Luc Huyghens

Mild hypothermia induced by a helmet device: a clinical feasibility study.

STUDY OBJECTIVEnTo test the feasibility and the speed of a helmet device to achieve the target temperature of 34 degrees C in unconscious after out of hospital cardiac arrest (CA).nnnMETHODSnPatients with cardiac arrest due to asystole or pulseless electrical activity (PEA) who remained unconscious after restoration of spontaneous circulation (ROSC) were enrolled in the study and randomised into two groups: a normothermic group (NG) and a hypothermic group (HG). Bladder and tympanic temperature were monitored every 15 min. A helmet device was used to induce mild hypothermia in the HG. Later on, the effect of mild hypothermia on the haemodynamics, electrolytes, lactate, arterial pH, CaO2, CvO2 and O2 extraction ratio were analysed and compared to the values obtained from the NG.nnnRESULTSnThirty patients were eligible for the study, 16 were randomised into the HG and 14 were randomised into the NG. The median tympanic temperature at admission in both groups was 35.5 degrees C (range: 33.3-38.5 degrees C) and the median tympanic temperature after haemodynamic stabilisation was 35.7 degrees C (range: 33.6-38.2 degrees C). In the HG, the core and the central target temperature of 34 degrees C were achieved after a median time of 180 and 60 min, respectively after ROSC. At the start of the study, no significant differences between the NG and HG were seen. At the end of the study, lactate concentration and O2 extraction ratio were significantly lower in the HG; however the CvO2 was significantly lower in the NG.nnnCONCLUSIONSnMild hypothermia induced by a helmet device was feasible, easy to perform, inexpensive and effective, with no increase in complications.

Elevated serum levels of S-100β protein and neuron-specific enolase are associated with brain injury in patients with severe sepsis and septic shock

Objective:We investigated whether serum levels of neuron-specific enolase (NSE) and S-100&bgr; protein could be used to evaluate cerebral injury and to predict outcome in severe sepsis and severe septic shock. Design:Prospective study. Setting:University hospital. Patients and Measurements:In 170 consecutively enrolled patients with severe sepsis and septic shock, serum S-100&bgr; and NSE were measured daily during four consecutive days after intensive care unit admission. Admission Glasgow Coma Scale before sedation and daily Sequential Organ Failure Assessment scores were recorded in all patients. Acute encephalopathy was defined as either a state of agitation, confusion, irritability, and convulsions (type A) or characterized by somnolence, stupor, and coma (type B) and persistently observed during 72 hrs after withdrawing sedation. When clinically indicated, contrast computed tomography or magnetic resonance imaging were performed to evaluate brain injury. Main Results:S-100&bgr; and NSE increased in, respectively, 72 (42%) and 90 (53%) patients. High biomarker levels were associated with the maximum Sequential Organ Failure Assessment scores (p = .001), and the highest values were found in patients who died early, within 4 days of inclusion (p = .005). Low consciousness encephalopathy type B was more frequently observed in patients with elevated S-100&bgr; (p = .004). S-100&bgr; levels of ≥4 &mgr;g/L were associated with severe brain ischemia or hemorrhage, and values of <2 &mgr;g/L were found in patients with diffuse cerebral embolic infarction lesions. High S-100&bgr; levels were associated with higher intensive care unit mortality (p = .04) and represented the strongest independent predictor of intensive care unit survival, whereas NSE and the Glasgow Coma Scale failed to predict fatal outcome. Conclusions:S-100&bgr; and NSE are frequently increased and associated with brain injury in patients with severe sepsis and septic shock. S-100&bgr; levels more closely reflected severe encephalopathy and type of brain lesions than NSE and the Glasgow Coma Scale.

Gastric emptying in critically ill patients is accelerated by adding cisapride to a standard enteral feeding protocol : results of a prospective, randomized controlled trial

OBJECTIVEnTo investigate the effect of cisapride, a relatively new prokinetic agent, on gastric emptying in critically ill patients.nnnDESIGNnProspective, randomized, controlled study.nnnSETTINGnAdult medical/surgical intensive care unit in a university hospital.nnnPATIENTSnTwenty-one consecutively enrolled patients, requiring prolonged mechanical ventilation and enteral feeding.nnnINTERVENTIONSnPatients were randomized to receive either no cisapride or 10 mg of cisapride four times daily, which was added to a standard enteral nutrition feeding protocol.nnnMEASUREMENTS AND MAIN RESULTSnGastric emptying was evaluated by daily measurements of gastric residue and on days 5 through 7 by bedside scintigraphy. Normal values for gastric clearance of a tracer-labeled test meal and for measurements obtained in the supine position were determined in ten healthy volunteers. The mean time at which 50% of the technetium 99m-labeled test meal was eliminated from the stomach (T 1/2) in this control group was 31 +/- 15 mins. In ten critically ill patients (enteral nutrition group), gastric emptying was markedly delayed after 5 to 7 days of enteral feeding (mean T 1/2 = 78 +/- 40 mins; p < .002 as compared with the control group). In contrast, patients treated with cisapride (cisapride group) showed an accelerated gastric emptying (mean T 1/2 = 18 +/- 7 mins; p > .05 as compared with controls; p < .005 as compared with enteral nutrition group). The mean gastric residue over a 1-wk period was also significantly lower in the cisapride group than in the enteral nutrition group (17.7 +/- 8.9 vs. 94.5 +/- 33.4 mL; p < .001).nnnCONCLUSIONSnThe data indicate that gastric emptying in critically ill, sedated, and mechanically ventilated patients can be significantly improved by adding cisapride to a routine enteral feeding protocol.

S-100 protein as early predictor of regaining consciousness after out of hospital cardiac arrest.

BACKGROUND AND PURPOSEnPatients resuscitated from cardiac arrest (CA) have a high mortality rate. Prognostic evaluation based on clinical observations is uncertain and would benefit from the use of biochemical markers of hypoxic brain damage. The purpose of the study was to validate the use of the serum astroglial protein S-100 levels at admission with regard to regaining consciousness after out of hospital CA.nnnMETHODSnFifty-eight patients resuscitated from out-of-hospital CA were followed up until they regained consciousness or until their death or permanent vegetative state occurred. Serum samples for measurement of S-100, using an immunoradiometric assay, were obtained at admission.nnnRESULTSnAt admission, the mean value+/-standard error of the mean of serum S-100 protein was significantly higher in patients who did not regain consciousness compared with patients who regained consciousness, respectively 4.66+/-0.61 microg/l and 0.84+/-0.21 microg/l. A serum S-100 value of >0.7 microg/l at admission was found to be a predictor that consciousness would not be regained, with a specificity of 85%, a sensitivity of 66.6%, a positive predictive value of 84%, a negative predictive value of 78% and an accuracy of 77.6%.nnnCONCLUSIONSnSerum S-100 protein at admission gives reliable and independent information concerning the short term neurological outcome after resuscitation; and could be a good marker of brain cell damage.

Open chest cardiopulmonary resuscitation in out-of-hospital cardiac arrest

Because closed chest cardiopulmonary resuscitation (CCCPR) achieve restoration of spontaneous circulation (ROSC) in less than 50% of cases, and because of the apparent physiological superiority of open-chest cardiopulmonary resuscitation (OCCPR), we evaluated OCCPR in out-of hospital cardiac arrest in cases who did not respond to standard external cardiopulmonary resuscitation with advanced life support. Over a period of 12 years, OCCPR was performed in 33 patients with out-of-hospital cardiac arrest arising from different causes, after unsuccessful attempts to achieve ROSC with CCCPR efforts over 7-121 min (median 25 min). With OCCPR, ROSC was achieved in 13/33 patients. Of these, two recovered to discharge (one with no neurological deficit and one with mild brain damage). The other 11 rearrested either in the emergency department after a median period of 70 min of resuscitation, or in the intensive care unit after a median period of 104 h. One case of iatrogenic cardiac injury was observed. The OCCPR attempts were well accepted by the public. Our data suggest that OCCPR is more effective than CCCPR in achieving ROSC outside hospital in patients with major cardiac disease and prolonged arrest. OCCPR is feasible in the out-of-hospital setting. Survival without neurological deficit cannot be expected when CCCPR with no-flow is continued beyond 25 min.

A prospective, open, single blind, randomized study comparing four analgesics in the treatment of peripheral injury in the emergency department.

&NA; The efficacy of four analgesics, distinct concerning analgesic power and mechanism of action, was evaluated for pain relief in patients suffering from single peripheral injury. Patients were randomly allocated to receive either propacetamol (the pro‐drug of paracetamol) 20 mg/kg i.v., piritramide 0.25 mg/kg i.m., tramadol 1 mg/kg i.v. or diclofenac 1 mg/kg i.v. Pain scores were measured by the patient using the visual analogue scale (VAS) and by an observer using a 4‐point verbal rating scale (VRS). Cardiorespiratory variables and side effects were recorded. One hundred and sixty patients were included, 131 completed the study. Groups matched for demography and baseline pain levels. In general pain scores decreased with time. No significant differences were found between groups at any particular time point. VAS scores were significantly (p < 0.02) lower than baseline scores 30 minutes after injection in all treatment groups except for the piritramide group where significance (p < 0.01) was reached after 60 minutes. VRS score analysis showed a similar trend although significances differed. In the piritramide group significantly more side effects were noted than in the other groups (p < 0.05). We conclude that intravenous propalcetaminil tramadol and diclofenac are equally efficatious for emergency analgesic treatment of single peripheral trauma.

Bedside Calculation of Energy Expenditure Does Not Guarantee Adequate Caloric Prescription in Long-Term Mechanically Ventilated Critically Ill Patients: A Quality Control Study

Nutrition is essential in critically ill patients, but translating caloric prescriptions into adequate caloric intake remains challenging. Caloric prescriptions (P), effective intake (I), and caloric needs (N), calculated with modified Harris-Benedict formulas, were recorded during seven consecutive days in ventilated patients. Adequacy of prescription was estimated by P/N ratio. I/P ratio assessed accuracy of translating a prescription into administered feeding. I/N ratio compared delivered calories with theoretical caloric needs. Fifty patients were prospectively studied in a mixed medicosurgical ICU in a teaching hospital. Basal and total energy expenditure were, respectively, 1361 ± 171u2009kcal/d and 1649 ± 233u2009kcal/d. P and I attained 1536 ± 602u2009kcal/d and 1424 ± 572u2009kcal/d, respectively. 24.6% prescriptions were accurate, and 24.3% calories were correctly administered. Excessive calories were prescribed in 35.4% of patients, 27.4% being overfed. Caloric needs were underestimated in 40% prescriptions, with 48.3% patients underfed. Calculating caloric requirements by a modified standard formula covered energy needs in only 25% of long-term mechanically ventilated patients, leaving many over- or underfed. Nutritional imbalance mainly resulted from incorrect prescription. Failure of “simple” calculations to direct caloric prescription in these patients suggests systematic use of more reliable methods, for example, indirect calorimetry.

Reversible cardiac failure in an adolescent after prolonged exposure to carbon monoxide

We describe the case of an adolescent who developed a severe but fully reversible cardiac dysfunction with low blood levels of carboxy haemoglobin (COHb = 10%) after a prolonged exposure to carbon monoxide. A 15-year-old male was admitted with a Glasgow Coma Scale of 8/15 with suspected postictal state and postanoxic encephalopathy. The cardiorespiratory failure which he developed soon after admission mandated mechanical ventilation, inotropic support and ultimately left ventricular support by intra-aortic balloon counterpulsation. The cardiac dysfunction was documented by radionuclide imaging and echocardiography. The patient fully recovered without neurological deficit. A low blood COHb concentration is a poor safety indicator since high tissue levels of accumulated carbon monoxide can be associated with coma and fulminant cardiorespiratory failure requiring advanced life support facilities.

Serum S100B Protein Could Help to Detect Cerebral Complications Associated with Extracorporeal Membrane Oxygenation (ECMO)

BackgroundTo investigate if serum S100B protein levels could early detect cerebral complications under treatment extracorporeal membrane oxygenation (ECMO).MethodsSerum S100B levels were measured over 5xa0days in 32 patients with cardiogenic and septic shock, including 15 patients who treated by ECMO and 17 who did not. Cerebral complications included hemorrhage, stroke, encephalopathy with myoclonus, and brain death. Delirium was identified by the positive Confusion Assessment Method in the ICU.ResultsS100B levels were elevated in 24/32 patients (75xa0%) at ICU admission. Five patients developed cerebral complications (2 hemorrhages with 1 brain death, 1 encephalopathy with myoclonus in the ECMO group and 2 strokes in the non-ECMO group). At day 5, S100B levels were higher in the 5 patients with cerebral complications than in the 27 without cerebral complications, regardless of ECMO (0.426 [0.421, 0.652] vs. 0.102 [0.085, 0.135] μg/L, pxa0=xa00.011). S100B levels were also more elevated in 3 patients with than in 12 without cerebral complications associated with ECMO (0.799 [0.325, 0.965] vs. 0.102 [0.09, 0.607] μg/L, pxa0=xa00.033). S100B levels were not associated with delirium after sedation withdrawal.ConclusionsMeasurement serum S100B could be useful to detect cerebral complications in deeply sedated patients associated with ECMO but not for monitoring delirium after sedation withdrawal.

Anticholinergic Treatment for Choreoathetosis in a Child After Induction with Propofol

We present a case of extrapyramidal side effects during administration of induction of anesthesia dose of propofol in a child and their treatment. A boy, 7 yr old, was admitted to the pediatric intensive care unit for supraventricular tachycardia. He had been electrically cardioverted previously using etomidate. No premeditation was given. During intravenous (IV) administration of propofol, he complained of pain on the injection site. This was accompanied by movements of the head, arms, and legs. After a dose of 3 mg/kg, the patient became unconscious and required mechanical ventilation via mask. He presented involuntary movements of the four limbs in a violent twisting motion, which necessitated restraining. A few minutes later, the movements were dystonic and choreiform with flexion, twist, or extension of the arms or legs. They were most often bilateral but not strictly symmetric. No trismus was present. No urine loss was observed. The dose of propofol was increased to 4 mg/kg, without changing the involuntary movements. The subsequent titrated administration of 18 mg etomidate did not alter these movements. Since the body motion hindered the safe performance of external electrical cardioversion, succinylcholine 25 mg IV was given. Once paralyzed, 30 joules were administered and prompt sinus rhythm occurred. Three minutes later, the extrapyramidal signs reappeared while the patient was unconscious and still required controlled ventilation. Biperiden 1 mg was slowly given IV. The movements disappeared within a few minutes. The patient regained spontaneous breathing and consciousness without any further adverse effects. He did not report (un)pleasant dreams or any awareness during the procedure. A higher incidence of spontaneous movements during induction of anesthesia with propofol was observed in children compared with adults (1,2). In seven out of seven children, Borgeat et al. (2) found spontaneous movements after induction with propofol (3 mg/kg followed by 0.1 mg . kg-’ * mini). These movements showed interindividual differences in intensity and lasted less than 50 s. The dystonic and choreiform nature of these movements and the absence of electroencephalographic abnormalities suggested a subcortical origin. In the above case, the involuntary movements lasted for several minutes and were successfully controlled by the injection of the anticholinergic drug. The latter suggests an effect of propofol at the level of the basal ganglia, where an imbalance between the cholinergic and dopaminergic activity can induce acute idiosyncratic dyskinesia including choreoathetosis. We did not observe a beneficial effect of increasing the dose from 3 to 4 mg/kg, although it was demonstrated that increasing the dose of propofol (to 5 mg/kg) reduces the incidence of the involuntary movements at induction (2). Excitatory adverse effects (including seizures) of propofol are known (3,4) and rare (5). Ries et al. (3) discussed the treatment strategy for nonepileptic excitatory events such as opisthotonos suggesting the use of diazepam or physostigmine to restore the neuronal inhibition by glycine and y-aminobutyric acid to counteract these phenomena. In this case, neither opisthotonos nor tonic-clonic movements were present and administration of etomidate, increasing GABA-ergic inhibitory action, did not alter the clinical presentation. We conclude that an induction dose of propofol may induce choreoathetosis-like movements in children, which in rare cases may be severe and may last for several minutes, possibly leading to physical harm if the patient is not restrained. Treatment with an anticholinergic drug can quickly result in the disappearance of this side effect.