S-adenosyl-L-methionine (SAMe) for the treatment of acetaminophen toxicity in a dog

An 8-month-old, spayed female Shetland sheepdog presented 48 hours after ingesting acetaminophen (1 gm/kg body weight). On presentation, the dog was laterally recumbent and hypovolemic. The dog had brown mucous membranes, severe Heinz-body hemolytic anemia, bleeding tendencies, and a red blood cell (RBC) glutathione (GSH) concentration that was 10% of reference values, despite a regenerative erythroid response. Treatment with s-adenosyl-l-methionine (SAMe) as a GSH donor successfully rescued this dog, despite the animal's late presentation after drug ingestion. A loading dose (40 mg/kg body weight) of a stable SAMe salt per os was followed by a maintenance dose (20 mg/kg body weight) sid for 7 days. Additional therapeutic interventions included an intravenous (i.v.) infusion of one unit of packed RBCs (on admission), i.v. fluid support (3 days), and famotidine (7 days) to reduce gastric acidity. Sequential assessment of RBC GSH concentrations and RBC morphology documented response to antidote administration within 72 hours. This case suggests that SAMe may provide a therapeutic option for treatment of acetaminophen toxicosis in dogs capable of retaining an orally administered antidote and maintaining adequate hepatic function for metabolism of SAMe to its thiol substrates.     

Mechanical Ventilation of a Dog with Pentobarbital Intoxication

A 9-year old spayed female American bulldog presented 5 hours after ingesting a portion of a recently euthanized sheep carcass. The dog was comatose, intubated and manually ventilated on arrival. On physical examination, the dog had stable cardiovascular parameters but was hypothermic. Cranial nerve reflexes were absent and spinal reflexes were depressed. Mechanical ventilation was initiated and maintained for 18 hours before spontaneous respiration returned. Elevated serum pentobarbital concentration (19.1 mg/ml) confirmed pentobarbital intoxication as the cause of neurological signs. This is the first report of a dog with pentobarbital toxicity that was successfully managed with mechanical ventilation. Neurologic and functional recovery was complete and the dog was discharged 48 hours after admission. (J Vet Emerg Crit Care 2001; 11(1):33–37)     

Laparoscopic Splenectomy in Goats

Objective— To report laparoscopic splenectomy in goats.
Study Design— Experimental study.
Animals— Healthy female goats (n=9); aged, 10–18 months; weighing, 22–30 kg.
Methods— Food was withheld for 24 hours and water for 10 hours. Anesthetized right laterally recumbent goats had a laparoscopic portal and 3 instrumental portals created in the left flank. Splenic attachments were dissected with monopolar electrocautery and blunt dissection through 2 instrument portals. Exposure and isolation of splenic vessels was performed with laparoscopic "right-angle" preparation forceps. Vessels were ligated with a medium-titanium clip and 2 silk sutures and then transected between the silk sutures. The detached spleen was manipulated into a specimen retrieval bag, morcellated, and the bag retrieved through an enlarged portal. Repeat laparoscopic examination was performed at 1 month.
Results— Laparoscopic splenectomy required 70 minutes (range, 52–88 minutes) and was successful without major intraoperative and postoperative complications. Postoperatively, all goats had signs of mild abdominal discomfort. On repeat laparoscopy, with the exception of 1 goat that had a focal omental adhesion to the enlarged portal site, no other abnormalities were identified.
Conclusions— Laparoscopic splenectomy can be accomplished in goats using 4 portals in the left flank and a combination of monopolar cautery dissection of splenic attachments, ligation of vessels using metal clips and intracorporeal ligatures, and intra-abdominal morcellation of the detached spleen in a specimen retrieval bag.
Clinical Relevance— Laparoscopic splenectomy is an effective and safe technique in goats.     

Therapy and outcome of suspected alpha lipoic acid toxicity in two dogs

Objective – To report a suspected toxicity in 2 dogs; to discuss therapy and prognosis.
Series Summary – Suspected alpha lipoic acid (ALA) toxicity was diagnosed based on clinical history and compatible laboratory findings in 2 dogs. Case 1 was presented within 10 hours of ALA ingestion, with initial behavioral changes likely due to hypoglycemia. During the course of hospitalization, hypoglycemia persisted and evidence of acute hepatic insult developed. With aggressive supportive care (including IV fluids with dextrose supplementation, hepatoprotective medications, and a plasma transfusion), he made a full recovery. Case 2 was presented approximately 60 hours after ALA ingestion, and was found to be in oliguric renal failure. She was treated with IV fluids, gastroprotective medications, and furosemide, but her condition deteriorated and she was ultimately euthanized within 16 hours of admission to the hospital.
New or Unique Information Provided – ALA is an uncommon but serious toxin that should be considered in cases presenting with hypoglycemia, acute renal failure, or acute hepatic insult.     

Ivermectin toxicosis in a dog

A 5-year-old male Doberman Pinscher was examined after ingesting an equine paste dewormer containing approximately 115 mg of ivermectin. Clinical signs consisted of profound hypothermia, mild dehydration, dilated unresponsive pupils, localized muscle group fasciculations around the face and hind limbs, and no response to any external stimuli. Twelve days after parenteral administration of isotonic fluids and IV administration of dexamethasone and dimethyl sulfoxide, the dog returned to a clinically normal neurologic state. Ivermectin toxicosis has been reported frequently in Collies; however, other breeds may have idiosyncratic reactions to low doses. Patients with severe toxicosis should eventually recover completely if given appropriate intensive care.     

Accidental 5-Fluorouracil Exposure in a Dog

objective: To demonstrate the range of toxicities with 5-Fluorouracil (5-FU).
Case Summary: A one-year-old male castrated Labrador Retriever presented to the University of Minnesota Veterinary Teaching Hospital Emergency Service following accidental ingestion of a 5% 5-Fluorouracil (5-FU) topical antineoplastic cream. The animal presented with status epilepticus and later demonstrated additional clinical signs consistent with 5-FU toxicosis including mucositis and diarrhea, profound but transient leukopenia, and thrombocytopenia.
New Information Provided: The calculated ingested dosage was 46 mg/kg. The dog responded well to intensive therapy, recovering uneventfully.     

Atypical Reaction to Acetaminophen Intoxication in a Dog

Objective: To report an unusual manifestation of acetaminophen intoxication in a dog.
Case Summary: A Miniature Pinscher was presented for evaluation of lethargy and facial swelling after ingestion of 500–750 mg/kg of acetaminophen. Laboratory testing revealed eccentrocytes, Heinz bodies, hemoglobinemia, and a declining packed red cell volume consistent with oxidative damage to the erythrocytes. Hepatocellular damage, as monitored by serum alanine aminotransferase, was not documented. The dog responded well to therapeutic intervention, and was discharged from the hospital. The dog returned to the hospital 2 days later with clinical signs and diagnostic tests consistent with acute keratoconjunctivitis sicca, which was assumed to be due to a toxic etiology. The dog responded well to therapy, regaining normal levels of tear production within six weeks.
New or Unique Information Provided: Acetaminophen intoxication may be associated with severe erythrocytic oxidative damage in the absence of detectable hepatic injury in dogs. Acetaminophen intoxication may have the potential to cause acute keratoconjunctivitis sicca in dogs. ( J Vet Emerg Crit Care 2001; 11(2): 123–126 )     

Critical illness-related corticosteroid insufficiency in a dog with septic shock

Objective – To describe a case of hydrocortisone-responsive hypotension and critical illness-related corticosteroid insufficiency (CIRCI) in a dog with septic shock.
Case Summary – A dog with aspiration pneumonia developed septic shock with pressor-refractory hypotension. A standard ACTH stimulation test was performed that showed a blunted cortisol response consistent with CIRCI. Reversal of shock was achieved within 2 hours of hydrocortisone administration, and complete weaning from pressors was accomplished over the subsequent 8 hours. The patient recovered and was discharged from the hospital. An ACTH stimulation test performed 1 month after hospital discharge showed normal adrenal responsiveness consistent with resolution of CIRCI.
New or Unique Information Provided – This case is the first published report of hydrocortisone-responsive hypotension and transient CIRCI associated with naturally occurring septic shock in a dog.     

Combined Gemcitabine and Carboplatin Therapy for Carcinomas in Dogs

Background: Response and adverse reactions to combined gemcitabine (GEM) and carboplatin (CARBO) therapy in dogs with carcinomas are not documented.
Hypothesis: GEM and CARBO are safe for the treatment of dogs with carcinomas.
Animals: Thirty-seven dogs with histologically or cytologically confirmed carcinomas.
Methods: Prospective clinical trial. Dogs were treated with GEM (2 mg/kg, 20–30-minute infusion IV) on Days 1 and 8 and 4 hours later, CARBO (10 mg/kg IV) on Day 1. The cycle was repeated on Day 22.
Results: Thirty-seven dogs (29 with measurable tumor) received a median of 2 cycles (range 0.5–6) for a total of 101 cycles administered. Twelve dogs (32%) developed neutropenia (3 Grade 3, and 5 Grade 4) and 9 (24%) thrombocytopenia (2 Grade 3, and 1 Grade 4). Dogs >20 kg were twice as likely to develop thrombocytopenia ( P = .023). Twenty-seven dogs (73%) had evidence of gastrointestinal (GI) toxicosis, but most signs were of mild to moderate severity and self-limiting. One dog died of treatment-related complications. Overall tumor response rate was 13%. One dog with metastatic prostatic carcinoma achieved a complete remission and 1 dog with intestinal adenocarcinoma and 1 with tonsillar squamous cell carcinoma achieved partial remission. Twelve dogs achieved stable disease for a median of 72 days.
Conclusion and Clinical Importance: GEM and CARBO combination causes mild to moderate hematologic and GI toxicosis in dogs with carcinoma. Response rate in this study was modest, and optimization of dosing of this combination is required.     

Hypothalamic-pituitary axis deficiency following traumatic brain injury in a dog

Objective – To describe endocrine dysfunction associated with traumatic brain injury in a dog.
Summary – A 12-week-old dog presented with traumatic brain injury and did not respond to traditional supportive care. Continued hypothermia, electrolyte derangements, hypotension, and hyposthenuria prompted screening for and detection of several hypothalamic-pituitary disorders including: hypoadrenocorticism, central diabetes insipidus, hypothyroidism, and growth hormone deficiency. Electrolyte abnormalities, urine osmolarity, and blood pressure improved with treatment for the associated disorders.
New or Unique Information Provided – This is the first report of generalized hypothalamic-pituitary dysfunction or panhypopituitarism following traumatic brain injury in a dog.     

Zinc-associated acute pancreatitis in a dog

Zinc-induced haemolytic anaemia is a common phenomenon in dogs in the USA following the ingestion of pennies minted after 1982. A case of acute pancreatitis secondary to zinc toxicosis in a dog is described. Acute pancreatitis has been reported in humans, following the ingestion of liquid zinc chloride, but zinc-associated pancreatitis has not been reported previously in the dog. The mechanism of toxicity is unknown, although the pathophysiology may relate to the role of the pancreas in zinc excretion. Acute pancreatitis as a sequela to zinc toxicosis in the dog represents a complication that may prolong hospitalisation and worsen the prognosis.     

Fatal systemic phaeohyphomycosis caused by Ochroconis gallopavum in a dog (Canis familaris)

A 5-year-old Shetland Sheepdog was presented with a history of weakness, ataxia, anemia, thrombocytopenia, and occasional seizures. The dog had been treated for 6 months with prednisone for inflammatory bowel disease. A positive titer for Ehrlichia canis was detected 6 months before referral. The initial physical examination revealed a weak, laterally recumbent dog with pale mucous membranes. Neurologic examination revealed multiple neurologic deficits. A complete blood cell count (CBC) revealed normochromic, normocytic, nonregenerative anemia; lymphopenia; thrombocytopenia; and neutrophilic and monocytic leukocytosis. Urinalysis revealed proteinuria, with a specific gravity of 1.045. The dog was unresponsive to treatment and died. At necropsy, there was severe serofibrinous peritonitis and pleuritis, with randomly scattered dark brown necrotic foci present in multiple organs, including liver, spleen, kidney, and pancreatic lymph node. Histologically, there were extensive regions of parenchymal necrosis surrounded by neutrophils admixed with epithelioid macrophages, lymphocytes, and pigmented fungal organisms. Numerous brown, 2 to 6 microm in diameter, septate, branching hyphae, subsequently identified as Ochroconis gallopavum (formerly Dactylaria constricta var. gallopava), were observed.     

Copper toxicosis in a Boer goat

A 1‐year‐old female Boer goat was presented with a 1‐day history of pigmenturia, anorexia, and shivering. Anemia was not present initially, but progressive hemolytic anemia developed subsequently and was characterized by the finding of Heinz bodies in both intact RBCs and in ghost cells and the presence of atypical fusiform RBCs. Plasma biochemical analysis revealed increased activities of aspartate aminotransferase and gamma‐glutamyltransferase, hyperbilirubinemia, and azotemia. Histopathologic examination of a liver biopsy revealed necrosis of individual hepatocytes and intracytoplasmic rhodamine‐positive granules, consistent with copper. Copper concentration in ante‐mortem hepatic tissue was increased, and a diagnosis of copper toxicosis was made. Despite supportive therapy, the goat continued to decline and was euthanized. Necropsy findings included hepatic necrosis and hemoglobinuric nephrosis. Freshly collected specimens of liver and kidney had markedly increased copper concentrations. The mineral composition of the water, grass hay, and goat chow was evaluated, and toxins and significant mineral imbalances were not found. The underlying cause of the hepatic accumulation and subsequent release of copper remains unclear in this goat. Recently, Boer goats have been recognized as being prone to copper toxicosis and may be more susceptible than other breeds; similar to sheep, Boer goats may experience a hemolytic crisis secondary to copper toxicosis.     

Fatal propylene glycol toxicosis in a horse

Toxicosis attributable to propylene glycol (1,2-propanediol) was suspected in an 8-year-old 450- to 500-kg male Quarter Horse. Clinical signs of toxicosis developed within 15 minutes of the accidental iatrogenic oral administration of 3.8 L of propylene glycol. Clinical signs of toxicosis included salivation, sweating, ataxia, and signs of pain. Additionally, at 24 hours after propylene glycol ingestion, the horse became increasingly atactic, had an abnormal breath odor, developed rapid shallow breathing, and was cyanotic. The horse died of apparent respiratory arrest 28 hours after the propylene glycol ingestion. Analysis of serum and combined urine and blood from the kidneys confirmed the presence of propylene glycol. Propylene glycol is used for the treatment and prevention of bovine ketosis, and is similar in appearance to mineral oil. The accidental administration of propylene glycol to horses may result in fatal poisoning.     

Metabolic changes associated with anaesthesia and cherry poisoning in a pony

Observations  A case of a pony with severe cyanide intoxication as a result of cherry ingestion is presented. General anaesthesia was performed for colic surgery. Severe metabolic lactate acidosis in combination with a high arterial oxygen partial pressure and clinically good peripheral perfusion parameters were the remarkable signs during anaesthesia. Severe hypothermia was obvious during recovery. Ten hours post-surgery the pony was euthanized as a result of neurological signs. The diagnosis of cyanide intoxication was made post-mortem.
Conclusion  Cherry ingestion can lead to lethal cyanide intoxication in horses indicated by severe nonhypoxic lactic acidosis during anaesthesia.     

Suspected lily-of-the-valley (Convallaria majalis) toxicosis in a dog

Objective: To describe successful treatment of third-degree atrioventricular (AV) block using temporary noninvasive transthoracic pacing and placement of a permanent transvenous pacemaker in a case of suspected lily-of-the-valley ( Convallaria majalis ) intoxication in a dog.
Case summary: A 2-year-old neutered male Beagle weighing 17.8 kg was presented to the emergency service for treatment of bradycardia, vomiting, and lethargy. An electrocardiogram revealed third-degree AV block that was nonresponsive to atropine. Ten hours after admission, the dog became obtunded. Treatment initially consisted of temporary noninvasive transthoracic pacing and eventually placement of a permanent transvenous pacemaker. The initial history did not suggest that the dog had access to any known cardiotoxins. However, C. majalis , which contains cardiac glycosides, was identified within the dog's environment and the dog's serum did contain digoxin or an immunologically cross-reactive compound.
New or unique information provided: This is the first reported successful management of C. majalis toxicosis in a dog. Temporary noninvasive transthoracic pacing was used in the management of this case as a safe and effective bridge to permanent pacemaker implantation.     

Acute, fatal illness in cattle exposed to boron fertilizer

Twenty-six cows died after accidental exposure to boron fertilizer. Cows developed diarrhea, weakness, ataxia, signs of depression, and died, usually within a few hours. Seizure-like behavior was noticed in 2 cows, and 2 were suspected of aborting. High boron concentrations in tissues from affected cows confirmed ingestion of an appreciable amount of boron fertilizer. In an attempt to confirm the diagnosis of boron poisoning, boron fertilizer was administered to goats. A kid goat given 3.6 g of fertilizer/kg of body weight developed clinical signs similar to those seen in the cattle. Boron compounds such as sodium borate and boric acid have been considered generally nontoxic, and reports of livestock toxicosis are uncommon. This case report suggests that these compounds may be palatable under certain circumstances leading to ingestion of toxic quantities.     

Adverse events associated with pericardiocentesis in dogs: 85 cases (1999–2006)

Objective – To quantify the frequency of adverse events occurring during or post pericardiocentesis and to determine if adverse events are related to the cause of the pericardial effusion or frequency of pericardiocentesis.
Design – Retrospective study.
Setting – Referral hospital.
Animals, Intervention and Measurements – Medical records of 85 dogs that underwent 112 episodes of pericardiocentesis were reviewed. Any adverse events during pericardiocentesis and in the 48 hours post pericardiocentesis were noted. The frequency of adverse events was compared between dogs with a suspected neoplastic cause and a suspected nonneoplastic cause of their pericardial effusion and also between the first and subsequent pericardiocenteses.
Main Results – The incidence of adverse events was 10.7% within 1 hour of pericardiocentesis and 15.2% within 48 hours. There was no significant difference in the frequency of adverse events between the groups. Most adverse events identified were dysrhythmias. Forty-one percent of those dogs with adverse events were euthanized or died within 48 hours.
Conclusion – The incidence of adverse events seen within 48 hours of pericardiocentesis was 15.2%.     

Pneumothorax secondary to pulmonary thromboembolism in a dog

Objective – To describe a case of spontaneous pneumothorax secondary to pulmonary thromboembolism possibly associated with pituitary dependent hyperadrenocorticism.
Case Summary – A 7-year-old spayed female Collie weighing 26 kg was referred for evaluation of spontaneous pneumothorax. An exploratory thoracotomy was performed and revealed 2 lung lobes to be diffusely hemorrhagic and they were resected. Histologic examination of multiple sections documented diffuse thromboembolism. A 2–3 cm thrombus was visualized distal to the bifurcation of the pulmonary artery during an echocardiographic examination postoperatively. The dog was discharged to the owner after recovery from surgery. The thrombus had resolved at the 4-week recheck examination. Diagnosis of pituitary dependent hyperadrenocorticism was confirmed based on follow-up endocrine testing.
New or Unique Information Provided – This is the first report of pulmonary thromboembolism causing spontaneous pneumothorax in the dog.     

Diagnosis and treatment of thallium toxicosis in a dog

A case of chronic thallium toxicosis in a dog is described. The difficulties in diagnosis in the absence of a history of known ingestion of the agent are discussed and a method of increasing urinary thallium to detectable levels is described.