Pancreatic beta cell tumor in a ferret

A ferret with clinical and laboratory signs of hypoglycemia was found at surgery to have a beta cell tumor of the pancreas. There had been recurrent episodes of weakness, ataxia, dehydration, and hypothermia. A fasting blood glucose content was 43 mg/dl and the amended insulin/glucose ratio was 362.5. The tumor was removed, yet hypoglycemia persisted postoperatively. Clinical signs related to hypoglycemia did not recur following application of medical treatment and frequent feedings. The histologic appearance of the tumor closely resembles that which has been seen in other species.     

Characterization of renal defects in dogs with a syndrome similar to the Fanconi syndrome in man.

Ten adult dogs with multiple spontaneous defects of renal tubular reabsorption were studied. Clinical signs included polydipsia, polyuria, and glycosuria for 2 to 12 months. Eight of the dogs were Basenjis. Urinalyses revealed hyposthenuria, glycosuria, and amino aciduria in most dogs. Renal function was normal in 5 dogs and slightly reduced in the remainder. Moderate metabolic acidosis had developed in 3 dogs. Renal clearance studies revealed reduced tubular reabsorption of glucose, phosphate, sodium, potassium, and uric acid. Abnormal glucose tubular maximal curves were found. Results of oral glucose tolerance tests were normal. Two patterns of abnormal amino aciduria were evident: generalized amino aciduria and a pattern similar to that of cystinuria in dogs. Radiography of long bones and bone densitometry did not reveal any skeletal abnormalities. Five of the dogs died within 90 days of diagnosis; death was due to acute renal failure associated with profound dehydration, acidosis, and papillary necrosis. The other dogs remained stable without treatment after 18 months. Histopathology of kidneys did not reveal uniform abnormalities; some dogs had variable and nonspecific changes and others were normal. Electron microscopy did not reveal ultrastructural abnormalities in renal tubular cells. It was concluded that the syndrome in these dogs represents a new entity of renal disease in dogs, similar to idiopathic Fanconi syndrome in man.     

Clinical, clinicopathologic, radiographic, and ultrasonographic characteristics of intestinal lymphangiectasia in dogs: 17 cases (1996-1998)

OBJECTIVE: To characterize the clinical, clinicopathologic, and imaging findings in dogs with intestinal lymphangiectasia and to compare the histologic grade of lymphangiectasia with clinicopathologic and imaging abnormalities. DESIGN: Retrospective study. ANIMALS: 17 dogs with a histologic diagnosis of intestinal lymphangiectasia. PROCEDURE: Medical records of dogs with a histologic diagnosis of intestinal lymphangiectasia were reviewed for signalment, history, clinical signs, results of exploratory laparotomy, and clinicopathologic, radiographic, ultrasonographic, and histologic findings. RESULTS: Mean age of dogs was 8.3 years; the most common clinical signs were diarrhea, anorexia, lethargy, vomiting, and weight loss. Abnormal physical examination findings included dehydration, ascites, and signs of pain on palpation of the abdomen. The most notable clinicopathologic findings were low serum ionized calcium concentration and hypoalbuminemia. Abdominal ultrasonography was performed in 12 dogs and revealed intestinal abnormalities in 8 dogs and peritoneal effusion in 7 dogs. Exploratory laparotomy revealed abnormalities in 9 of 16 dogs including thickened small intestine, dilated lacteals, lymphadenopathy, and adhesions. On histologic examination of the small intestine, concurrent inflammation was observed in 15 of 17 dogs, crypt ectasia in 5 of 17, and lipogranulomas in 2 of 17. CONCLUSIONS AND CLINICAL RELEVANCE: Intestinal lymphangiectasia in dogs appears to be a heterogeneous disorder characterized by various degrees of panhypoproteinemia, hypocholesterolemia, lymphocytopenia, and imaging abnormalities. In most dogs, the severity of hypoalbuminemia appears to offer the best correlation with severity of histologic lesions of lymphangiectasia. Imaging abnormalities are common in dogs with intestinal lymphangiectasia but are not specific enough to differentiate this disorder from other gastrointestinal disorders, nor are they predictive of histologic severity.     

Clinical, haematological and biochemical findings in milk-fed calves with chronic indigestion

The principal clinical signs in 59 milk-fed calves with chronic indigestion were general malaise and depression, poor appetite, poor body condition, dehydration, a dull and scaly hair coat, alopecia and clay-like faeces. All the calves had metabolic acidosis, which was associated with an inability to stand up in more than half of them. There were significant differences in the severity of acidosis between the calves that could stand and those that could not. Other signs in some of the calves were dehydration, leucocytosis, and increased activities of liver enzymes.     

Fluid and electrolyte balance in critical patients

Recognition and appropriate management of fluid and electrolyte disorders in critical patients is extremely important. In many cases, these secondary problems are more complicated and more serious than the initiating disease process. A severely ill diabetic patient, for example, is more likely to die from dehydration, hyperosmolality, metabolic acidosis, hypokalemia or hypophosphatemia than from hyperglycemia or lack of insulin therapy. Proper fluid therapy and treatment of electrolyte abnormalities make a major difference in the survival rate of critically ill animals.     

Listeria monocytogenes septicemia in a Thoroughbred foal.

Listeria monocytogenes septicemia was diagnosed in a 6-day-old Thoroughbred foal. Primary clinical signs included fever, depression, diarrhea, and respiratory distress. Hematologic abnormalities included leukopenia, neutropenia, degenerative left shift, and hyperfibrinogenemia. Clinical chemistry and blood gas abnormalities included metabolic acidosis, hypoxemia, hypocapnia, hypoglycemia, and hyponatremia. Despite aggressive therapeutic intervention and intensive care, the foal died within 12 hours of admission. A postmortem examination was performed, and the primary gross lesion was bilaterally severe, focally extensive bronchopneumonia. Histopathology revealed severe subacute multifocal suppurative bronchopneumonia with necrotizing vasculitis and intralesional coccobacilli. Cultures of blood collected at admission and immediately prior to death were positive for L. monocytogenes, as were cultures obtained from lung and liver at necropsy. Immunohistochemical examination of formalin-fixed tissues revealed abundant intra- and extracellular L. monocytogenes antigen within the lung and intravascularly in multiple organs.     

A retrospective study of the relationship between clinical signs and severity of acidosis in diarrheic calves

A retrospective study of 123 calves under two months of age with signs of diarrhea was performed to investigate the relationships among the calf's demeanor, dehydration, rectal temperature, and base deficit. The severity of dehydration, hypothermia, and metabolic acidosis were associated with level of depression. Clinical signs and age of calf could be used to predict the severity of acidosis. Acidosis was more severe in calves over eight days of age and also increased in severity with the degree of depression. The most severe metabolic acidosis was seen in calves over eight days of age presented in sternal or lateral recumbency; the base deficit in these groups was 16.3 ± 8.3 (means ± 1SD) and 20.3 ± 10.1 mmol/L respectively, and on average these calves require 2.4 and 3.0 L respectively of 1.3% sodium bicarbonate solution to correct the acidosis.     

Management of feline diabetes mellitus.

Up to one quarter of diabetic cats can be well controlled with oral hypoglycemic drugs, although at least 75% require insulin therapy. Most available insulins provide good clinical control but only moderate glycemic control. Because mild to moderate hyperglycemia is well tolerated by cats receiving insulin but hypoglycemia can be life threatening, conservative insulin dosing is recommended. Clinical signs and water intake indicate whether a dose adjustment is required, but serial blood glucose measurements are usually needed to determine the direction of the adjustment. Starting doses of 0.3 to 0.5 IU/kg administered twice daily (rounded down to the nearest whole unit) are usually safe. Dose adjustments should not exceed 1 IU per cat every 2 to 4 weeks unless clinical hypoglycemia has occurred. Cats with clinical hypoglycemia need to be reassessed to see if they are in remission. If not, a 50% to 75% reduction in dose is advised. Approximately 30% of cats go into diabetic remission 1 to 4 months after an adequate treatment protocol is instituted.     

4-Methylpyrazole as treatment for naturally acquired ethylene glycol intoxication in dogs

Eight dogs with ethylene glycol intoxication were treated with 4-methylpyrazole, an alcohol dehydrogenase inhibitor. Dogs had clinical signs referable to ethylene glycol ingestion including ataxia, depression, vomiting, polyuria, and dehydration. Metabolic abnormalities included high anion gap metabolic acidosis, serum hyperosmolality, isosthenuria, and monohydrate and dihydrate calcium oxalate crystalluria. Serum and urine ethylene glycol concentrations were determined to confirm ingestion of ethylene glycol. A 50-mg/ml solution of 4-methylpyrazole in propylene glycol was administered iv as follows: initial treatment, 20 mg/kg of body weight; at 17 hours after admission, 15 mg/kg; at 25 hours after admission, 5 mg/kg. By 24 hours after admission, all dogs had clinical and metabolic improvement. Of the 8 dogs, 7 were released within 3 days of admission. Four of the 8 dogs returned for follow-up evaluation, at which time biochemical or hematologic abnormalities were not observed.     

Abnormalities of the brainstem auditory response of the dog associated with equilibrium deficit and seizure

The brainstem auditory evoked response (BAER) was recorded from 20 dogs, 10 exhibiting vestibular deficit, and 10 presented with a history of seizures. Two dogs exhibited both types of signs. Abnormalities of the BAER, prolonged interwave latency, were seen in 8 of the 10 animals with vestibular problems, and in 7 of the 10 animals with seizure history. Several different diagnosis were associated with BAER abnormalities in both groups of animals. In 55.5% of the cases exhibiting abnormalities of the BAER, postmortem evidence of brainstem pathology was not detected. The electroencephalogram (EEG) was normal in three instances of abnormalities of the BAER. The BAER was normal in three dogs with abnormalities of the EEG. The BAER is presented as a useful diagnostic tool for brain lesions in animals with vestibular deficit and seizure history, but appears most useful when used in conjuction with the EEG. Correlations of abnormalities of the BAER and clinical course of disease are discussed.Publication No. 1707, School of Veterinary Medicine, Auburn University, AL 36849     

Pancreatic necrosis in New World camelids: 11 cases (1990-1998)

OBJECTIVE: To determine clinical, clinicopathologic, and postmortem abnormalities in New World camelids with pancreatic necrosis. DESIGN: Retrospective study. ANIMALS: 10 llamas and 1 alpaca. PROCEDURES: Medical records of animals in which a diagnosis of pancreatic necrosis had been made on the basis of histologic examination of necropsy specimens or on the basis of clinical signs and results of clinicopathologic testing were reviewed. RESULTS: The initial owner complaint varied, and various other conditions were diagnosed. Clinical and clinicopathologic abnormalities were vague. Amylase activity was higher in abdominal fluid than in serum in 5 of 7 animals, and lipase activity was higher in abdominal fluid than in serum in all 7. Four animals survived, and 7 died or were euthanatized. Only 1 of the animals that died had marked inflammation of the pancreatic parenchyma. All 7 had necrosis and saponification of fat in and surrounding the pancreas. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that pancreatic necrosis may develop in New World camelids, but clinical signs are vague, and the condition may easily be confused with other diseases. The only laboratory test that appeared to be helpful in the antemortem diagnosis of pancreatic necrosis was comparison of amylase and lipase activities in abdominal fluid and serum.     

Hypoglycemia: a factor associated with low survival rate of neonatal piglets infected with transmissible gastroenteritis virus.

The main purpose of this work was to study changes in the balance of fluids, electrolytes and blood metabolites in neonatal piglets with severe transmissible gastroenteritis. Six two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as normal controls. Blood samples were collected in heparin when the infected piglets were moribund. The following variables were measured: packed red cell volume, total plasma protein and bicarbonate, blood pH, blood urea nitrogen and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets and they were moribund one or two days later. Before becoming moribund, most of the piglets fell rapidly into a lethargic and comatose state. The most evident changes in their blood variables were an increase in packed cell volume, total protein, blood urea nitrogen, phosphorus and magnesium levels and a decrease in pH and bicarbonate concentration as well as a severe hypoglycemia. The results suggest that severe hypoglycemia coupled with metabolic acidosis and dehydration might be an important factor contributing to the high mortality rates caused by transmissible gastroenteritis in neonatal piglets. The hypoglycemia results from a combination of the inadequate glucose metabolism inherent to neonatal piglets and the acute maldigestion and malabsorption resulting from the diffuse and severe villous atrophy induced by the virus.     

Simulated small intestinal volvulus in the anesthetized horse

Experimental closed loop small intestinal volvulus was studied in the anesthetized horse. Volvulus was simulated by ligation of the mesenterial veins to a segment of small intestine. Physical signs and hemodynamic, hematologic, clinical chemical, bacteriologic and peritoneal fluid values were examined. Compared to conscious horses anesthesia highly delayed and modified the clinical signs of shock (changes in mucosal colour, dehydration, decreased skin temperature, elevated pulse rate, low blood pressures) and of small intestinal volvulus (altered peristalsis, gastric dilation). Plasma glucose response to shock was also modified by unconsciousness. However, a dose response relationship was indicated between the extent of small intestinal damage and clinical symptoms. The same was applicable to changes in blood pressures, blood acid-base balance, lactate, potassium, chloride, glucose, inorganic phosphorus, creatinine, creatine kinase, red blood cell and total white blood cell counts and serum total protein. The relationship was also indicated in the following peritoneal fluid values: volume, lactate, pH, total white cell counts, alkaline phosphatase and bacteriology. Changes related to shock (insufficient tissue perfusion) were low blood pressures and metabolic acidosis due to anaerobic glycolysis with accumulation of lactic acid. Also low plasma glucose and elevated plasma potassium, creatinine, inorganic phosphorus and creatine kinase were regarded as consequences of shock.     

Clinical findings and treatment of listeriosis in 67 sheep and goats

This paper describes the clinical findings and treatment of 67 sheep and goats with listeriosis. In 55 of them the diagnosis was made on the basis of the typical signs, which included vestibular ataxia, circling, head tilt and unilateral cranial nerve deficits, but in 12 animals a definitive diagnosis was made only after postmortem examination. The most significant haematological and biochemical findings were a high haematocrit in 16 animals, a high concentration of total protein in 33, a high concentration of bilirubin in 39 and a high concentration of urea nitrogen in 28 animals. Twenty-eight of the animals had a metabolic acidosis. Thirty-nine animals were treated with antibiotics, intravenous sodium chloride and glucose solutions and sodium bicarbonate. Ten of them survived and the others were euthanased because their condition deteriorated. Of the 10 that survived, nine were able to stand when they were first examined and one was in lateral recumbency. Of 15 animals treated with chloramphenicol, one survived; of 11 animals treated with oxytetracycline, two survived; and of nine animals treated with gentamicin and ampicillin, six survived.     

Tricyclic antidepressant toxicosis

Accidental ingestions of TCAs by companion animals often occur. During the past 4 years, over 450 cases have been reported to the IAPIC. At least 7% of the animals that displayed clinical signs of toxicosis eventually died. Overdoses of TCAs adversely affect the cardiovascular, parasympathetic, and central nervous systems. The cardiovascular system is involved most seriously and ventricular arrhythmias with severe hypotension are believed to be the primary cause of death. Animals that ingest a potentially lethal dose (over 15 mg/kg) may die within 1 to 2 hours if appropriate treatment is not administered. Treatment involves the use of initial life-supportive measures (control of seizures, maintenance of an airway, ventilation, and so on), detoxification of the animal (enterogastric lavage, activated charcoal, etc.), and the intravenous use of sodium bicarbonate (2-3 mEq/kg) to control signs of acidosis, hypotension, tachycardia, bradycardia, and other cardiac conduction abnormalities. The animal must then be monitored closely for the return of the clinical signs and sodium bicarbonate therapy should be repeated as needed. In addition, to enhance removal of the TCAs from the gastrointestinal tract and, ultimately, from the body, activated charcoal should be repeated at 3-hour intervals until the animal is asymptomatic.     

Hypoglycemia in Four Dogs With Smooth Muscle Tumors

Tumor-associated hypoglycemia has been reported in dogs with pancreatic β-cell tumors, hepatic tumors, and, rarely, with other neoplasms. This article describes 4 dogs with marked hypoglycemia associated with smooth muscle tumors (jejunal leiomyoma, gastric leiomyoma and leiomyosarcoma, and splenic leiomyosarcoma). Presenting clinical signs included grand mal seizures, lethargy, weakness, ataxia, and, in 1 dog, polyuria/polydipsia. The serum insulin concentration was low in 1 dog and normal in the other dog evaluated. Immunohistochemical staining for insulin was negative in the 4 tumors; the 3 tumors arising from the stomach and jejunum stained diffusely positive for glucagon. Blood glucose concentrations rapidly returned to normal after complete surgical resection of the tumors, and clinical signs associated with hypoglycemia resolved. Long-term follow-up available in 3 of the 4 dogs found no recurrence of clinical signs related to hypoglycemia at 15, 31, and 38 months after surgery, respectively.     

Effects of trenbolone acetate and propylene glycol on pregnancy toxaemia in ewes

Eleven ewes with pregnancy toxaemia were monitored clinically and biochemically after daily treatment with trenbolone acetate (30 mg) and propylene glycol (twice daily 100 ml), for at least one week. The clinical signs of pregnancy toxaemia at first examination were less severe than those described in ewes in other countries. After the first treatment, the appetite improved in nine ewes, blood glucose levels increased in 10 ewes and blood ketone body concentrations decreased in nine animals. A statistically significant decrease in mean ketone body levels was found between the day of first examination and the second day thereafter. Four animals recovered before lambing (group 1). One animal lambed one day after the first treatment and recovered. In the remaining ewes clinical and biochemical improvement did not last long. Three of these animals did not recover until after lambing (group 2) and three animals died (group 3). In three animals of group 2 and two animals of group 3 an increase of serum activities of lactate dehydrogenase, sorbitol dehydrogenase, gamma glutamyl transferase and alkaline phosphatase was found. In two necropsied animals of group 3 a severe fatty degeneration of the liver was found. Treatment of pregnancy toxaemia with trenbolone acetate and propylene glycol appeared to have some positive effect in mild cases. In more advanced cases the time of parturition is the crucial factor leading to recovery.     

Hypoglycemia spiking mortality syndrome in broilers with rickets and a subsequent investigation of feed restriction as a contributing factor

Several cases of elevated mortality with neurologic signs in 14-to-16-day-old broilers were presented to the Poultry Diagnostic and Research Center from one local integrated company. Suspected of "spiking mortality" associated with hypoglycemia, blood glucose levels were <150 mg/dl overall, with several birds with blood glucose levels as low as 30 mg/dl. Tissues, submitted for histopathology, revealed rickets in 50% of the birds. Virus isolation and serology for reovirus and infectious bursal disease virus were negative. After evaluation of these cases, a brief investigation was conducted to determine the effects of feed restriction on the induction of rickets and resulting hypoglycemia. One-hundred 1-day-old broilers were randomly assigned to three treatment groups of: 1) ad libitum feed, 2) 25% restriction, and 3) 50% restriction. Restriction began on the fifth day of age and continued to 21 days of age. Samples collected during the course of the study included whole blood for blood glucose measurements and proximal tibiotarsus for histopathologic examination for rickets. We were unable to reproduce the clinical signs of spiking mortality, neurologic changes, or hypoglycemia experimentally. Histopathology of the growth plates of the proximal tibiotarsus did indicate mild changes consistent with rickets, but the changes were not significant between treatment groups.     

Fanconi syndrome in four non-basenji dogs exposed to chicken jerky treats

Four small-breed dogs were diagnosed with acquired Fanconi syndrome. All dogs ate varying amounts of chicken jerky treats. All dogs were examined for similar clinical signs that included, but were not limited to, lethargy, vomiting, anorexia, diarrhea, and altered thirst and urination. The quantity of chicken jerky consumed could not be determined; however, based on the histories obtained, the chicken jerky treats were a significant part of the diet and were consumed daily by all dogs. Extensive diagnostic testing eliminated other causes of the observed clinical signs, such as urinary tract infection and rickettsial disease. Glucosuria in the face of euglycemia or hypoglycemia, aminoaciduria, and metabolic acidosis confirmed the diagnosis of Fanconi syndrome. All dogs received supportive care, including IV fluids, antibiotics, gastroprotectants, and oral nutritional supplements. Three dogs exhibited complete resolution of glucosuria, proteinuria, and the associated azotemia; however, one dog remained azotemic, resulting in a diagnosis of chronic kidney disease.     

Hypoglycemia associated with nonislet cell tumor in 13 dogs

Hypoglycemia associated with nonislet cell tumor was found in 13 dogs. In each dog, clinical signs were related directly to adrenergic and neuroglucopenic effects of hypoglycemia and included collapsing episodes, tremors, restlessness, weakness, and grand mal seizures that were responsive to glucose administration. Eight of the dogs had hepatocellular carcinoma; surgical resection of the tumor achieved remission of clinical signs in 3 of these dogs. Other hepatic tumors associated with hypoglycemia included leiomyosarcoma and hemangiosarcoma involving solitary lobes of the liver. Nonhepatic tumors included splenic hemangiosarcoma, diffuse metastatic melanoma, and salivary gland adenocarcinoma.