Massive pulmonary embolism leading to cardiac arrest is associated with consumptive coagulopathy presenting as disseminated intravascular coagulation.

SUMMARY BACKGROUND: A consumptive coagulopathy resembling disseminated intravascular coagulation (DIC) has been seen in patients with massive pulmonary embolism (PE). We hypothesized that a DIC-like condition is relevant in patients whose pulmonary embolism leads to cardiopulmonary arrest and cardiopulmonary resuscitation (CPR). METHODS: This hypothesis was tested by the use of a database consisting of all cases of PE diagnosed at the Department of Emergency Medicine from June 1993 to October 2007. Out of 1018 cases with PE, 113 patients underwent CPR. In this cohort study, the resuscitated patients were compared with those with PE but without CPR. RESULTS: Patients with PE and CPR had 3-fold higher D-dimer, prolonged prothrombin time (PT), reduced platelet counts and lower fibrinogen and antithrombin (AT) levels compared with PE patients without cardiac arrest (P < 0.001 for all). Among patients with PE and CPR, D-dimer was abnormal in 100%, PT in 44%, AT in 53%, fibrinogen in 19% and platelets in 25%. In comparison, PE without CPR was associated with abnormal D-dimer in 99%, abnormal PT in 15%, low AT in 6%, low fibrinogen in 1% and low platelets in 2%. Nine per cent of the resuscitated patients had a DIC score >or= 5, indicating overt DIC. The DIC score highly correlated with 1-year and in-hospital mortality. CONCLUSIONS: Massive PE leading to CPR is associated with consumptive coagulopathy and overt DIC. In resuscitated patients, DIC markers may indicate pulmonary embolism as the underlying cause of arrest.

Troponin T predicts in-hospital and 1-year mortality in patients with pulmonary embolism.

We aimed to determine the prognostic value of troponin T (TNT) for in-hospital and 1-yr mortality in a large sample of patients with pulmonary embolism (PE). Patients presenting at the emergency department of a tertiary care centre from January 1998 to December 2006 with PE were included. A blood sample was taken at the time of presentation. To determine in-hospital and 1-yr mortality, data from the hospital records and the national death register were used. TNT was determined in 563 out of 737 patients with proven PE. TNT was elevated (>0.03 ng x mL(-1)) in 27%. In-hospital survival was 79% in TNT-positive patients compared with 94% in TNT-negative patients (p<0.001). 1-yr survival was 71% in TNT-positive patients compared with 90% in TNT-negative patients (p<0.001). Elevated TNT levels meant a four-times higher risk of in-hospital death and a three-times higher risk of 1-yr mortality, even after adjustment for the other most important risk factors of death in this population. Elevated TNT independently predicts in-hospital and 1-yr mortality in patients with acute PE.

Value of negative spiral CT angiography in patients with suspected acute PE: analysis of PE occurrence and outcome.

The aim of this study was to analyze pulmonary embolism (PE) occurrence and retrospective clinical outcome in patients with clinically suspected acute PE and a negative spiral CT angiography (SCTA) of the pulmonary arteries. Within a 35-month period, 485 consecutive patients with clinical symptoms of acute PE underwent SCTA of the pulmonary arteries. Patients with a negative SCTA and without anticoagulation treatment were followed-up and formed the study group. Patient outcome and recurrence of PE was evaluated retrospectively during a period of 6 months after the initial SCTA, and included a review of computerized patient records, and interviews with physicians and patients. Patients were asked to fill out a questionnaire concerning all relevant questions about their medical history and clinical course during the follow-up period. Special attention was focused on symptoms indicating recurrent PE, as well as later confirmation and therapy of PE. Of the 485 patients, 325 patients (67%) had a negative scan, 134 (27.6%) had radiological signs of PE, and 26 (5.4%) had an indeterminant result. Of 325 patients with a negative scan, 269 (83%) were available for follow-up. The main reasons for loss to follow-up were change of address, name, or phone number, or non-resident patients who left abroad. Of 269 patients available for follow-up, 49 patients (18.2% of 269) received anticoagulant treatment because of prior or recent deep venous thrombosis (32.6%) or a history of PE (34.7%), cardiovascular disease (18.4%), high clinical probability (8.2%), positive ventilation-perfusion scan (4.2%), and elevated D-dimer test (2%). The remaining 220 patients, who did not receive anticoagulant medication, formed the study group. Of this study group, 1 patient died from myocardial infarction 6 weeks after the initial SCTA, and the postmortem examination also detected multiple peripheral emboli in both lungs ( p=0.45%; 0.01-2.5, 95% confidence interval). The PE did not occur in any other patient. In patients with suspected PE and negative SCTA without anticoagulant therapy, the risk of recurrent PE in this study was less than 1% and similar to that in patients after a negative pulmonary angiogram. Therefore, we conclude that patients can be managed safely without anticoagulation therapy; however, this approach may not be appropriate for critically ill patients and those with persistent high clinical suspicion of acute PE.

Acute phase reactants in patients with abdominal aortic aneurysm.

BACKGROUND: There is increasing evidence that an inflammatory process is present in abdominal aortic aneurysms (AAAs) to varying degrees. The aim of this study was to compare acute phase reactants in patients with asymptomatic AAA, symptomatic AAA without rupture and ruptured AAA. METHOD: Two hundred and twenty-five consecutive patients treated because of AAA were included in this case-control study. Polynomial logistic regression analysis was applied to compare admission C-reactive protein (CRP) and white blood count (WBC) measured in 111 asymptomatic outpatients, 52 symptomatic patients without rupture and 62 patients with rupture of the aneurysm. We adjusted for the potentially confounding effect of age, sex, haemoglobin levels and aneurysm diameter. RESULTS: Patients with symptomatic AAA and patients with ruptured AAA had significantly elevated CRP (p=0.002) and WBC (p<0.0001) levels compared to asymptomatic patients. There was no statistically significant difference in CRP and WBC between patients with symptomatic AAA and ruptured AAA. Median CRP values of asymptomatic, symptomatic and ruptured AAA were <0.5 (interquartile range (IQR) <0.5-0.85), 1.1(IQR <0.5-4.0) and 2.4 mg/dl (IQR 0.65-8.6), respectively, and median WBC values were 6.5 (IQR 5.5-8.0), 8.7 (IQR 6.8-11.2) and 13.2 (IQR 10.5-17.0), respectively. CONCLUSION: A significant elevation of CRP and WBC could be found in patients who presented with symptoms or rupture of an AAA. These indicators of inflammation were not observed in asymptomatic patients with AAA.

Cardiopulmonary resuscitation performed by bystanders does not increase adverse effects as assessed by chest radiography.

UNLABELLED: Important adverse effects of bystander cardiopulmonary resuscitation (CPR) are well known. We describe the number of nonmedical professional CPR-related complications in patients surviving cardiac arrest, as assessed by chest radiograph. Within 2 yr, all consecutive patients admitted to the department of emergency medicine at a university hospital who had a witnessed, nontraumatic, normothermic cardiac arrest were studied. Radiologically evaluated adverse effects were compared with Mann-Whitney U-tests between patients who received bystander basic life support (Bystander group) and patients who did not receive bystander basic life support before advanced life support was started (ALS group). For assessment of bystander CPR-associated complications, chest radiographs were used. Of 224 patients, 173 were eligible. The median age was 58 yr (interquartile range, 51-71 yr), and 126 patients (73%) were men. The incidence of adverse effects associated with assisted-ventilation maneuvers and external chest compressions did not differ significantly between groups (severe gastric insufflation, 17% vs 18% between the Bystander group [n = 59] and the ALS group [n = 96], respectively; suspicion of aspiration, 22% vs 17%, respectively; soft tissue emphysema, 2% vs 1%, respectively; and serial rib fractures, 8% vs 8%, respectively). CPR administered by nonmedical personnel did not increase the number of life support-related adverse effects in patients surviving cardiac arrest as assessed by means of chest radiograph on admission. IMPLICATIONS: Complications related to cardiopulmonary bypass (CPR) are not increased when CPR is administered by nonmedical personnel, as assessed by chest radiograph. These data may be valuable in motivating lay people to perform basic life support.

Sepsis-associated purpura fulminans in adults.

Sepsis-associated purpura fulminans is defined as septicemia, shock, disseminated intravascular coagulation and circulatory failure leading to multiple organ dysfunction. 40-70% of patients with sepsis-associated purpura fulminans die. Early prognostic factors in adults have not been well delineated yet. Aim of our study was 1) to evaluate currently used scoring systems for meningococcal septicemia in the setting of sepsis-associated purpura fulminans and 2) to assess if other parameters are feasible as early prognostic factors. From 1.1 1994-31.12.1998 twelve patients (female: 7; mean age: 31 (21; 43) years) were studied. Six patients (50%) died within 2 hours and 7 days after admission despite standard intensive treatment. On admission non-survivors had a more pronounced degree of disseminated intravascular coagulation compared to survivors (platelet count 18000 (15000; 45000) G/l vs. 119.000 (111000; 152000) G/l, (p = 0.03); fibrinogen 67 (50; 108) mg/dl vs. 356 (234; 483) mg/dl, (p = 0.02); PTZ 28% (20%; 30%) vs. 44% (35%; 51%), (p = 0.05); aPTT 120 (120; 128) sec vs. 46 (44; 69) sec, (p = 0.001). Severity of lactic acidosis was significantly higher in non-survivors than in survivors (pH 7.08 (6.92; 7.21) vs. pH 7.4 (7.25; 7.4), (p = 0.02); lactate 13.5 (11; 15) mval/l vs. 6.0 (4.4; 6) mval/l, (p = 0.02); data presented as median (25-75% interquartile range). In our patients the Glasgow Meningococcal Septicemia Prognostic Score (GMSPS) and the Niklasson-Score failed to distinguish between survivors and non-survivors (GMSPS 7 (6; 11) vs 7.5 (7; 9) out of 15; predicted mortality according to Niklasson-Score 73% vs 88%). There was no difference in the APACHE II Score (22 (18.5, 24) vs 22 (20.25, 26)). The severity of disseminated intravascular coagulation assessed by routine laboratory parameters and the degree of lactic acidosis on admission were the strongest predictors of outcome in patients with sepsis-associated purpura fulminans. Scoring systems developed for patients with meningococcal septicemia are of limited value in the setting of sepsis-associated purpura fulminans.

Termination of recent-onset atrial fibrillation/flutter in the emergency department: a sequential approach with intravenous ibutilide and external electrical cardioversion.

Safety and effectiveness are the goals in treating patients with arrhythmias. In an open prospective study, we observed the efficacy and safety of up to 2 mg intravenous ibutilide, a new class III antiarrhythmic agent in haemodynamically stable patients presenting in the emergency department (ED) with symptoms of recent-onset (<48 h) atrial fibrillation/flutter. Arrhythmia termination within 90 min, haemodynamic parameters and proarrhythmic effects were assessed. Non-responders to the ibutilide infusion underwent external electrical cardioversion. We included 51 patients. In 31 patients therapeutic intervention with intravenous ibutilide was successful within 90 min (61%). In another seven patients conversion to sinus rhythm occurred after 90 min without any other intervention (14%). Blood pressure remained stable and no relevant proarrhythmic effects were observed. The 13 patients who did not respond to ibutilide treatment underwent successful external electrical cardioversion. The overall conversion rate was 100%. Forty-seven patients (92%) were discharged within a median of 9 h and managed as outpatients. In conclusion, in haemodynamically stable patients with recent-onset atrial fibrillation/flutter intravenous ibutilide and external electrical cardioversion for conversion to sinus rhythm turned out to be effective and safe. The short duration of admission makes this strategy attractive for use in the ED.

Pulmonary embolism as a cause of cardiac arrest: presentation and outcome.

BACKGROUND: Pulmonary embolism (PE) is a possible noncardiac cause of cardiac arrest. Mortality is very high, and often diagnosis is established only by autopsy. METHODS: In a retrospective study, we analyzed clinical presentation, diagnosis, therapy, and outcome of patients with cardiac arrest after PE admitted to the emergency department of an urban tertiary care hospital. RESULTS: Within 8 years, PE was found as the cause in 60 (4.8%) of 1246 cardiac arrest victims. The initial rhythm diagnosis was pulseless electrical activity in 38 (63%), asystole in 19 (32%), and ventricular fibrillation in 3 (5%) of the patients. Pronounced metabolic acidosis (median pH, 6.95, and lactate level, 16 mmol/L) was found in most patients. In 18 patients (30%), the diagnosis of PE was established only postmortem. In 42 (70%) it was diagnosed clinically, in 24 of them the diagnosis of PE was confirmed by echocardiography. In 21 patients, 100 mg of recombinant tissue-type plasminogen activator was administered as thrombolytic treatment, and 2 (10%) of these patients survived to hospital discharge. Comparison of patients of the thrombolysis group (n = 21) with those of the nonthrombolysis group (n = 21) showed a significantly higher rate of return of spontaneous circulation (81% vs 43%) in the thrombolysis group (P=.03). CONCLUSIONS: Mortality related to cardiac arrest caused by PE is high. Echocardiography is supportive in determining PE as the cause of cardiac arrest. In view of the poor prognosis, thrombolysis should be attempted to achieve return of spontaneous circulation and probably better outcome.

Restoration of coronary blood flow by single bolus injection of the GPIIb/IIIa receptor antagonist c7E3 Fab in a patient with acute myocardial infarction of recent onset.

It has been debated that primary coronary angioplasty could be more effective if immediate antithrombotic therapy would contribute to a faster recanalization of the infarct-related artery. This is the first report of a patient who presented at the emergency department with acute anterolateral myocardial infarction, in whom a single bolus injection of c7E3 Fab (0.25 mg/kg body weight) led to complete reperfusion of the infarct-related coronary artery during organization time for planned acute coronary angioplasty. Pain relief 15 min after initiation of therapy and ST-segment resolution of > 50%, as well as occurrence of idioventricular rhythm 30 min thereafter, were suggestive of successful recanalization before the coronary intervention was started. Diagnostic coronary angiography at 90 min revealed TIMI-grade 3 flow in the infarct-related coronary artery with only moderate luminal irregularities. Bolus administration of c7E3 Fab could be effective for dissolving platelet-rich thrombi in the early stage of acute myocardial infarction (AMI) and may therefore represent a promising "bridging" therapy in patients with AMI elected for primary coronary angioplasty.

Cyclosporin A-induced ocular flutter after marrow transplantation.

Ocular flutter is a rare neurologic condition occurring in patients suffering from viral encephalitis, intracranial neoplasia, paraneoplastic syndrome or intoxications. Neurotoxicity is a recognized complication of cyclosporin A (CsA) therapy, but ocular flutter has not been reported in association with CsA administration to date. We describe a 17-year-old female patient who developed ocular flutter 51 days after transplantation with marrow from an unrelated donor, for acute myeloid leukemia. After discontinuation of cyclosporin, which was given for prophylaxis of graft-versus-host disease, the clinical symptoms resolved within 3 weeks, but a slightly abnormal electrooculogram persisted for more than 10 months.

Severity assessment of acute pulmonary embolism with spiral CT: evaluation of two modified angiographic scores and comparison with clinical data.

Spiral computed tomography (CT) has shown promising results in the detection of acute pulmonary embolism. The aim of this study was to investigate whether the severity of acute pulmonary embolism could be quantitatively assessed with spiral CT examinations and to test the potential clinical impact of this information. In a consecutive series of 123 patients screened with spiral CT for suspected acute pulmonary embolism, 31 patients (25%) had evidence of emboli. The severity of pulmonary arterial obstruction in those 31 spiral CT examinations was evaluated by two independent observers using angiographic scores previously described by Walsh (29) and Miller (30), adapted to the needs of spiral CT. Clinical patient subgroups were defined according to oxygen saturation, heart rate, and echocardiographic signs of right ventricular strain. CT severity scores were then correlated to each other and to clinical parameters using the Spearman rank test. Interobserver agreement was calculated using the analysis of variance. Both modified Walsh and Miller scores were readily reproducible and showed interobserver agreements of 0.85 and 0.96, respectively (p = 0.001). Patients with mild and marked clinical abnormalities showed statistically significant differences between CT severity scores. Differences between severity scores of patients with moderate and marked clinical abnormalities were somewhat significant. No significant mean severity score differences were seen between patients with mild and moderate clinical abnormalities. Although correlations of severity scores and detailed clinical parameters within the defined subgroups were moderate to poor, threshold scores greater than 10 (Miller) and greater than 11 (Walsh) always indicated marked clinical abnormalities. The modified scores presented in this study constitute a readily reproducible method for the quantitative assessment of acute pulmonary embolism severity on spiral CT examinations.

Radiographic detection of intrabronchial malpositions of nasogastric tubes and subsequent complications in intensive care unit patients.

OBJECTIVE: The aim of our study was to illustrate the radiographic spectrum of the intrabronchial malposition of nasogastric tubes and subsequent complications, and to discuss the role of radiography in the detection of such malpositions. DESIGN: Retrospective clinical investigation. SETTING: Tertiary care university teaching hospital. PATIENTS AND METHODS: We reviewed chest radiographs of 14 intensive care patients with nasogastric tubes malpositioned in the tracheobronchial tree. The site and anatomic location of the malposition were recorded. Complications due to tube malpositioning were monitored on follow-up radiographs and on computed tomographic examinations, which were available in 4 patients. RESULTS: Nine of 14 nasogastric tubes were inserted in the right and 5 in the left tracheobronchial tree. Tube tips were malpositioned in the lower lobe bronchi (50%), the intermediate bronchus (36%), and the main bronchi (14%). There was perforation of the bronchial system with subsequent pneumothorax in 4 patients. In 4 other patients, pneumonia developed at the former site of the malpositioned tube tip. Radiographic detection of nasogastric tube malpositioning was prompt in 9 patients and delayed in 5 patients. CONCLUSIONS: Whereas clinical signs of nasogastric tube malpositioning in intensive care patients may be absent or misleading, chest radiography can accurately detect nasogastric tube malpositions in the tracheobronchial tree, may prevent complications, and avoid the use of further costly or invasive diagnostic techniques.

Mild resuscitative hypothermia and outcome after cardiopulmonary resuscitation.

Recovery without residual neurological damage after cardiac arrest with global cerebral ischemia is still a rare event. Severe impairment of bodily or cognitive functions is often the result. The individual, emotional, and social aspects of brain damage and rehabilitation are seldom taken into account. Efforts to improve the prevention of brain damage immediately after successful resuscitation of patients are missing. The efficacy of hypothermia in preserving neurologic function when instituted before and during certain no-flow cardiovascular states has been well documented both clinically and experimentally since the 1950s. Most studies have used moderate (28-33 degrees C) to deep (20-28 degrees C) hypothermia to demonstrate these protective effects. Considering the use of hypothermia for preservation and resuscitation, the lack of controlled outcome trials, the long period of time required to reach therapeutic hypothermia, and the incidence of rewarming complications such as infection, arrhythmia, and coagulopathy have made it difficult to apply these methods to emergency situations such as cardiac arrest. Recent experimental evidence in dogs has shown that hypothermia induced after cardiac arrest does indeed mitigate the effects of the postresuscitation syndrome and improves neurologic function and reduces histologic brain damage. More importantly, such benefits can be demonstrated with mild (34-36 degrees C) hypothermia, thus minimizing complications and requiring less time for induction of hypothermia. Ice water nasal lavage, direct carotid infusion of cold fluids, use of a cooling helmet, and peritoneal cooling are promising techniques for clinical cerebral cooling. External auditory canal temperature (e.g., tympanic membrane temperature changes) could provide an approximation to brain temperatures. For accurate temperature monitoring, however, a central pulmonary artery thermistor probe should be inserted. Temperature monitoring is needed to avoid temperature < 30 degrees C. Mild hypothermia may prove to be an important and secure component for cerebral preservation and resuscitation during and after global ischemia; it may also prove to be a useful method of cerebral resuscitation after global ischemic states, thereby promoting the prevention of neuromental diseases.

Possibilities of brain protection with tirilazad after cardiac arrest.

Cardiac arrest and resuscitation often create a cerebral insult caused by the initial cessation of blood flow, followed by the incomplete ischemia of cardiopulmonary resuscitation (low flow), and, following the return of spontaneous circulation, by the post-resuscitation syndrome. A cascade of physiologic, vascular, and biochemical events is set in motion, including changes in neuropeptides, electrolytes such as calcium and magnesium, excitatory neurotransmitters such as glutamate and acetylcholine, lymphokines such as interleukin-1, and arachidonic acid metabolites such as prostaglandins and leukotrienes; and formation of oxygen free radicals and lactic acid. Oxygen free radical-induced lipid peroxidation appears to increase tissue injury during and after brain ischemia. The 21-aminosteroid U74006F (tirilazad mesylate) is a novel inhibitor of lipid membrane peroxidation induced by oxygen free radicals, which has been shown, in animal models of subarachnoid hemorrhage, central nervous system trauma, and cerebral ischemia, to limit the extent of secondary tissue damage, thus improving functional recovery. Since tirilazad appears to have little or no behavioral or physiologic side effects, it appears to be an ideal agent for widespread brain ischemia prophylaxis. Tirilazad mesylate studies in out-of-hospital cardiac arrest are currently being planned.

Near infrared spectroscopy during and after cardiac arrest--preliminary results.

OBJECTIVE: To evaluate if regional cerebrovascular oxygen saturation (rSO2) is linked to systemic oxygenation and if impaired regional cerebral oxygenation affects outcome in cardiac arrest patients. DESIGN: Prospective, observational study. SETTING: Emergency department of a University Hospital. SUBJECTS: Patients during cardiac arrest or after restoration of spontaneous circulation. INTERVENTIONS: To measure rSO2 an infrared light-emitting probe was applied to the patient's forehead after arrival in the emergency department. Data were collected continuously together with blood pressure and pulse oximetry. Each variable measured immediately after arrival was used for calculation. ENDPOINTS: Best outcome (cerebral performance category) or death within one week. MEASUREMENTS AND MAIN RESULTS: Regional SO2 was measured in 18 consecutive patients. Six patients presented with cardiac arrest on arrival and rSO2 was measured during chest compression. Twelve patients had achieved restoration of spontaneous circulation before they arrived in the emergency department. No association was found between rSO2 and pulse oximetry or rSO2 and blood pressure. All patients surviving for one week (n = 9) achieved a significantly higher median rSO2 on arrival than nonsurvivors (n = 9) (63% and 46%, respectively; p = 0.003). Median rSO2 was lower in the group arriving without spontaneous circulation (n = 6) than in patients after restoration of spontaneous circulation (n = 12) (44% and 63%, respectively; p = 0.009). This difference was not found in pulse oximetry readings. Patients with restoration of spontaneous circulation surviving the first week after cardiac arrest (n = 8) had a higher rSO2 than patients with restoration of spontaneous circulation who did not survive (n = 4) (65% and 48%, respectively). Time from restoration of spontaneous circulation to arrival was not different between the two groups. CONCLUSION: By showing that low rSO2 readings after cardiac arrest are associated with a higher mortality, this new, non-invasive and easily applicable technique might help to prognosticate outcome and offers new insights into monitoring cerebral oxygenation after cardiac arrest.

Sudden cardiac death of a teenage girl.

Anomalies of coronary artery origin can be of little clinical significance and only an incidental autopsy finding. However recent case reports have shown that a wide range of potential pathologic alterations of congenital coronary anomalies are associated with clinical symptoms and exercise related sudden death. We describe the case of a 16-year-old girl who sustained a cardiac arrest and died after cardiopulmonary resuscitation (CPR) of intractable cardiogenic shock. The sporty and previously healthy girl suddenly fainted after swimming in a tributary of the Danube. Autopsy revealed an anomalous origin of the left coronary artery from the anterior sinus of Valsalva and its course between aorta and pulmonary artery. The cause of this anomalous origin and possible mechanism for sudden death is discussed. We conclude that this congenital anomaly should be considered in cases of major cardiac events in young people.