Identification of risk factors for death from tetanus in Pernambuco, Brazil: a case-control study Identificação de fatores de risco para morte por tétano em Pernambuco, Brasil: um estudo de caso-controle

A case-control study was conducted to identify risk factors for death from tetanus in the State of Pernambuco, Brazil. Information was obtained from medical records of 152 cases and 152 controls, admitted to the tetanus unit in the State University Hospital, in Recife, from 1990 to 1995. Variables were grouped in three different sets. Crude and adjusted odds ratios, p-values and 95% confidence intervals were estimated. Variables selected in the multivariate analysis in each set were controlled for the effect of those selected in the others. All factors related to the disease progression - incubation period, time elapsed between the occurrence of the first tetanus symptom and admission, and period of onset - showed a statistically significant association with death from tetanus. Similarly, signs and/or symptoms occurring on admission or in the following 24 hours (second set): reflex spasms, neck stiffness, respiratory signs/symptoms and respiratory failure requiring artificial ventilation (third set) were associated with death from tetanus even when adjusted for the effect of the others.<br>Um estudo de caso-controle foi conduzido no Estado de Pernambuco, Brasil, para identificar fatores de risco para morte por tétano. As informações foram obtidas dos prontuários médicos de 152 casos e 152 controles, admitidos na Unidade de Tétano do Hospital Universitário Oswaldo Cruz, na cidade do Recife, de 1990 a 1995. As variáveis foram agrupadas em três diferentes conjuntos. Foram estimados os "odds ratios" brutos e ajustados, o intervalo de confiança de 95% e o valor de "p". As variáveis selecionadas na análise multivariada em cada conjunto, foram controladas para os efeitos daquelas selecionadas nos demais. Todos os fatores relacionados à progressão da doença - período de incubação, tempo decorrido entre o primeiro sintoma de tétano e a admissão no hospital, e período de progressão - mostraram uma associação estatisticamente significante com morte por tétano. De modo semelhante, o segundo conjunto de variáveis - sinais e/ou sintomas que ocorreram à admissão ou nas primeiras 24 horas: espasmos, rigidez de nuca, sinais e sintomas respiratórios - bem como as variáveis do terceiro conjunto - insuficiência respiratória que necessitou de respiração artificial foram associadas com morte por tétano, mesmo quando ajustadas com os efeitos das demais variáveis

Anemia and transfusion after subarachnoid hemorrhage

Delayed cerebral ischemia after subarachnoid hemorrhage (SAH) may be affected by a number of factors, including cerebral blood flow and oxygen delivery. Anemia affects about half of patients with SAH and is associated with worse outcome. Anemia also may contribute to the development of or exacerbate delayed cerebral ischemia. This review was designed to examine the prevalence and impact of anemia in patients with SAH and to evaluate the effects of transfusion. A literature search was made to identify original research on anemia and transfusion in SAH patients. A total of 27 articles were identified that addressed the effects of red blood cell transfusion (RBCT) on brain physiology, anemia in SAH, and clinical management with RBCT or erythropoietin. Most studies provided retrospectively analyzed data of very low-quality according to the GRADE criteria. While RBCT can have beneficial effects on brain physiology, RBCT may be associated with medical complications, infection, vasospasm, and poor outcome after SAH. The effects may vary with disease severity or the presence of vasospasm, but it remains unclear whether RBCTs are a marker of disease severity or a cause of worse outcome. Erythropoietin data are limited. The literature review further suggests that the results of the Transfusion Requirements in Critical Care Trial and subsequent observational studies on RBCT in general critical care do not apply to SAH patients and that randomized trials to address the role of RBCT in SAH are required

Hemodynamic management of subarachnoid hemorrhage

Hemodynamic augmentation therapy is considered standard treatment to help prevent and treat vasospasm and delayed cerebral ischemia. Standard triple- H therapy combines volume expansion (hypervolemia), blood pressure augmentation (hypertension), and hemodilution. An electronic literature search was conducted of English-language papers published between 2000 and October 2010 that focused on hemodynamic augmentation therapies in patients with subarachnoid hemorrhage. Among the eligible reports identified, 11 addressed volume expansion, 10 blood pressure management, 4 inotropic therapy, and 12 hemodynamic augmentation in patients with unsecured aneurysms. While hypovolemia should be avoided, hypervolemia did not appear to confer additional benefits over normovolemic therapy, with an excess of side effects occurring in patients treated with hypervolemic targets. Overall, hypertension was associated with higher cerebral blood flow, regardless of volume status (normo- or hypervolemia), with neurological symptom reversal seen in two-thirds of treated patients. Limited data were available for evaluating inotropic agents or hemodynamic augmentation in patients with additional unsecured aneurysms. In the context of sparse data, no incremental risk of aneurysmal rupture has been reported with the induction of hemodynamic augmentation

Endocrine function following acute SAH

Disruption of the hypothalamic-pituitary-adrenal axes may occur after aneurysmal subarachnoid hemorrhage, resulting in hypopituitarism. An electronic literature search was conducted to identify articles with English-language abstracts published between 1980 and March 2011, which addressed hypothalamic-pituitary-adrenal axis insufficiency and hormone replacement. A total of 18 observational and prospective, randomized studies were selected for this review. Limited data are available, evaluating pituitary effects during the acute stage after subarachnoid hemorrhage, with inconsistent results being reported. Overall, after acute subarachnoid hemorrhage, cortisol levels may initially be supranormal, decreasing toward normal levels over time. During the months to years after subarachnoid hemorrhage, pituitary deficiency may occur in one out of three patients. Limited data suggest modest outcome benefits with fludrocortisone and no benefit or harm from corticosteroids