Neurologic causes of cardiac arrest and outcomes.

BACKGROUND: Sudden cardiac arrest as a complication of neurologic disorders is rare, occasionally acute neurologic events present with cardiac arrest as initial manifestation. OBJECTIVE: Our aim was to describe neurologic disorders as a cause of cardiac arrest in order to enable better recognition. METHODS: We retrospectively analyzed prospectively collected resuscitation data of all patients treated between 1991 and 2011 at the emergency department after cardiac arrest caused by a neurologic event, including diagnosis, therapy, and outcomes. RESULTS: Over 20 years, 154 patients suffered cardiac arrest as a result of a neurologic event. Out-of-hospital cardiac arrest occurred in 126 (82%) patients, 78 (51%) were male, median age was 51 years (interquartile range 17 to 89 years). As initial electrocardiogram rhythm, pulseless electrical activity was found in 77 (50%) cases, asystole in 61 (40%), and ventricular fibrillation in 16 (10%) cases. The most common cause was subarachnoid hemorrhage in 74 (48%) patients, 33 (21%) patients had intracerebral hemorrhage, 23 (15%) had epileptic seizure, 11 (7%) had ischemic stroke, and 13 (8%) had other neurologic diseases. Return of spontaneous circulation was achieved in 139 (90%) patients. Of these, 22 (14%) were alive at follow-up after 6 months, 14 (9%) with favorable neurologic outcome, 8 of these with epileptic seizure, and most of them with history of epilepsy. CONCLUSIONS: Subarachnoidal hemorrhage is the leading neurologic cause of cardiac arrest. Most of the patients with cardiac arrest caused by neurologic disorder have a very poor prognosis.

Cardiac arrest caused by acute intoxication-insight from a registry.

INTRODUCTION: The aim of the study was to evaluate the epidemiology and outcome after cardiac arrest caused by intoxication. METHODS: A retrospective analysis of 1991 to 2010 medical record of patients experiencing cardiac arrest caused by self-inflicted, intentional intoxication was performed. The setting was an emergency department of a tertiary care university hospital. The primary end point was the presentation of epidemiologic data in relation to favorable neurologic outcome, defined as cerebral performance categories 1 or 2 and 180-day survival. Furthermore, the patients were subdivided into a single-substance and polysubstance group, depending on the substances causing the intoxication. RESULTS: Of 3644 patients admitted to our department, 99 (2.7%) with a median age of 26 (interquartile range, 19-42) years (37% female) were included. Cardiac arrest was witnessed in 62 cases (63%). Eleven patients (11%) received basic life support by bystanders, and 11 (11%) had a shockable rhythm in the initial electrocardiogram. The combined end point "good survival" was achieved by 34 patients (34%). Cardiac arrest occurred out of hospital in 73 patients (74%) and in-hospital in 26 patients (26%). A single substance causing the intoxication was found in 56 patients (56%). Opiates were the leading substance, with 25 patients (25%) using them. CONCLUSION: Cardiac arrest caused by intoxication is found predominately in young patients. Overall, favorable neurologic survival was achieved in 34%. Opiate-related cardiac arrest was associated with poor survival and a high incidence of neurologic deficits.

The effect of percutaneous coronary intervention in patients suffering from ST-segment elevation myocardial infarction complicated by out-of-hospital cardiac arrest on 30 days survival.

AIM OF THE STUDY: To question the beneficial effects of the recommended early percutaneous coronary intervention (PCI) after out-of-hospital cardiac arrest on 30-day survival with favourable neurological outcome. METHODS: Prospectively collected data of 1277 out of hospital cardiac arrest patients between 2005 and 2010 from a registry at a tertiary care university hospital were used for a cohort study. RESULTS: In 494 (39%) arrest patients ST-segment elevation was identified in 249 (19%). Within 12h after restoration of spontaneous circulation catheter laboratory investigations were initiated in 197 (79%) and PCI in 183 (93%) (78% got PCI in less than 180 min). Adjustment for a cumulative time without chest compressions <2 min, initial shockable rhythm, cardiac arrest witnessed by healthcare professionals, and a higher core temperature at time of hospitalization reduced the effect of PCI on favourable neurological outcome at 30 days (OR 1.40; 95% CI, 0.53-3.7) compared to the univariate analysis (OR 2.52; 95% CI, 1.42-4.48). CONCLUSION: This cohort study failed to demonstrate the beneficial effects of PCI as part of post-resuscitation care on 30-day survival with a favourable neurological outcome.

Causes of in-hospital cardiac arrest and influence on outcome.

AIM OF THE STUDY: To evaluate the relationship between cause and outcome of in-hospital cardiac arrest. METHODS: Retrospective analysis of resuscitation data, causes of cardiac arrest and outcome with a follow-up to 6 months of a cardiac arrest registry in an emergency department of a tertiary care hospital, covering a 17.5-year period. RESULTS: Of 1041 patients, 653 were male (63%), the median age was 64 years (IQR 53-73), 51% suffered cardiac arrest in the emergency department. The first recorded rhythm showed PEA in 432 (41%), ventricular fibrillation in 404 (39%) and asystole in 205 (20%) patients. Cardiac arrest of cardiac origin occurred in 63% of all patients, with 35% of them due to acute myocardial infarction. Non-cardiac causes were mostly due to pulmonary causes (15% of all patients). Aortic dissection/rupture, exsanguination, intoxication and adverse drug reactions, metabolic, cerebral, sepsis and accidental hypothermia each ranged between 1 and 4% of the cohort. Of all patients, 376 (36%) were discharged in good neurologic condition. Overall, patients with cardiac causes had a significantly better outcome than those with non-cardiac causes (44% vs. 23%, p<0.01). Patients with pulmonary causes survived in 24%. The other subgroups showed widely divergent survival results (3-65%). Patients who had suffered cardiac arrest in the emergency department had a better outcome then patients of the regular ward or radiology department. CONCLUSION: In hospital cardiac arrest is caused mainly by cardiac and pulmonary causes, outcome depends on the cause, with a big variability.

Cardiopulmonary resuscitation-associated major liver injury.

AIM: To evaluate the frequency, presentation, treatment and outcome of cardiopulmonary resuscitation-associated major liver injury in patients after non-traumatic in- or out-of-hospital cardiac arrest. MATERIALS AND METHODS: Retrospective analysis of a cardiac arrest registry in a tertiary care hospital emergency department. We reviewed patients charts, laboratory data, diagnostic imaging studies and autoptic findings. RESULTS: Within 14.5 years, major liver injury (rupture/laceration, haemorrhage/haematoma) was found in 15 of 2558 cardiac arrest victims (0.6%). Eleven were male (73%), median age was 58 (IQR 53-67). In seven, resuscitation was started out-of-hospital. In 9 of the 15 patients, liver injury was correctly diagnosed intra vitam. In 5, haematocrit level was low on admission, in 8 haematocrit dropped significantly during observation; haemostasis was compromised in 13 patients, 4 of them receiving thrombolytic therapy. Bedside abdominal sonography showed free intra-peritoneal fluid in 8 of 9 cases examined. In 11 patients, we found liver rupture/laceration, in 4 liver haemorrhage/haematoma. The site of injury was the left liver lobe in 11, six underwent emergent surgery. Two of 15 patients survived to 6 months in good neurological condition, 1 after emergency surgery. No patient died from bleeding due to liver injury. CONCLUSION: Our single centre observation confirms that resuscitation-associated major liver injury is infrequent and shows that most patients had compromised haemostasis. Low or dropping haematocrit should trigger suspicion. Bedside sonography reveals intra-peritoneal fluid or liver injury. A conservative therapeutic approach or emergency surgery may be warranted. Major liver injury alone scarcely appears to influence overall outcome.

Non-traumatic aortic dissection or rupture as cause of cardiac arrest: presentation and outcome.

OBJECTIVE: To evaluate the frequency, presentation and outcome of non-traumatic aortic dissection/rupture as a cause of cardiac arrest. DESIGN: Retrospective analysis of a cardiac arrest registry in a tertiary care hospital emergency department. RESULTS: Over 11.5 years, aortic dissection/rupture was identified as the immediate cause of cardiac arrest in 46 (2,3%) out of 1990 patients with sudden cardiac arrest, primarily affecting the abdominal aorta in 25 and the thoracic aorta in 21 cases. The characteristics of the 46 patients were as follows: male gender (74%), median age 71 years (IQR 59-76), high co-morbidity (89%), previously known aortic aneurysm (33%), pulseless electric activity (70%) as initial cardiac rhythm. When performed, bedside abdominal sonography or echocardiography was almost always diagnostic. Patients with abdominal aortic dissection/rupture had abdominal (52%) and/or flank pain (32%). Patients with thoracic aortic dissection/rupture complained of chest pain (48%) or dyspnoea (19%). Return of spontaneous circulation occurred in 12 (26%) of 46 patients, emergency surgery was performed in eight of these patients, 2 (4%) survived to discharge in good neurological condition. CONCLUSIONS: Cardiac arrest caused by aortic dissection/rupture is rare, and mortality remains very high, even when circulation can be restored initially. Common features such as previously known aortic aneurysm, old age, male gender and pulseless electrical activity as initial cardiac rhythm should increase suspicion of the condition.

Major bleeding complications in cardiopulmonary resuscitation: the place of thrombolytic therapy in cardiac arrest due to massive pulmonary embolism.

OBJECTIVE: Thrombolytic therapy in patients with massive pulmonary embolism (MPE) and prolonged cardiopulmonary resuscitation (CPR) is subject to debate. This study was performed to determine whether (1) thrombolytic treatment increases the risk of bleeding complications, (2) if the risk of bleeding is influenced by the duration of CPR and if (3) thrombolytic therapy improves outcome. DESIGN: Retrospective cohort study. SETTING: Emergency department of a tertiary care university hospital. PATIENTS AND METHODS: Sixty-six patients with cardiac arrest (CA) due to MPE admitted between July 1993 and December 2001. Thirty-six patients received thrombolysis (TL) and were compared with 30 patients without thrombolytic therapy. Bleeding complications were assessed by clinical evidence or autopsy. RESULTS: Major bleeding complications appear to occur more frequently in patients treated with thrombolytics (9/36 (25%) vs. 3/30 (10%)) even though the difference was statistically not significant (P=0.15). It appears that CPR duration >10 min has no adverse impact on major bleeding complications. No difference in the rate of major bleeding complications between thrombolyzed patients who had a CPR duration of 10 min could be observed (2/8 (25%) vs. 7/28 (25%), P=0.99). In thrombolyzed patients a return of spontaneous circulation could be achieved more frequently (24/36 (67%) vs.13/30 (43%) in controls, P=0.06) and survival after 24 h was higher (19/36 (53%) vs. 7/30 (23%), P=0.01). Survival to discharge was also higher in the TL group (7/36 (19%) vs. 2/30 (7%)), but not statistically significant (P=0.15). CONCLUSION: Although severe bleeding complications tend to occur more frequently in patients undergoing TL, the benefit of this treatment might outweigh the risk of bleeding.

Clinical signs of pulmonary congestion predict outcome in patients with acute chest pain.

BACKGROUND: Pulmonary congestion is associated with poor outcome in patients with acute coronary syndromes. In consecutive patients presenting with acute unexplained chest pain to a primary care facility, the prognostic impact of pulmonary congestion is indeterminate. Therefore, we assessed the predictive value of clinical signs of pulmonary congestion in patients presenting with acute chest pain to an emergency department with regard to the origin of the symptoms. METHODS: 1288 consecutive patients with acute chest pain were prospectively assessed for clinical signs of pulmonary congestion. The diagnosis was confirmed by chest radiography. The association of pulmonary congestion and short- and intermediate-term mortality in patients with coronary (n = 381) and non-coronary (n = 907) causes of chest pain was determined using multivariate Cox regression analysis. RESULTS: 108 (8%) patients had clinical signs of pulmonary congestion. Within the mean follow-up period of 23 months (SD 4) 67 patients died, mainly within the first 6 months. Of 108 patients with pulmonary congestion, 82 (76%) had coronary and 26 (24%) had non-coronary chest pain. Pulmonary congestion was independently associated with mortality in patients with coronary chest pain (hazard ratio 6.4, 95% confidence interval 2.5 to 16.1, p < 0.0001), both in patients with acute coronary syndromes or angina pectoris. However, in patients with non-coronary chest pain we observed no independent association of pulmonary congestion with outcome. CONCLUSION: Clinical signs of pulmonary congestion indicate an increased risk for poor outcome in patients with chest pain due to myocardial ischemia. Mortality of these patients is high, particularly in the first months after presentation. Therefore, hospital admission is warranted, including patients with angina pectoris, who otherwise may be candidates for early discharge.