Early achievement of mild therapeutic hypothermia and the neurologic outcome after cardiac arrest.

BACKGROUND: Mild therapeutic hypothermia (MTH) achieved by endovascular cooling has emerged as a new treatment strategy to reduce hypoxic brain injury after cardiac arrest (CA). It remains to be established how the time interval between CA and MTH impacts the neurologic outcome. We hypothesized that a more rapid achievement of MTH (time to target temperature [TTT], time to coldest temperature [TCT]) improves the outcome after CA. METHODS: Forty-nine consecutive patients successfully resuscitated from CA were enrolled. MTH with a body core temperature between 32.0 and 34.0 degrees C (target temperature: 33.0 degrees C) over 24 h was achieved using a closed-loop endovascular system. Based on the neurologic outcome at discharge, the patient group was dichotomized into good (no/mild cerebral disability) and poor (severe disability, coma/vegetative state, brain death) outcomes. Serum neurone specific enolase (NSE) as biochemical marker of brain damage was sampled at 24, 48, and 72 h after CA. RESULTS: Twenty-eight patients were discharged with a good outcome. Multivariate stepwise regression showed TTT (odds ratio for every h TTT: 0.69 [95% confidence interval: 0.51-0.98]) or, if entered into the model, TCT (odds ratio for every h TCT: 0.72 [95% confidence interval: 0.56-0.94]) to be independent predictors for good outcome. Further independent determinants were age, BMI, asystole as presenting rhythm, and thrombolysis during resuscitation. However, TCT was the only variable to correlate with maximum NSE values after CA (r=0.32, P<0.05). CONCLUSIONS: Early achievement of MTH by endovascular cooling appears to reduce hypoxic brain injury and to favour a good neurologic outcome after CA.

MARS dialysis in decompensated alcoholic liver disease: a single-center experience.

Acute decompensation of chronically stable alcoholic liver disease (ALD) is the most common cause of terminal liver failure in developed countries. Molecular adsorbent recirculation system (MARS) is increasingly used as artificial liver support to facilitate spontaneous organ recovery. However, the experience to date and the evidence to justify this therapeutic strategy in acutely decompensated ALD are still insufficient. We report our clinical experience with MARS in 14 patients with acutely decompensated ALD (6 male subjects; median age [interquartile range], 51 [47-56] years; Child-Pugh score, 12 [10-13]; Acute Physiology and Chronic Health Evaluation (APACHE) II score, 20 [18-24]) and severely impaired liver function whose disease was unresponsive to conventional supportive care. At least 3 sessions were applied in any patient (48 sessions in total). Under MARS treatment, the following levels decreased: bilirubin (544 [489-604] to 242 [178-348] micromol/L; P<0.001), creatinine (212 [112-385] to 91 [66-210] micromol/L; P=0.002), cholestatic parameter gamma-glutamyl transpeptidase (5.9 [1.8-13.1] to 4.6 [1.8-8.3] micromol/L) (P<0.001), blood urea nitrogen (56 [32-91] to 34 [21-68] mmol/L; P=0.044), and platelet count (176 [85-241] to 84 [31-145] Gpt/L; P=0.004). In contrast, MARS failed to improve daily urine output (P=0.846), ammonia levels (P=0.340), or thromboplastin time (P=0.775). Only 3 patients survived the hospital stay (mortality 78.6%). Although MARS improved laboratory parameters of hepatic detoxification and renal function in patients with acutely decompensated ALD, the patients' mortality remained unsatisfactorily high. Our experience does not support the indiscriminative use of MARS in acutely decompensated ALD without further controlled studies.

Severe septic inflammation as a strong stimulus of myocardial NT-pro brain natriuretic peptide release.

BACKGROUND: Septic shock (SS) has recently been identified as stimulus of N-terminal pro-brain natriuretic peptide (NT-proBNP) release. We tested whether SS mediates NT-proBNP release through cardiomyocyte necrosis. Moreover, the discriminative value of NT-proBNP for the distinction between SS and non-septic shock (NSS) was assessed. METHODS: The study included 50 ICU patients with SS (n=25) and NSS (n=25), 40 patients with acute coronary syndrome and elevated troponin-I (ACStrop+) and 16 patients with unstable angina and normal troponin-I (UAtrop-). Eleven subjects without inflammation or cardiac disease served as controls. NT-proBNP levels of coronary patients were measured on admission, those of ICU patients 48 h after onset of shock symptoms. RESULTS: ACStrop+ (1525 [25th-75th percentile: 790-3820] pg/L) and NSS (687 [254-1552]) patients showed increased NT-proBNP levels above those of UAtrop- patients (107 [43-450], p<0.001) and controls (52 [42-99], p<0.001), but SS patients exhibited still higher levels (11,335 [4716-25,769], p<0.001 vs all others). Among ICU patients with shock symptoms, NT-proBNP discriminated SS and NSS with high sensitivity and specificity (area under ROC curve: 0.946 [95% confidence interval, 0.872-1.019]). NT-proBNP correlated with troponin-I, as marker of cardiomyocyte damage, among ACStrop+ (p<0.001) and SS patients (p=0.013). But, whereas SS patients showed the greatest NT-proBNP values, ACStrop+ patients had higher troponin-I levels (p<0.001), suggesting different mechanisms by which myocardial ischemia and SS mediate NT-proBNP release. CONCLUSIONS: SS is a more potent stimulus of NT-proBNP release than myocardial ischemia. NT-proBNP reliably distinguishes SS from other forms of shock. SS-related NT-proBNP release appears to involve cardiomyocyte damage but not genuine cardiomyocyte necrosis.

Acute reversible cardiomyopathy with cardiogenic shock in a patient with Addisonian crisis: a case report.

A 42 year-old female, admitted to the ICU, with Addisonian crisis developed acute cardiopulmonary failure after hydrocortisone therapy was initiated. An echocardiogram showed severe reduction in the left-ventricular ejection fraction. Additionally, profound ECG abnormalities with diffuse ST-elevation and decreased QRS-amplitudes occurred, whereas Troponin-I was only moderately increased. Chest X-ray displayed bilateral pulmonary edema. The patient's condition culminated in respiratory failure and cardiogenic shock requiring catecholamines and ventilatory support. After a week, she had recovered uneventfully.