Istepan Kürkciyan

acute Renal Infarction: Clinical Characteristics of 17 Patients

We analyzed the medical records of patients with an established diagnosis of acute renal infarction to identify predictive parameters of this rare disease. Seventeen patients (8 male) who were admitted to our emergency department between May 1994 and January 1998 were diagnosed by contrast-enhanced computed tomography (CT) as having acute renal infarction (0.007% of all patients). We screened the records of the 17 patients for a history with increased risk for thromboembolism, clinical symptoms, and urine and blood laboratory results known to be associated with acute renal infarction. A history with increased risk for thromboembolism with 1 or more risk factors was found in 14 of 17 patients (82%); risk factors were atrial fibrillation (n = 11), previous embolism (n = 6), mitral stenosis (n = 6), hypertension (n = 9), and ischemic cardiac disease (n = 7). All patients reported persisting pain predominantly from the flank (n = 11), abdomen (n = 4), and lower back (n = 2). On admission, elevated serum lactate dehydrogenase was found in 16 (94%) patients, and hematuria was found in 12 (71%) of 17 patients. After 24 hours all patients showed an elevated serum lactate dehydrogenase, and 14 (82%) had a positive test for hematuria. Our findings suggest that in all patients presenting with the triad--high risk of a thromboembolic event, persisting flank/abdominal/lower back pain, elevated serum levels of lactate dehydrogenase and/or hematuria within 24 hours after pain onset--contrast-enhanced CT should be performed as soon as possible to rule out or to prove acute renal infarction.

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 or >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.

Accuracy and Impact of Presumed Cause in Patients With Cardiac Arrest

BACKGROUND International guidelines recommend differentiation between cardiac and noncardiac causes of cardiac arrest. The aim of this study was to find the rate of agreement between primarily postulated and definitive causes of cardiac arrest. METHODS AND RESULTS We retrospectively analyzed the primarily presumed cause of cardiac arrest as determined by the emergency room physician on admission in all patients admitted to the emergency department of one urban tertiary care hospital. This was compared with the definitive cause as established by clinical evidence or autopsy. Within 4 years, the initially presumed cause was unclear in 24 (4%) of 593 patients. In the remaining 569 patients, the presumed cause was correct in 509 (89%) and wrong in 60 (11%) cases. Cardiac origin was presumed in 421 (71%) and the definitive cause in 408 (69%) cases. Noncardiac origin was presumed in 148 (25%) and the definitive cause in 185 (31%) patients. Presumed cardiac cause was sensitive (96%) but less specific (77%). Noncardiac causes such as pulmonary embolism, cerebral disorders, or exsanguination were those most frequently overlooked. Asystole occurred significantly more often in patients in whom presumed cause remained undetermined or differed from the definitive cause. CONCLUSIONS Cause of cardiac arrest is not as easily recognized as anticipated, especially when the initial rhythm is different from ventricular fibrillation. This might affect comparability of study results, therapeutic strategies, prognosis, and outcome. Patients in whom the presumed cause was confirmed as being correct had significantly better survival and neurological outcome.

Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest

OBJECTIVE Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest. DESIGN We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features. RESULTS Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome. CONCLUSIONS Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.

Measurement of myocardial contractility following successful resuscitation: quantitated left ventricular systolic function utilising non-invasive wall stress analysis

After successful resuscitation from cardiac arrest, prolonged contractile failure has been demonstrated in animal experiments. No systematic evaluation of myocardial contractility following successful resuscitation after human cardiac arrest exists. The aim of this study was to assess left ventricular contractility following human cardiac arrest with successful resuscitation. In 20 adult patients after cardiac arrest and in four control patients, the relation between meridional wall stress (MWS) and rate-corrected mean velocity of circumferential fibre shortening (Vcf(c)), a load independent and rate corrected index of left ventricular contractility was measured within 4 h after return of spontaneous circulation and after 24 h by means of transoesophageal echocardiography. As the normal values of Vcf(c) depend on MWS, a normal deviate (z) was calculated. A normal z-score is defined as 0+/-2, < -2 indicates reduced contractility, > + 2 increased contractility. Data are presented as median and the interquartile range (IQR). For the comparison of related samples the Wilcoxon sign test was used. In most patients after cardiac arrest contractility was severely impaired within 4 h after successful resuscitation [z - 7.0 (IQR - 8.9 - (-2.5))]. Contractility did not significantly improve within the observational period [z after 24 h - 3.7 (IQR - 7.9 - (-1.8))] (P = 0.3). The four control patients had normal left ventricular contractility on arrival (z 0.0, range - 0.9-0.8) and after 24 h (z 0.7, range - 1.5-2.7). In conclusion non-invasive wall stress analysis can be applied to quantitate systolic left ventricular function, which was severely compromised in most patients within the first 24 h after successful resuscitation. Whether depression of left ventricular function is caused by cardiac arrest itself or by the underlying disease remains speculative.

Creatine kinase and creatine kinase-MB release after nontraumatic cardiac arrest

The aim of the study was to describe the course of serum creatine kinase (CK) and its MB fraction (CK-MB) in patients surviving cardiac arrest, and to identify factors influencing CK and CK-MB release. The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation, collected within a period of 33 months, were evaluated retrospectively and compared with laboratory blood investigations collected prospectively (on admission and after 6, 12, and 24 hours) in 107 adult patients surviving a witnessed cardiac arrest for 24 hours. CK and CK-MB were elevated in >75% of the patients within 24 hours. Release of CK and CK-MB was mainly associated with electrocardiographic evidence of acute myocardial infarction (AMI) cumulative energy administered during defibrillation, and duration of chest trauma by compression. The CK-MB/CK ratio was elevated in 32% of the patients. Of patients with electrocardiographic evidence of AMI, only 49% had an elevated CK-MB/CK ratio. In conclusion, the elevation in serum CK and CK-MB fraction in patients after nontraumatic cardiac arrest is a frequent finding, and is associated with ischemic myocardial injury, as well as physical trauma to the chest. This should be considered when interpreting the course of CK and CK-MB fraction for the diagnosis of AMI.

A New Preparation of Nifedipine for Sublingual Application in Hypertensive Urgencies

A new preparation of nifedipine for sublingual application in hypertensive urgencies was investigated in a prospective study. Patients admitted to the Emergency Department with a persistent elevation of systolic blood pressure (SBP) greater than 190 mm Hg and/or a diastolic blood pressure (DBP) greater than 100 mm Hg received nifedipine 10 mg sublin gual with a sprayer. A second dose was administrated fifteen minutes later if an adequate response defined as a stable reduction of SBP below 180 mm Hg and DBP below 100 mm Hg had not occurred. Of 30 patients, 21 (70%) responded to the first nifedipine appli cation, 7 responded to the second dose, and 2 nonresponders had to be treated with urapidil. Overall mean SBP was 206 ± 19 mm Hg and mean DBP was 113 ± 15 mm Hg before treatment, and a significant antihypertensive effect was noted within fifteen minutes after nifedipine spray (p < 0.05). The maximum antihypertensive effect was for SBP in sixty minutes (146 ±19 mm Hg) and for DBP after one hundred twenty minutes (78 ± 18 mm Hg). The average reduction in SBP was 29% and in DBP 31%. In first-dose responders (n = 21) a significant antihypertensive effect was noted within fifteen minutes. SBP declined from 205 ±21 to a minimum of 142 ±15 mm Hg (22.3%) after sixty minutes and DBP from 113 ± 13 to a minimum of 77 ±11 mm Hg (22.2%) after one hundred twenty minutes. In second-dose responders (n = 7) a significant antihypertensive effect was noted within thirty minutes. SBP declined from 214 ±20 to a minimum of 151 ± 18 mm Hg (29.5%) after sixty minutes and DBP from 123 ± 14 to a minimum of 92 ±31 mm Hg (24.9%) after one hundred twenty minutes. After treatment with sublin gual nifedipine spray the authors could not observe any clinically significant side effects. Overall the heart rate decreased significantly from 100 ±21 beats per minute to a minimum of 84 ± 15 beats per minute after one hundred twenty minutes. The authors conclude that sublingual nifedipine spray application offers a new, highly effective, safe, and convenient method of treating patients with hypertensive urgencies.

Mild resuscitative hypothermia and outcome after cardiopul monary 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°C) to deep (20–28°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 histologie brain damage. More importantly, such benefits can be demonstrated with mild (34–36°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°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.

Spontaneous pneumomediastinum in a patient with diabetic ketoacidosis.

A 27-year-old male patient was admitted to the emergency department because of polyuria, polydipsia and loss of weight. On admission, pronounced hyperventilation was noted. In the laboratory exams, while blood glucose was 311 mg/dl, arterial blood gas analysis indicated a metabolic ketoacidosis with a base excess of –21 and a pH of 7.19. The chest X-ray (left Fig.) showed a 2–3 mm wide transradiant zone around the left border of the heart without fluid level, sharply demarcated by the 1 mm line shadow of the parietal pericardium which went parallel to the heart shadow with a lateral convex curve. No signs of a pneumothorax were evident. Computed tomography of the thorax (right Fig.) confirmed the diagnosis, but did not explain the cause of the pneumomediastinum. The patient did not show respiratory discomfort, and the pneumomediastinum vanished within two weeks without therapeutical intervention. In the absence of other causes such as chest trauma, iatrogenic etiology, etc., we suggest that forced breathing manoeuvres during hyperventilation led to microtrauma of the trachea, causing pneumomediastinum. A spontaneous pneumomediastinum is a rare event and the exact site of entry of air into the mediastinum is often unknown. Even in those cases that have come to autopsy there has been no obvious source of pneumomediastinum. A literature search revealed that similar cases have been reported in diabetic ketoacidosis [1–5]. As a rule, spontaneous pneumomediastinum is benign and self-limiting within a few weeks. No specific therapy appears to be indicated.