Hemodialysis as emergency treatment of a severe baclofen intoxication in a 3 kg dog.

OBJECTIVE: To describe the clinical efficacy and drug removal kinetics of hemodialysis (HD) as emergency treatment in a small size dog with severe baclofen intoxication. CASE DESCRIPTION: A 2-year-old dog was presented in stupor to the emergency service a few hours after ingestion of up to 25 mg of baclofen. Medical stabilisation was attempted but was unsuccessful in improving the neurological condition and the patient rapidly progressed to coma. A 4-h session of HD was performed in emergency with near complete resolution of neurological signs and only mild disorientation by the end of the treatment. No adverse side effects occurred during HD. Baclofen concentration was measured serially during the session. Drug extraction ratio, clearance and mass removal by the dialyser were calculated. Dialytic elimination rate constant (Kd ) was seven times higher than the intrinsic elimination rate constant (Kintr ) and the half-life (t½) during HD was nearly nine times shorter than the endogenous one. NEW OR UNIQUE INFORMATION PROVIDED: This is the first case report providing pharmacokinetic data associated with HD treatment of severe baclofen intoxication in a dog.

Retrospective characterization of coma and stupor in dogs and cats presenting to a multicenter out-of-hours service (2012-2015): 386 animals.

OBJECTIVE: To describe the signalment, etiology, and short-term outcome of dogs and cats presenting in a coma or stupor. DESIGN: Retrospective study conducted between May 2012 and February 2015. SETTING: Multicenter out-of-hours emergency service provider. ANIMALS: Three hundred eighty-six patients presenting in a coma or stupor to a multicenter out-of-hours emergency care provider. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Records were reviewed to determine the most likely etiology of coma or stupor. Short-term outcomes were defined as deceased (died or euthanized) or transferred (case handed over to a daytime clinic or discharged). There were 168 dogs (coma n = 112, stupor n = 56) and 218 cats (coma n = 148, stupor n = 70) identified. Coma and stupor were more prevalent in cats compared to dogs, and Chihuahuas were over represented. Blood glucose concentrations were frequently outside established reference intervals. Excluding undetermined causes, the most common causes in dogs included traumatic brain injury (TBI) 16.0% (n = 27, deceased n = 22), hypoglycemia 10.7% (n = 18, deceased n = 8), shock 10.1% (n = 17, deceased n = 16), seizure 9.5% (n = 16, deceased n = 13), and renal or hepatic dysfunction 5.3% (n = 9, deceased n = 7). For cats, the most common causes included TBI 21.6% (n = 47, deceased n = 38), renal or hepatic dysfunction 13.3% (n = 29, deceased n = 25), intoxication 10.1% (n = 22, deceased n = 18), hypoglycemia 6.0% (n = 13, deceased n = 4), and shock 5.0% (n = 11, deceased n = 8). When treatment was attempted, 46.0% of dogs (n = 44/96) and 41.2% of cats (n = 35/85) survived to be transferred. Compared to all other etiologies, death was less likely when coma or stupor was attributed to hypoglycemia. CONCLUSION: In cases where a cause was determined, TBI was the predominant etiology of coma and stupor for both species. With the exception of coma and stupor attributed to hypoglycemia, the overall short-term prognosis was poor.

Treatment of ibuprofen toxicity with serial charcoal hemoperfusion and hemodialysis in a dog.

OBJECTIVE: To describe the efficacy of serial charcoal hemoperfusion and hemodialysis in removing ibuprofen from a dog with severe clinical signs of toxicity. CASE SUMMARY: A dog ingested a minimum of 2,200 mg/kg of ibuprofen resulting in progressive neurologic dysfunction that progressed to a comatose state by the time of presentation. Extracorporeal charcoal hemoperfusion coupled serially with hemodialysis was performed to remove ibuprofen from this patient. Serial charcoal hemoperfusion and hemodialysis therapy resulted in complete reversal of the neurologic dysfunction in this dog. No evidence of acute kidney or hepatic injury was observed. Serum ibuprofen concentrations confirmed the efficacy of this treatment. NEW INFORMATION PROVIDED: This report details the technique for extracorporeal extraction of ibuprofen, a methodology that could be employed for other toxicities due to substances with similar pharmacokinetics. Complications and limitations (eg, saturation of the charcoal cartridge) of the therapy are discussed.

Severe seizures associated with traumatic brain injury managed by controlled hypothermia, pharmacologic coma, and mechanical ventilation in a dog.

OBJECTIVE: To describe the management and outcome of a dog presenting with intractable seizures associated with traumatic brain injury. CASE SUMMARY: A spayed female Wheaten Terrier was presented to an emergency clinic with neurologic deficits (modified Glasgow coma scale of 10) shortly after a road traffic accident. Seizures were uncontrolled despite aggressive pharmacologic intervention. Controlled hypothermia to achieve a rectal temperature of 33-35 degrees C (91.4-95 degrees F) was initiated as a protective measure to reduce intracranial pressure and cerebral metabolic rate, and to assist with seizure control. Intubation and mechanical ventilation were required to protect the airway and manage hypercapnia associated with hypoventilation. The patient went on to make a full recovery, although behavioral changes were noted by the owners for an 8-week period following injury. NEW OR UNIQUE INFORMATION PROVIDED: To the author's knowledge, this is the first instance of therapeutic hypothermia reported in the veterinary literature. A short review of this treatment modality is provided.

Sequential magnetic resonance imaging of an intracranial hematoma in a dog.

An 8-year-old Yorkshire terrier developed acute onset coma and seizure after cranial trauma. Intracranial hemorrhage was suspected from the clinical signs and history. Low-field magnetic resonance (MR) imaging revealed a round mass within the right cerebral hemisphere, compressing the right lateral ventricle and displacing the longitudinal fissure to the left. The lesion was hypointense on T1-weighted images and hyperintense on T2-weighted images, consistent with an acute hemorrhage. MR imaging was performed every 24 h for 6 days from 1 h after the injury, and then on day 14 of hospitalization. With time, the signal intensity changed to hyperintense on Ti-weighted images. On T2-weighted images the center of the mass changed to hypointense, and then to hyperintense with a hypointense rim. These changes of signal intensity were related to hemoglobin oxidation.

Myxedema coma leading to respiratory depression in a dog.

A 10-year-old, intact male, cocker spaniel was presented with hypothermia, without shivering, and progressive stupor leading to coma. Myxedema coma, potentially precipitated by diuretic therapy, was tentatively diagnosed and treatment initiated, but progressive respiratory depression led to the decision to euthanize. Postmortem findings supported the diagnosis of myxedema coma.

Acute endosulfan poisoning in cattle.

Endosulfan poisoning was observed in cattle where the owner applied the insecticide topically as ectoparasitic control. Two of 11 cattle died in 2 d with rapid and difficult breathing, foamy exudates in the mouth, tremors, exophthalmos and coma. At necropsy, hemorrhages were on the serosal membranes of the visceral organs and lungs, and there was severe edema and emphysema in the lungs. The levels of endosulfan in the liver, kidney, lungs and muscle were 13.1, 4.0, 1.6 and 0.8 ppm, respectively.

A review of moxidectin overdose cases in equines from 1998 through 2000.

Moxidectin is a macrolide endectocide available as a 2% equine oral gel in the US. This report presents clinical signs of moxidectin toxicosis and its treatment in equines as reported to the ASPCA Animal Poison Control Center (APCC) from January 1998 to December 2000. Nine cases of moxidectin overdose in equines occurred: 5 had signs of toxicosis such as coma, dyspnea, depression, ataxia, tremors, seizures, or weakness. The approximate dose of moxidectin at which these signs were observed ranged from 1.0 to 5.1 mg/kg. The 4 equines that ingested moxidectin between 0.9 mg/kg to 1.7 mg/kg did not show signs of toxicosis. Clinical signs were seen within 6-22 h and lasted for 36-168 h. Only 1/5 clinical equines was an adult, the others were < 4 month of age. This study supports earlier report that young foals are more susceptible to moxidectin toxicosis. All 4 equines with known outcomes recovered with treatment that included decontamination, seizure control, thermoregulation, fluid therapy, and supportive care.

Coma and apnea in a dog with hydroxyzine toxicosis.

Hydroxyzine is a commonly prescribed H1-receptor antagonist in small animal practice. The most common adverse effect reported after therapeutic dosing is mild sedation; severe reactions resulting in coma have occasionally been reported in children. We present a case of large po hydroxyzine exposure causing in coma and apnea in a dog. Exposure was confirmed with gas chromatography/mass spectrometry analysis of urine. Extensive therapeutic measures to enhance drug elimination and assist ventilation were required for 11 d. The positive outcome justifies critical care of similarly exposed animals. Veterinarians should be aware of the potential for coma and apnea secondary to hydroxyzine exposure.

Intravenous administration of levothyroxine for treatment of suspected myxedema coma complicated by severe hypothermia in a dog.

A 7-year-old male English Coonhound with suspected myxedema coma complicated by severe hypothermia and metabolic abnormalities was treated with a combination of active external and core rewarming techniques, i.v. and oral administration of levothyroxine, supplemental oxygen, and administration of fluids (0.9% NaCl solution). Myxedema coma develops as a consequence of severe hypothyroidism and is characterized by a hypometabolic, stuporous state. Myxedema coma is associated with a high mortality rate, and most reported cases have involved Doberman Pinschers. Intravenous administration of levothyroxine can be used successfully in combination with oral administration to restore normal metabolic function and assist in warming and thermoregulation, although dosages should be conservative to avoid adverse cardiovascular effects.

[Moxidectin poisoning in a foal?]. / Moxidectine intoxicatie bij een veulen?

A 2 day old foal was presented with central nervous depression (coma) after moxidectin overdose. Moxidectin belongs to the milbemycin anthelmintics which elicit their working mechanism through a GABA (gamma-aminobutyric acid)-stimulatory mode of action. The foal developed profound hypothermia, bradycardia and hypoventilation. Absence of urine voiding and mild abdominal distension suggested a ruptured bladder, which was confirmed by transabdominal ultrasound and clinical-pathologic parameters. Repeat auscultation of the ventral lung parts and the occurrence of gastric reflux were suggestive of an aspiration pneumonia. The foal underwent surgical bladder repair, however, did succumb due to mixed acidosis and early signs of sepsis postoperatively. The findings in this foal are suggestive for moxidectin overdosing. The GABAergic working mechanism of moxidectin does explain the development of profound central nervous depression and its sequels hypothermia, bradycardia, hypoventilation and paralytic ileus. Dyssynergia was unexpected, however, has to be related to a central nervous problem, rather than a peripheral nervous problem.

Presumed moxidectin toxicosis in three foals.

Outcome and complications associated with administration of moxidectin gel to 3 foals < 4 months old are described. Two foals became comatose but survived following supportive treatment. One foal died following loss of consciousness associated with moxidectin administration. Risk of moxidectin overdose exists, because horse owners often fail to read or comprehend the package insert instructions pertaining to use of the syringe-locking mechanism. In addition, moxidectin should not be administered to foals < 4 months old, because it is likely that treated foals will become comatose.

Central nervous system disorders after renal transplantation in cats.

OBJECTIVE: This study describes the incidence and severity of postoperative central nervous system (pCNS) disorders in feline renal transplant recipients. STUDY DESIGN: A retrospective study based on the medical records of cats that received renal allografts from 1987 to 1996. ANIMALS OR SAMPLE POPULATION: Fifty-seven client-owned cats received renal allografts for the treatment of renal failure. METHODS: The frequency, duration, severity, and treatment of episodes of pCNS disorders were recorded from the medical records. RESULTS: Twelve (21%) of 57 cats had pCNS disorders 1 hour to 5 days after the surgical procedure. Seven cats survived; four had single or multiple seizure episodes, and two had seizure episodes or disorientation followed by a period of coma. One cat became temporarily ataxic and blind after restraint for venipuncture. Five cats died; all had episodes of disorientation or seizures, or both, that progressed to a nonrecoverable comatose state, respiratory arrest or cardiac arrest, or both. There were no significant differences between the two groups in preoperative serum creatinine, blood urea nitrogen, or cholesterol levels, and intraoperative blood pressure measurements. There were no significant differences in the postoperative serum glucose levels, electrolytes levels, or osmolality between the two groups. The cats with pCNS disorders had a mean preoperative trough cyclosporine A (CyA) whole blood level of 429 ng/mL; cats without pCNS disorders had a significantly (P = .0116) higher mean preoperative trough CyA whole blood level of 736 ng/mL. CONCLUSION: Central nervous system disorders are a common and often fatal complication of renal transplantation in cats. CLINICAL RELEVANCE: Recognition of pCNS disorders, and possible causes, will help develop hypotheses to investigate the problem.

Suspected poisoning of puppies by the mushroom Amanita pantherina.

Amanita pantherina poisoning is suspected as the cause of a severe, transient neurological disorder in three 5-week-old German shepherd puppies. There was very strong circumstantial evidence that this mushroom had been eaten, and the signs encountered were similar to those described in confirmed field cases of intoxication in dogs. It was also in many respects consistent with the syndrome seen in humans. A veterinary perspective on the hallucinogenic Amanita spp. is given and the veterinary literature on mushroom intoxication is briefly reviewed as, in contrast to humans, it is not often reported in animals. This is the 1st report of suspected mushroom intoxication of animals in South Africa.

Experimental Aujeszky's disease in blue foxes (Alopex lagopus).

Blue foxes were inoculated orally with Aujeszky's disease virus. Several foxes were killed at the onset of clinical signs and other animals spontaneously died. The incubation period ranged from 3 to 6 days and was followed by a short illness characterized by anorexia, depression and coma. At autopsy, no specific gross findings were observed. Microscopically, lesions included a non-suppurative meningoencephalitis with neuronal necrosis, gliosis, neuronophagia and mononuclear cell cuffing. Viral antigen was detected by immunoperoxidase technique.

Utilization of medium-chain triglycerides by neonatal pigs: effects of emulsification and dose delivered.

Four trials were conducted using 86, 24-h-old pigs to evaluate the utilization of medium-chain triglycerides (MCT). Effects of emulsification and amount of MCT fed were examined. After a 4-h period during which feed was withheld, pigs were force-fed MCT (containing 75% octanoate and 25% decanoate), marking time 0 of the experiment. Blood samples were obtained at 1 and 2 h for subsequent medium-chain fatty acid (MCFA) analysis. In Trials 1 (six pigs/treatment) and 2 (four pigs/treatment) the response to three emulsifying agents was compared to a nonemulsified (NE) control. Twenty milliliters of a 30% (vol/vol) emulsion of MCT or 6 mL of NE MCT was administered. Concentrations of MCFA at 1 h in pigs receiving a Tween 80 (polyoxy-ethylene [20] sorbitan monooleate) emulsion were 3- to 19-fold higher than concentrations in animals administered a gum arabic/gum tragacanth emulsion, a lecithin emulsion, or NE MCT. Trials 3 (eight pigs/treatment) and 4 (six pigs/treatment) were conducted to determine the plasma MCFA concentrations resulting from feeding increasing levels of NE (3, 6, 9, or 12 mL of MCT) or emulsified MCT oil (2, 4, 6, or 8 mL in a 30% Tween 80 emulsion). Plasma octanoate concentrations measured at 1 h increased linearly (P < .05) with increasing MCT dosage through 9 mL of NE and 6 mL of emulsified MCT. A transient narcosis was observed in 8 of 12 animals that received 6 or 8 mL of emulsified MCT and was most pronounced 1 to 2 h after feeding, which roughly corresponded to peak plasma MCFA concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Emulsification and fatty-acid chain length affect the utilization of medium-chain triglycerides by neonatal pigs.

Three experiments were conducted using 52 pigs between 22 and 35 h of birth to determine the effects of emulsification and fatty-acid chain length on utilization of medium-chain triglycerides (MCT). After a 4-h period during which feed was withheld, pigs were force-fed 6 mL of nonemulsified (NE) MCT or 20 mL of a 30% (vol/vol) Tween 80-(polyoxy-ethylene [20] sorbitan monooleate) MCT emulsion, marking time 0, and serial blood samples were drawn throughout 8 h for analysis of medium-chain fatty acid (MCFA) concentrations by HPLC. In Exp. 1, pigs received either NE or emulsified Tri-C4, -C5, -C6, or -C7. The emulsified treatments were discontinued due to deaths caused by coma resulting from high concentrations (up to 12 mM) of plasma MCFA. Concentrations in pigs fed emulsified MCT were 2.5-fold higher than those in pigs fed NE MCT. In pigs fed NE MCT, concentrations of even-chain-length MCFA were higher than those of odd-chain-length MCFA (P < .001), with a tendency for C6 to be higher than C4 (P < .1). In Exp. 2 and 3, pigs received an equimolar mixture of MCT in either emulsified or NE form. In Exp. 2, the mixture contained Tri-C4 through Tri-C7; whereas, in Exp. 3 the mixture contained Tri-C4, -C6, -C8, and -C10. A three-way interaction (emulsion x fatty acid x sample time; P < .05) was observed in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracranial dysfunctions: stupor and coma.

Coma and stupor are pathologic neural states whose signs arise from either massive cortical or brainstem disease or toxicity. A variety of pathological processes can cause brain disease. Often one has to begin treatment before the diagnosis of the cause of the problem is made. At all stages of treatment, great care must be taken to avoid precipitating an intracranial crisis. The physiological derangements that may aid in the diagnosis include arousability, pupil reactivity, various reflexes, breathing patterns, and cardiovascular function. The treatment needs to be both specific and general; i.e., the condition itself must be treated, if possible, and the intracranial pressure must be lowered if it has been raised by the condition. Treatments for raised intracranial pressure include hyperventilation, diuretics, corticosteroids, avoidance of jugular vein compression, coughing, and any change of the position of the head and neck from normal. When sedating or anesthetizing these patients, one should avoid drugs that increase cerebral blood flow such as ketamine and inhaled anesthetics, using instead drugs that lower cerebral blood flow such as thiopental, lidocaine, and narcotics (with ventilation).