Lactate as an early prognostic indicator in yellow phosphorus rodenticide-induced acute hepatic failure: a retrospective observational study in a tertiary care hospital.

INTRODUCTION: Acute hepatic failure due to yellow phosphorus rodenticide ingestion is often lethal. This study aimed to analyze demographic characteristics and prognostic indicators, focusing on hyperlactataemia as a potential early indicator of mortality in patients poisoned with yellow phosphorus rodenticide. MATERIALS AND METHODS: This was a retrospective study of 96 patients poisoned with a yellow phosphorus-containing rodenticide (Ratol paste, which contains 3% yellow phosphorus). We examined demographic details, clinical symptoms, and biochemical markers to identify prognostic indicators. RESULTS: Demographics were similar among survivors and non-survivors. Mortality (36.5%) correlated with a higher ingested dose and treatment delays, with a mean (±SD) of 5.26 ± 2.2 survival days among those who died. Symptoms, including gastrointestinal and neurological features, typically appeared 48 h after ingestion. Non-survivors developed increased aminotransferase activities (74.3%), prolonged prothrombin time (65.7%), and hyperbilirubinaemia (65.7%) during hospitalization, significantly more commonly compared to survivors (P < 0.0001). Hyperlactataemia (lactate concentration >2 mmol/L) was present in 97.1% of non-survivors, with increased serial lactate concentrations observed in 88.6%. The median (interquartile range) admission lactate concentration among non-survivors was 4.6 mmol/L (3.36-7.53 mmol/L), and their peak median (interquartile range) lactate concentration was 6.1 mmol/L (8.74-10.6 mmol/L). In non-survivors, an increased lactate concentration preceded increased aminotransferase activities and prolonged prothrombin time. Logistic regression and receiver operating characteristic curve analysis confirmed that a 24 h lactate concentration ≥2.67 mmol/L predicted death with 94.3% sensitivity and 91.8% specificity. DISCUSSION: The majority of patients who ingest yellow phosphorus remain asymptomatic initially and typically present to hospital following the onset of gastrointestinal symptoms, usually a day later. As progression to death occurs within a week of yellow phosphorus ingestion in most cases, determining prognosis as early as possible enables swift referral to a liver transplant centre. Based on our study, a 24 h lactate concentration ≥2.67 mmol/L appears to be an early prognostic indicator of death. In another study, a lactate concentration >5.8 mmol/L was found to be a poor prognostic indicator. CONCLUSIONS: Hyperlactataemia on admission and increased serial lactate concentrations appear to be early poor prognostic signs in patients with yellow phosphorus-induced liver failure.

Diagnostic Accuracy of Optic Nerve Sheath Diameter (ONSD) using Ultrasonography for Raised Intracranial Pressure in Pediatric Patients - A Systematic Review and Meta-analysis.

PURPOSE: Detecting increased intracranial pressure early in pediatric patients is essential, as early initiation of therapy prevents morbidity and mortality. The objective of this study was to determine the diagnostic accuracy of the ONSD measured via ultrasound for the prediction of increased intracranial pressure. METHODS: Four databases, namely, PubMed, EMBASE, Scopus & CINAHL, were searched for this systematic review and meta-analysis. The study's predefined inclusion criteria considered diagnostic accuracy, cross-sectional, prospective observational, and retrospective studies with a focus on children with elevated intracranial pressure from causes such as traumatic brain injury and cerebral edema, the diagnostic accuracy of the optic nerve sheath diameter measured using ultrasound was assessed. The primary outcome measures included sensitivity, specificity. The study included invasive monitoring (EVD) and noninvasive measures as the gold standards for increased intracranial pressure. Two authors extracted and reviewed the data. Baseline data, outcome measures, and diagnostic accuracy data were extracted. RESULTS: Twenty-five studies with 1,591 patients and 3,143 ONSD measurements via ultrasound were analyzed. The pooled sensitivity and specificity of the ONSD measured via ultrasound for the prediction of increased intracranial pressure were 92% (86-96%) and 89% (77-96%), respectively. The pooled positive and negative likelihood ratios were 8.6 and 0.08, respectively. CONCLUSION AND RELEVANCE: Optic nerve ultrasonography stands out as a precise and valuable diagnostic tool applicable across diverse patient populations and clinical scenarios. We recommend routine ocular ultrasound for optic nerve sheath diameter measurement in pediatric patients to increase the accuracy of diagnosing increased intracranial pressure.

Mechanodefibrillator dissociation due to prolonged sinus arrest / Mecano disociación del desfibrilador debido a un paro sinusal prolongado

To the editor, Sinus arrest and cardiac arrest are two different terms which are often confused by many. This confusion often leads to inappropriate cardiopulmonary resuscitation (CPR) when patient is connected to defibrillator. Sinus arrest is defined as transient pause in Sino-atrial firing for more than 3 s1. When sinus arrest occurs, other latent pacemakers (atrial myocardium, cells nearby atrioventricular node, and His purkinje system) usually starts firing until Sino-atrial node recover. Sinus arrest can be prolonged till other pacemakers starts firing2. Cardiac arrest occurs when these latent pacemakers does not take up the job of alternate firing. Prolonged sinus arrest in a defibrillator may look like a cardiac arrest which might lead to unnecessary CPR. Here, we would like the put forward a new term “mechano - defibrillator dissociation” which occurs because of prolonged sinus arrest. We should be aware this, so that inappropriate CPR could be avoided. We, emergency physician also faced similar situation while resuscitating a patient because of mechano - defibrillator dissociation caused by prolonged sinus arrest/pseudo cardiac arrest. A 52-year-old male diabetic, hypertensive, and chronic alcoholic came to our emergency department (ED) with history of giddiness, syncope, and palpitation. On arrival to ED, patient was drowsy, diaphoretic, and hypotensive. Patient was connected to defibrillator which showed a heart rate of 35/min and saturation was 90% in room air. ECG showed complete heat block (CHB) and point of care echocardiography showed reduced ejection fraction.