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Fatal hyponatremia in a young woman after ecstasy
Kamyar Kalantar-Zadeh*, Minhtri K Nguyen, Roger Chang and Ira Kurtz

This article offers the opportunity to earn one Category 1 credit toward the AMA Physician’s Background A 20-year old, otherwise healthy, female college student
presented in an unresponsive state with respiratory distress after ingesting
ecstasy (3,4-methylenedioxymethamphetamine). She had initial plasma

sodium concentration of 117 mmol/l.
In 2002, a 20-year-old, Asian American woman Investigations Physical examination, blood chemistry panel, urinary
was brought to the emergency room at Harbor- osmolality and electrolytes, arterial blood gas, chest X-ray, and CT scan of
the brain.
multiple tablets of ecstasy (3,4-methylene- Diagnosis Hyponatremia associated with noncardiogenic pulmonary
edema and cerebral edema.
quantities of water while dancing and drinking excessively during a party the night before. She Management Administration of a total of 6.8 l of isotonic saline and 0.245 l
did not report any symptoms upon returning of 3% hypertonic saline with sporadic administration of intravenous
home after the party. In the morning, however, furosemide. The patient died approximately 12 h after admission.
she was found unresponsive and foaming at the KEYWORDS ecstasy, estrogen, hyponatremic encephalopathy, MDMA,
noncardiogenic pulmonary edema

mouth although no seizures were reported. She had rapid and shallow breathing, a weak pulse and did not respond to painful stimuli. The patient was otherwise healthy, with no medical or surgical history or significant family history. She was not taking any medications and was a college student of good standing. In the emergency room the patient was found to be in respiratory distress (respiratory rate 30–35 breaths per minute), hypothermic (temperature 34.7 °C), tachycardic (pulse 123 beats per minute), hypotensive (blood pressure 88/49 mmHg), hypoxemic (oxygen saturation 80% on a non rebreather mask), and nonedematous. Her pupils were symmetrically dilated and minimally reactive to light. No jugular venous distention was K Kalantar-Zadeh is an Associate Professor of Medicine and Pediatrics and noted. Chest auscultation revealed diffuse crackles Director of the Dialysis Expansion Program and Epidemiology at Harbor-UCLA bilaterally. The patient was intubated.
Division of Nephrology and Hypertension, MK Nguyen (co-primary author) Table 1 shows results of initial plasma electro- is an Assistant Professor of Medicine and Director of Consultative Nephrology lyte measurements and arterial blood gas analy ses in the Division of Nephrology, and I Kurtz is Chief of Nephrology, Professor of and how these results changed over time with Medicine, Factor Chair in Molecular Nephrology, and Director of the Molecular Physiology and Biophysics Transport Laboratory at UCLA, Torrance, CA. treatment. Initial laboratory examination also R Chang is a hospitalist at St Joseph’s Hospital in Orange, CA, USA. revealed a blood urea nitrogen (BUN) level of 6.4 mmol/l, a serum glucose level of 5.75 mmol/l, Correspondence
and a serum calcium level of 1.95 mmol/l. *Harbor-UCLA Medical Center, UCLA David Geffen School of Medicine, 1124 W Carson St, C-1 Annex, Box 406, Torrance, CA 90502-2064, USA The patient had an initial serum osmolality of 245 mOsm/kg, urine specific gravity of 1.015, a white blood cell count of 18,300 cells/mm3, Received 1 July 2005 Accepted 20 February 2006
a hemoglobin concentration of 133 g/l, and a platelet count of 310,000 cells/mm3. The chest 2006 Nature Publishing Group
Table 1 Chronologic course of events in the patient after ecstasy (3,4-methylenedioxymethamphetamine) ingestion.
Chemistry panel
Arterial blood gas
Events and
Na (mmol/l;
Cl (mmol/l;
pO (mmHg;
range: 135–
range: 95–
range: 80–
145 mmol/l)
105 mmol/l)
range: 22–
range: 50–
range: 38–
100 mmHg)
26 mmol/l)
120 μmol/l)
Approximately 1 l normal saline in the ambulance normal saline upon arrival in emergency room 20 ml 3% hypertonic saline in intensive care unit saline plus furosemide following nephrology consultation pressure increased to 23 cm, intravenous fluids discontinued GLOSSARY
X-ray showed severe pulmonary edema (Figure 1). concentration [Na+] increased to 129 mmol/l NONCARDIOGENIC
A CT scan of the head showed evidence of after 10 h of hospitalization, but the patient’s PULMONARY EDEMA
hemodynamic status remained unstable; 12 h A status of pulmonary vascular congestion and/or The patient was given a total of 6.8 l of isotonic after admission, she was found to have wide- saline and 0.245 l of 3% hypertonic saline with complex tachycardia, which was followed by intermittent administration of furosemide and pulseless electrical activity. Resuscitation efforts 60 g of mannitol (Table 1). Plasma sodium were unsuccessful, and the patient expired.
KALANTAR-ZADEH ET AL. MAY 2006 VOL 2 NO 5 2006 Nature Publishing Group
Hyponatremia can lead to increased intracranial
pressure, which might trigger the development
of neurogenic pulmonary capillary leak and
result in noncardiogenic pulmonary edema.
Cardiogenic pulmonary edema is highly unlikely
in a young woman with no medical history of
cardiovascular, pulmonary or renal disease.
Encephalopathy is thought to result from brain
edema caused by movement of water into the
brain cells. Hyponatremic encephalopathy can
also manifest as hypercapnic respiratory failure.1
Even in chronic symptomatic hyponatremia,
hypoxia can play a crucial role in morbidity
and mortality.2 The encephalopathic patient
with hyponatremia usually presents with head-
ache, nausea, vomiting, abdominal pain, confu-
sion, and seizures, which can lead to permanent
neurologic sequelae and imminent death due to
brain edema and subsequent herniation.
Several factors that might contribute to Figure 1 Chest X-ray of 20-year-old woman with a plasma sodium concentration
in Box 1. Profuse sweating at a ‘rave party’ can of 117 mmol/l after ecstasy (3,4-methylenedioxy methamphetamine) ingestion. lead to excessive water intake, which ultimately Note the cephalization of pulmonary vasculature consistent with pulmonary results in a decreased concentration of sodium edema, which is noncardiogenic in this case.
in the blood.3 Up to 2 l of perspiration can be lost per hour in a hot environment, especially during intense physical activity such as dancing.4 Box 1 Factors that might contribute to fatal hyponatremia following ecstasy
If MDMA in some way also inhibits perspira- (3,4-methylenedioxymethamphetamine [MDMA]) ingestion. tion, hyponatremia is more likely to occur. A Excessive fluid intake in response to central polydipsia (effect of MDMA on the central nervous system) or polydipsia as a result of perspiration during also stimulate thirst and cause primary poly- rigorous physical activity (e.g. dancing) dipsia independent of perspiration or ambient Fluid third-spacing in the GI tract (ileus) with subsequent abrupt water temperature.5 Moreover, partygoers are usually encouraged to drink large volumes of water to avoid dehydration.4 As in marathon runners, excess antidiuretic Overproduction and/or release of antidiuretic hormone either in response to, hormone (ADH, also known as vasopressin) or independent of, rigorous physical activity release can result from rigorous physical activity Administration of hypotonic or isotonic intravenous fluids such as dancing. MDMA can trigger inappro-priate secretion of ADH independent of the degree of physical activity. In a study of eight healthy drug-free male volunteers Fallon et al. Estrogenic hormones (in menstruating women) showed that concentrations of plasma argi-nine vasopressin increase significantly after Higher intracellular brain volume (relative to older women) or absence of In MDMA users, gastrointestinal motility can decrease, resulting in a large static volume of electrolyte-free water in the lumen of the gastro-intestinal tract.4,7 An ileus with a 2-cm radius would lead to a 7-l water intake and its retention of physical activity (e.g. at the end of a dance in the lumen of the stomach and small intestine.4 This retained water might be absorbed abruptly through the gastrointestinal tract upon cessation hyponatremia have been reported;8–12 most of MAY 2006 VOL 2 NO 5 KALANTAR-ZADEH ET AL. 2006 Nature Publishing Group
Table 2 Comparison of clinical and laboratory findings, course of events, and management and outcome of three hyponatremic
MDMA user
Marathon runner
Post-surgical patient
preoperatively and postoperatively to avoid hypoglycemia no jugular venous distention, bilateral basilar crackles on chest auscultation discontinued, 40 mg intravenous furosemide administered in 6 h) with no sequelae, discharged after 1 day MDMA, 3,4-methylenedioxymethamphetamine; [Na+], sodium concentration; SG, urine specific gravity; UOsm, urine osmolality. these cases were premenopausal women.8–12 reported to be 30 times greater for women than This finding is consistent with the findings of for men, and 25 times greater for menstruant ‘Ayus–Arieff syndrome’, in which women of females than for postmenopausal females.13 The this age develop noncardiogenic pulmonary higher morbidity and mortality rates among edema, hypoxemia and brain edema.13,14 The relative risk of death or permanent neurological to the effects of estrogenic hormones, via damage from hyponatremic encephalopathy is two possible mechanisms: (1) inhibition of KALANTAR-ZADEH ET AL. MAY 2006 VOL 2 NO 5 2006 Nature Publishing Group
cerebral Na+/K+-ATPase activity, which impairs Are there signs and symptoms of pulmonary edema the ability of brain cells to extrude sodium (dyspnea, hypoxemia, congestion) or cerebral edema (headache)? in the initial defense of cell volume; and (2) increased vasoconstriction of cerebral blood vessels by vasopressin, which leads to decreased brain perfusion.15,16 The gender discrepancy could also be due to the fact that women have less muscle mass than men. As half of total body water is located in skeletal muscle cells, an individual with low muscle mass is at high risk for development of severe hyponatremia when a given volume of electrolyte-free water is retained.4 Individuals Figure 2 Algorithm for treatment of premenopausal women with hyponatremia.
with muscle atrophy resulting from illness or a nutritional problem (e.g. anorexia nervosa) are also at risk. In addition, differences in brain adaptation could account for part of the gender Box 2 The Nguyen-Kurtz equation can predict post-intervention plasma
discrepancy—women are less able to adapt to sodium concentration based on pre-intervention plasma sodium concentration, total body water and other factors including the type and amount of administered fluid, urine output and urinary electrolytes.17,18 natremia-associated morbidity. Young patients seem to be affected to a greater degree than older patients, possibly because of the absence of age-related brain cell atrophy and the resulting higher intracellular brain volume. If acute hypo-natremia develops, a larger intracellular brain EMB = (Na+ + K+)input–output = mass balance of Na+ + K+ in a chosen duration of time.
volume could result in a greater increase in cell = [E]IVF × VIVF + [E]oral × Voral + [E]tube feed × Vtube feed + [E]TPN × VTPN volume within the confined space of the skull. − [E]urine × Vurine − [E]GI × VGI − [E]sweat × Vsweat DISCUSSION OF TREATMENT OPTIONS
VMB = Vinput – Voutput = mass balance of H2O in a chosen duration of time.
In edematous patients with otherwise asympto- = VIVF + Voral + Vtube feed + VTPN + Voxidation − Vurine − VGI matic hyponatremia, combined water restric- tion and loop diuretics or vasopressin-receptor antagonists are appropriate treatment options. y = 23.8 + (1.6/100)([G] − 120) where [G] = plasma glucose concentration.
In patients with acute or symptomatic hypo- In patients with euglycemia, y1 = y2 = 23.8 for the sake of simplification.
natremia, however, the administration of a loop , [Na+ + K+] in the administered total parenteral nutrition; [Na+] diuretic plus intravenous saline is often neces- , post-intervention plasma sodium concentration; sary to achieve a higher rate of correction of the water produced as a result of oxidation; V Table 2 outlines two nonfatal cases of hypo- natremia in premenopausal women who had signs and symptoms similar to those of our patient but had favorable outcomes. These to proceed with hypertonic fluid treatment was patients were treated primarily with hypertonic reached after the team reviewed relevant litera- saline or with the diuretic furosemide, and their ture.10 In the setting of non cardiogenic pulmo- symptoms resolved within 48 h. The decision to nary edema and cerebral edema, treatment administer hypertonic saline (plus furosemide of the hyponatremia should be aimed at both therapy) to patients with pulmonary and cerebral correcting dysnatremia and achieving negative edema is counterintuitive and might be ques- tioned by many physicians. Indeed, in the case In the fatal case presented here, the patient’s presented here, the recommendation of hyper- tonic fluid made by the consulting nephrolo- gist was questioned by the emergency room after administra tion of intravenous fluids. The physicians and by the intensivist. Agreement relative contributions of isotonic saline and MAY 2006 VOL 2 NO 5 KALANTAR-ZADEH ET AL. 2006 Nature Publishing Group
hypertonic saline to correction of this patient’s References
hyponatremia can be determined quantitatively 1 Ayus JC and Arieff AI (1995) Pulmonary complications of hyponatremic encephalopathy: noncardiogenic EQUATION
pulmonary edema and hypercapnic respiratory failure. An equation for predicting changes in plasma sodium (Box 2).15 Administration of 6.8 l of isotonic Chest 107: 517–521
saline is predicted to have raised plasma [Na+] 2 Ayus JC and Arieff AI (1999) Chronic hyponatremic by 3.6 mmol/l, whereas infusion of 0.245 l hyper- association of therapies with morbidity and mortality. tonic saline is predicted to have increased plasma JAMA 281: 2299–2304
[Na+] by 3.4 mmol/l. For a given urinary output, et al. (2002) The health effects of ecstasy: a literature review. Drug Alcohol Rev 21: 53–63
the volume of isotonic saline required to raise 4 Cherney DZ et al. (2002) Acute hyponatraemia and the plasma [Na+] to a target value will be signifi- ‘ecstasy’: insights from a quantitative and integrative cantly greater than that of hypertonic saline. In analysis. QJM 95: 475–483
et al. (2004) Polydipsia as another the setting of hyponatremia asso ciated with cere- mechanism of hyponatremia after ‘ecstasy’ (3,4 bral and pulmonary edema, this additional fluid methyldioxymethamphetamine) ingestion. Eur J will worsen volume overload, as was the case Emerg Med 11: 302–304
Rosenthal Foundation, and the Fredrika Taubitz Fund. with this patient. Administration of hypertonic et al. (2002) Action of MDMA (ecstasy) and its metabolites on arginine vasopressin release. Ann saline and furosemide is therefore preferable to NY Acad Sci 965: 399–409
Competing interests
infusion of isotonic saline and furosemide, as 7 Haldane JS and Priestley JG (1916) The regulation of The authors declared they have no competing the former approach facilitates attainment of excretion of water by the kidneys. J Physiol London
50: 296–303
negative water balance by limiting the amount of infusate needed to increase the plasma [Na+] amphetamine (“Ecstasy”) abuse. Am J Med Sci 326:
et al. (2002) Hyponatraemic states CONCLUSIONS
following 3,4-methylenedioxymethamphetamine Nephrologists are often consulted on the manage- (MDMA, ‘ecstasy’) ingestion. QJM 95: 431–437
10 Balmelli C et al. (2001) Fatal brain edema after ment of patients with MDMA-associated hypo- ingestion of ecstasy and benzylpiperazine. Dtsch Med natremia. At the dawn of the 21st century, however, Wochenschr 126: 809–811
many nephrologists, as well as emergency room 11 Parr MJ et al. (1997) Hyponatraemia and death after “ecstasy” ingestion. Med J Aust 166: 136–137
physicians, cardiologists and intensivists, might 12 O’Connor A et al. (1999) Death from hyponatraemia- still be unaware of the potentially fatal outcome induced cerebral oedema associated with MDMA and might not feel comfortable recommending (“Ecstasy”) use. NZ Med J 112: 255–256
13 Ayus JC et al. (2000) Hyponatremia, cerebral edema, administration of hypertonic saline in the pres- and noncardiogenic pulmonary edema in marathon ence of noncardiogenic pulmonary edema. This runners. Ann Intern Med 132: 711–714
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tion) and signs and symptoms of noncardiogenic pulmonary edema (e.g. dyspnea, hypoxemia and 16 Ayus JC et al. (1992) Postoperative hyponatremic pulmonary congestion or edema) in a young encephalopathy in menstruant women. Ann Intern woman with mild to moderate hyponatremia, Med 117: 891–897
17 Kurtz I and Nguyen MK (2003) A simple quantitative should prompt immediate hospitalization (prefer- approach to analyzing the generation of the ably in the intensive care unit) and administra- dysnatremias. Clin Exp Nephrol 7: 138–143
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KALANTAR-ZADEH ET AL. MAY 2006 VOL 2 NO 5 2006 Nature Publishing Group


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