A clinical and EEG scoring system that predicts early cortical response (N20) to somatosensory evoked potentials and outcome after cardiac arrest.

BACKGROUND: Anoxic coma following cardiac arrest is a common problem with ethical, social, and legal consequences. Except for unfavorable somatosensory-evoked potentials (SSEP) results, predictors of unfavorable outcome with a 100% specificity and a high sensitivity are lacking. The aim of the current research was to construct a clinical and EEG scoring system that predicts early cortical response (N20) to somatosensory evoked potentials and 6-months outcome in comatose patients after cardiac arrest. METHODS: We retrospectively reviewed the records of all consecutive patients who suffered cardiac arrest outside our hospital and were subsequently admitted to our facility from November 2002 to July 2006. We scored each case based on early clinical and EEG factors associated with unfavorable SSEPs, and we assessed the ability of this score to predict SSEP results and outcome. RESULTS: Sixty-six patients qualified for inclusion in the cohort. Among them, 34 (52%) had unfavorable SSEP results. At day three, factors independently associated with unfavorable SSEPs were: absence of corneal (14 points) and pupillary (21 points) reflexes, myoclonus (25 points), extensor or absent motor response to painful stimulation (28 points), and malignant EEG (11 points). A score >40 points had a sensitivity of 85%, a specificity of 84%, and a positive predictive value (PPV) of 85% to predict unfavorable SSEP results. A score >88 points had a PPV of 100%, but a sensitivity of 18%. Overall, this score had an area under ROC curves of 0.919. In addition, at day three, a score > 69 points had a PPV of 100% with a sensitivity of 32% to predict death or vegetative state. CONCLUSION: A scoring system based on a combination of clinical and EEG findings can predict the absence of early cortical response to SSEPs. In settings without access to SSEPs, this score may help decision-making in a subset of comatose survivors after a cardiac arrest.

Angiotensin converting enzyme insertion/deletion genetic polymorphism: its impact on renal function in critically ill patients.

OBJECTIVE: Previous clinical studies have suggested an association between the insertion/deletion (I/D) genetic polymorphism of angiotensin converting enzyme and acute or chronic diseases. We aimed to test the prognostic value of the I-allele, which is associated with lower angiotensin converting enzyme activity, on acute kidney injury. DESIGN: Prospective 6-month noninterventional study. SETTING: Intensive care unit of a University Hospital. PATIENTS AND METHODS: One hundred eighty consecutive admitted white patients for an expected intensive care unit stay >48 hr. Angiotensin converting enzyme genetic polymorphism was screened for genotype (I/D polymorphism analysis by polymerase chain reaction amplification) and phenotype (measurement of the circulating rate of angiotensin converting enzyme by spectrophotometry). Acute kidney injury was assessed according to Risk, Injury, Failure, Loss, and End-stage Kidney classification. INTERVENTION: None. RESULTS: II, ID, and DD genotype frequencies were 25%, 48%, and 27%, respectively. II and ID genotypes were associated with lower baseline circulating rates of angiotensin converting enzyme (20 +/- 14 and 22 +/- 18 U/L, respectively, vs. 30 +/- 23 U/L for DD genotype; p = 0.04). Repartition of angiotensin converting enzyme genotypes were different in patients with and without acute kidney injury (p < 0.0001), with greater II genotype proportion in acute kidney injury patients (42% vs. 13% for those without acute kidney injury). After adjustment on the identified prognostic factors, II genotype was independently associated with increased risk of acute kidney injury (adjusted odds ratio, 6.5; 95% confidence interval, 2.4-17.7; p = 0.0002), then death among patients with acute kidney injury (adjusted odds ratio, 1.7; 95% confidence ratio, 1.1-2.6; p = 0.02). CONCLUSION: These data confirm the key role of the renin-angiotensin system to maintain glomerular filtration rate, and highlight an association between a genetic factor and susceptibility to and prognosis of acute kidney disease.

Hyperreninemic hypoaldosteronism syndrome, plasma concentrations of interleukin-6 and outcome in critically ill patients with liver cirrhosis.

OBJECTIVE: To investigate the relation between the adrenal production of gluco- and mineralocorticoids, the inflammatory status and the outcome in critically ill patients with liver cirrhosis. DESIGN: Prospective descriptive study. SETTING: Medical intensive care unit (ICU) in a university hospital. PATIENTS: Fifty consecutive patients with liver cirrhosis. INTERVENTIONS: A corticotropin stimulation test within 12h following ICU admission. Plasma cortisol concentration was measured before and after the test. Renin and aldosterone concentrations, as well as interleukin-6 (IL-6) level to assess the pro-inflammatory status, were measured only before the test. Impaired adrenal function was defined as cortisol response to the test less than 9microg/dl. Hyperreninemic hypoaldosteronism syndrome was defined as basal renin over aldosterone ratio (RRA) higher than 2. MEASUREMENTS AND RESULTS: Forty-one (82%) patients had impaired adrenal function, and 26 patients (52%) presented with RRA > 2. Patients with RRA > 2 exhibited greater disease severity and organ dysfunction scores at baseline, higher levels of serum renin and IL-6, and a greater ICU mortality rate, but risk-adjusted mortality rates were not different between the two groups. Renin and IL-6 plasma concentrations were positively correlated. Finally, in a Cox regression analysis, independent predictors of 30-day mortality were hyperreninemic hypoaldosteronism syndrome, IL-6 higher than 400pg/ml and severe renal failure. CONCLUSIONS: Adrenal dysfunction was common in critically ill cirrhotic patients. Hyperreninemic hypoaldosteronism syndrome was related to a greater pro-inflammatory status and degree of acute organ failure, and was independently associated with a worse prognosis.

Refractory shock and asystole related to tramadol overdose.

INTRODUCTION: Tramadol use is largely considered safe. However, several lethal cases of tramadol intoxication were reported, suggesting an underestimated toxicity. We report for a tramadol overdose case in combination with other central nervous system depressants, leading to refractory shock requiring extracorporeal life support. CASE REPORT: A 33-year-old man was admitted in our intensive care unit for drug intoxication with coma, seizures, and hypotension without signs of heart failure. A few hours later, he developed a ventricular tachycardia, followed by a brief cardiac arrest in asystole with refractory shock requiring an extracorporeal life support, vasopressors, and hemofiltration. With this aggressive support, his overall status gradually improved. Repeated echocardiography showed an improvement in the cardiac function. The patient was weaned off extracorporeal life support on day eight and discharged on day 12. On admission, a urine analysis, using gas chromatography-mass spectrometry, showed high peaks of tramadol and desmethyltramadol with the presence of hydroxyzine, gabapentine, and clonazepam. The tramadol blood concentration measured by the high-performance liquid chromatography method-diode array detector was 23.9 mg/L, much higher than many previously reported fatal overdoses. No other drugs with potential cardiac toxicity, such as beta-blockers, calcium antagonists, antiarrythmic, antidepressants, meprobamate, or other xenobiotics were detected. CONCLUSION: This case illustrates that tramadol overdose may cause refractory shock and asystole when taken in combination with CNS depressants, and reminds all physicians to be vigilant with regard to the potential toxic effects of tramadol.