Giora Meron

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.

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.

Analysing calls by lay persons reporting cardiac arrest

Prior to establishing a protocol for pre-arrival instructions for cardio-pulmonary resuscitation in the Vienna emergency medical system dispatch centre, a study was performed to determine whether any problems exist which may compromise guidance for basic life-support on the telephone. To evaluate the feasibility of prearrival instructions, a retrospective analysis of cardiac arrest calls was performed. We reviewed the Vienna emergency medical services dispatch centre tape recordings, ambulance run sheets and the hospital charts of 114 patients suffering from atraumatic cardiac arrest. Analysis showed that in 59 cases the arrest occurred in the victims home. The telephone and the patient were either in the same or in adjoining rooms in 55% of the calls. We did not experience any technical or language difficulties. The caller and victim were related in 51 cases. The callers were completely calm in 77% and fairly calm in an additional 15%. Not one caller was distraught. Our data show that most objections to the feasibility of pre-arrival instructions can be refuted. We conclude that in Vienna the setting and location of arrest will impose few problems on the performance of bystander-cardio-pulmonary resuscitation using pre-arrival instructions given by dispatchers.

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.