Title : Unmasking of Type-1 Brugada syndrome in a case of Aluminium Phosphide (Celphos) poisoning: An unusual phenomenon
Abstract:
A 21 year old female was brought to the emergency department of our hospital with alleged history of celphos consumption an hour back at home. Following consumption, she had 2 episodes of vomiting. On arrival in the emergency, she was irritable and in gasping condition. Endotracheal intubation was done and was put on mechanical ventilation. On examination, her vitals were- BP- 70/40 mmHg, pulse- 88/ min, SpO2- 56% @ room air. Old hesitant marks were present on left forearm. No fresh ligature marks or cuts seen. Immediately gastric lavage was done with normal saline and coconut oil. Patient was shifted to ICU where inotropes & vasoconstrictor drugs were given along with mechanical ventilation. When asked about past history, the attendees of the patient replied that she had also attempted suicide 5 years back, citing family issues.
A 12 lead ECG taken at the time of arrival showed normal sinus rhythm with inverted T waves in lead III (Fig. 1). Changes appeared in serial ECGs were recorded (fig. 3, 4,5). The changes were suggestive of ongoing myocarditis and typical ST Segment coving in V1, V2 suggestive of Type 1 Brugada. Arterial blood gas (ABG) done at the time of admission showed pH of 6.96, pCO2 of 37.6 mmHg, Bicarbonate 10.4 mmol/l, Calcium 1.11 mmol/l. Blood reports showed Hemoglobin of 8.9 gm%, Total Leukocyte count 12,300 per cumm, Platelet 3.48 lac/cumm, Serum urea 0.92 mg/dl, Serum creatinine 0.92 mg/dl, Serum Sodium 148 mmol/l, Serum potassium 2.6 mmol/l, Total bilirubin 0.8 mg/dl, SGOT of 15 U/l, SGPT 10 U/l and Serum albumin 2.1 gm/dl.
ECHO/Color Doppler showed Right ventricular hypokinesia, jerky inter-ventricular septum, dilated Right atrium, dilated Right ventricle, Left ventricular ejection fraction approx. 40%, dilated and <50% collapse of Inferior vena cava on inspiration. Bicarbonate infusion was initiated. Intravenous Magnesium Sulphate infusion was also given. Despite maximal hemodynamic support, the patient remained in refractory shock after admission. She did not develop any instances of ventricular arrhythmia during hospitalization and succumbed after 15 hours due to toxic effects of Aluminium Phosphide.
Audience Takeaway
- Better understanding of pathophysiologic effects of Aluminium Phosphide poisoning on body. The patient discussed here did not develop any arrhythmia but the presence of subtle changes in ECG could predict poor outcomes. Electrocardiographic changes in Aluminium phosphide poisoning have been studied in past. Atrial fibrillation, supraventricular and ventricular tachycardia, ST-T changes, atrio-ventricular conduction defects, bundle branch blocks have been reported in various studies. Studies are also available that show ECG changes that have been uncommonly seen, like
- Aluminium phosphide poisoning carries >70% mortality. The incidences of poisoning are on rise, especially in developing countries. Cardiac complications are seen in approximately 40% patients and are predominant cause of death in these patients. Physicians, intensivists, residents working in critical care & emergency departments and nurses working in ICU settings should understand and anticipate such possible grave complications while managing patients with Aluminium Phosphide poisoning. Careful monitoring and timely intervention with drugs like Quinidine, Magnesium sulfate can have potential to improve outcome.
- Yes, Researchers working at tertiary institutions can work on animal models. The mechanism behind pathogenesis of Brugada syndrome has been described as disequilibrium between Ito and ICa currents that results in loss of dome of action potential in the right ventriclular epicardium. Factors that increase potassium current precipitate Brugada waveform of ST segment elevation while factors that increase calcium current suppress it. Normally, magnesium inhibits the efflux of potassium by acting as a cofactor for the Na-K ATPase in cardiac cells. Thus, decrease in serum Magnesium precipitates ST segment elevation. Aluminium phosphide poisonings carries high mortality. Brugada syndrome is a life threatening phenomenon. Faculty at academic institutions can provide broad knowledge based on these observations.
- Rather than providing a practical solution, it is important to work more on the understanding of the Aluminium phosphide poisoning. In Asian countries, Aluminium phosphide (better known by Celphos) is a common agent to commit suicide. Patients arrive at hospital in dire emergencies but by the time the emergency management starts, patients land up with mortality. The margin between identification of effects of Poisoning on ECG and start of emergency treatment is very narrow. In fact better understanding in this regard can actually open a window for primary care physicians or for doctors managing patients while in ambulance.
- Yes, it has huge clinical implications. For developing countries where health infrastructure is poor and research at genomic levels is close to nil, this can provide new management and life saving options.
- My vision is to bring our understanding to a level where a junior doctor or a nurse posted in primary health care settings can provide immediate management to patients with Aluminium phosphide poisoning like the way they manage acute coronary syndromes, dehydration, etc. This can only be possible with continuous reporting of all the possible observations related to the disease process and continuously working on animal models with respect to the same.
