Clinical analysis of penehyclidine hydrochloride combined with hemoperfusion in the treatment of acute severe organophosphorus pesticide poisoning.

This study aimed to observe the clinical curative effect of penehyclidine hydrochloride (PHC) combined with hemoperfusion in treating acute severe organophosphorus pesticide poisoning. We randomly divided 61 patients with severe organophosphorus pesticide poisoning into an experimental group (N = 31) and a control group (N = 30), and we compared the coma-recovery time, mechanical ventilation time, healing time, hospital expenses, and mortality between the two groups. The coma-recovery time, mechanical ventilation time, and healing time were lower in the experimental group than in the control group (P < 0.05), while the hospitalization expenses were higher in the experimental group than in the control group (P < 0.01); moreover, no significant difference was observed in the mortality rate between the two groups. Thus, PHC combined with hemoperfusion exerts a better therapeutic effect in acute severe organophosphorus pesticide poisoning than PHC alone.

Coma blisters after poisoning caused by central nervous system depressants: case report including histopathological findings.

Blister formation and eccrine sweat gland necrosis is a cutaneous manifestation associated with states of impaired consciousness, most frequently reported after overdoses of central nervous system depressants, particularly phenobarbital. The case of a 45-year-old woman who developed "coma blisters" at six distinct anatomic sites after confirmed (laboratory) phenobarbital poisoning, associated with other central nervous system depressants (clonazepam, promethazine, oxcarbazepine and quetiapine), is presented. A biopsy from the left thumb blister taken on day 4 revealed focal necrosis of the epidermis and necrosis of sweat gland epithelial cells; direct immunofluorescence was strongly positive for IgG in superficial blood vessel walls but negative for IgM, IgA, C3 and C1q. The patient was discharged on day 21 with no sequelae.

Coma blisters after poisoning caused by central nervous system depressants: case report including histopathological findings / Bolhas do coma pós-intoxicação por depressores do sistema nervoso central: relato de caso incluindo achados histopatológicos

Blister formation and eccrine sweat gland necrosis is a cutaneous manifestation associated with states of impaired consciousness, most frequently reported after overdoses of central nervous system depressants, particularly phenobarbital. The case of a 45-year-old woman who developed "coma blisters" at six distinct anatomic sites after confirmed (laboratory) phenobarbital poisoning, associated with other central nervous system depressants (clonazepam, promethazine, oxcarbazepine and quetiapine), is presented. A biopsy from the left thumb blister taken on day 4 revealed focal necrosis of the epidermis and necrosis of sweat gland epithelial cells; direct immunofluorescence was strongly positive for IgG in superficial blood vessel walls but negative for IgM, IgA, C3 and C1q. The patient was discharged on day 21 with no sequelae.

Formação de bolhas e necrose de glândula sudoríparas écrinas é uma manifestação cutânea associada com estados de diminuição da consciência, mais frequentemente relatada após superdosagens de depressores do sistema nervoso central, particularmente fenobabital. Relatamos o caso de uma paciente de 45 anos que desenvolveu "bolhas do coma" após tentativa de suicídio por fenobarbital (confirmada laboratorialmente), associada a outros depressores do sistema nervoso central (clonazepam, prometazina, oxcarbazepina e quetiapina). Biópsia da bolha do 1o quirodáctilo esquerdo no 4o dia de internação revelou necrose focal da epiderme e necrose de células epiteliais de glândula sudorípara; a imunofluorescência direta foi fortemente positiva para IgG na parede superficial dos vasos sanguíneos, mas negativa para IgM, IgA, C3 e C1q. A paciente teve alta no 21o dia, sem seqüelas.

Extradural haematoma and diffuse axonal injury in victims of fatal road traffic accidents.

Seven cases of victims of road traffic accidents with extradural haematoma (EH) and diffuse axonal injury (DAI) are reported. Such cases are part of a total of 120 victims of fatal road traffic accidents that were subjected to pathological study. The association of the two lesions occurred in 5.8% of the patients and all cases of EH were associated with DAI. The latter explains the immediate coma (absence of lucid interval) and the grave prognosis for all seven patients. It was noted that EH is relatively infrequent in road traffic accidents, but in such cases it is more severe since it is frequently associated with DAI and immediate coma.

Iatrogenic Wernicke's encephalopathy in allogeneic bone marrow transplantation: a study of eight cases.

Wernicke's encephalopathy (WE) is a neuropsychiatric condition generally caused by acute thiamine deficiency and classically involves the triad of altered mentation, ataxia and ophthalmoplegia. It is most common among alcoholics, but several other causes have been identified, including total parenteral nutrition (TPN) use. We present eight cases of WE in patients undergoing allogeneic BMT, where thiamine deficiency was caused by a lack of vitamin supplementation during TPN administration. Clinically, WE presented as a severe refractory metabolic acidosis, preceded by 'raspberry tongue', and ophthalmologic and neurologic dysfunction. The sites most affected were the periventricular structures and the thalamus, and no mammilary bodies lesions were found.

[Acute postinfectious encephalomyelitis. A case report]. / Encefalomielitis aguda postinfecciosa. Informe de un caso.

Acute disseminated encephalomyelitis, an infrequent demyelinating disease, complicates some common infections of childhood and is sometimes seen after vaccination particularly after rabies vaccination. We describe a six years old girl who had an upper respiratory tract infection two weeks prior to death. In a retrospective analysis we found that she also had received 14 doses of rabies vaccine eight months before her illness. The clinical and pathological features of this disease and its relationship with experimental allergic encephalomyelitis are analyzed.

Coma and death in unrecognized Wernicke's encephalopathy. An autopsy study.

Eleven out of 36 autopsied cases of Wernicke's encephalopathy had developed coma. None of these patients had the diagnosis during life. There were six men and five women with ages ranging from 26 to 50 years (mean 36.6). Seven of these patients were heavy drinkers, three exhibited signs of severe malnutrition, whereas one was being evaluated for a disseminated gastric cancer and one was in treatment of hyperemesis gravidarum. Two patients were brought to the hospital after found unconscious at home. Neuropathological examination disclosed gross changes in the mammillary bodies in eight cases and microscopic changes in all cases. In one case there was atrophy of the anterior superior part of the vermis. Petechial hemorrhages were observed particularly in the walls of the third ventricle. Microscopically there were in addition to hemorrhages, glial proliferation, endothelial hypertrophy and necrosis of nerve cells and myelin. Central pontine myelinolysis was observed in one case. Wernicke's encephalopathy is a clinically underdiagnosed condition. Coma may mask its classical clinical picture or even be the sole manifestation. Although coma points to a poor outlook it may be reversed by thiamine administration. Any patient with coma of unknown etiology should be given parenteral thiamine.

Hemorrhagic shock and encephalopathy: clinical, pathologic, and biochemical features.

To further define the clinical, pathologic, and biochemical features of hemorrhagic shock and encephalopathy syndrome, we studied 25 affected children (aged 3 months to 14 years) admitted to a single center between 1982 and 1985. A prodromal illness comprising vomiting, diarrhea, listlessness, and fever was present in 84% of the cases. Acute onset of shock, convulsions and coma, bleeding (or laboratory evidence of disseminated intravascular coagulation), elevated plasma activity of hepatic enzymes, acidosis, and impaired renal function was present in every case. Twenty patients died, and all the survivors are neurologically damaged. At postmortem examination, intravascular microthrombi coexisting with hemorrhages and petechiae were found in most organs. Centrilobular liver necrosis and cerebral edema were prominent features. No microbiologic cause for the disorder was identified, but decreased plasma levels of the protease inhibitors alpha 1-antitrypsin and alpha 2-macroglobulin, together with increased levels of circulating proteolytic enzymes, were frequently present. An overrepresentation of the uncommon variant phenotypes of alpha 1-antitrypsin was found in first-degree relatives of affected patients (four had the MZ phenotype, and one each the MS or MC phenotype, of 19 relatives studied). Abnormal accumulation of alpha 1-antitrypsin was detected immunohistochemically in the livers of six of the patients. Defective protease inhibitor production or release may be involved in the pathogenesis of the disorder.