Successful treatment of a severe 5-hydroxytrytophan intoxication using carbon hemoperfusion, hemodiafiltration, and mechanical ventilation in a dog.

OBJECTIVE: To describe the successful use of carbon hemoperfusion and hemodiafiltration in combination with mechanical ventilation (MV) to treat a severe intoxication of 5-hydroxytryptophan (5-HTP) in a dog. CASE SUMMARY: A dog ingested a minimum of 550 mg/kg of extended-release 5-HTP, resulting in serotonin syndrome that progressed to a comatose state and severe hypoventilation requiring MV. Extracorporeal carbon hemoperfusion coupled with hemodiafiltration was performed to remove 5-HTP from this patient. A carbon hemoperfusion cartridge was placed in series upstream in the extracorporeal circuit from the hemodialyzer. A total of 46.5 L of blood (4.89 L/kg) was processed during a 4.85-hour treatment. Serial plasma samples were obtained at 0, 60, 90, and 150 minutes during the session and 14 hours after the session. These samples were later analyzed for 5-HTP and serotonin concentrations. The extraction ratio of 5-HTP was 93.6%-98.9% through the carbon filter. The dog was weaned from MV within 8 hours after extracorporeal therapy and, after a full recovery, was successfully discharged. NEW OR UNIQUE INFORMATION PROVIDED: Despite an extensive review of the available literature, this appears to be the first reported case of using a carbon hemoperfusion, hemodiafiltration, and MV to treat severe serotonin syndrome secondary to 5-HTP intoxication in a dog. The combination of carbon hemoperfusion and hemodiafiltration can significantly reduce plasma 5-HTP concentrations after acute intoxication and may serve to decrease morbidity and mortality in patients with severe intoxication.

Dexmedetomidine to control signs associated with lisdexamfetamine dimesylate toxidrome in a cat.

A 5-month-old intact female domestic shorthaired cat had mydriasis, agitation, and increased locomotion after ingestion of lisdexamfetamine, 10.3 mg/kg body weight (BW). Despite treatment with IV fluids, IV acepromazine, oral cyproheptadine and intravenous lipid emulsion the patient's clinical signs worsened. Dexmedetomidine administered at 2 µg/kg BW and continued at 0.5 µg/kg BW per hour rapidly controlled the patient's signs. An episode of vomiting and hematuria developed. Follow-up 5 days after discharge revealed that the cat appeared normal.

Dexmédétomidine pour contrôler les signes associés à la toxidrome à la lisdexamfétamine dimesylate chez une chatte. Une chatte domestique intacte âgée de 5 mois présentait de la mydriase, de l'agitation et une locomotion accrue après avoir ingéré de la lisdexamfétamine, 10,3 mg/kg poids corporel (PC). Malgré le traitement à l'aide de solutions intraveineuses, d'acépromazine intraveineuse, de cyproheptadine orale et d'émulsion de lipides intraveineux, les signes cliniques de la patiente s'étaient aggravés. La dexmédétomidine administrée à 2 µg/kg PC et maintenue à 0,5 µg/kg PC l'heure a rapidement contrôlé les symptômes de la patiente. Un épisode de vomissements et d'hématurie s'est développé. Un suivi 5 jours après le congé a révélé que la chatte semblait normale.(Traduit par Isabelle Vallières).

Serotonin Syndrome from 5-Hydroxytryptophan Supplement Ingestion in a 9-Month-Old Labrador Retriever.

INTRODUCTION: 5-Hydroxytryptophan (5-HTP) supplements are available over the counter and labeled as sleeping aids and anxiolytics for human use. 5-HTP is a serotonin precursor and overdose can lead to serotonin syndrome. CASE REPORT: A 9-month-old female Labrador retriever was evaluated after ingestion of a 5-HTP supplement. Signs of agitation developed within 1 h of ingestion, and emesis was attempted by the owner with  3% hydrogen peroxide (H2O2) orally. On presentation, the dog was obtunded, bilaterally mydriatic and salivating. Physical exam revealed tachypnea, tachycardia, hyperthermia, and hypertension. Eighteen hours post presentation, the dog developed melena, hematemesis, and pigmenturia. A hemogram revealed mild anemia with evidence of oxidative erythrocyte damage (eccentrocytes, Heinz bodies, and siderocytes). A chemistry panel revealed markedly elevated creatine kinase and hyperbilirubinemia, supporting hemolytic anemia. A urinalysis revealed pigmenturia. Hemolytic anemia was presumed to be caused by oxidative damage secondary to gastrointestinal ulceration and circulatory embolism of H2O2. Treatment included fluid therapy, a mannitol constant rate infusion, antiemetics, gastroprotectants, and cyproheptadine as a serotonin antagonist. The patient responded well to treatment and was discharged within 48 h of presentation. DISCUSSION: Serotonin syndrome is an increasingly common toxic syndrome in veterinary medicine with the availability of over-the-counter medications that alter serotonin metabolism. The importance of appropriate client education regarding emesis with H2O2 is highlighted.

Tramadol toxicity in a cat: case report and literature review of serotonin syndrome.

OVERVIEW: Tramadol toxicity has not previously been reported in a cat. CASE SUMMARY: This report describes the clinical signs, diagnosis and treatment of tramadol toxicity, manifesting as serotonin syndrome, in a cat in Australia. PRACTICAL RELEVANCE: For any cat with suspicion of serotonin syndrome, in particular secondary to tramadol overdose, it is recommended that decontamination, monitoring and supportive care are instituted as soon as clinical signs develop. Prolonged hospitalisation may be required in the event of a severe overdose. LITERATURE REVIEW: The literature relating to the pharmacology of tramadol and tramadol overdose, clinical manifestations of tramadol overdose, and serotonin syndrome in cats, humans and dogs is reviewed. Recommended treatment for tramadol overdose and serotonin syndrome is also discussed.

5-Hydroxytryptophan toxicosis in dogs: 21 cases (1989-1999).

OBJECTIVE: To determine epidemiologic characteristics, clinical findings, and treatment outcome of 5-hydroxytryptophan (5-HTP) toxicosis in dogs. DESIGN: Retrospective study. ANIMALS: 21 dogs with evidence of accidental 5-HTP ingestion. PROCEDURE: Information was retrieved from the National Animal Poison Control Center database. Records of dogs ingesting 5-HTP between January 1989 and February 1999 were reviewed for information on signalment, dose ingested, clinical signs (onset, severity, duration), treatments administered, and outcome. RESULTS: Clinical signs of toxicosis developed in 19 of 21 (90%) dogs. Neurologic signs included seizures (9 dogs), depression (6), tremors (5), hyperesthesia (5), and ataxia (4). Gastrointestinal tract signs included vomiting or diarrhea (12 dogs), signs of abdominal pain (3), and hypersalivation (2). Other clinical signs were hyperthermia (7 dogs) and transient blindness (3). Three dogs died. No important clinical laboratory or necropsy findings were reported. The doses of 5-HTP ingested ranged from 2.5 to 573 mg/kg (1.1 to 260 mg/lb) of body weight; the minimum toxic dose reported in our study was 23.6 mg/kg (10.7 mg/lb), and the minimum lethal dose was 128 mg/kg (58.1 mg/lb). Onset of signs ranged from 10 minutes to 4 hours after ingestion, and signs lasted up to 36 hours. Of 17 dogs with clinical signs of toxicosis that received treatment, 16 recovered; treatment consisted of decontamination, seizure control, thermoregulation, fluid therapy, and supportive care. CONCLUSIONS AND CLINICAL RELEVANCE: Ingestion of 5-HTP in dogs can result in a potentially life-threatening syndrome resembling serotonin syndrome in humans, which requires prompt and aggressive care.