Induced hypothermia in comatose survivors of asphyxia: a case series of 14 consecutive cases.

BACKGROUND: Induced hypothermia is widely used for comatose survivors of cardiac arrest. Other causes of hypoxic brain injury carry a poor prognosis when treated using traditional methods. At our hospital, hypothermia has also been used for the management of all comatose survivors of asphyxiation. The aim of the present study was to report the results of the management of these patients. METHODS: Hospital charts of all patients admitted unconscious after asphyxiation during a 7-year period were reviewed. This included patients after hanging, drowning, carbon monoxide intoxication and other gas intoxications. In all patients, hypothermia with a target temperature of 32-34 degrees C was induced with external or intravascular cooling for 24 h. The primary outcome was neurologic function at discharge. RESULTS: Fourteen male patients were treated with hypothermia, eight after hanging, three after drowning, two after carbon monoxide intoxication and one after methane intoxication. All were deeply comatose (Glasgow Coma Score 3-5) on arrival to hospital. Nine had been resuscitated from cardiac arrest. There were nine survivors (65%), all with good neurological recovery (Cerebral Performance Category 1-2). Four out of five non-survivors showed cerebral edema already on arrival computed tomographic (CT) scan while none of the nine survivors did. CONCLUSIONS: The results of this study suggest that an early abnormal CT scan of the brain in patients resuscitated after asphyxiation carries an adverse prognosis. The favorable outcome of the patients in the present study suggests that a randomized clinical trial on the use of induced hypothermia in patients exposed to severe asphyxia might be warranted.

Outcome, timing and adverse events in therapeutic hypothermia after out-of-hospital cardiac arrest.

BACKGROUND: Therapeutic hypothermia (TH) after cardiac arrest protects from neurological sequels and death and is recommended in guidelines. The Hypothermia Registry was founded to the monitor outcome, performance and complications of TH. METHODS: Data on out-of-hospital cardiac arrest (OHCA) patients admitted to intensive care for TH were registered. Hospital survival and long-term outcome (6-12 months) were documented using the Cerebral Performance Category (CPC) scale, CPC 1-2 representing a good outcome and 3-5 a bad outcome. RESULTS: From October 2004 to October 2008, 986 TH-treated OHCA patients of all causes were included in the registry. Long-term outcome was reported in 975 patients. The median time from arrest to initiation of TH was 90 min (interquartile range, 60-165 min) and time to achieving the target temperature (< or =34 degrees C) was 260 min (178-400 min). Half of the patients underwent coronary angiography and one-third underwent percutaneous coronary intervention (PCI). Higher age, longer time to return of spontaneous circulation, lower Glasgow Coma Scale at admission, unwitnessed arrest and initial rhythm asystole were all predictors of bad outcome, whereas time to initiation of TH and time to reach the goal temperature had no significant association. Bleeding requiring transfusion occurred in 4% of patients, with a significantly higher risk if angiography/PCI was performed (2.8% vs. 6.2%P=0.02). CONCLUSIONS: Half of the patients survived, with >90% having a good neurological function at long-term follow-up. Factors related to the timing of TH had no apparent association to outcome. The incidence of adverse events was acceptable but the risk of bleeding was increased if angiography/PCI was performed.

Scandinavian clinical practice guidelines for therapeutic hypothermia and post-resuscitation care after cardiac arrest.

BACKGROUND AND AIM: Sudden cardiac arrest survivors suffer from ischaemic brain injury that may lead to poor neurological outcome and death. The reperfusion injury that occurs is associated with damaging biochemical reactions, which are suppressed by mild therapeutic hypothermia (MTH). In several studies MTH has been proven to be safe, with few complications and improved survival, and is recommended by the International Liaison of Committee on Resuscitation. The aim of this paper is to recommend clinical practice guidelines for MTH treatment after cardiac arrest from the Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI). METHODS: Relevant studies were identified after two consensus meetings of the SSAI Task Force on Therapeutic Hypothermia (SSAITFTH) and via literature search of the Cochrane Central Register of Controlled Trials and Medline. Evidence was assessed and consensus opinion was used when high-grade evidence (Grade of Recommendation, GOR) was unavailable. A management strategy was developed as a consensus from the evidence and the protocols in the participating countries. RESULTS AND CONCLUSION: Although proven beneficial only for patients with initial ventricular fibrillation (GOR A), the SSAITFTH also recommend MTH after restored spontaneous circulation, if active treatment is chosen, in patients with initial pulseless electrical activity and asystole (GOR D). Normal ethical considerations, premorbid status, total anoxia time and general condition should decide whether active treatment is required or not. MTH should be part of a standardized treatment protocol, and initiated as early as possible after indication and treatment have been decided (GOR E). There is insufficient evidence to make definitive recommendations among techniques to induce MTH, and we do not know the optimal target temperature, duration of cooling and rewarming time. New studies are needed to address the question as to how MTH affects, for example, prognostic factors.

Brain natriuretic peptide is a good predictor for outcome in cardiac surgery.

BACKGROUND AND AIM: The heart secretes brain natriuretic peptide (BNP) in response to myocardial stretch. The aim of this study was to determine whether adverse effects after cardiac surgery were associated with higher serum BNP levels pre-operatively. METHODS: One hundred and thirty-five patients undergoing various cardiac procedures were included in the study, and N-terminal pro-BNP (NT-pro-BNP) was measured pre-operatively. Post-operative complications were defined as follows: (i) a post-operative length of stay in the intensive care unit (ICU) exceeding 48 h; (ii) mortality at 28 days; (iii) the need for inotropic agents and/or intra-aortic balloon pump (IABP); and (iv) renal failure. Serum NT-pro-BNP values were compared for patients with and without complications. The serum NT-pro-BNP level was also correlated with the euroSCORE and ejection fraction (EF). RESULTS: Pre-operative serum NT-pro-BNP levels were significantly higher in patients with an ICU length of stay of more than 2 days or death prior to post-operative day 28 (3118 ng/l vs. 705 ng/l; P < 0.001). Pre-operative serum NT-pro-BNP levels were also significantly higher in patients needing inotropic agents (2628 ng/l vs. 548 ng/l; P < 0.001) or IABP insertion (3705 ng/l vs. 935 ng/l; P = 0.001) or developing renal failure (2857 ng/l vs. 945 ng/l; P < 0.001) post-operatively. The correlation between the serum NT-pro-BNP level and euroSCORE was good (r = 0.658; P < 0.001). The receiver operating characteristic (ROC) curves were used to assess the ability of serum NT-pro-BNP, euroSCORE and EF to predict outcome after cardiac surgery. This revealed an area under the ROC curve for the length of stay in the ICU or mortality at 28 days of 0.829 for serum NT-pro-BNP, 0.814 for euroSCORE and 0.328 for EF assessed by transesophageal echocardiography, indicating that the pre-operative serum NT-pro-BNP level is a good prognostic indicator for outcome after cardiac surgery. CONCLUSION: Serum NT-pro-BNP is a good predictor for complications after cardiac surgery, and is as good as euroSCORE and better than EF.

Training trauma teams in the Nordic countries: an overview and present status.

BACKGROUND: During the last decade there has been an increased interest in the organisation and quality of trauma care in the Nordic countries. Still, most patients are initially cared for at hospitals with low caseloads of severe trauma. More than 200 hospitals offer initial care to trauma patients. Training of trauma teams using simulators or simulated patients has evolved in the same period, as one important factor to overcome lack of practical training. This overview describes the present state of trauma team training in the Nordic countries. METHODS: Members of a Nordic working group on the use of simulation in medicine reviewed present literature on training with simulation and described the present use of team training in their own countries during winter 2004. RESULTS: There is an increasing amount of evidence indicating that training of teams with simulation reduces treatment errors and improves performance. The training activities do not need to be complex, but skilled debriefing seems necessary. Few Nordic hospitals train their trauma teams. The training activities vary considerably between and within countries. CONCLUSION: There is considerable evidence supporting an increased use of experience gained in other high-risk domains where training in communication, leadership and decision-making is the focus for safety and improvement efforts. There is a need for more widespread training of trauma teams. The different training activities actually undertaken should be scientifically evaluated.

Atrial natriuretic peptide attenuates pacing-induced myocardial ischemia during general anesthesia in patients with coronary artery disease.

UNLABELLED: Atrial natriuretic peptide (ANP) exerts a dilatory effect on coronary arteries in humans. We investigated the effects of ANP on pacing-induced myocardial ischemia during enflurane anesthesia in patients with coronary artery disease (CAD). In 20 patients with CAD, myocardial ischemia was induced by atrial pacing before and after an i.v. infusion of ANP (50 mg x kg(-1) min(-1), n = 10) or placebo (n = 10). We studied the effects of ANP or placebo on pacing-induced changes in central hemodynamics, myocardial blood flow and regional myocardial indices of lactate uptake (RMLU), and oxygen consumption (RMVO2) and extraction (RMO2E). ST-segment depression was less pronounced during pacing with ANP compared with control pacing (-0.09 +/- 0.01 vs -0.24 +/- 0.02 mV; P < 0.001). RMLU decreased to -11.1 micromol/min during control pacing compared with -0.7 micromol/min during pacing with ANP (P < 0.01). ANP did not affect pacing-induced changes in RMVO2, RMO2E, or the rate pressure product. Placebo did not affect pacing-induced changes in ST-segment depression or RMLU. In conclusion, ANP attenuates ischemic ST-segment depression and lactate release during pacing-induced myocardial ischemia in patients with CAD. The antiischemic effect of ANP was not accompanied by any improvement in the regional myocardial oxygen supply/demand relationship. IMPLICATIONS: We evaluated the effects of i.v. atrial natriuretic peptide (50 ng x kg(-1) x min(-1)) on pacing-induced myocardial ischemia during general anesthesia in patients with coronary artery disease. In contrast to placebo, atrial natriuretic peptide attenuated ST-segment depression and myocardial lactate production and improved left ventricular function during pacing-induced ischemia.

Myocardial circulatory and metabolic effects of atrial natriuretic peptide after coronary artery bypass grafting.

The purpose of this study was to examine the effects of incremental infusion rates of human atrial natriuretic peptide (ANP), 25, 50, 100 ng.kg-1. min-1, on myocardial blood flow and metabolism (n = 10), and to compare the effects of ANP on these variables with those of equipotent infusion rates of sodium nitroprusside (SNP) (n = 9) 1-3 h after coronary artery bypass grafting (CABG). ANP induced a dose-dependent decrease in mean arterial blood pressure and systemic vascular resistance. There were no changes in cardiac index, heart rate, or cardiac filling pressures. ANP caused no changes in myocardial blood flow or its distribution, and caused no changes in myocardial oxygen extraction. Regional myocardial lactate uptake (RMLU) and extraction (RMLE) increased significantly (P < 0.05) at 50 ng.kg-1.min-1 (10.2 +/- 3.8 mumol/min and 8.2% +/- 3.0%, respectively) as compared to control (-1.1 +/- 3.0 mumol/min and -1.3% +/- 3.3%, respectively). RMLE and RMLU were significantly (P < 0.05) higher with ANP (5.7% +/- 2.5% and 6.8 +/- 3.7 mumol/min, respectively) compared to SNP (-1.5% +/- 2.1% and -0.1 +/- 3.7 mumol/min, respectively). We conclude that ANP has no dilatory effects on coronary vascular resistance vessels and thus lacks the potential to maldistribute flow, and that ANP improves myocardial lactate metabolism after CABG.

Effects of atrial natriuretic peptide on acute renal impairment in patients with heart failure after cardiac surgery.

OBJECTIVE: To investigate the effects of IV infusion of atrial natriuretic peptide (human ANP 1-28) on renal function in patients with acute heart failure and renal impairment after cardiac surgery. DESIGN: Pharmocodynamic dose-effect investigation. SETTING: Cardiothoracic Intensive Care Unit of a university hospital. PATIENTS: Twelve patients (mean age 68 years, range 44-78 years) treated with inotropic drugs and an intra-aortic balloon pump (n = 8) were studied 1-3 days after cardiac surgery. Patients had acute renal impairment, defined as a rise in serum creatinine of more than 50% compared to preoperative values. Patients were receiving dopamine and furosemide infusion to increase urine flow. INTERVENTIONS: Baseline measurements of glomerular filtration rate (GFR) and renal blood flow (51Cr-EDTA and PAH clearance) were first performed during two 30-min periods. ANP was then administered for two consecutive 30-min periods (25 and 50 ng/kg per min), followed by two control periods. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure decreased by 6% at the highest ANP dose. Urine flow, GFR and RBF increased 62%, 43% and 38%, respectively, while renal vascular resistance decreased 30%. At this dose level, circulating ANP concentrations were on the average eight fold higher than preinfusion levels. CONCLUSIONS: ANP improved renal function and decreased elevated renal vascular resistance in patients with renal dysfunction after cardiac surgery. The improvement in renal blood flow and glomerular filtration rate may be of potential therapeutic value to prevent or treat exaggerated renal vasoconstriction in patients with acute renal impairment following cardiac surgery.

Effects of atrial natriuretic peptide on renal function after cardiac surgery and in cyclosporine-treated heart transplant recipients.

The study investigated the effects of intravenous infusion of atrial natriuretic peptide (human ANP 99-126) on renal function and central hemodynamics after coronary artery bypass grafting (CABG), and the ability of ANP to reverse the acute nephrotoxic effects of cyclosporine after heart transplantation. Ten patients with an EF > 0.5 and normal renal function were studied 2 to 4 hours after CABG surgery. Furthermore, six heart transplant recipients receiving cyclosporine for immunosuppression who developed renal dysfunction 2 to 4 days after transplantation were studied. Standard urinary clearance of 51Cr-EDTA and PAH was used to study the effects of ANP on glomerular filtration rate (GFR) and renal blood flow (RBF). Baseline measurements were first performed during two 30-minute periods. Incremental infusion rates of ANP were then administered for three consecutive 30-minute periods (25, 50, and 100 ng/kg/min), followed by two 30-minute post-ANP control periods. Marked increases in urinary flow (UF), GFR, filtration fraction (FF), and fractional urinary excretion of Na+ were observed in the CABG patients with increasing doses of ANP, while RBF was unchanged. Mean arterial pressure decreased by around 15% at the highest ANP dose. In the heart transplant recipients, baseline GFR was markedly reduced compared to pretransplantation values (-65%). UF, GFR, and RBF increased 240%, 69%, and 53%, respectively, while renal vascular resistance decreased 45% during the highest dose of ANP infused. At this ANP dose level, circulating ANP concentrations were sixfold to eightfold higher than the preinfusion control level.(ABSTRACT TRUNCATED AT 250 WORDS)