Management following resuscitation from cardiac arrest: recommendations from the 2003 Rocky Mountain Critical Care Conference.

PURPOSE: To propose a strategy for the management of patients admitted to critical care units after resuscitation from cardiac arrest. SOURCE: Prior to the conference relevant studies were identified via literature searches and brief reviews circulated on the following topics: glucose and blood pressure management; therapeutic hypothermia; prearrest outcome prediction; post-arrest outcome prediction; and management of myocardial ischemia. Two days were devoted to assessing evidence and developing a management strategy at the conference. Consensus opinion of conference participants [intensive care unit (ICU) physicians] was used when high grade evidence was unavailable. Additional literature searches and data grading were performed post-conference. PRINCIPAL FINDINGS: High grade evidence was lacking in most areas. Specific goals of treatment were proposed for: general care; neurologic care; respiratory care; cardiac care; and gastrointestinal care. There was adequate evidence to recommend therapeutic hypothermia for comatose patients who had witnessed ventricular fibrillation or ventricular tachycardia arrests. Conference participants supported extending therapeutic hypothermia to other presenting rhythms in selected circumstances. Additional goals included mean arterial pressure 80 to 100 mmHg, glucose 5 to 8 mmol.L(-1) using insulin infusions, and PaO(2) > 100 mmHg for the first 24 hr. Absent withdrawal to pain 72 hr after resuscitation should prompt consideration of palliative care. The level of evidence for other recommendations was low. CONCLUSIONS: The proposed management strategy represents an approach to manage patients in the ICU following resuscitation from cardiac arrest. Most of the recommendations are based on low grade evidence. Additional research is needed to improve the evidence base. A standard post-arrest management strategy could help facilitate future research.

A novel missense homozygous inactivating mutation in the fourth transmembrane helix of the luteinizing hormone receptor in leydig cell hypoplasia.

Loss-of-function mutations/inactivating mutations of the human chorionic gonadotropin/luteinizing hormone receptor (hCG/LHR), a G-protein coupled receptor, lead to impaired Leydig cell differentiation. Leydig cell hypoplasia/agenesis/dysplasia (LCH) is one of the causes of male pseudohermaphroditism (MPH). We studied a 19-year-old MPH patient with female phenotype and 46,XY karyotype. Testicular histology and hormonal profile of the patient is typical of LCH. Nucleotide sequencing of exon 11 of hLHR identified a novel T1505C transversion mutation. The mutation is homozygous in the patient and is heterozygous in both parents. The single base mutation caused the substitution of a conserved leucine at 502 position to proline in transmembrane helix (TM) IV of the hLHR. This is the first LCH causing mutation identified in TM IV of the hLHR. Expression study of the mutated hLHR in human embryonic kidney (HEK)293 cells showed reduced cAMP production and ligand binding. Receptor trafficking was not affected by the mutation when the green fluorescence protein conjugated mutated receptor was expressed in HEK293 cells. The mutation caused inactivation of the hLHR and resulted in LCH in the patient.