Intra-aortic balloon pump in toxic myocarditis due to aluminum phosphide poisoning

Latha M. Siddaiah 0 MBBS 0 Srilakshmi M. Adhyapak 0 DNB 0 Santosh M. Jaydev 0 DNB 0 Gurappa G. Shetty 0 DM 0 Kiron Varghese 0 DM 0 Chandrakanth B. Patil 0 DM 0 Shamanna S. Iyengar 0 DM 0 0 Department of Cardiology, St. John's Medical College Hospital , Bangalore, India Introduction: Aluminum phosphide (ALP) is a pesticide that is highly toxic. It is a mitochondrial toxin that causes death by cardiac and metabolic toxicity. The most ominous effect is cardiac toxicity, which may range from minor electrocardiographic abnormalities to severe depression of cardiac contractility secondary to toxic myocarditis. There is no documented report of the use of Intra-aortic Balloon Pump (IABP) for toxic myocarditis from ALP poisoning, although it has been used effectively for toxic myocarditis due to other toxins. Case Report: We are reporting a young female who presented with ALP poisoning, in cardiogenic shock due to myocarditis. We used an IABP for cardio-circulatory support until the effects of ALP resolved. She is the only reported survivor of ALP poisoning, presenting with cardiogenic shock. Discussion: Several reports describe the use of IABP for cardiogenic shock due to toxic myocarditis. There is no report in the medical literature using IABP for cardiogenic shock caused by ALP toxin-induced myocarditis. Our patient presented with cardiocirculatory shock, necessitating the use of inotropes and mechanical ventilation. As she did not improve despite ventilation and maximal doses of inotropes, IABP was used for cardio-circulatory support until the effects of ALP resolved. - fields were clear. She brought a container of the toxin, thus a tox- IU/hour as prophylaxis for deep vein thrombosis. Prophylactic icological screen was not obtained. Her arterial blood gas (ABG) broad spectrum antibiotics were administered: magnamycin 1-g revealed the following: pH 7.321; sodium bicarbonate (HCO3), IV every 6 hours and Amikacin 500-mg IV every 6 hours. 11.8 meq; base excess (BE), 14; and SaO2, 97%. She was given 12 On day 5 of admission, the patient continued to be tachymEq IV sodium bicarbonate of 7.5% strength (12 ml, 1 mEq = cardic [heart rate (HR),152/min] and hypotensive (systolic BP, 1ml) over 4 hours, started on IV fluids 0.9-N normal saline at a 70 mmHg) with maximal doses of inotropes (dobutamine 1520 rate of 100 ml/hour (2 L/day), inotrope infusion of dobutamine g/kg/minute and noradrenaline 0.8 mg to 1 mg/minute). Be24 g/kg per minute, and noradrenaline 0.04 mg/minute. Five cause of continued hypotension and signs of decreased perfuhours after admission, oxygen desaturation occurred with wors- sion (decreased urine output of 250 ml in 24 hours), IABP was ening shock and the patient was intubated and received mechan- inserted after assessing its risks and benefits. On insertion of ical ventilation. IABP, there was improvement in her BP to 110/70 mmHg, with Admission electrocardiogram (ECG) showed sinus tachycardia a mean BP of 80 mmHg. Perfusion to vital organs improved, with ST depression in II, III, AVF, V4V6 (Figure 1). A chest radi- with an increase in urine output to 2.3 L/day. On day 8, her Hb, ograph showed a small right-sided pleural effusion. Echocardiog- TLC, DC, PC, and serum potassium decreased (Hb 7.8 g/dl, TC raphy revealed normal valves, dilatation of all chambers, global 8600/mm2, PC 41.000/mm2, and serum potassium was 3.9 hypokinesia, and left ventricular ejection fraction (LVEF) of 35%. mEq/L). Her liver function tests (LFT) were abnormal, with rises Her admission hemogram and biochemistry were normal. Her in AST, ALT, and alkaline phosphatase: 556 U/L, 356 U/L, and hemoglobin was 14.7 g/dl; total leukocyte count (TLC), 10,800 110 U/L, respectively. Hypocalcemia and hypomagnesemia percells/mm3; platelet count (PC), 2.2 cells/mm3; blood urea, 26 sisted. She was transfused with 2 U of packed cells and platelet mg/dl; creatinine, 0.7 mg/dl; sodium, 141 mEq/L; potassium, 4.1 rich plasma and received IV potassium chloride 20 ml (40 mEq/L; chloride, 106 mEq/L; International Normalized Ratio, 1.8; mEq) of 15% strength in 500-ml saline, magnesium sulphate 2 transaminasesALT and AST37 and 53 IU, respectively; tro- g in 100-ml saline, and calcium gluconate 10 ml (1.375 g calponin I, 0.05 IU (normal 0.04). Serum calcium was 7.9 mg/dl and cium) in 10% strength. magnesium was 1.9 mg/dl. These electrolyte abnormalities were On day 10 (i.e., day 5 of IABP), her BP stabilized at 120/60 corrected. Intravenous magnesium sulfate 2 g in 100-ml saline was mmHg. Repeat echocardiogram revealed mild LV global hypokiadministered over 1 hour and was repeated the next day. Intra- nesia with left ventricular ejection fraction (LVEF) of 35% to 45%. venous unfractionated heparin was initiated at a dose of 1000 IABP was weaned and discontinued. On day 15, she improved clinically with heart rate of 92/min, BP 128/68 mmHg, and good urine output. She was extubated on the same day, and inotropes were tapered and stopped. Her hematological and biochemical parameters normalized. Echocardiogram on day 16 of admission showed normal chambers and LVEF of 65%. The ECG on day 16 of admission showed sinus tachycardia with no significant ST segment or T wave abnormalities (Figure 2). She subsequently recovered and was discharged on day 22 of hospitalization. ALP is a synthetic substance with a garlic odor, available as tablets (3 g) and pellets (0.6 g) [1,2], with trade names such as Quickphos, Celphos, and Alphos. The fatal dose for an adult is 0.5 g [2,3]. On contact with moisture, ALP releases phosphine, which inhibits cytochrome oxidase of mitochondria, blocking the electron transfer chain and oxidative phosphorylation. It also inhibits catalase and induces superoxide dismutase in humans, leading to free radical stress, causing hypoxic cell injury [4]. Clinical features include gastrointestinal disturbances, shock, acute respiratory distress syndrome, acute renal failure, hemorrhage, disseminated intravascular coagulation, acidosis, and cerebral anoxia [2]. The most ominous clinical manifestation is cardiovascular toxicity in the form of toxic chemical myocarditis, leading to severe left ventricular dysfunction [5,6]. Minor ECG changes such as ST segment elevation or depression, PR prolongation, broad QRS complexes, right bundle branch block (RBBB), left bundle branch block (LBBB), complete heart block (CHB), supraventricular ectopic beats, or atrial fibrillation may occur [5]. Biochemical abnormalities including elevated AST, creatine phosphokinase (CPK MB), and lactate dehydrogenase (LDH) can also occur. Diagnosis is by definitive history or silver nitrate test [1]. To date there is no antidote available for ALP poisoning [2)], the mainstay of treatment being supportive care. Gastric lavage using saline, sodium bicarbonate, potassium permanganate, and coconut oil have been reported to be effective in anecdotal reports (7). Shock has been managed in various centers with IV saline, dopamine, a (...truncated)