Southern Medical Journal 95(2002):1047.
by Amy Stevens, MD, D. Paul Robinson, MD, Julie Turpin, RD, Ted Groshong, MD, Joseph D. Tobias, MD
Sudden Cardiac Death of an Adolescent During Dieting
Reprint requests to Joseph D. Tobias, MD, University of Missouri, Department of Child Health, M658 Health Sciences Center, One Hospital Dr, Columbia, MO 65212.
Dr. Tobias is the Russell and Mary Shelden Chair of Pediatric Intensive Care Medicine at the University of Missouri Medical Center. He is the editor of Pediatric Critical Care and is Board Certified in Pediatrics, Anesthesiology, Critical Care Medicine - Pediatrics, Critical Care Medicine - Anesthesiology, and Pain Management.
We describe a 16-year-old girl who had sudden onset of cardiorespiratory arrest while at school. She had recently attempted weight loss using a low-carbohydrate/high-protein, calorie-restricted dietary regimen that she had initiated on her own. During resuscitation, severe hypokalemia was noted. At postmortem examination, no other causes for the cardiac arrest were identified. Toxicologic findings were negative. The potential role of the dietary regimen as a contributing factor to the hypokalemia and subsequent cardiac arrest are discussed.
The pressures to meet our society’s definition of beauty may lead young women to jeopardize their health to lose weight and stay thin. More than 40% of female adolescents in the United States have been on a diet at some point, and 80% of teenagers report that they diet to look better. We present the case of an adolescent who was following a low-carbohydrate, high-protein diet and who had sudden onset of cardiorespiratory arrest. Laboratory evaluation during resuscitation revealed severe hypokalemia. Other potential causes for the condition were ruled out by parental history, autopsy findings, and postmortem toxicologic evaluation.
Emergency teams were summoned to a local high school to care for a 16-year-old girl who had suddenly collapsed. She was 5 feet 8 inches tall and weighed approximately 80 to 85 kg (176 to 187 lb). The patient had been in good health with no known history of medical problems. She had started a low-carbohydrate/high-protein diet 1 or 2 weeks earlier in an effort to lose weight. She had learned about the diet from video tapes, purchased from an advertisement on television. Her mother had been on the same diet. She had complied with the dietary regimen, eating meat, cheese, and salads without fasting. When the paramedics arrived, the girl was pulseless and apneic. The electrocardiogram revealed ventricular fibrillation. The patient’s trachea was intubated and cardiopulmonary resuscitation was initiated. Resuscitative measures, including defibrillation, were without effect. On arrival in the emergency department, the patient remained pulseless, with no evidence of cardiac activity. Arterial blood gas analysis revealed a pH of 6.89, with a base deficit of -19.8. Other laboratory values were serum sodium 142 mEq/L, ionized calcium 1.12 mEq/L, and serum potassium 3.8 mEq/L. Further resuscitative efforts were without effect. Postmortem and toxicologic examinations revealed no apparent cause for the death. Subsequent cardiologic evaluation of the patient’s 12-year-old sibling including echocardiography and electrocardiography was within normal limits.
Low-carbohydrate/hig h-protein diets have fallen in and out of popularity since the 1960s, resurfacing in various forms including the Stillman diet, the Scarsdale diet, the Zone diet, the carbohydrate addicts’ diet, and the Atkins diet. The Atkins diet was developed by Robert C. Atkins, MD, in 1970 and has gained recent popularity once again with the release of the revised and updated book Dr. Atkins’ New Diet Revolution.
Low-carbohydrate/high-protein plans seem attractive to many dieters because these diets set no limit on the amount of certain types of foods one can eat, exclude hunger from the dieting experience, reduce appetite, and at times, produce steady weight loss, even after dramatic failures or weight gain on other diets.
With a high-protein/high-fat intake, there is the release of cholecystokinin, a known appetite suppressant. The lack of glucose in the diet also avoids the 1-hour postprandial insulin surge associated with stimulation of neurogenic feeding centers. Additionally, the increased reliance on fat to meet the metabolic demands results in the production of ketone bodies and systemic ketosis, which may also suppress the appetite and curb feelings of hunger.
However, low-carbohydrate/high-protein diets are not without the potential for adverse biochemical and physiologic consequences. Ketone bodies compete with uric acid for renal tubular excretion, which can exacerbate disease in patients with gouty diathesis. Bloom and Azar reported that postural hypotension can develop in subjects on low-carbohydrate diets. Using an isolated, perfused rat heart model, Russell and Taegtmeyer showed that the beating heart loses contractile function (more than 50% in 60 minutes) when oxidizing acetoacetate alone.
Although results are contradictory, some studies have linked these diets to increases in serum triglycerides and low-density lipoprotein cholesterol.[5,6] Elevated levels of free fatty acids may promote both vascular thrombosis and cardiac arrhythmias.[7,8] Plasma lipolysis and infusion of albumin-bound free fatty acids have been associated with the development of serious arrhythmias in dogs, possibly through a detergent effect on mitochondrial and cell membranes. These diets have also been associated with hypothyroidism characterized by a decrease in thyrotropin and a marked decrease in triiodothyronine, as well as alterations in the metabolism of diuretics and cholesterol medications.
More importantly, deaths associated with other specialized diets have been reported. In the 1960s and 1970s, liquid protein diets were associated with several deaths. Some of these deaths were related to QT prolongation with pathologic findings of myocardial atrophy and myocarditis. Other findings in patients who had sudden cardiac death related to liquid protein diets included electrolyte disturbances such as hypokalemia, hypocalcemia, and hypomagnesemia. Restriction of caloric intake to less than the basal needs results in the catabolism of protein and glycogen stores, which have a high water content, leading to a diuretic effect with the loss of free water and electrolytes. Ketone bodies undergo urinary excretion with a cation to maintain electrical neutrality, resulting in the additional loss of cations, including calcium, magnesium, and potassium. When compounded by inadequate intake, deficiencies of these cations may ensue. Caloric restriction is not generally recommended on most low carbohydrate diets, including the Atkins diet, further emphasizing the dangers of using these diets without strict adherence to their recommendations.
Our patient’s sudden onset of cardiorespiratory arrest occurred without an underlying cause identified by history or on postmortem examination. Initial electrocardiogram revealed ventricular fibrillation, an unusual presenting arrythmia in a 16-year-old adolescent without underlying cardiac disease or electrolyte disturbance. During resuscitation, with a pH of 6.89, the serum potassium level was 3.8 mEq/L, suggesting profound hypokalemia if corrected for the pH. The ionized calcium level was 1.12 mEq/L (normal, 1.10 to 1.22 mEq/L). As with serum potassium, correction for the pH would indicate significant hypocalcemia. Serum magnesium level was not measured. Because potassium and magnesium undergo similar handling mechanisms in the renal tubules, hypomagnesemia is another potential cause of our patient’s cardiorespiratory arrest. When considering the potential causes of these electrolyte disturbances in an otherwise healthy female adolescent, questions arise regarding the potential role of the low-carbohydrate/high-protein diet compounded by a period of inadequate caloric intake and the resultant catabolic state. It is also possible, although no such history was obtained in this case, that associated problems such as bulimia, anorexia, and diuretic or laxative abuse can cause or potentiate electrolyte losses in such patients.
In light of the previous reports of mortality related to liquid protein diets and the lack of information on electrolyte and physiologic changes during low-carbohydrate, high-protein diets, we do not recommend such dieting regimens. We continue to suggest moderate caloric restriction with a balanced macronutrient and micronutrient intake and increased physical activity under a physician’s guidance. While it is possible that the patient’s dietary regimen had nothing to do with her sudden cardiovascular collapse, continued surveillance for similar cases is suggested.
Sidebar: Key Points
*More than 40% of female adolescents in the United States have been on a diet at some point, and 80% of teenagers report that they diet to look better.
Low-carbohydrate/high-protein plans seem attractive to many dieters because these diets set no limit on the amount of certain types of foods one can eat.
Plasma lipolysis and infusion of albumin-bound free fatty acids have been associated with the development of serious arrhythmias in dogs, possibly through a detergent effect on mitochondrial and cell membranes.
Ketone bodies undergo urinary excretion with a cation to maintain electrical neutrality, resulting in the additional loss of cations, including calcium, magnesium, and potassium.
In light of the previous reports of mortality related to liquid protein diets and the lack of information on electrolyte and physiologic changes during low-carbohydrate, high-protein diets, we do not recommend such dieting regimens.
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- Russell RR III, Taegtmeyer H: Changes in the citric acid cycle flux and anaplerosis antedate the functional decline in isolated rat hearts. J Clin Invest 1991; 87:384-390
- Council on Foods and Nutrition: A critique of low-carbohydrate ketogenic weight reduction regimens. JAMA 1973; 224:1415-1419
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