Cause Of Sudden Unexpected Death Research Articles

Sudden unexpected death in persons

This study retrospectively assesses the underlying causes of sudden unexpected death and the occurrence of prodromal symptoms in 162 subjects (aged 9 to 39 years) over a 10-year period (1976 to 1985). Underlying cardiac diseases accounted for sudden death in 73% and noncardiac causes in 15% of subjects. In 12% of subjects, the causes were unidentifiable. Myocarditis (22%), hypertrophic cardiomyopathy (22%) and conduction system abnormalities (13%) were the major causes in 32 subjects aged <20 years. Major causes of 46 deaths in subjects 20 to 29 years were atherosclerotic coronary artery disease (24%), myocarditis (22%) and hypertrophic cardiomyopathy (13%). The largest number of deaths in 84 subjects aged ≥30 years was attributed to coronary artery disease (58%), followed by myocarditis (11%). Among noncardiac causes of sudden death, intracranial hemorrhage was the most frequent (5%), followed by infectious disease (4%). Prodromal symptoms were reported by 54% of subjects; most frequent were chest pain (25%) in subjects aged ≥20 years, and dizziness (16%) in those aged <20. Sudden death, which occurred during routine daily activity in 49% and during sleep in 23% of subjects, was related to physical exercise in 23% and emotional upset in 6%. Sudden unexpected death in the young is still an unresolved medical problem. The early recognition of prodromal symptoms could be crucial in the prevention of sudden death, specifically when exercise-related.

Recurrent cyanotic episodes with severe arterial hypoxaemia and intrapulmonary shunting: a mechanism for sudden death.

The pathophysiology of recurrent cyanotic episodes has been investigated in 51 infants and children. Episodes began at a median age of 7 weeks (range 1 day to 22 months, 39 at less than 4 months). They were characterised by the rapidity of onset and progression of severe hypoxaemia with early loss of consciousness from cerebral hypoxia. The most common precipitating factor was a sudden naturally occurring stimulus from pain, fear, or anger. In uncontrolled trials, cyanotic episodes were reduced in frequency and severity by tetrabenazine (n = 15) and additional inspired oxygen (n = 10). Eight patients died suddenly and unexpectedly (four during cyanotic episodes). Twenty eight patients underwent physiological studies during cyanotic episodes. There was no evidence of seizure activity at the onset and although prolonged absence of inspiratory effort with continued expiratory efforts was common, breathing sometimes continued. Episodes were not caused by upper airway obstruction and sometimes occurred during positive airway pressure ventilation. The rapidity of fall in arterial oxygen pressure and continued breathing suggested a right to left shunt of sudden onset. The results of contrast echocardiography and lung imaging studies confirmed that this was occurring within the lungs. These cyanotic episodes included both intrapulmonary shunting and prolonged expiratory apnoea. They are best explained by interactions between central sympathetic activity, brainstem control of respiration and vasomotor activity, reflexes arising from around and within the respiratory tract, and the matching of ventilation to perfusion in the lungs. They are a cause of sudden unexpected death in infancy and early childhood.

Cardiac asystole associated with epileptic seizures: a case report with simultaneous EEG and ECG.

Cardiac arrhythmias occurring in association with epileptic seizures are a potential source of diagnostic confusion and a possible cause of sudden unexpected death in epilepsy. A case is described in which simultaneous ambulatory electroencephalography and electrocardiography revealed periods of asystole coinciding with epileptic seizures. The aystole appeared to precede obvious changes in the scalp recorded electroencephalogram (EEG), but clinical attacks and EEG seizure activity were not altered by pacemaker correction of the cardiac arrhythmias.

Department of Corrections

In the December issue (Pediatr Rev 1987;9:203), question 1 should have read: "... the most likely cause of sudden unexpected death in the adolescent athlete..." (not "least likely"). The correct answer is "A. Cardiac disease."

Myocardial ischemia and infarction: Anatomic and biochemical substrates for ischemic cell death and ventricular arrhythmias

Myocardial ischemia is a widespread cause of morbidity and the number one cause of death in the economically developed countries of the world. In the United States, approximately 25 per cent of all deaths are at tr ibuted to hear t attacks; of these deaths, about one half occur suddenly outside the hospital setting. Although there are many possible causes of sudden unexpected death, the majority undoubtedly are cardiogenic, owing to ventricular arrhythmias that occur either in the setting of transient myocardial ischemia or in some phase of an evolving myocardial infarct. Following hospitalization for an acute myocardial infarct, the majority of deaths have anatomically definable explanations (i.e., loss of sufficient myocardium to cause cardiac pump failure or specific anatomic complications of infarction such as cardiac rupture). In addition, despite the development of many potent antiarrhythmic drugs, some patients still die of ventricular fibrillation during the acute phase of myocardial infarction; others, even after the infarct has undergone replacement by scarring, st iffer f rom recu r r en t chronic ventr icular tachycardia that can lead to hemodynamic collapse and/or ventricular fibrillation. The reduction of overall cardiac pump function in myocardial infarction may have several contributory causes; the most important cause surely is the loss of contractile mass. It has been shown, for example, that among patients with fatal myocardial infarcts, those who had died o f cardiogenic shock usually had lost at least 30 per cent and often 40 per cent or more of their left ventricular mass) Some of the gross anatomic determinants of myocardial infarct size are known, as are many subcellular biochemical and structural consequences of acute ischemic injury. However, the subcellular conditions dictating that an ischemic myocyte has become irreversibly and thus destined for necrosis have not been defined completely. The electrophysiologic explanations for most ventricular arrhythmias are reentrant conduction, enhanced automaticity of an injured focus, or triggered activity of an injured focus. 2 However, the underlying anatomic and/or biochemical explanations

Sudden Unexpected Death from Primary Pulmonary Hypertension

Five cases of sudden unexpected death from primary pulmonary hypertension (PPH) are reviewed. Right ventricular myocardial hypertrophy and a dilated pulmonary conus may be the only findings at the initial gross examination. Characteristic microscopic changes in the lungs are primarily those of plexiform vascular lesions. The pathophysiology and morphologic alterations of PPH are discussed, and the association of this entity with collagen vascular diseases and mixed connective tissue disease is emphasized. It is concluded that PPH is an unusual cause of sudden unexpected death and its diagnosis may be difficult because prior signs or symptoms may be absent. The increased familial incidence of PPH underscores the necessity of considering this entity in cases of sudden unexpected death of obscure cause.

Chronic tonsillar herniation: an attempt at classifying chronic hernitations at the foramen magnum.

A system is presented for the classification of chronic herniations of the cerebellar tonsils in the absence of space-occupying intracranial lesions, based on a survey of the literature and 13 own cases. The Arnold-Chiari malformation in adults typically involves herniation of the cerebellar tonsils instead of herniation of the vermis as is typical when it occurs in infancy. Identification of chronic tonsillar herniation with the Arnold-Chiari malformation in adults was thought to require at least one other sign of the Arnold-Chiari complex, e.g. a medullary deformity. Cases for which chronic herniation and sclerosis of the cerebellar tonsils present as the only nervous lesion are classified as "chronic tonsillar herniation". Such cases may manifest with neurological symptoms during adult life, or they may be found incidentally at autopsy. Attention is drawn to the occurrence of chronic tonsillar herniation in 7 infants and children where it apparently represents a cause of sudden unexpected death. The overlap between chronic tonsillar herniation and the Arnold-Chiari malformation of adults is discussed in regard to the frequence of associated osseous anomalies, hydrocephalus and syringomyelia.

Nasal obstruction, a cause of sudden unexpected death?

Nasal obstruction, a cause of sudden unexpected death?

Congenital heart disease as a cause of sudden unexpected death in children under one year of age: Levinson, S. A.: Am. J. Clin. Path. 11: 741, 1941

Mechanical ventilation is widely recommended for reptiles during anesthesia, and while it is well-known that their low ectothermic metabolism requires much lower ventilation than in mammals, very little is known about the influence of ventilation protocol on the recovery from anesthesia. Here, 15 ball pythons (Python regius) were induced and maintained with isoflurane for 60 min at one of three ventilation protocols (30, 125, or 250 ml min− 1 kg− 1 body mass) while an arterial catheter was inserted, and ventilation was then continued on 100% oxygen at the specified rate until voluntary extubation. Mean arterial blood pressure and heart rate (HR) were measured, and arterial blood samples collected at 60, 80, 180 min and 12 and 24 h after intubation. In all three groups, there was evidence of a metabolic acidosis, and snakes maintained at 30 ml min− 1 kg− 1 experienced an additional respiratory acidosis, while the two other ventilation protocols resulted in normal or low arterial PCO2. In general, normal acid-base status was restored within 12 h in all three protocols. HR increased by 143 ± 64% during anesthesia with high mechanical ventilation (250 ml min− 1 kg− 1) in comparison with recovered values. Recovery times after mechanical ventilation at 30, 125, or 250 ml min− 1 kg− 1 were 289 ± 70, 126 ± 16, and 68 ± 7 min, respectively. Mild overventilation may result in a faster recovery, and the associated lowering of arterial PCO2 normalised arterial pH in the face of metabolic acidosis.