Coconut crab intoxication in New Caledonia from January 2016 to April 2022

Abstract

Coconut crab intoxication is known in New Caledonia, it is defined by the occurrence in the following twelve hours after crustacean consumption, of digestive clinical signs such as nausea, vomiting, diarrhea. This intoxication could as well, presents more severe clinical signs such as cardiac issues that require sometimes the use of the antidote, digitalis antibodies and in fewer cases could cause death. The intoxication is caused by the crustacean consumption of mango tree Cerbera manghas that contained cardiotonic glycosides such as neriifoline. Neriifoline owns a cardiac toxicity and provokes in some patients, conduction troubles that may progress towards asystolia. This work reports 14 cases of crab intoxication by coconut crab in New Caledonia. The objective is to report the crab intoxications, to search if there are some factors that could be the cause of severe forms. It is a retrospective study that covers a timeframe from January 2016 to April 2022. It follows a first study made from January 2008 to December 2015. Clinical, biological, toxicological characteristics of each patient have been collected and analysed. They are extracted from hospitalised patient at the CHT in Noumea's clinical files. First clinical signs of the intoxication are the digestives ones. In fact, nausea and vomiting are found in every patient in this study. They could be associated with diarrhea for six cases, or asthenia, or headaches for five cases. Cardiac signs are presents in ten cases and appears after digestive signs. The most common manifestation is bradycardia, in between 38 to 50 pulse per minute, for eight cases. On the fourteen patients, twelve had bloodword to look for cardenolides of Cerbera manghas and nine patients had urinary level works. There is no correlation between clinical severity and neriifoline blood levels. Indeed, one patient with bradycardia at 41 ppm presented a nerifoline blood concentration of 0.12 ng/mL and urinary concentration < 0.1 ng/mL. As well, there is no correlation between hyperkaliema and neriifoline blood concentration. Indeed, for one patient that had a kaliemia of 8.0 mmol/L, we found a neriifoline blood concentration < 0.1 ng/mL and a urinary concentration of 0.1 ng/mL. There are several parts of the crab that could be eaten. We can eat the crab in totality, or we can only eat the clamp or the cephalothorax. In the study, 3 patients ate only the crab claws, 2 ate only the cephalothorax, 8 ate the whole crab and 1 case is undocumented. Preexisting conditions such as, advanced age, renal insufficiency, diabetes, cardiovascular pathology were associated with severe intoxications. Indeed, in this study, patient who presented the most severed forms, with antibodies injection, were patients with the most comorbidities associated. In agreement, this study finds digestives clinical signs for every patient. In fact, a digestive impairment is one the characteristics of a cardenolides intoxication. This is actually those digestives signs that motivated patient to consult. The non-correlation between clinic and blood concentrations, and hyperkaliemia and blood concentrations are in accordance with the previous study. It confirms the uselessness to dose in emergency, blood level of cardenolides. The only predictive factor of toxicity is kaliemia. Following tradition in the loyalty island, a traditional preparation, consisting in removing the digestive tube after the crab cooking, would prevent the intoxication. If the logical would follow, the people eating only crab clamp should not be intoxicated. However, in this study, several patients who only ate clamp were intoxicated. The cephalothorax consumption, seems to expose to severe forms. Nevertheless, cardiotonic glycosides could be presented, in significant quantity in every part of the crab. Severe intoxication needing the use of antibodies is linked with patients comorbidities.