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Objectives Neutrophil gelatinase-associated lipocalin (NGAL) is secreted by various tissues in pathologic states. Previous studies reported that post-cardiac arrest serum NGAL levels correlate with short-term neurologic outcomes and survival. The aim of this study was to examine the associations between NGAL levels post-cardiac arrest and long-term outcomes and survival. Methods This prospective observational study and retrospective review included adult out-of-hospital cardiac arrest survivors who were treated by hypothermia-targeted temperature management. Serum NGAL was assessed at 0, 24, 48, and 72 h after return of spontaneous circulation. The primary outcome was poor outcome at six months after cardiac arrest, defined as cerebral performance category score of 3–5. The secondary outcome was six-month mortality. Results In total, 76 patients were analyzed. The patients with poor outcomes showed significantly higher NGAL levels at 24, 48 and 72 h after cardiac arrest than the patients with good outcomes. Long-term survival rates were significantly lower in the high-NGAL group than in the low-NGAL group at each time point. Subgroup analysis of patients who survived 72 h showed that only serum NGAL 72 h after cardiac arrest had prognostic value for long-term outcomes (area under the receiver operating characteristic curve = 0.72; p = 0.02). Conclusions Post-cardiac arrest serum NGAL is associated with long-term outcomes and survival; particularly, three days post-cardiac arrest is the optimal time point for predicting long-term outcomes. However, the predictive power of NGAL is unsatisfactory, and it should be regarded as an additional prognostic modality.

We report a case of atypical cerebellar infarction following accidental inhalation of toluene mixed paint. An unconscious 57-year-old housewife with hypertension arrived at our emergency department by ambulance. She had been rescued from a basement (30 m3) 12 h after exposure to paint containing toluene (34%). On arrival, she was comatose (E1V1M1) with a mild fever (37.4 °C). Physical examination showed chemical burns on her buttocks and rales on the left lung. Initial arterial blood gas with 15 L/min of oxygen showed a pH of 7.142, PCO2 of 47.3 mmHg, and PaO2 of 204.7 mmHg. She received endotracheal intubation and mechanical ventilation. Laboratory tests showed elevated white blood cells (26.86 × 109/L), C-reactive protein (0.18 mg/dL), glucose (238 mg/Dl), and CPK (1389 U/L). At 5.5 h after arrival, she became responsive to verbal commands. On day 3, after removal of the endotracheal tube, she began to complain of an occipital headache without neurologic abnormalities. Brain magnetic resonance angiography (MRA) performed on day 6 showed a tiny acute infarction on the right cerebellar hemisphere. We serially measured urinary hippuric acid concentrations (reference range, ≤2.5 g/g creatinine) from 74 h (3.88) after hospital arrival to 218 h (0.5). She was discharged on day 14. Herein we presented a near fatal toluene intoxication (>45,000 mg/m3 estimated based on the basement volume and quantity of paint used) with atypical cerebellar infarction, compared with prior findings of bilateral involvement or reversibility.

Objective Therapeutic hypothermia is now regarded as the only effective treatment of global ischemic injury after cardiac arrest. Numerous studies of the neuroprotective effects of 17 β -estradiol have yielded conflicting results depending on administration route and dose. Herein, we investigated the neuroprotective effect of postischemic 17 β -estradiol administration combined with therapeutic hypothermia. Methods Twenty-one rats were randomly divided into 4 groups: control (group I), therapeutic hypothermia (group II), 17 β -estradiol treatment (group III), and therapeutic hypothermia combined with 17 β -estradiol treatment (group IV). One rat was assigned to a sham operation group. With the exception of the sham-operated rat, all animals underwent transient global cerebral ischemia for 20 minutes by the 4-vessel occlusion method. Hypothermia was maintained at 33°C for 2 hours in groups II and IV, and 17 β -estradiol (10 μ g/kg) was intraperitoneally administered to rats in groups III and IV. Neurologic deficit scores and hippocampal cornu ammonis 1 neuronal injury were assessed 72 hours postischemia. Results The neurologic deficit score was not significantly different among the groups. The percentage of normal neurons in the hippocampal cornu ammonis 1 was 7.32% ± 0.88% in group I, 53.65% ± 2.52% in group II, 51.6% ± 3.44% in group III, and 79.79% ± 1.6% in group IV. The neuroprotective effect in the combined treatment group was markedly greater than in the single treatment groups, which suggests that hypothermia and 17 β -estradiol work synergistically to exert neuroprotection. Conclusion Postischemic administration of low-dose 17 β -estradiol appears to be neuroprotective after transient global ischemia, and its effect is potentiated by therapeutic hypothermia.

Benzodiazepines are widely used for many diseases, and benzodiazepine overdose is globally increasing in proportion to its prescriptions. Although most benzodiazepine overdoses are known to be safe and nonfatal without coingestions, morbidity or mortality after benzodiazepine overdose is closely related with the duration of unconsciousness or depth of compromised airway. Proper use of flumazenil, a potent antidote of benzodiazepine, seems to accelerate the recovery from the toxicity after benzodiazepine overdose.However, as the case we present demonstrates, careful attention and repetitive evaluations before and after use of flumazenil may be needed in benzodiazepine overdose because resedation occurs in approximately 30% of total flumazenil-treated cases, which suggests that the risk of aspiration or incidental death after administrating flumazenil might be significant without careful monitoring.

Hypothermia increases clotting time, which is known as hypothermic coagulopathy. However, prothrombin time and activated partial thromboplastin time prolongation associated with therapeutic hypothermia is usually mild and thus, hypothermic coagulopathy is not considered to cause clinically significant bleeding. On the other hand, PT and aPTT do not seem to reflect the severity of hypothermic coagulopathy. Serious bleeding complications of therapeutic hypothermia has not been reported previously. Herein, we introduce a case of spontaneous brain stem hemorrhage as a complication of therapeutic hypothermia-induced coagulopathy.