Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state.
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Diabetic ketoacidosis and the hyperglycemic hyperosmolar state are the most serious complications of diabetic decompensation and remain associated with excess mortality. Insulin deficiency is the main underlying abnormality. Associated with elevated levels of counterregulatory hormones, insulin deficiency can trigger hepatic glucose production and reduced glucose uptake, resulting in hyperglycemia, and can also stimulate lipolysis and ketogenesis, resulting in ketoacidosis. Both hyperglycemia and hyperketonemia will induce osmotic diuresis, which leads to dehydration. Clinical diagnosis is based on the finding of dehydration along with high capillary glucose levels with or without ketones in the urine or plasma. The diagnosis is confirmed by the blood pH, serum bicarbonate level and serum osmolality. Treatment consists of adequate correction of the dehydration, hyperglycemia, ketoacidosis and electrolyte deficits. (+info)
Neurological outcome of prolonged coma survivors of out-of-hospital cardiac arrest.
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Nine adult survivors of out-of-hospital presumed cardiogenic cardiac arrest, who remained unresponsive for longer than their third hospital day and who eventually were discharged from the acute care hospital, are reported. Their neurological outcome fell into three distinct categories: (a) a persistent vegetative state, (b) able to follow some simple commands but requiring total nursing care, and (c) able to perform most activities of daily living but unemployable because of marked organic deficits. (+info)
Severe anaemia in childhood cerebral malaria is associated with profound coma.
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BACKGROUND: Severe anaemia in children with cerebral malaria has been associated with respiratory distress secondary to lactic acidosis and/or hypoxia. The ensuing metabolic derangement may further depress the level of consciousness culminating in presentation with profound coma. This association has poorly been studied. OBJECTIVE: To determine the relationship between profound coma at presentation and the presence of severe anaemia in children with cerebral malaria. METHODS: This cross-sectional study involved 100 children with cerebral malaria who were consecutively recruited at admission in the Paediatric emergency unit of Mulago hospital in Uganda from July to December 2000. Clinical and laboratory evaluation was done using the hospital's guidelines for the management of severe malaria. The exposure factor of interest was severe anaemia (Hb < 5.0 g/dl) and occurrence of profound coma (Blantyre coma Scale 0) was the outcome measure. RESULTS: Severe anaemia and profound coma were seen in 20% and 9% of the children respectively. Severe anaemia was independently associated with profound coma, adjusted OR 1.34 (CI 1.17 - 1.95), p = 0. 002 and age < 3 years, adjusted OR 1.42 (CI 1.13 - 1.54), p = 0.001). Thirty percent of those with severe anaemia had deep sighing (acidotic) breathing compared to only 15% of those with haemoglobin (Hb) > 5 g/dl, OR 1.21 (CI 0.90 - 1.64), p = 0.118. There was no association between the malaria parasite density and severe anaemia. A similar proportion of those with severe anaemia regained consciousness within 24 hours compared to those with Hb > 5 g/dl (30 vs 42.5%), OR 1.56 (0.65 - 3.71), p = 0.307. CONCLUSIONS: The findings suggest that profound coma in cerebral malaria may not only result from primary malaria encephalitis but possibly also from a metabolic dysfunction due to severe anaemia. (+info)
Neuroanatomical correlates of brainstem coma.
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The brainstem tegmentum, including the reticular formation, contains distinct nuclei, each of which has a set of chemical, physiological and anatomical features. Damage to the brainstem tegmentum is known to cause coma, the most radical disturbance of consciousness. However, it has remained unclear which nuclei within the tegmentum are crucial for the maintenance of consciousness in humans. Accordingly, we initiated a retrospective study of MRIs obtained from 47 patients with brainstem stroke. The lesion boundaries were charted on patient MRIs and transferred onto a corresponding series of 4.7 T MRIs obtained from a control brainstem specimen that later was cut on a freezing microtome and analysed histologically. In addition, medical charts and available post-mortem materials were used to obtain relevant clinical and anatomical data to verify the MRI readings in each case. We found that in the 38 patients who did not have coma, brainstem damage either was located outside the tegmentum (n = 29) or produced a very small and unilateral compromise of the tegmentum (n = 9). In contrast, in patients who had coma (n = 9), the lesions in the tegmentum were mostly bilateral (n = 7) and were located either in the pons alone (n = 4) or in the upper pons and the midbrain (n = 5). The maximum overlap territory of the lesions coincided with the location of the rostral raphe complex, locus coeruleus, laterodorsal tegmental nucleus, nucleus pontis oralis, parabrachial nucleus and the white matter in between these nuclei. We also found that four coma subjects developed hyperthermia and died in the absence of any infections. In these cases, the maximum lesion overlap was centred in the core of pontine tegmentum. Our findings suggest that lesions confined to the upper pons can cause coma in humans even in the absence of damage to the midbrain. The findings also point to the brainstem nuclei whose lesions are likely to be associated with loss of consciousness and fatal hyperthermia in humans. (+info)
Expensive cerebral blood flow measurements alone are useless and misinformative in comatose patients: a comprehensive alternative.
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Since the first report addressing quantification of cerebral blood flow (CBF), concomitant assessment of cerebral oxygen consumption was also carried out. Over the years, however, some investigators have emphatically and mistakenly addressed cerebral ischemia in comatose patients, on the basis of CBF measurements alone. In contrast, we have repeatedly reported that ischemia in these patients must be precisely evaluated based on CBF-metabolism coupling or uncoupling, rather than CBF alone. Based on these previous findings, we therefore propose a comprehensive alternative approach, namely the evaluation of brain ischemia in comatose patients based on cerebral metabolic parameters, such as cerebral extraction of oxygen or cerebral lactate release, without expensive CBF measurements. (+info)
Dural arteriovenous malformation and sinus thromboses in a patient with prostate cancer: an autopsy case.
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A 67-year old man with prostate cancer showed Balint's syndrome, memory disturbance, anosognosia and hallucinations after having been comatose. Radiological findings indicated bilateral dural arteriovenous malformation (DAVM) and thrombosis at the bilateral transverse sinuses and superior sagittal sinus. Pathological findings showed abnormally dilated veins, diffuse neuron loss and gliosis in the parieto-occipital lobe. The chlormadinone and prostate cancer are speculated to have caused the dural sinus thrombosis which probably induced the DAVM. (+info)
Aceruloplasminemia with juvenile-onset diabetes mellitus caused by exon skipping in the ceruloplasmin gene.
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We herein report a case of aceruloplasminemia in a 27-year-old man who had a 10-year history of diabetes mellitus. The patient developed a convulsion, most likely as a result of hypoglycemia. Unexpectedly, this episode left him in a prolonged state of unconsciousness, which necessitated neurological testing and imaging. Brain MRI showed bilateral hypo-intensities in the basal ganglia and thalamus. Molecular analysis revealed a novel splicing mutation in the ceruloplasmin (CP) gene that would result in the skipping of exon 3 during transcription. This case suggests that diabetes associated with aceruloplasminemia can become manifest in the teens. (+info)
Role of Glasgow Coma Scale in pediatric nontraumatic coma.
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OBJECTIVE: To assess the relationship between Modified Glasgow Coma Scale (MGCS), its components and survival in children with acute coma. DESIGN: Prospective observational study. SETTING: Tertiary care referral hospital. PATIENTS: Consecutive children (n = 270) with acute nontraumatic coma between 2 months to 12 years. METHODOLOGY: MGCS and brainstem reflexes were assessed at 6 hourly intervals for 72 hours from the time of admission. The lowest score of the MGCS and worst brain stem reflexes were used for the analysis. MAIN OUTCOME MEASURE: Survival. RESULTS: Total score (Spearman rank correlation coefficient IRI = O.577, ocular response (IRI = O.641), motor response (IRI = O.729), verbal response (lRI = 0.608), brain stem response (lRI = O.843) were all found to be associated with adverse outcome. Multivariate regression analysis revealed that ocular response and motor response were individually predictive of short-term outcome. CONCLUSION: A score incorporating the brain stem reflexes, ocular response and motor response in the assessment and prognostication of comatose patients needs to be evaluated. (+info)