In trouble with Tetrodotoxin


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tetrodotoxin ingestion by a dog

Maci, a seven-year-old female speyed Staffordshire bull terrier mix, was with her family at the Maroochy River near the Sunshine Coast when she started vomiting and became weak. Despite no snakes in the area, her owners did notice there were pufferfish in the car park and along the river. Before this, Maci had no pre-existing conditions. 

Maci was rushed to Animal Emergency Service Tanawha, where on arrival she presented as dull and non-ambulatory. She was carried to the crash bench, where she was unable to maintain sternal recumbency. 

tetrodotoxin ingestion by a dog

Maci’s vital signs included tachycardia with a heart rate of 164 beats per minute and a grade 3/6 left systolic murmur, with synchronous pulses and normal pulse pressure. Respiration was normal with 20 breaths per minute with a normal effort, and mild hypothermia with a temperature of 37.1°C. Her mucous membranes were pink and moist with a capillary time of two seconds.  

Minutes after arriving and receiving an initial assessment, Maci’s mucous membranes turned cyanotic and then respiratory and cardiac arrest were identified. Chest compressions were performed using the cardiac compression technique (due to her narrow thoracic shape), she was intubated, and positive pressure ventilation (PPV) was commenced with 100% oxygen at 10 breaths per minute. This was performed continuously in two-minute cycles. Initially, adrenaline was administered via the ET tube and then once a peripheral IV catheter was placed, it was repeated intravenously.    

tetrodotoxin ingestion by a dog
Soon after a diagnosis of tetrodotoxin ingestion, Maci was placed on a ventilator (above) and intubated (above).

Although return of spontaneous circulation (ROSC) was obtained after four and a half minutes, there remained no voluntary respiration and PPV continued. A snake venom detection test was performed but returned negative, so at this point, the veterinarian suspected a diagnosis of tetrodotoxin ingestion. Full blood tests were performed including blood gas, coagulation profile, PCV/TP, biochemistry and CBC. Abnormalities included mild haemoconcentration at 57%, mild acidaemia at 7.33 with metabolic acidosis, mild hypoalbuminaemia (15), hypophosphatemia (0.87), and elevated creatinine (129).  

As Maci remained apnoeic, a decision was made to place her on mechanical ventilation. Initially, the ventilator settings were set with PCV+, a fio2 of 100% and inspiratory pressure of 13cm H20. The patient received constant monitoring of anaesthetic depth, ECG, SPO2, ETC02, and blood pressure (initially non-invasively but once stable on the ventilator this was switched to invasive through a dorsal pedal artery catheter). An arterial blood gas was performed, whereupon it was deemed there was both adequate ventilation and oxygenation, and the fio2 was gradually reduced to 40% over several hours. 

The patient was started on a Midazolam and Fentanyl CRI; no additional anaesthesia agents were required at this time. An indwelling urinary catheter was placed and urine output was monitored via a closed collection system. Crystalloid fluids were commenced at maintenance rates due to Maci’s heart murmur with her hydration status regularly reassessed. Full ventilator nursing care was commenced to provide gold-standard care.  

After approximately 12 hours on the ventilator, Maci started to initiate occasional spontaneous breaths. Over the next few hours, the ventilator mode was changed to synchronised intermittent mandatory ventilation (SIMV) to allow her voluntary respiration attempts to be synchronised with the ventilator. As her respiration efforts improved, Maci was placed on continuous positive airway pressure (CPAP) therapy for a few hours. 

Approximately 18 hours after being placed on the ventilator, a weaning attempt was made. Unfortunately, it was unsuccessful with the patient becoming apnoeic. She was placed back on CPAP for another six hours before being able to be successfully liberated from the ventilator approximately 24 hours after ventilation commenced. Maci remained intubated for a few hours before being successfully extubate. At this point she was able to maintain an SPO2 of 99% on room air.  

Once extubated, Maci was showing signs of being distressed and anxious, attempting to move despite tetraparesis. Additional sedation was added with Butorphanol and a micro-dose of Medetomidine CRI. Recumbent nursing care continued, and Maci was able to maintain her oxygenation as signs of tetraparesis gradually reduced. 

The veterinary team and her owners excitedly watched her regain enough strength to sit unaided, begin taking tentative supported steps and be able to eat and drink safely. Three days after admission, Maci had recovered enough to be discharged from hospital.  

tetrodotoxin ingestion by a dog
Maci, three days after admission.

Tetraodontidae is a family of primarily marine and estuarine fish. There are 57 species of pufferfish, 48 of them found in Queensland waterways. The majority of these species are toxic and some are among the most poisonous vertebrates in the world. Tetrodotoxin is produced by various species of bacteria and animals that carry tetrodotoxin absorb and accumulate it through the food chain. The toxin can be found in internal organs such as the liver, gastrointestinal tract, gonads and sometimes the skin of these animals, as little as 1-4mg of toxin can kill an adult. 

It is a highly selective and potent blocker of voltage sodium-dependent channels in both the central and peripheral nervous systems, with brain and skeletal muscle sodium channels more sensitive than cardiac sodium channels. Clinical signs can include vomiting, hypersalivation, ataxia, dilated pupils, muscle tremors/seizures, respiratory distress and failure, tetraparesis, coma and death. These clinical signs can advance rapidly depending on the amount of toxin ingested.  

There is no antidote and treatment involves rapid identification of the suspected toxin ingestion. If very recent ingestion has occurred, emesis, gastric lavage or endoscopic removal of any parts of the fish may be helpful if not clinically contraindicated. Respiratory support and other supportive care should be provided until the tetrodotoxin is excreted in the urine. Although not widely available, haemodialysis may also be helpful.

Kate Tinney, RVN, AVN, Cert IV TAE, Dip VN (ECC), VTS (ECC), Animal Emergency Service Tanawha

tetrodotoxin ingestion by a dog

Kate Tinney has been a veterinary nurse for over 20 years with most of her career spent in an emergency and referral hospital setting. She currently works full-time for Animal Emergency Services at Tanawha in Queensland. 

She has completed a Diploma in Veterinary Nursing in Emergency and Critical Care, Certificate IV in Training and Assessment and is currently a registered and accredited veterinary nurse through the VNCA. 

She was a finalist for VNCA’s Veterinary Nurse of the year in 2017, and in 2019 achieved her Veterinary Technician Specialist in Emergency and Critical Care through AVECCTN in America, a career highlight. 

Kate has presented at both local and national conferences, and was recently involved in the development and delivery of Improve International Australia’s Emergency Veterinary Nursing Course. Her interests include transfusion medicine, toxicities, neonatal care, and mechanical ventilation. 


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