Blocking vicious cycle of cardiac dysfunction by external cardiopulmonary resuscitation is the key to rescue acute aluminium phosphide poisoning

Perfusion ◽  
2021 ◽  
pp. 026765912110468
Author(s):  
Yan Shen ◽  
Daishan Jiang ◽  
Ting Wang ◽  
Mengqiu Li ◽  
Yayun Wang ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Metabolic Acidosis ◽  
Renal Replacement Therapy ◽  
Ventricular Fibrillation ◽  
Cardiac Dysfunction ◽  
Clinical Manifestations ◽  
Vicious Cycle ◽  
Refractory Shock ◽  
Aluminium Phosphide ◽  
Cellular Hypoxia

Aluminium phosphide (ALP) and aluminium zinc phosphide (ZnP), the two main ingredients of fumigation drugs, are commonly used to kill insects or rodents in grain. When exposed to water, highly toxic phosphine gas is released and absorbed through the respiratory or digestive tract. Phosphine gas could non-selectively block cytochrome oxidase, inhibit electron transfer and suppress oxidative phosphorylation, leading to cellular hypoxia and organ dysfunction. The characteristic clinical manifestations are refractory shock and metabolic acidosis with high mortality. However, patients with ALP poisoning have a chance to be cured. Here, we report a case of oral ALP poisoning that was successfully treated by extracorporeal membrane oxygenation (ECMO) combined with continuous renal replacement therapy (CRRT) during frequent ventricular fibrillation and cardiac dysfunction.

scholarly journals Interleukin-1 receptor-induced PGE2 production controls acetylcholine-mediated cardiac dysfunction and mortality during scorpion envenomation

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mouzarllem B. Reis ◽  
Fernanda L. Rodrigues ◽  
Natalia Lautherbach ◽  
Alexandre Kanashiro ◽  
Carlos A. Sorgi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Dysfunction ◽  
Acetylcholine Release ◽  
Interleukin 1 ◽  
Clinical Manifestations ◽  
Prostaglandin E ◽  
High Dose ◽  
Scorpion Envenomation ◽  
Risk Of Death ◽  
Include Heart Failure

Abstract Scorpion envenomation is a leading cause of morbidity and mortality among accidents caused by venomous animals. Major clinical manifestations that precede death after scorpion envenomation include heart failure and pulmonary edema. Here, we demonstrate that cardiac dysfunction and fatal outcomes caused by lethal scorpion envenomation in mice are mediated by a neuro-immune interaction linking IL-1 receptor signaling, prostaglandin E2, and acetylcholine release. IL-1R deficiency, the treatment with a high dose of dexamethasone or blockage of parasympathetic signaling using atropine or vagotomy, abolished heart failure and mortality of envenomed mice. Therefore, we propose the use of dexamethasone administration very early after envenomation, even before antiserum, to inhibit the production of inflammatory mediators and acetylcholine release, and to reduce the risk of death.

Abstract 15210: Do Idiopathic Ventricular Fibrillation and Brugada Syndrome Patients Have Favor Outcomes in the Targeted Temperature Management Era?

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Eisuke Kagawa ◽  
Masaya Kato ◽  
Noboru Oda ◽  
Eiji Kunita ◽  
Michiaki NAGAI ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Survival Rate ◽  
Ventricular Fibrillation ◽  
Brugada Syndrome ◽  
Cardiac Dysfunction ◽  
Targeted Temperature Management ◽  
Temperature Management ◽  
Circulatory Support ◽  
Idiopathic Ventricular Fibrillation ◽  
Coronary Syndrome

Introduction: Idiopathic ventricular fibrillation (IVF) including Brugada syndrome (BS) is one of causes of cardiac arrest without prior overt cardiac dysfunction. Hypothesis: We assessed the hypothesis that patents of IVF had favor outcomes than those of non-IVF after cardiac arrest treated with targeted temperature management (TTM). Methods: Patients who were treated with TTM after cardiac arrest between 2000 and 2019 were enrolled in the study. Patients were divided into 2 groups according to whether the patients were diagnosed as IVF or not. The patients treated with TTM were routinely performed coronary angiography. Results: Among the study patients (N = 306), 35 (11%) patients were IVF and 7 were BS. The patients of the IVF group were significantly younger (median 53 y vs. 64 y) than those of the non-IVF group. The prevalence of initial rhythm was shockable (69% vs. 47%, P = 0.02) was significantly higher in the patients of the IVF group than those of the non-IVF group. Among the patients in the non-IVF group, 114 patients (42%) were diagnosed as acute coronary syndrome and 93 patients (35%) were treated with coronary revascularization. The prevalence of male sex (77% vs 74%, P = 0.70) and witnessed to arrest (80% vs. 81%, P = 0.87), and low-flow time (29 min vs. 38 min [20 - 43 min vs. 21 - 52 min, P = 0.15]) were similar between the 2 groups. The prevalence of performing extracorporeal resuscitation (9% s 43%, P < 0.001) were lower in the patients of the IVF group. The 8-y survival rate were shown in the figure. All of the BS patients were witnessed arrest and were discharged without severe neurological deficit. The IVF as the cause of arrest was independently associated with 8-y survival. Conclusions: The patients of IVF had favor outcomes than those of non-VF. One of causes may be the lower prevalence of requiring extracorporeal circulatory support due to less cardiac dysfunction. The patients of BS had the tendency toward higher survival rate than those of non-BS IVF patients.

Abstract 13618: Negative Association of H558r Polymorphism and Ventricular Fibrillation in Patients With Brugada Syndrome

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hiroya Matsumura ◽  
Yukiko Nakano ◽  
Masaaki Toshishige ◽  
Hidenori Ochi ◽  
Takehito Tokuyama ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Membrane Trafficking ◽  
Brugada Syndrome ◽  
Clinical Manifestations ◽  
Taqman Assay ◽  
Nonsynonymous Mutation ◽  
Study Population ◽  
The Common ◽  
Electrocardiogram Ecg ◽  
Normal Controls

BACKGROUND: The common SCN5A polymorphism H558R has been reported as a genetic modulator that improves sodium channel activity in mutated channels by repairing abnormal channel gating kinetics and membrane trafficking. We investigated the possible effects of H558R on the clinical manifestations of Brugada syndrome. METHODS: The study population comprised 95 Brugada syndrome patients (mean age 42 ± 14 years, 91 males and 4 females) and 1,875 normal controls. H558R was genotyped by TaqMan assay in all subjects. The SCN5A gene mutation was screened by resequencing. We evaluated the PR, QRS, and QTc intervals from lead II and the J-point amplitude from leads V1 and V2 of a 12-lead electrocardiogram (ECG). We also evaluated signal-averaged ECG and electrophysiological parameters. RESULTS: H558R was less frequent in patients with Brugada syndrome than normal controls (4.7% vs. 10.3%, P = 0.01). Surprisingly, H558R (minor allele A) was not observed in patients with Brugada syndrome without ventricular fibrillation (VF; n = 60), whereas 7.5% of patients with VF had H558R (n = 35). Nonsynonymous mutation of SCN5A was not detected in patients with H558R. The H558R carriers showed lower J-point elevation in lead V1 than noncarriers (1.8 ± 0.4 vs. 3.3 ± 0.3 mV, P = 0.04). Other parameters in the 12-lead and signal-averaged ECG were similar in patients with and without H558R. CONCLUSION: We demonstrated that the H558R polymorphism was a strong protective genetic modulator even in Brugada syndrome patients without SCN5A mutation.

Aluminium Phosphide Poisoning

1992 ◽  
Vol 22 (4) ◽  
pp. 155-157 ◽  
Author(s):  
S N Khosla ◽  
R Handa ◽  
P Khosla
Keyword(s):  
Abdominal Pain ◽  
Metabolic Acidosis ◽  
Conventional Treatment ◽  
Indian Subcontinent ◽  
Serum Biochemistry ◽  
Organ Damage ◽  
Severe Metabolic Acidosis ◽  
Aluminium Phosphide ◽  
The Common ◽  
Electrocardiographic Abnormalities

Aluminium phosphide is a solid fumigant pesticide widely used in the Indian subcontinent as a grain preservative. Over the last 5 years there has been a dramatic increase in the number of cases of aluminium phosphide poisoning in India. Ninety-two patients with aluminium phosphide poisoning due to ingestion were studied over a period of 3 years. Abdominal pain, vomiting and restlessness were the common initial features followed by alteration in sensorium and shock unresponsive to conventional treatment. Electrocardiographic abnormalities were very common and highly variable. Routine serum biochemistry was usually unremarkable. Severe metabolic acidosis was common and mortality high (49%). The survivors recover completely without any residual organ damage. There is no known antidote.

scholarly journals Cardiac dysfunction in pediatric patients on renal replacement therapy

2012 ◽  
Vol 27 (9) ◽  
pp. 1603-1604
Author(s):  
Dorota Polak-Jonkisz ◽  
Malgorzata Sobieszczanska
Keyword(s):  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Cardiac Dysfunction ◽  
Pediatric Patients

Six Patients with MethylmalonicAcidemia and Their Outcome: A Literature Review and Case Series

2020 ◽  
Author(s):  
Naser Ali Mirhosseini ◽  
Sana Taghiyar ◽  
Mahdieh Saatchi
Keyword(s):  
Metabolic Acidosis ◽  
Quantitative Analysis ◽  
Progressive Failure ◽  
Clinical Manifestations ◽  
Case Series ◽  
Failure To Thrive ◽  
Feeding Problems ◽  
Urinary Organic Acid ◽  
Severe Metabolic Acidosis ◽  
Recurrent Vomiting

Background: Methylmalonic acidemia (MMA) is a congenital disorder due to the defects in the propionate pathway. It results from a deficiency in methylmalonyl coenzyme A mutase or one of the steps of the synthesis of the cobalamin (B12) cofactors for the enzyme. There is deficiency of methylmalonylcoAmutase (MCM) in the classic MMA. It presents with severe metabolic acidosis in the first month of life, progressive failure to thrive, feeding problems, recurrent vomiting, dehydration, hepatomegaly, lethargy, seizures, and developmental delay. Quantitative analysis of urinary organic acid patterns by GC-MS is used in MMA diagnosis. Treatment with large doses of hydroxocobalamin is helpful in some cases of MMA.                                                                                        Case presentation:We Reported 6 patients with MMA with a variety of clinical manifestations and outcomes. Conclusion: The overall prognosis of classic MMA remains doubtful, whereas vitamin B12 responsive MMA has a reasonable outcome.

scholarly journals Metformin-Associated Lactic Acidosis following Intentional Overdose Successfully Treated with Tris-Hydroxymethyl Aminomethane and Renal Replacement Therapy

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Ngan Lam ◽  
Gurbir Sekhon ◽  
Andrew A. House
Keyword(s):  
Metabolic Acidosis ◽  
Renal Replacement Therapy ◽  
Lactic Acidosis ◽  
Serum Creatinine ◽  
Replacement Therapy ◽  
Delayed Diagnosis ◽  
Complete Recovery ◽  
Nondiabetic Patient ◽  
Severe Metabolic Acidosis ◽  
Metformin Concentration

A 43-year-old woman was brought to the hospital with severe metabolic acidosis (pH 6.56, bicarbonate 3 mmol/L, and lactate 18.4 mmol/L) and a serum creatinine of 162 μmol/L with a serum potassium of 7.8 mmol/L. A delayed diagnosis of metformin-associated lactic acidosis was made, and she was treated with tris-hydroxymethyl aminomethane (THAM) and renal replacement therapy (RRT). Following a complete recovery, she admitted to ingesting 180 tablets (90 grams) of metformin. Her peak serum metformin concentration was 170 μg/mL (therapeutic range 1-2 μg/mL). Our case demonstrates an intentional metformin overdose resulting in lactic acidosis in a nondiabetic patient who was successfully treated with THAM and RRT.

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