An unconscious man with profound drug-induced hypoglycaemia.

INTRODUCTION: Hypoglycaemia has been reported as an unusual complication of tramadol use and in a few cases of tramadol poisoning, but the exact mechanism is not known. CASE DESCRIPTION: An ambulance crew was dispatched to an unconscious 46-year old man. A glucometer point-of-care measurement revealed a profound hypoglycaemia (1.9 mmol/L). Treatment with intravenous glucose was started and the patient was transported to the hospital. The patient had several episodes of pulseless electrical activity requiring cardiopulmonary resuscitation in the ambulance and upon arrival in the hospital. Despite continuous glucose infusion the hypoglycaemia was difficult to correct during the next few hours and the patient developed hypokalaemia. Further investigation to identify the cause of hypoglycaemia revealed that insulin and C-peptide were inappropriately raised. A toxicological investigation revealed the presence of tramadol and its metabolites in lethal concentrations. Also acetaminophen, ibuprofen and lormetazepam were present. Ethanol screening was negative (< 0.1 g/L) and no sulfonylurea were detected. The patient developed multiple organ failure, but eventually recovered. WHAT HAPPENED: The hypoglycaemia was caused by inappropriate stimulation of insulin secretion in a patient intoxicated with tramadol. The sudden hypokalaemia was caused by a massive intracellular shift of potassium in response to the hyperinsulinemia, triggered by the intravenous administration of glucose. MAIN LESSON: To our knowledge, we are the first to document a significant rise in endogenous insulin production in a hypoglycaemic patient presenting with tramadol intoxication. Our observation suggests that hyperinsulinemia could be the cause of the hypoglycaemia associated with tramadol use.

Feasibility of absolute cerebral tissue oxygen saturation during cardiopulmonary resuscitation.

INTRODUCTION: Current monitoring during cardiopulmonary resuscitation (CPR) is limited to clinical observation of consciousness, breathing pattern and presence of a pulse. At the same time, the adequacy of cerebral oxygenation during CPR is critical for neurological outcome and thus survival. Cerebral oximetry, based on near-infrared spectroscopy (NIRS), provides a measure of brain oxygen saturation. Therefore, we examined the feasibility of using NIRS during CPR. METHODS: Recent technologies (FORE-SIGHT™ and EQUANOX™) enable the monitoring of absolute cerebral tissue oxygen saturation (SctO2) values without the need for pre-calibration. We tested both FORE-SIGHT™ (five patients) and EQUANOX Advance™ (nine patients) technologies in the in-hospital as well as the out-of-hospital CPR setting. In this observational study, values were not utilized in any treatment protocol or therapeutic decision. An independent t-test was used for statistical analysis. RESULTS: Our data demonstrate the feasibility of both technologies to measure cerebral oxygen saturation during CPR. With the continuous, pulseless near-infrared wave analysis of both FORE-SIGHT™ and EQUANOX™ technology, we obtained SctO2 values in the absence of spontaneous circulation. Both technologies were able to assess the efficacy of CPR efforts: improved resuscitation efforts (improved quality of chest compressions with switch of caregivers) resulted in higher SctO2 values. Until now, the ability of CPR to provide adequate tissue oxygenation was difficult to quantify or to assess clinically due to a lack of specific technology. With both technologies, any change in hemodynamics (for example, ventricular fibrillation) results in a reciprocal change in SctO2. In some patients, a sudden drop in SctO2 was the first warning sign of reoccurring ventricular fibrillation. CONCLUSIONS: Both the FORE-SIGHT™ and EQUANOX™ technology allow non-invasive monitoring of the cerebral oxygen saturation during CPR. Moreover, changes in SctO2 values might be used to monitor the efficacy of CPR efforts.

Cerebral tissue oxygen saturation during therapeutic hypothermia in post-cardiac arrest patients.

AIM OF THE STUDY: This observational study was performed to assess the cerebral tissue oxygen saturation during and after therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest. METHODS: We performed a prospective observational study on the cerebral tissue oxygen saturation (SctO(2)) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO(2) (measured by near-infrared spectroscopy) was non-invasively and continuously measured in 28 post-cardiac arrest patients during hypothermia and active rewarming. RESULTS: At the start of mechanically induced TH, SctO(2) was 68% (65-72) and PaCO(2) was 47.2 mmHg (36.9-51.4). SctO(2) and PaCO(2) significantly decreased to 59% (57-64; p=0.006) and 36.6 mmHg (33.9-44.7; p=0.002), respectively, within the first 3h of mechanically induced TH. Cerebral tissue oxygen saturation was significantly lower in non-survivors (n=10) compared with survivors (n=18) at 3h after induction of hypothermia (p=0.02) while the decrease in PaCO(2) was similar in both groups. During TH maintenance, SctO(2) gradually returned to baseline values (69% (63-72)) at 24h, with no differences between survivors and non-survivors (p=0.65). Carbon dioxide remained within the range of mild hypocapnia (32-38 mmHg) throughout the hypothermic period. During rewarming, SctO(2) further increased to 71% (67-78). CONCLUSIONS: Induction of TH in comatose post-CA patients changes the balance between oxygen delivery and supply. The decrease in SctO(2) was less pronounced in patients surviving to hospital discharge.

The effect of anti-L-selectin (aselizumab) in multiple traumatized patients--results of a phase II clinical trial.

OBJECTIVE: The objectives of this study were to evaluate safety (primary) and clinical efficacy (secondary) of the humanized monoclonal anti-L-selectin antibody aselizumab in severely injured patients. DESIGN: Prospective phase II, parallel group, double-blind, randomized, placebo-controlled clinical trial. SETTING: Fourteen medical intensive care units or trauma units in level I trauma centers in Belgium, Germany, and Poland. PATIENTS: Eighty-four patients with a sustained trauma due to a blunt or penetrating injury and a total Injury Severity Scale score of > or =25. INTERVENTIONS: Patients received either aselizumab at dosages of 0.5, 1, or 2 mg/kg or placebo within 6 hrs of the traumatic event and were followed for 6 wks. MEASUREMENTS AND MAIN RESULTS: The number of expeditable adverse events increased dose dependently over the aselizumab groups compared with placebo. There were no statistically significant differences between all groups regarding leukopenia and risk of infection. No immunologic response following infusion of aselizumab was noted. The number of patients with multiple organ failure, defined as a median value of the total Goris Multiple Organ Failure score of > or =5 on > or =2 consecutive days within 14 days, was not significantly different for the 0.5 mg/kg, 1 mg/kg, 2 mg/kg, and placebo groups. There were no statistically significant differences in time of mechanical ventilation, length of stay in an intensive care unit, and total duration of hospitalization between treatment groups. CONCLUSIONS: Aselizumab was associated with a higher rate of infections and leucopenia; however, this difference was not significantly different compared with placebo. For all efficacy variables, aselizumab presented no significant trends but only a few scattered statistically significant differences between groups.