Super-Vasmol, a cheap, freely-available hair dye is emerging as a major cause of suicidal poisoning in India. It contains potential toxins including paraphenylene diamine, resorcinol, sodium ethylenediaminetetraacetic acid and propylene glycol which can result in multiorgan dysfunction. A retrospective study was conducted over 3.5 years (January 2006-July 2009) of 13 consecutive patients with Super-Vasmol poisoning admitted to a tertiary care, referral hospital in South India. A chart review including records of clinical presentations, laboratory findings and treatment details was carried out. Eleven of the patients were women and the mean age was 27.2 years. The predominant clinical features were cervico-facial oedema and pain, cola-coloured urine and oliguria. Laboratory investigations revealed elevated hepatic transaminases (100%), leucocytosis (92.3%), elevated creatinine phosphokinase (92.3%), metabolic acidosis (84.6%), hypocalcaemia (61.5%), hyperphosphataemia (46.2%) and renal failure (38.5%). Eight of the patients were discharged with complete recovery. Trends towards a poor outcome were evident among the following patients: late presentation at our centre; when no gastric lavage was done at the primary-care centre; those requiring tracheostomy/intubation at the primary centre; presentation with a low Glasgow Coma Score or seizures; established renal failure; and those who subsequently require dialysis, mechanical ventilation or intensive care. Hair dye poisoning classically presents with cervico-facial oedema, severe rhabdomyolysis and renal failure. Early therapy with tracheostomy and aggressive forced diuresis are essential in order to prevent the high mortality associated with this toxin. It is imperative to raise public awareness of the potential toxicity of the dye as well as to educate physicians about the need for aggressive and early treatment.

Background and Aims:Scrub typhus, a zoonotic rickettsial infection, is an important reason for intensive care unit (ICU) admission in the Indian subcontinent. We describe the clinical profile, organ dysfunction, and predictors of mortality of severe scrub typhus infection.Materials and Methods:Retrospective study of patients admitted with scrub typhus infection to a tertiary care university affiliated teaching hospital in India during a 21-month period.Results:The cohort (n = 116) aged 40.0 ± 15.2 years (mean ± SD), presented 8.5 ± 4.4 days after symptom onset. Common symptoms included fever (100%), breathlessness (68.5%), and altered mental status (25.5%). Forty-seven (41.6%) patients had an eschar. Admission APACHE-II score was 19.6 ± 8.2. Ninety-one (85.2%) patients had dysfunction of 3 or more organ systems. Respiratory (96.6%) and hematological (86.2%) dysfunction were frequent. Mechanical ventilation was required in 102 (87.9%) patients, of whom 14 (12.1%) were solely managed with non-invasive ventilation. Thirteen patients (11.2%) required dialysis. Duration of hospital stay was 10.7 ± 9.7 days. Actual hospital mortality (24.1%) was less than predicted APACHE-II mortality (36%; 95% Confidence interval 32-41). APACHE-II score and duration of fever were independently associated with mortality on logistic regression analysis.Conclusions:In this cohort of severe scrub typhus infection with multi-organ dysfunction, survival was good despite high severity of illness scores. APACHE-II score and duration of fever independently predicted mortality.

In acute OP poisoning, the generic scoring systems APACHE-II and SAPS-II outperform the PSS. These tools may be used to predict the mortality rate in OP poisoning.

Although confounded by the varying quantity of chlorpyrifos and cypermethrin in the different formulations, patients with mixed poisoning appear to have shorter ventilator-free days than patients poisoned by either of the pesticides alone. Further studies are required comparing patients poisoned by formulations with similar quantities of OP and pyrethroid or with analysis of blood pesticide concentration on admission.

There is a constant search for new and potent insecticides nontoxic to humans. We describe fatal toxicity with one such insecticide considered relatively safe.A 34-year-old male from rural India was brought following the deliberate consumption of imidacloprid in a suicide attempt. At presentation, he was comatose with dilated nonreacting pupils, diaphoretic, and cyanosed. His blood pressure was unrecordable, and his heart rate was 50/min. Following intubation and stabilization of hemodynamics with crystalloids, a gastric lavage was performed. Subsequently, he was referred to our hospital. On arrival, 2 h later, he continued to be unconscious with fixed dilated pupils. His blood pressure was 130/80 mmHg and pulse rate 86/min.Following transfer to intensive care, he required epinephrine infusion to maintain blood pressure. Deterioration of renal function was noted from the second day with progressive oligoanuria (peak creatinine 6.9 mg/dl) and severe metabolic acidosis necessitating dialysis. Creatinine phosphokinase levels of 67,980 U/L (reference<170 U/L) suggested rhabdomyolysis. Hospital stay was further complicated by the development of liver dysfunction, ventilator-associated pneumonia, and refractory septic shock. Despite appropriate supportive therapy, he succumbed on day12.Neonicotinoids, agonists at the nicotinic acetylcholine receptors (nAChRs), induce neuromuscular paralysis. The high selectivity for nAChRs (particularly the a4b2 subtype) in insects compared with mammals results in their favorable toxicological profile [1,2]. Imidacloprid, the commonest neonicotinoid used in South Asia, was recently reported to have a 0% case fatality in a series of 68 patients presenting with poisoning [3]. Despite their safety profile, other publications have described rhabdomyolysis [4], neuropsychiatric manifestations [4], ventricular fibrillation [5], and deaths with imidacloprid [5][6][7].This patient manifested neurological dysfunction and rhabdomyolysis. The initial neurological dysfunction, probably due to central nicotinic stimulation, was compounded by ischemic and metabolic encephalopathy. Renal injury was perpetuated by rhabdomyolysis, hypotension, and toxin. Progressive deterioration and eventual demise was due to multiple organ dysfunction syndrome and not the toxin per se. Serum imidacloprid level would have helped elucidate causality, but was unavailable. This report of imidacloprid toxicity sensitizes clinicians to an emerging cause of poisoning and highlights the need for a careful review of its toxicity profile. Conflict of interestThe authors declare that they have no conflict of interest. There was no funding for this report.