32 research outputs found
Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients
One life ends, another begins: Management of a brain-dead pregnant mother - A systematic review -
Background: An accident or a catastrophic disease may occasionally lead to brain death (BD) during pregnancy. Management of brain-dead pregnant patients needs to follow special strategies to support the mother in a way that she can deliver a viable and healthy child and, whenever possible, also be an organ donor. This review discusses the management of brain-dead mothers and gives an overview of recommendations concerning the organ supporting therapy. Methods: To obtain information on brain-dead pregnant women, we performed a systematic review of Medline, EMBASE and the Cochrane Central Register of Controlled Trials (CENTRAL). The collected data included the age of the mother, the cause of brain death, maternal medical complications, gestational age at BD, duration of extended life support, gestational age at delivery, indication of delivery, neonatal outcome, organ donation of the mothers and patient and graft outcome. Results: In our search of the literature, we found 30 cases reported between1982 and 2010. A nontraumatic brain injury was the cause of BD in 26 of 30 mothers. The maternal mean age at the time of BD was 26.5 years. The mean gestational age at the time of BD and the mean gestational age at delivery were 22 and 29.5 weeks, respectively. Twelve viable infants were born and survived the neonatal period. Conclusion: The management of a brain-dead pregnant woman requires a multidisciplinary team which should follow available standards, guidelines and recommendations both for a nontraumatic therapy of the fetus and for an organ-preserving treatment of the potential donor
Procalcitonin: a new parameter for the diagnosis of bacterial infection in the peri-operative period
Gene expression analysis of human islets in a subject at onset of type 1 diabetes
Swollen islet cells have been repeatedly described at onset of type 1 diabetes, but the underlying mechanism of this observation, termed hydropic degeneration, awaits characterization. In this study, laser capture microdissection was applied to extract the islets from an organ donor that died at onset of type 1 diabetes and from an organ donor without pancreatic disease. Morphologic analysis revealed extensive hydropic degeneration in 73% of the islets from the donor with type 1 diabetes. Expression levels of genes involved in apoptosis, ER stress, beta cell function, and inflammation were analyzed in isolated and laser-captured islets by qPCR. The chemokine MCP-1 was expressed in islets from the donor with type 1 diabetes while undetectable in the control donor. No other signs of inflammation were detected. There were no signs of apoptosis on the gene expression level, which was also confirmed by negative immunostaining for cleaved caspase-8. There was an increased expression of the transcription factor ATF4, involved in transcription of ER stress genes, in the diabetic islets but no further signs of ER stress were identified. In summary, on the transcription level, islets at onset of type 1 diabetes in which many beta cells display hydropic degeneration show no obvious signs of apoptosis, ER stress or inflammation supporting the notion that these cells are responding normally to high glucose and eventually succumbing in beta cell exhaustion. Also, this study validates the feasibility of performing qPCR analysis of RNA extracted from islets from subjects with recent onset T1D and healthy controls by laser capture microdissection
Wait, treat and see: echocardiographic monitoring of brain-dead potential donors with stunned heart
<p>Abstract</p> <p>Background</p> <p>Heart transplantation is limited by a severe donor organ shortage. Potential donors with brain death (BD) and left ventricular dysfunction due to neurogenic stunning are currently excluded from donation – although such abnormalities can be reversible with aggressive treatment including Hormonal Treatment (HT) and deferred organ retrieval.</p> <p>Aim</p> <p>To assess the recovery of left ventricular dysfunction in potential brain-dead donors with hemodynamic instability treated by aggressive treatment and HT.</p> <p>Methods</p> <p>In a single-center, observational study design, we evaluated 15 consecutive brain-dead potential donors (DBD) (8 males, age = 48 ± 15 years) with hemodynamic instability. All underwent standard hemodynamic monitoring and transthoracic 2-dimensional echo (2-DE) with assessment of Ejection Fraction (EF). Measurements were obtained before BD and after BD within 6 h, at 24 h and within 48 h. HT (with insulin, methylprednisolone, vasopressin and T3) was started as soon as possible to treat hemodynamic instability and avoid administration of norepinephrine (NE). Eligible potential heart donors underwent coronary angiography.</p> <p>Results</p> <p>After HT, we observed a normalization of hemodynamic conditions with improvement of mean arterial pressure (pre = 68 ± 8 mmHg vs post = 83 ± 13 mmHg, p < .01), cardiac index (pre = 2.4 ± 0.6 L/min/m<sup>2</sup> vs post 3.7 ± 1.2 L/min/m<sup>2</sup>, p < .05), EF (pre = 48 ± 15 vs post = 59 ± 3%, p < .01) without administration of norepinephrine (NE) in 67% of cases. Five potential donors were excluded from donation (opposition, n = 3, tubercolosis n = 1, malignancy n = 1). At pre-harvesting angiography<b>,</b> coronary artery stenosis was present in 2 of the 10 consented donors. Eight hearts were uneventfully transplanted. No early graft failure occurred and all eight recipients were alive at 6-month follow-up.</p> <p>Conclusion</p> <p>In BD donors, intensive treatment including HT is associated with improvement of regional and global LV function and reverse remodeling detectable by transthoracic 2DE. Donor hearts with recovered LV function may be eligible for uneventful heart transplant. The wait (in brain death), treat (with HT) and see (with 2D echo) strategy can help rescue organs suitable for heart donation.</p
Vasopressin serum levels and disorders of sodium and water balance in patients with severe brain injury Níveis séricos de vasopressina e distúrbios de sódio e água em pacientes com lesão cerebral grave
BACKGROUND: Disorders of water and sodium balance are frequently seen in patients with severe brain injury (SBI), and may worsen their prognosis. PURPOSE: To evaluate vasopressin (AVP) serum levels and sodium and water balance disorders during the first week post-injury in patients with SBI. METHOD: Thirty-six adult patients with SBI (admission Glasgow Coma Scale score < 8) and an estimated time of injury < 72 hours were prospectively studied. Clinical and laboratory data were recorded and AVP was measured in venous blood samples collected on the 1st, 2nd, 3rd and 5th days following inclusion. RESULTS: AVP serum levels remained within the normal range in SBI patients (either traumatic or non-traumatic), although tended to be greater in non-survivor than in survivor patients (p=0.025 at 3rd day). In-hospital mortality was 43% (15/36), and serum sodium and plasma osmolality variabilities were greater in non-survivor than in survivor patients during the observation period (p<0.001). CONCLUSION: AVP serum levels remained within the normal range values in these SBI patients, but those who died have shown higher incidence of abnormal sodium and water balance during the first week post-injury.<br>ANTECEDENTES: Desordens do balanço de água e sódio são frequentemente vistas em pacientes com lesão cerebral grave (LCG), podendo agravar o prognóstico. OBJETIVO: Avaliar os níveis séricos de vasopressina (AVP) e a incidência de distúrbios da água e sódio na primeira semana pós-lesão em pacientes com LCG. MÉTODO: Trinta e seis pacientes adultos com LCG (pontuação inicial na escala de coma de Glasgow < 8) e tempo estimado de lesão < 72h foram estudados prospectivamente. Dados laboratoriais e clínicos foram registrados e os níveis séricos de AVP foram mensurados no 1º, 2º, 3º e 5º dias pós-inclusão. RESULTADOS: A AVP manteve-se dentro da faixa de normalidade nestes pacientes, mas mostrando-se proporcionalmente mais elevada nos pacientes que não sobreviveram (p=0,025 no 3º dia). A mortalidade intra-hospitalar foi 43% (15/36) e as variações do sódio e osmolalidade plasmáticos foram maiores nos pacientes que não sobreviveram durante o período de observação (p<0,001). CONCLUSÃO: Os níveis séricos de AVP mantiveram-se dentro da faixa de normalidade nestes pacientes com LCG, mas aqueles não sobreviventes mostraram maior incidência de anormalidades do balanço de água e sódio durante a primeira semana de evolução
