Observations on blood coagulation after snakebite in dogs and cats

Blood samples from 13 cases of snakebite, 6 in dogs and 7 in cats, were tested for activated partial thromboplastin time (APTT), prothrombin time (PT) and fibrin/fibrinogen degradation products (FDP). Four cases were tested for fibrinogen concentration. Based on the results of a commercially available ELISA test, 9 cases were caused by tiger snakes (Notechis scutatus) and 1 case by a brown snake (Pseudonaja textilis). Three other cases had clinical signs and increased creatine phosphokinase values which suggested tiger snake envenomation. Although the period post-envenomation varied, results indicated a marked prolongation of the APTT and PT in 5 of 6 dogs. Three of these 5 dogs also had increased FDP values and 3 (of 3 examined) were hypofibrinogenaemic. Clinical manifestations of this coagulopathy were: haematoma formation after venepuncture (3 cases), gingival petechiae (1 case) and hyphaema (1 case). In contrast, there was minimal or no prolongation of the APTT and PT values, and no increase in FDP, in all 7 cats. Furthermore, no cat exhibited clinical signs of a coagulopathy.     

Acute renal failure associated with contrast medium administration in a dog.

Intravenous administration of an ionic radiographic contrast medium was believed to have caused acute oliguric renal failure in a young dog. Intravenous pyelography was done on a healthy 14-month-old female Lhasa Apso prior to reconstructive surgery for pseudohermaphroditism. Within 24 hours of the radiographic procedure, acute oliguric renal failure developed. Cause for the renal failure was not found other than the recent IV administration of radiographic contrast medium. Treatment with fluids, furosemide, and dopamine was successful in returning renal function to normal. Various adverse reactions to IV administration of contrast media in human beings and animals have been reported; however, to our knowledge, acute renal dysfunction induced by IV administration of contrast material has not been reported in dogs.     

Acute intrinsic renal failure in cats: 32 cases (1997-2004)

OBJECTIVE: To determine patient demographics, clinicopathologic findings, and outcome associated with naturally acquired acute intrinsic renal failure (ARF) in cats. DESIGN: Retrospective case series. ANIMALS: 32 cats with ARF. PROCEDURES: Cats were considered to have ARF if they had acute onset of clinical signs (< 7 days), serum creatinine concentration > 2.5 mg/dL (reference range, 0.8 to 2.3 mg/dL) and BUN > 35 mg/dL (reference range, 15 to 34 mg/dL) in conjunction with urine specific gravity < 1.025 or with anuria or increasing serum creatinine concentration despite fluid therapy and normal hydration status, and no signs of chronic renal disease. Cases were excluded if cats had renal calculi or renal neoplasia. RESULTS: Causes of ARF included nephrotoxins (n = 18 cats), ischemia (4), and other causes (10). Eighteen cats were oliguric. For each unit (mEq/L) increase in initial potassium concentration, there was a 57% decrease in chance of survival. Low serum albumin or bicarbonate concentration at initial diagnosis was a negative prognostic indicator for survival. Initial concentrations of BUN, serum creatinine, and other variables were not prognostic. Seventeen (53%) cats survived, of which 8 cats had resolution of azotemia and 9 cats were discharged from the hospital with persistent azotemia. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that survival rates of cats with ARF were similar to survival rates in dogs and that residual renal damage persisted in approximately half of cats surviving the initial hospitalization.     

Tumoral calcinosis in a dog with chronic renal failure

A 2-year-old male German shepherd dog in poor bodily condition was evaluated for thoracic limb lameness due to a large, firm mass medial to the left cranial scapula. Radiography revealed several large cauliflower-like mineralized masses in the craniomedial left scapula musculature, pectoral region and bilaterally in the biceps tendon sheaths. Urinalysis, haematology and serum biochemistry showed that the dog was severely anaemic, hyperphosphataemic and in chronic renal failure. The dog was euthanased and a full post mortem performed. A diagnosis of chronic renal failure with secondary hyperparathyroidism was confirmed. The mineralised masses were grossly and histopathologically consistent with a diagnosis of tumoral calcinosis. Tumoral calcinosis associated with chronic renal failure that does not involve the foot pads is rarely seen.     

Hemodialysis of a dog with acute renal failure

A dog with oliguric acute renal failure presumed to have been caused by ethylene glycol ingestion was treated by hemodialysis for 1 month. Hemodialysis was effective in controlling azotemia, hyperphosphatemia, and hyperkalemia when performed on a daily or alternate-day basis. The major complications during treatment were infection and severe weight loss. Serial renal biopsies disclosed a progression from initial acute tubular necrosis to severe diffuse interstitial fibrosis and mononuclear cell inflammation. Infection, cachexia, development of end-stage renal lesions, and terminal hyperkalemia contributed to the eventual death of the dog.     

Anuric renal failure in a dog after red-bellied black snake (Pseudechis porphyriacus) envenomation

A case of Red-bellied Black snake envenomation resulting in intravascular haemolytic anaemia, rhabdomyolysis and anuric renal failure is described in the dog. A 12-year-old female desexed Golden Retriever was presented with a 15 hour history of profuse salivation, progressive lethargy, obtundence, inappetence and collapse. Significant findings on clinical examination were pallor, icterus, tachypnoea and dyspnoea with increased respiratory sounds and crackles in all lung fields. Generalised abdominal and muscular pain was apparent and dark red-brown urine was present around the perineal region. A diagnosis of Red-bellied Black snake (Pseudechis porphyriacus) envenomation was made and the dog was treated with intravenous fluid therapy, Tiger/Brown snake antivenom, packed red cell transfusions and Intermittent Positive Pressure Ventilation. Continued clinical deterioration occurred and a diagnosis of acute renal failure secondary to myohaemoglobinuric pigmenturia was made 12 hours after admission. Intensive treatment was attempted with diuresis and volume expansion. Oliguria and subsequent anuria ensued and the dog was euthanased due to a grave prognosis and lack of clinical response to treatment. Necropsy examination revealed muscular necrosis, accumulation of fluid in the thoracic and peritoneal cavities, and marked renal tubular necrosis with intraluminal occlusion secondary to pigmentary casts.     

Acute pulmonary edema after diazepam-ketamine in a dog

An 8-year-old mixed-breed dog was anesthetized for colonoscopy. Moderate sedation was produced by premedication with glycopyrrolate, acepromazine, and hydromorphone, and anesthesia was induced by IV injection of diazepam and ketamine. Frothy, reddish-colored fluid flowed from the endotracheal tube immediately after endotracheal intubation but ceased after several minutes. Furosemide was injected IV. Anesthesia was maintained by sevoflurane in oxygen. Ventilation and arterial blood pressure were satisfactory, however, after oxygen was administered to maintain normal hemoglobin saturation. Radiography revealed changes consistent with a diagnosis of pulmonary edema. The following day, ventricular premature contractions developed and atrial dissociation, valvular regurgitation, and pulmonary hypertension were diagnosed on echocardiography. The proposed etiology is either profound transient hypotension and/or pulmonary hypertension induced by ketamine. The cardiac abnormalities that were present the following day suggest that myocardial dysfunction after induction of anesthesia was more severe than was apparent as assessed by routine physical examination and monitoring methods.     

Gentamicin-associated acute renal failure in the dog

Gentamicin-associated acute renal failure was diagnosed in 10 dogs. The disease was characterized by a poor prognosis and lengthy hospitalization. Hypoalbuminemia, disorders of potassium homeostasis, proteinuria, hematuria, and cylindruria were common during therapy for renal failure. Fever and dehydration were the most commonly identified potential predisposing factors.     

Acute toxoplasmosis following renal transplantation in three cats and a dog.

Three cats and 1 dog that had undergone renal transplantation because of end-stage renal disease were examined because of complications 3 to 6 weeks after surgery. One cat died prior to treatment of the complications; Toxoplasma cysts were found in sections of the renal allograft, and Toxoplasma tachyzoites were found in other organs. The other 2 cats and the dog died despite treatment, and protozoal cysts, as well as tachyzoites, were identified in other organs but not within the allografts, suggesting that reactivation of latent infection following immunosuppression was the most likely cause of disseminated toxoplasmosis. These cases illustrate that toxoplasmosis can be a fatal complication in renal transplant recipients. We currently recommend that feline and canine donors and recipients undergo serologic testing for toxoplasmosis prior to surgery. In addition, we suggest that seropositive donors not be used for seronegative recipients and that seropositive recipients and that seropositive recipients be monitored closely after surgery for clinical signs of toxoplasmosis.     

Hemodialysis in a dog with acute renal failure from currant toxicity

A 3 1/2-year-old Labrador retriever being presented for acute onset vomiting and lethargy was diagnosed with acute renal failure (ARF). The dog had ingested dried currants, a type of raisin. Hemodialysis was successfully performed to treat the ARE Raisin toxicity can cause ARF and warrants early recognition and aggressive treatment.     

Isoniazid-induced seizures with secondary rhabdomyolysis and associated acute renal failure in a dog

Isoniazid-induced seizures resulted in rhabdomyolysis and associated acute renal tubular necrosis in a dog. Rhabdomyolysis and myoglobinuric renal failure, although recognised in the dog, are reported infrequently as a consequence of seizures. The clinical presentation of isoniazid toxicity in a dog is described.     

Acute polyneuromyopathy with respiratory failure secondary to monensin intoxication in a dog

Objective

To describe a successfully managed case of polyneuropathy and respiratory failure secondary to presumed monensin intoxication.

Case Summary

A 9‐month‐old Australian Shepherd was evaluated for progressive generalized weakness and respiratory distress. Several days preceding presentation, the dog was seen playing with a monensin capsule, and had free access to a barn where the product was stored and where chewed capsules were subsequently found. The dog was presented with flaccid tetraparesis, hyperthermia, and severe respiratory distress. Bloodwork and urinalysis revealed marked increase in serum creatine kinase concentration and presumed myoglobinuria. Cardiac troponin I level was markedly increased. Management included mechanical ventilation for 5 days, fluid‐therapy, active cooling, antimicrobial therapy, analgesia, gastroprotectants, antiemetics, enteral feedings, continuous nursing care, and physiotherapy. Intravenous lipid rescue therapy was administered with lack of improvement in respiratory function and muscle strength. The patient completely recovered and was discharged after 12 days of hospitalization.

New or Unique Information Provided

Monensin intoxication should be considered in the differential diagnosis of acute polyneuromyopathy and respiratory failure in dogs with access to this compound. Respiratory failure secondary to monensin intoxication does not necessarily carry a poor prognosis if mechanical ventilation can be provided as a bridge until return of respiratory function is achieved.     

Managing fluid and electrolyte disorders in renal failure.

Because of the role of the kidneys in maintaining homeostasis in the body, kidney failure leads to derangements of fluid, electrolyte, and acid-base balance. The most effective therapy of a uremic crisis is careful management of fluid balance, which involves thoughtful assessment of hydration, a fluid treatment plan personalized for the specific patient, repeated and frequent reassessment of fluid and electrolyte balance, and appropriate changes in the treatment plan in response to the rapidly changing clinical situation of the patient that has renal failure. Disorders of sodium, chloride, potassium, calcium, and phosphorus are commonly encountered in renal failure and may be life threatening. Treatment of metabolic acidosis and nutritional support are frequently needed.     

Leukemoid blood response and bone infarcts in a dog with renal tubular adenocarcinoma

Neutrophilic leukocytosis (136,800 WBC/microliters) and multiple bone infarcts were detected in a dog with renal tubular adenocarcinoma. The causes of the leukocytosis and bone infarcts were not determined, but these syndromes appear to be uncommon manifestations of cancer in animal and human patients.