentesis or by catheterisation, and routine urinanalysis was performed. Snake venom testing was performed within 2 h of collection using a commercially available snake venom detection kit, which was observed continuously during the 10-min colour reaction phase for evidence of a visible colour indicating a positive test. Results No false-positive reactions occurred in any sample analysed. Conclusion The snake venom detection kit appears to have 100% specificity for using urine as a test sample.     

Brown recluse spider (Loxosceles reclusa) envenomation in small animals

Objective – To provide a comprehensive review of relevant literature regarding the brown recluse spider (BRS) and to define those criteria that must be satisfied before making a diagnosis of brown recluse envenomation.
Etiology – The complex venom of the BRS contains sphingomyelinase D, which is capable of producing all the clinical signs in the human and some animal models.
Diagnosis – There is no current commercially available test. In humans there are many proposed guidelines to achieve a definitive diagnosis; however, there are no established guidelines for veterinary patients.
Therapy – Currently, no consensus exists for treatment of BRS envenomation other than supportive care, which includes rest, thorough cleaning of the site, ice, compression, and elevation.
Prognosis – Prognosis varies based on severity of clinical signs and response to supportive care.     

Rattlesnake envenomation in 12 New World camelids

BACKGROUND: Rattlesnake envenomation of New World camelids is a seasonal problem with often dramatic clinical signs. HYPOTHESIS: The purpose of this study was to identify the clinical signs, laboratory results, treatment methods, and outcome for rattlesnake envenomation in New World camelids. ANIMALS: Medical records from 1988 to 2004 were searched for New World camelids presented for rattlesnake bite or clinical signs suspected to be related to recent envenomation. Twelve records were identified. METHODS: From these records a retrospective study was performed. RESULTS: Nine camelids presented for acute disease (2/9 arrived dead), whereas 3 presented for subacute onset of disease. Swelling of the lips, head and neck, tachypnea, dyspnea, tachycardia, and lethargy were the most common presenting signs. Snake bites were most commonly located to the muzzle (10/12). Common complete blood count (CBC) and serum biochemical abnormalities were neutrophilia, lymphopenia, increased muscle enzyme activity, hypoalbuminemia, hyperglycemia, hypokalemia, and thrombocytopenia. Treatment included combinations of intravenous fluid therapy, antimicrobials, anti-inflammatory drugs, tetanus prophylaxis, tracheostomy, supplemental oxygen, antivenom, total parenteral nutrition, and nursing care. Five of the 10 animals with acute onset of clinical signs survived, and all animals with subacute presentation died. The mortality rate for New World camelids with severe local tissue reaction and systemic signs of envenomation was 58%. CLINICAL IMPORTANCE: New World camelids that sustain rattlesnake envenomation and severe facial swelling precluding prehension and mastication have a guarded prognosis for survival. Aggressive treatment is recommended to optimize the chances of survival. Animals with less severe local tissue reaction and absence of systemic signs have a better prognosis.     

Clinicopathologic abnormalities associated with snake envenomation in domestic animals

Envenomation of domestic animals by snakes occurs frequently in certain geographic areas. However, reports describing clinical signs, clinicopathologic abnormalities, therapeutic approaches, and outcomes are sparse. This review summarizes various snake families, venom types associated with harmful snakes, and the significant hematologic, hemostatic, and biochemical abnormalities associated with envenomation. Hematologic abnormalities include RBC membrane abnormalities, hemolysis, hemoconcentration, leukogram changes, and platelet abnormalities, specifically thrombocytopenia. Coagulopathies associated with snake envenomation are well described in human medicine, and many studies have demonstrated properties of venoms that lead to both procoagulation and anticoagulation. As expected, similar abnormalities have been described in domestic animals. Biochemical abnormalities are associated with the effects of venom on tissues such as liver, skeletal and cardiac muscle, vascular endothelium, and kidney as well as effects on protein components and cholesterol. This comprehensive review of clinicopathologic abnormalities associated with envenomation and their relationships to characterized venom constituents should be useful both in the diagnosis and management of envenomation and should serve as a foundation for future research in this field.     

Toxic exotics.

The purpose of this article is to familiarize the reader with the basic venom components, the pathophysiologic responses of envenomated dogs and cats, and some brief treatment guidelines for envenomations by various exotic "pets." Representative toxic species of reptiles, amphibians, and arthropods are included. The growing trend toward the collection of exotic animals by private owners increases the likelihood that veterinarians will face the challenge of treating an exotic envenomation.     

Laryngeal paralysis in cats: 16 cases (1990-1999)

OBJECTIVE: To determine clinical signs, physical examination findings, radiographic features, and concurrent diseases in cats with laryngeal paralysis, as well as evaluate the outcome of medical or surgical management. DESIGN: Retrospective study. ANIMALS: 16 cats. PROCEDURE: Medical records from January 1990 to April 1999 were examined for cats with laryngeal paralysis. Signalment, clinical signs, physical examination findings, cervical and thoracic radiographic findings, laryngeal examination results, and clinical outcome were reviewed. RESULTS: No breed or sex predilection was identified in 16 cats with laryngeal paralysis. The most common clinical signs included tachypnea or dyspnea, dysphagia, weight loss, change in vocalization, coughing, and lethargy. Clinical signs were evident for a median of 245 days. Airway obstruction was apparent on cervical and thoracic radiographic views in 9 cats. Examination of the larynx revealed bilateral laryngeal paralysis in 12 cats and unilateral laryngeal paralysis in 4 cats. The 4 cats with unilateral disease were managed with medical treatment, and 3 of these had acceptable long-term outcomes. Seven of 12 cats with bilateral paralysis underwent surgery; procedures performed included left arytenoid tie back, bilateral arytenoid tie back and ventriculo-cordectomy, and partial left arytenoidectomy. One cat was euthanatized as a result of complications from surgery. CONCLUSIONS AND CLINICAL RELEVANCE: Laryngeal paralysis is an uncommon cause of airway obstruction in cats. Cats with less severe clinical signs (often with unilateral paralysis) may be successfully managed with medical treatment, whereas cats with severe airway obstruction (often with bilateral paralysis) may benefit from surgical intervention.     

Four cases of snake envenomation responsive to death adder antivenom

Death adder envenomation is rare in humans and there is only one brief report previously in dogs. This paper details three cases of canine common death adder (Acanthophis antarcticus) envenomation and one case of bardick (Echiopsis curta) envenomation which were responsive to death adder antivenom. The available literature on death adder envenomations is also reviewed. The main clinical sign in the four dogs was severe lower motor neuron paralysis. There was no clinical evidence of coagulopathy or myopathy. Use of a snake venom detection kit was essential for selection of appropriate antivenom. Death adder and bardick envenomation in dogs potentially has a good prognosis if sufficient antivenom is administered and intensive supportive care is available.     

Myotoxicity and nephrotoxicity of common tiger snake (Notechis scutatus) venom in the dog

SUMMARY The myotoxicity and neurotoxicity of common tiger snake (Notechis scutatus) venom are major factors in the pathogenesis of envenomation in the dog. Histological examination of the tissues of experimentally envenomed dogs has demonstrated the importance of muscle damage in affecting the clinical syndrome of tiger snake envenomation. Within one hour of injection of the venom into dogs, there was selective involvement of some muscles. Cardiac and smooth muscles were not significantly affected. The severity of myofibre damage was influenced by the amount of venom injected. Immobilisation under general anaesthesia resulted in significant protection against the myotoxic effects of high doses of venom. Lesions in the kidneys of experimentally envenomed dogs were acute tubular necrosis and the variable presence of a small amount of proteinaceous material in tubules. These lesions, which were similar to those in cases of natural snake bite, were indicative of a direct nephrotoxic effect, which could be complicated by the effects of myoglobinuria. These findings emphasise the need for supportive treatment aimed at maintenance of renal function in the treatment of dogs suffering from tiger snake envenomation.     

Clinical and echocardiographic findings of pulmonary artery stenosis in seven cats

ObjectivesDescribe the clinical, electrocardiographic (ECG), radiographic and echocardiographic findings in cats with isolated pulmonary artery stenosis. Assess the usefulness of systolic and diastolic Doppler measurements at predicting stenosis severity.BackgroundPulmonary artery stenosis is an infrequent congenital cardiac defect in humans that has not been reported in cats. In humans, pulmonary artery stenosis is usually seen in conjunction with other cardiac defects and may lead to clinical signs if severe.Animals, materials and methodsSeven cats with pulmonary artery stenosis were retrospectively evaluated. Medical records, radiographs, ECGs, echocardiograms and angiocardiograms were reviewed. Severity of stenosis was assessed by two-dimensional and color Doppler echocardiographic evaluation and clinical findings. Peak systolic and diastolic gradients across the stenosis, and systolic and diastolic pressure decay half-times were graded using echocardiography. In addition, the duration of antegrade flow during diastole was subjectively assessed. Univariate analyses were performed to assess the best variable to predict stenosis severity.ResultsConcurrent congenital defects were not identified. Only cats with severe obstruction showed clinical signs including exertional dyspnea and lethargy. Diastolic Doppler measurements were superior to systolic measurements at predicting severity of stenosis. Antegrade flow throughout diastole and/or a diastolic pressure half-time of >100 ms indicated severe obstruction. The prognosis for pulmonary artery stenosis appears to be good regardless of severity.ConclusionAmong cats with pulmonary artery stenosis, clinical signs are uncommon and prognosis is good. Doppler assessment of diastolic flow appears to be superior to systolic flow at predicting severity.     

SnakeMap: four years of experience with a national small animal snake envenomation registry

SnakeMap is a national cloud-based, veterinary snakebite registry. It was designed to prospectively collect data of the clinical circumstances and temporospatial information on cases of snake envenomation in dogs and cats. We herein introduce the project and summarise the data from the first 4 years of SnakeMap. The registry is a veterinary community-based online database allowing case entry from veterinary hospitals across Australia. Registry data comprise hospital characteristics, patient characteristics, envenoming snake type, treatment and outcome variables, including time and geolocation of the snake bite. We present summative information on select key variables from the SnakeMap registry (1 July 2015 to 30 June 2019). Twenty-eight hospitals from 6 states/territories entered 624 cases into the registry, including 419 dogs (67%) and 205 cats (33%). Bite time was available in 216 animals of which 90 (42%) were reported to be bitten in the 3 hours between 03:00 pm and 05:59 pm; median bite to presentation interval was 60 (interquartile range [IQR] 30, 211) minutes in dogs and 95 (IQR 41, 238) minutes in cats. Bites occurred in the owner's yard in 356 dogs (85%) and 53 cats (26%). A snake venom detection kit was used in 172 cases (28%) and antivenom was administered in 523 cases (85%). Most animals (n = 534, 88%) survived to discharge (median hospitalisation of 25 [IQR 16, 62] hours). SnakeMap effectively collects relevant clinical data from dogs and cats with presumed snake bite and provides locally specific information on the epidemiology of snake envenomation in small animals.     

Smoke exposure in cats: 22 cases (1986-1997).

OBJECTIVE: To review clinical findings and clinical course for cats exposed to smoke in residential fires and to determine clinical variables that may have prognostic importance. DESIGN: Retrospective study. ANIMALS: 22 cats admitted to our veterinary teaching hospital between 1986 and 1997 with a history of smoke exposure during a residential fire. PROCEDURE: Medical records were reviewed for history, clinical signs, physical examination findings, changes in respiratory tract signs, initial hematologic analysis, treatment, results of thoracic radiography, and outcome. RESULTS: Fifteen of 22 (68%) cats were categorized in the uncomplicated group, 5 (23%) in the complicated group, and 2 (9%) were discharged after a short period because of financial considerations. Twenty (91%) cats survived, but 2 (9%) were euthanatized because of severe respiratory compromise or neurologic changes. Predominant thoracic radiographic changes were diffuse interstitial pattern (6 cats) and focal alveolar pattern (5). The majority (8/13) of cats that were stable or had improved by the day after admission had an uncomplicated clinical course while hospitalized, whereas cats that were worse on the day after admission tended to have a complicated clinical course. CONCLUSIONS AND CLINICAL RELEVANCE: Cats that survive a residential fire and are admitted to a hospital have a good chance to be discharged. Cats that do not have signs of respiratory tract dysfunction at admission probably will not develop severe respiratory complications. For cats with signs of respiratory dysfunction at admission, better prognostic information will be determined by monitoring progression of the respiratory condition on the day after admission.     

Lead toxicosis in cats-a review

Although the incidence of lead toxicosis in small animals continues to decrease, it remains a significant malady. We have reviewed the literature of the past 45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis, pathology and treatment of feline lead toxicosis are reviewed. In 84% of these cases the source of lead was old paint usually from home renovation. The most common signs in cats are anorexia, vomiting, and seizures. The younger individuals seem more likely to show CNS signs. Since signs are often vague, lead toxicosis may be significantly under diagnosed in cats. The gold standard of diagnostic tests is blood lead concentration, although it does not necessarily correlate with total body burden of lead or with metabolic effects including clinical signs. Diagnostic tests including erythropoietic protoporphyrin (EPP), urine aminolevulinic acid, and others are discussed. Gross findings on necropsy are few and include a yellow-brown discoloration of the liver often with a nutmeg-like appearance. Histological examination may reveal pathognomonic inclusion bodies in liver and renal tissues. Characteristic histological changes in the CNS include neuronal necrosis and demyelination. Treatment of lead toxicosis in cats, as in any species, involves removing the exposure, decontaminating the individual and the environment, supportive care and chelation therapy. The most recently available chelator is succimer (meso 2,3-dimercaptosuccinic acid). Succimer given orally is well tolerated and has a wide margin of safety. A high index of suspicion of lead toxicosis is warranted in cats since they often present with vague and non-specific signs. With any consistent history owners need to be asked about home renovation. Early diagnosis and treatment affords a good prognosis.     

Occurrence of Problems after Three Techniques of Bilateral Thyroidectomy in Cats

Bilateral thyroidectomy was performed in 106 cats with hyperthyroidism by one of three techniques: original intracapsular, modified intracapsular, or modified extracapsular. Hypocalcemia was detected in the first 3 days after surgery in 11 (22%) of 50 cats treated by the intracapsular technique, 10 (33%) of 30 cats treated by the modified intracapsular technique, and 6 (23%) of 26 cats treated by the modified extracapsular technique. Hypocalcemia was classified as mild or severe. No signs of hypoparathyroidism developed in any of the 13 cats with mild hypocalcemia. Of the 14 cats with severe hypocalcemia, 8 had clinical signs of hypoparathyroidism before and during treatment with calcium and vitamin D, 3 were treated and no clinical signs developed, 2 were not treated but no clinical signs developed, and 1 was lost to follow-up. No cat required permanent calcium or vitamin D supplementation after surgery. Severe hypocalcemia and clinical signs of hypoparathyroidism occurred in 3 (6%) of the 50 cats treated by the intracapsular technique, 4 (13.3%) of the 30 cats treated by the modified intracapsular technique, and 1 (3.8%) of the 26 cats treated by the modified extracapsular technique. Twelve cats had recurrence of hyperthyroidism at a median time of 23 months. The intracapsular technique was used in 11 of these cats, and the modified extracapsular technique was used in 1. No clinical signs of hypothyroidism were detected in any of the cats. The modified intracapsular and modified extracapsular techniques of bilateral thyroidectomy are effective procedures for the treatment of feline hyperthyroidism.     

Feline exocrine pancreatic disorders.

Despite the uncommon clinical diagnosis, cats frequently suffer from disorders of the exocrine pancreas. Pancreatitis is the most common feline exocrine pancreatic disorder. Pancreatitis can be acute or chronic and mild or severe. The etiology of most cases of feline pancreatitis is idiopathic. Some cases have been associated with severe abdominal trauma, infectious diseases, cholangiohepatitis, and organophosphate and other drug intoxication. The clinical presentation of cats with pancreatitis is nonspecific. Vomiting and signs of abdominal pain, which are the clinical signs most commonly observed in humans and dogs with pancreatitis, are only uncommonly observed in cats with pancreatitis. Routine laboratory findings are also nonspecific. Abdominal ultrasonography is a valuable diagnostic tool in feline patients with pancreatitis. Serum activities of lipase and amylase are rarely increased in cats with pancreatitis; however, these cats often have elevated serum fTLI concentrations. The goals of management are removal of the inciting cause, provision of supportive and symptomatic therapy, and careful monitoring for and aggressive treatment of systemic complications. Exocrine pancreatic insufficiency is a syndrome caused by insufficient synthesis of pancreatic digestive enzymes by the exocrine portion of the pancrease. The clinical signs most commonly reported are weight loss, loose and voluminous stools, and greasy soiling of the hair coat. Serum fTLI is subnormal in affected cats. Treatment of cats with EPI consists of enzyme supplementation with powdered pancreatic extracts or raw beef pancreas. Many cats with EPI have concurrent small intestinal disease. Most cats with EPI also have severely decreased serum cobalamin concentrations and may require parenteral cobalamin supplementation. Pancreatic adenocarcinoma is the most common neoplastic condition of the exocrine pancreas in the cat. At the time of diagnosis, the tumor has already metastasized in most cases, and the prognosis is poor. Pancreatic pseudocyst, pancreatic abscess, pancreatic parasites, pancreatic bladder, and nodular hyperplasia are other exocrine pancreatic disorders, that are less commonly seen in cats.