Successful treatment of Solanum dulcamara intoxication in a Labrador retriever puppy

A 10-week-old intact male Labrador retriever dog was presented for acute onset of weakness, ataxia, and generalized muscle tremors. The puppy was suffering respiratory and central nervous system (CNS) depression, was mildly pyrexic, and vomited plant material that was identified as creeping nightshade (Solanum dulcamara). He responded well to supportive care and was discharged successfully. To the authors’ knowledge, this is the first report of Solanum dulcamara toxicity occurring in a dog.     

Rauwolfia serpentina toxicity in a dog

Objective– To describe the clinical manifestations and treatment of Rauwolfia serpentina toxicity in a dog. Case Summary– A 9‐month‐old intact male mixed breed dog was presented following ingestion of an antihypertensive medication containing alkaloids from R. serpentina. R. serpentina alkaloids cause depletion of the biologic amines: norepinephrine, dopamine, and serotonin. The dog experienced hypotension, mental depression, bradycardia, diarrhea, bronchoconstriction, and gastrointestinal ulceration similar to the adverse effects reported in humans. The dog was released from the hospital after 4 days of supportive care. New Information Provided– This is the first case of accidental R. serpentina toxicity in a dog reported in the literature. This case had a good clinical outcome with supportive care and monitoring of all the subsequent adverse effects.     

Two cases of acute polyradiculoneuritis in dogs consuming a raw poultry diet

A 9-year-old female mixed-breed dog presented with ascending flaccid tetraparesis, and a 5-year-old castrated male Poodle dog presented with ventroflexion of neck, dysphonia, and hindlimb weakness, which progressed to acute ascending tetraparesis. Both dogs were fed raw poultry for over 9 and 5 years, respectively. Blood examination and other test results were normal or unrelated to the present case. Fecal polymerase chain reaction analysis in the Poodle dog was positive for Clostridium perfringens and Campylobacter jejuni. Tetraparesis improved with supportive care in both dogs. Human IV immunoglobulin was only administered to the Poodle dog, which showed a shorter recovery (12 days compared to 34 days in the mixed-breed dog). Both dogs returned to normal conditions eventually.     

Airway obstruction in a dog after Dieffenbachia ingestion

Objective – To describe a case of Dieffenbachia ingestion in a dog presented for dysphagia and airway obstruction successfully treated with a temporary tracheostomy and supportive care beyond that reported in the veterinary literature. Case Summary – An 8‐year‐old male neutered Labrador Retriever, weighing 30 kg, was presented with the complaint of choking and gagging. Abdominal radiographs showed that he had a distended stomach full of foreign material and a gastrotomy was performed. After receiving preanesthetic medication, the dog developed inspiratory stridor and during anesthetic induction, marked oropharyngeal swelling complicated tracheal intubation. During surgery a large amount of dog bedding and Dieffenbachia plant material was removed. Because of the severity of the oropharyngeal swelling, the dog required a temporary tracheostomy and treatment for an acute allergic reaction related to the Dieffenbachia ingestion. The patient was discharged after 6 days in the hospital and had no significant complications. New or Unique Information Provided – To our knowledge, this is the first reported case of successful treatment of an airway obstruction related to the toxicity of Dieffenbachia ingestion.     

Evaluation of ifosfamide for treatment of various canine neoplasms

lfosfamide (3-[2-chloroethyl]-2[(2 chloroethyl)amino]tetrahydro-2H-1,3,2-oxazaphosphorine 2-oxide) is an alkylating agent with a broad spectrum of antitumor activity. The efficacy and toxicity of ifosfamide were evaluated in 72 dogs with spontaneously occurring tumors. Forty dogs (56%) had lymphoma, 31 (43%) had sarcomas, and 1 had a metastatic carcinoma. Five dogs received ifosfamide at dosages <350 mg/m2 IV. Neither toxicity nor response were observed, and the remaining dogs received ifosfamide at 350 mg/m2 (n = 18) and 375 mg/m2 body surface area IV (n = 49). Saline diuresis and the thiol compound mesna were used to prevent urothelial toxicity. Fifty-two dogs had measurable tumors and could be evaluated for response. Complete responses were seen in 1 dog with metastatic leiomyosarcoma of the urinary bladder and in 1 dog with metastatic cutaneous hemangiosarcoma. One dog with lymphoma had a partial response for 112 days. Six dogs with splenic hemangiosarcoma received ifosfamide postsplenectomy and their median survival time was 147 days. The acute dose limiting toxicity was neutropenia 7 days after administration of ifosfamide. The median and mean neutrophil counts 7 days after ifosfamide at 350 mg/m2 were 2,035 cells/microL and 4,773 cells/microL, respectively (n = 12). The median and mean neutrophil counts 7 days after ifosfamide at 375 mg/m2 were 2,500 cells/microL and 3,594 cells/microL, respectively (n = 37). No dog developed clinical or microscopic evidence of hemorrhagic cystitis. Ifosfamide appears safe to use in tumor-bearing dogs, and the evaluation of combination chemotherapy protocols that include ifosfamide should be considered.     

Treatment of traumatic cervical myelopathy with surgery, prolonged positive-pressure ventilation, and physical therapy in a dog

CASE DESCRIPTION: A 9-year-old dog was evaluated for traumatic cervical myelopathy after a surgical attempt to realign and stabilize the C2 and C3 vertebrae. CLINICAL FINDINGS: The dog could not ventilate spontaneously and was tetraplegic; positive-pressure ventilation (PPV) was maintained. Myelography and computed tomography revealed spinal cord compression with subluxation of the C2 and C3 vertebrae and extrusion of the C2-3 intervertebral disk. TREATMENT AND OUTCOME: Surgically, the protruding disk material was removed and the vertebrae were realigned with screws and wire. For PPV, assist control ventilation in volume control mode and then in pressure control mode was used in the first 6 days; this was followed by synchronized intermittent mandatory ventilation until 33 days after the injury; then only continuous positive airway pressure was provided until the dog could breathe unassisted, 37 days after the injury. Physical therapy that included passive range of motion exercises, neuromuscular electrical stimulation, and functional weight-bearing positions was administered until the dog was discharged 46 days after injury; the dog was severely ataxic and tetraparetic but could walk. Therapy was continued at home, and 1 year later, the dog could run and had moderate ataxia and tetraparesis. CLINICAL RELEVANCE: Hypoventilation with tetraparesis in traumatic spinal cord injury can be successfully treated with PPV exceeding 30 days, surgery, and physical therapy.     

A case of type B botulism in a pregnant bitch

A two‐year‐old pregnant Gordon setter presented with acute onset of flaccid tetraparesis and respiratory distress. Neurological examination revealed diffuse lower motor neuron dysfunction. Clostridium botulinum neurotoxin B was isolated from the dog's serum. The dog was hospitalised and received supportive care; respiratory function was monitored but positive‐pressure ventilation was not required. Recovery was complete within 1 month and parturition occurred without complication 49 days after admission. The puppies delivered lacked any obvious congenital defects and development during the first few months of life was normal. The source of contamination was suspected to be poorly conserved dry food. To the authors’ knowledge, this is the first report of C. botulinum neurotoxin B isolation in a dog and the first report of botulism in a pregnant bitch.     

Successful management of saltwater submersion injury in a dog using mechanical ventilation

Objective– To describe successful management of saltwater near-drowning in a dog using mechanical ventilation. Case Summary– A 7-year-old spayed female Golden Retriever weighing 37 kg was referred for mechanical ventilation after saltwater submersion injury. The dog had a history of rare seizures characterized by pre-ictal agitation. On the morning of the event, the dog became agitated and ran toward Puget Sound. The owners discovered the dog unconscious in approximately 25.4 cm (10 in) of water, with her head submerged. The owners estimated that the dog was submerged for approximately 30 seconds. The dog was presented immediately to the nearest emergency facility where initial diagnostic testing and treatment included venous blood gases, nasal oxygen, and IV fluids. The dog was dyspneic despite nasal oxygen administration and was referred for mechanical ventilation. Upon arrival the patient was cyanotic with an arterial partial pressure of oxygen of 38 mm Hg (reference interval 85–100 mm Hg) and oxygenation saturation of 62% (reference interval >95%). Thoracic radiographs were taken and revealed severe, bilateral pulmonary infiltrates. The patient was ventilated for 70 hours and was discharged 4 days later. Complications included pneumonia and phlebitis at the site of a cephalic IV catheter. Follow up thoracic radiographs 10 days after discharge were within normal limits and the owners report a full recovery at 1 year. New or Unique Information Provided– Submersion injury can result in acute respiratory distress syndrome in dogs. Mechanical ventilation provided critical support during pulmonary recovery in this dog.     

Xylitol intoxication associated with fulminant hepatic failure in a dog

Objective: To describe a case of xylitol intoxication causing fulminant hepatic failure in a dog. Case summary: A 2.5‐year‐old castrated male English Springer Spaniel weighing 26 kg, was presented after ingestion of half of a loaf of bread containing the sweetener xylitol. Toxic effects of the xylitol in this dog included vomiting, mild hypoglycemia and fulminant hepatic failure. Clinical management of acute hepatic failure and subsequent coagulopathy with supportive care and fresh frozen plasma is described. The dog was discharged 3 days after admission after a full clinical recovery. New or unique information provided: This paper describes the clinical consequence and successful treatment of fulminant hepatic failure in a dog following ingestion of xylitol.     

Sudden acquired retinal degeneration ('silent retina syndrome') in two dogs.

Two unrelated adult dogs developed idiopathic, acute-onset, bilateral total blindness. The ophthalmoscopic changes were minimal and no electroretinographic response could be detected in either dog. The retinas were examined ultrastructurally 10 days (dog 1) and two-and-a-half months (dog 2) after they became blind. There was widespread loss of the outer segments of rod and cone photoreceptors. Where the outer segments persisted, there was marked tubulovesicular change with loss of normal orientation in their lamellae. Second order neurons (bipolar cells) and ganglion cells were unaffected. The cause of this selective and massive disruption of rod and cone endings was not established, but acute toxicity is proposed as a possible mechanism.     

Diet‐associated hepatic failure and immune‐mediated hemolytic anemia in a Weimaraner

Objective: To describe the medical and nutritional management of a 4‐year‐old Weimaraner with acute hepatic failure and immune‐mediated hemolytic anemia (IMHA) associated with consuming a commercial dog food. Case summary: A 4‐year‐old male castrated Weimaraner developed signs of IMHA, hepatic failure, disseminated intravascular coagulopathy, and malnutrition after consuming a commercial dog food. During the course of hospitalization, medical management included immunosuppressive therapy and supportive care. Nutritional support consisted of both enteral and parenteral nutrition. The dog was discharged after 19 days of hospitalization and fully recovered by 6 months. An investigation by the Food and Drug Administration was not able to determine the exact cause of the acute hepatic failure and IMHA. New information provided: This is the first case report documenting the medical and nutritional management of a critically ill animal associated with ingestion of this commercial dog food.     

Toxicity of apolar and polar Lantana camara L. crude extracts in mice

Lantana camara L, widely used in folk medicine, presents toxicity for farm animals. The acute poisoning effects of the apolar and polar L. camara L. extracts in mice were done. The percentage of death during 7 days after treatment, the acute signs of toxicity as well as the general activity observed in open field were assessed. The extracts were administered by i.p. route at 1.5, 3.0 and 5.0 g/kg. Animals were evaluated during the first 2 h after the treatments to assess the acute signs of toxicity and daily observations were done for the presence of death. In the end of the experiment, at day 7, or immediately after death the animals had their organs removed, weighted and observed for macroscopic alterations. ¹H NMR and TLC analysis suggest the presence of triterpenoids in the apolar phase but not in the polar phase. Results showed also that both extracts produced similar percentage of death, mainly after 2 days of treatment; only the apolar extract presented a dose-dependent increased lethality. At necropsy, mice treated by both apolar and polar extracts were severely icteric, dehydrated and constipated, with hepatosis, showed congested heart and lung, and nephrosis; no skin lesions were shown. The main signs of toxicity revealed a decreased spontaneous general activity. In addition, it was observed a decreased duration of locomotion and animal rearing parallel to an increased immobility in the open field. The similarity of the signs related to the acute toxicity for both apolar and polar extracts suggested that the extracts have some of the active toxic principles in common. Data from open field behavior and spontaneous signs of toxicity suggest that the toxic principles have depressive properties on central nervous system.     

Calcipotriol toxicity in a dog

A six-month-old Labrador retriever was presented for investigation of acute polyuria, polydipsia and haematemesis six hours following ingestion of a tube of the topical antipsoriatic vitamin D analogue, calcipotriol. Transient hypercalcaemia, azotaemia, proteinuria, thrombocytopenia and ventricular arrhythmlas ensued. Abdominal ultrasonography and echocardiography revealed evidence of diffuse soft tissue mineralisation. Despite 13 days of intensive supportive care, the dog was euthanased due to continued haematemesis and anorexia. Necropsy confirmed mineralisation and necrosis of multiple organ systems consistent with vitamin D toxicity.     

Mycotic aneurysm caused by Graphium species in a dog

A 10-year-old castrated male mixed-breed dog exhibited vomiting, lethargy and anorexia. An abdominal ultrasound examination revealed a focal dilation of the abdominal aorta. The dog died 2 days after examination, and necropsy revealed a ruptured aneurysm at the abdominal aorta between the kidneys. Histological examination revealed severe granulomatous and necrotizing pan-arteritis with fungal organisms. Graphium species was identified through DNA sequence analysis of the PCR product from formalin-fixed paraffin-embedded samples. To our knowledge, this is the first report of aortic aneurysm caused by Graphium species in a dog.     

The recognition and treatment of the intermediate syndrome of organophosphate poisoning in a dog

Objective: To discuss a new clinical presentation of organophosphate toxicity called the intermediate syndrome in a dog. Case summary: A mixed breed dog presented with generalized weakness, hypoventilation and hypoxemia. The weakness was most marked in the thoracic limbs, cervical and respiratory muscles. The history revealed a likely exposure to an organophosphate compound. The other dog in the household demonstrated mild clinical signs of organophosphate toxicity. A blood cholinesterase level was markedly reduced. Therapy included placement of a tracheostomy tube and mechanical ventilation. The dog gradually improved over the following 8 days but had persistent cervical ventroflexion for a total of 4 weeks. New or unique information provided: Organophosphate toxicity can present as a paralysis following the acute cholinergic crisis. The muscular weakness predominantly affects the thoracic limb and neck muscles but cranial nerve deficits can also occur. Dogs can die from the associated respiratory depression. Oxime therapy is indicated in the treatment of this syndrome.     

Toxicity of Halogenated Oxyquinolines in Dogs. A Clinical Study: I. A Survey of Cases

A survey of 100 cases of oxyquinoline poisoning in dogs is presented. The disease, characterized by hyperexcitability of the CNS with convulsions as well as heart and liver injury, runs an acute course. The mortality (euthanized dogs included) was 30 %. Case-history data showed that the oxyquinoline treatment which preceded the disease was given because the dog had incidental diarrhoea. In most cases the drugs were administered for only 1 day before the dog fell ill. The median time from the last dose to onset of symptoms was 12 hrs. Old dogs were affected more often than expected and also showed higher mortality than did young dogs.     

Canine renal cortical necrosis and haemorrhage following ingestion of an Amitraz-formulated insecticide dip

Amitraz is a formamidine compound used in veterinary medicine as a topical dip to control ticks and mites on dogs and livestock. A 10-year-old female Scottish terrier was presented following the accidental oral administration of a dip containing amitraz. This case report describes the clinical signs, treatment and pathology of this dog. Clinical signs of toxicity from amitraz result from stimulation of alpha2-adrenergic receptors. Amitraz is seldom fatal because the effects can be reversed by alpha2-adrenergic antagonists. The dog recovered from the amitraz toxicity but died 5 days later from acute renal failure.     

Influence of ascorbic acid on BUN, creatinine, resistive index in canine renal ischemia-reperfusion injury

Renal ischemia as a course of renal transplantation is a common cause of renal dysfunction as renal failure. The purpose of this study was to investigate the influence of ascorbic acid on blood urea nitrogen (BUN), creatinine (Cr) and resistive index (RI) for dog models with renal ischemia-reperfusion (I/R) injury. Renal ischemia was induced on 6 Beagle dogs. The left kidney was exposed to normothermic ischemia for a short period at 30 min followed by reperfusion. On the blood Cr level and RI, there was no significant difference comparing both groups. 14 days after I/R injury a significant reduction on the blood BUN level was observed in the vehicle group (34.06 mg/dl) compared to that of ischemia induced treated group (10.3mg/dl) (p < 0.05). In conclusion, administration of ascorbic acid for renal ischemic-reperfusion injury had influence on blood BUN level, but it was not revealed the influence on blood Cr and RI.     

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 )     

Reversal of ethylene glycol-induced nephrotoxicosis in a dog

Ethylene glycol-induced nephrotoxicosis was diagnosed in a dog with acute renal failure. Histologically, the dog had proximal tubular degeneration and necrosis, intraluminal calcium oxalate crystals, generally intact tubular basement membranes, and evidence of tubular regeneration. After 20 days of peritoneal dialysis and diuresis, renal function was adequate to maintain homeostasis without supportive care. Nine weeks after onset of the ethylene glycol-induced renal failure, the dog's kidneys were histologically and functionally normal.