Markers of immune-mediated inflammation in the brains of young adults and adolescents with type 1 diabetes and fatal diabetic ketoacidosis. Is there a difference?

Due to the limited data on diabetic ketoacidosis and brain edema (DKA/BE) in children/adolescents and the lack of recent data on adults with type 1 diabetes (T1D), we addressed the question of whether neuroinflammation was present in the fatal DKA of adults. We performed immunohistochemistry (IHC) studies on the brains of two young adults with T1D and fatal DKA and compared them with two teenagers with poorly controlled diabetes and fatal DKA. C5b-9, the membrane attack complex (MAC) had significantly greater deposits in the grey and white matter of the teenagers than the young adults (p=0.03). CD59, a MAC assembly inhibitory protein was absent, possibly suppressed by the hyperglycemia in the teenagers but was expressed in the young adults despite comparable average levels of hyperglycemia. The receptor for advanced glycation end products (RAGE) had an average expression in the young adults significantly greater than in the teenagers (p=0.02). The autophagy marker Light Chain 3 (LC3) A/B was the predominant form of programmed cell death (PCD) in the teenage brains. The young adults had high expressions of both LC3A/B and TUNEL, an apoptotic cell marker for DNA fragmentation. BE was present in the newly diagnosed young adult with hyperglycemic hyperosmolar DKA and also in the two teenagers. Our data indicate that significant differences in neuroinflammatory components, initiated by the dysregulation of DKA and interrelated metabolic and immunologic milieu, are likely present in the brains of fatal DKA of teenagers when compared with young adults.

Sudden cardiac arrest as a presentation of Brugada syndrome unmasked by thyroid storm.

An 18-year-old man suffered a sudden cardiac arrest with ventricular fibrillation and was successfully resuscitated. He had neither a medical nor family history of cardiac disease/sudden death, but was known to have Graves' disease, for which he was treated with radioactive iodine. Recently, block-and-replacement therapy had been discontinued to evaluate thyroid functioning. On admission, thyroid hormone levels were markedly elevated, suggesting thyroid storm due to residual Graves' disease. The patient was treated with propylthiouracil, hydrocortisone and Lugol solution. ECG showed repolarisation patterns suggestive of an underlying type 1 Brugada syndrome (BS). These findings were confirmed by an additional ajmaline test. An implantable cardioverter defibrillator was implanted to prevent future arrhythmias. The patient underwent total thyroidectomy 9 months later and recovered completely. To the best of our knowledge, this is the first reported case of a sudden cardiac arrest as a presentation of BS unmasked by thyroid storm.

An unusual neurological consequence of massive wasp stings.

Although rare, central and peripheral neurological manifestations after single or multiple wasp stings have been reported. The authors describe a 45-year-old man who developed periods of sudden loss of consciousness with a Glasgow Coma Scale of 6 after being stung by fifty wasps. These periods were seen directly after being stung and were continuing months later. Different mechanisms and pathophysiological findings of neurological sequela reported after wasp stings are being reviewed.

Haemodynamic consequences of mild therapeutic hypothermia after cardiac arrest.

BACKGROUND AND OBJECTIVE: Mild therapeutic hypothermia (MTH) is used after out-of-hospital cardiac arrest (OHCA) to minimize cerebral damage. Induced hypothermia may further interfere with cardiac function and influence haemodynamics after OHCA. METHODS: This was a prospective study of haemodynamic variables in 50 consecutive patients with OHCA treated with MTH. Patients were cooled to a core body temperature of 32.5 degrees C for 24 h. Induction and maintenance of cooling was accomplished via infusion of 2 l of cold isotonic saline (4 degrees C) and a cooling blanket. Rewarming was performed to 36 degrees C at a rate of 0.3 degrees C per hour. Haemodynamic data were analysed and compared in individual patients during different temperature phases. RESULTS: Heart rate dropped from a mean of 85 to 60 beats per min (P=0.001) during hypothermia. Mean arterial pressure dropped from 79 to 72 mmHg, despite a rise in vasopressors and inotropes. Lactate levels were elevated throughout the induction (mean+/-SD) and maintenance phase (mean+/-SD); however, this did not correlate with a decrease in SVO2. Pulmonary artery pressures decreased during induction of hypothermia despite rapid infusion. CONCLUSION: MTH after OHCA lowered the heart rate. Despite induction of hypothermia with cold fluids, filling pressures decreased. Lower mean arterial pressure and cardiac output were observed during MTH, without deleterious effect on ScVO2. Lactate levels were elevated during MTH; however, levels did not correlate with outcome. Although the need for vasopressors and inotropes increases, this hypothermia-induced metabolic beta-blocker-like effect seems to have no negative effect on oxygen consumption and only temporarily affects anaerobic metabolism. No association of haemodynamic changes during MTH with outcome was found.

[Mild therapeutic hypothermia following resuscitation; experience and results in the first two years after introduction]. / Milde therapeutische hypothermie na reanimatie. Ervaringen en resultaten van de eerste 2 jaar na implementatie.

OBJECTIVE: To describe the results of mild therapeutic hypothermia (MTH) following resuscitation in the 'Gelderse Vallei' hospital, Ede, the Netherlands. DESIGN: Descriptive, retrospective. METHOD: Patient data was collected from patients who had undergone MTH during the first two years following introduction of this treatment in the intensive care department of the 'Gelderse Vallei' hospital, Ede. Information used in the description included patient characteristics, heart arrest type (ventricular fibrillation or other arrhythmias), place of onset (in hospital or elsewhere), resuscitation data, side effects of the treatment, mortality and neurological outcome. RESULTS: 67 patients were treated with MTH in the period April 2005 to July 2007. The hospital mortality rate within this group was 81%. The mortality rate in the subgroup presenting with ventricular fibrillation as initial arrhythmia was 76%, compared with 89% in the subgroup with other arrhythmias. The mortality rate of patients who were resuscitated outside the hospital was comparable with that for patients resuscitated in hospital (80% versus 83%). Patients who could be discharged from hospital had a good neurological outcome (average Cerebral Performance Category score 1.9; 95%-CI: 1.6-2.2). The most important complications during MTH were electrolyte imbalances and ventilator associated pneumonia. CONCLUSION: The introduction of MTH in the intensive care department of the "Gelderse Vallei" has taken place without major problems. Although the mortality rate following cardiopulmonary resuscitation was relatively high, the neurological outcome in those patients who were discharged from hospital alive was good.

Progressive respiratory distress due to neck mass.

The present report describes the case of an 80-year-old woman who presented at the emergency department with progressive respiratory distress caused by a massive anterior neck mass with tracheal deviation and compression. A CT scan showed diffuse enlargement of the thyroid gland. The patient underwent a left-sided hemithyroidectomy. Pathology unexpectedly revealed a primary thyroid lymphoma. Treatment with prednisone and vincristine was initiated to reduce tumour size and preserve the airway, resulting in rapid volume reduction and airway expansion. Primary thyroid lymphoma is a rare entity that requires adequate diagnosis and rapid initiation of treatment to reduce tumour volume and to prevent airway compromise.

Extracorporeal elimination in acute valproate intoxication.

Severe poisoning with valproate may result in coma and death. The management of valproate intoxication is principally supportive. Valproate is scarcely excreted renally and is mainly protein bound and, therefore, not considered to be amenable for extracorporeal elimination. Despite these unfavourable pharmacokinetic properties, several case reports showed successful treatment of valproate intoxication with haemodialysis and/or haemoperfusion. We describe a male patient (57 years) after ingestion of 64 g of valproate. The patient was successfully treated with haemodialysis for 6 h. Haemodialysis was followed by continuous venovenous haemodiafiltration (CVVH-D) for 18 h to prevent a rebound phenomenon. This report confirms the benefit of haemodialysis in serious valproate overdose. A review of the literature shows that haemodialysis followed by CVVH-D is the treatment of choice in severe valproate intoxication.