RE: MDMA-Associated Cerebral Edema Resembling Psychogenic Polydipsia?

RE: MDMA-Associated Cerebral Edema Resembling Psychogenic Polydipsia?

The Journal of Emergency Medicine, Vol. 48, No. 1, pp. 81–84, 2015 Copyright Ó 2015 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ ...

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The Journal of Emergency Medicine, Vol. 48, No. 1, pp. 81–84, 2015 Copyright Ó 2015 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ - see front matter

Letters to the Editor , OSMOREGULATORY MECHANISMS DIFFERENTIATE MDMA-ASSOCIATED HYPONATREMIA FROM PSYCHOGENIC POLYDIPSIA

ical features of hyponatremic MDMA users (eg, urine sodium level) could be different from those typical clinical scenarios in which the decrease in solute-free water clearance is exclusively due to overproduction of ADH (eg, lung mass). Concerning the point on the use of mannitol for treatment of MDMA-induced acute symptomatic hyponatremia, osmotic diuresis is not advocated as the first line of therapy in this clinical setting. As mentioned in our article, the rarity of this phenomenon precludes any evidence-based specific consensus for its management, and current recommendations are primarily based on extrapolation of available data on any state of acute hyponatremia. Although a variety of regimens, including saline solutions, furosemide, and water restriction, have been used for the previously reported cases of MDMAassociated hyponatremia, mannitol has rarely been used in this setting. Therefore, based on the biological plausibility and the clinical success of the two reported cases, it would be sound to consider its use in cases where other therapeutic options are not readily available.

, To the Editor: Dr. Ligtenberg and colleagues have raised two interesting points regarding the diagnosis and treatment of 3,4-methylenedioxymethamphetamine (MDMA) associated hyponatremia. In order to maintain the plasma osmolality within a very narrow range (i.e., 275 290 mosmol/kg), despite significant variations that exist in the fluid and solute intake of a normal individual, kidneys show an amazing capability to substantially modify water clearance and urine osmolality on a continuous basis; urine osmolality can vary from 50 to 1200 mosmol/kg in normal adults. In psychogenic polydipsia and excessive water intake, where the osmoregulatory mechanisms are intact, plasma hypo-osmolality results in suppression of antidiuretic hormone (ADH), which then leads to significant excretion of free water through maximally diluted urine to correct hyponatremia. Therefore, urine osmolality typically falls to < 100 mosmol/kg (and specific gravity to < 1.003) in these cases. In contrast, values greater than these in a hyponatremic patient point to aberrancy in the osmoregulatory mechanisms and the inability of the kidneys to excrete solute-free water (aquaresis), most commonly driven by elevated levels of ADH. In our patient with severe hyponatremia, urine osmolality was found to be as high as 505 mosmol/kg (and a specific gravity of 1.013). This indicates lack of appropriate suppression of ADH levels, despite plasma hypoosmolality, and is incompatible with a diagnosis of psychogenic polydipsia. These laboratory data further supported the clinical findings, including hyperthermia, dilated pupils, recent MDMA use, and lack of any psychiatric history. It is also noteworthy that while nonosmotic release of ADH is considered a major cause for hyponatremia in MDMA users, several other mechanisms have also been implicated, including MDMA-induced polydipsia, hyperthermia, rigorous physical activity, and excessive perspiration. Therefore, the biological and clin-

Amir Kazory, MD Division of Nephrology Hypertension, and Renal Transplantation University of Florida Gainesville, FL http://dx.doi.org/10.1016/j.jemermed.2014.07.055 , RE: MDMA-ASSOCIATED CEREBRAL EDEMA RESEMBLING PSYCHOGENIC POLYDIPSIA? , To The Editor: In the June issue of the Journal, Ghatol and Kazory describe a case of cerebral edema after excessive fluid intake during 3,4-methylenedioxymethamphetamine (MDMA) use in a 20-year-old previously healthy woman (1). They review current knowledge about the mechanisms by which MDMA may cause hyponatremia and cerebral edema, and suggest that there might be a role 81

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for mannitol causing osmotic diuresis in similar cases. Previously, we described a 38-year-old previously healthy woman, who, after 1 day of anxiety and paranoid hallucinations, compulsively drank 6 L of water in a few hours. She did not use any medications. Cerebral computed tomography (CT) scan showed diffuse cerebral edema and cerebellar herniation. Administration of mannitol did not result in any improvement (2). Goldman et al. found impairment of maximal urine dilution capacity, and free water clearance that could not be attributed to inadequate suppression of vasopressin in psychiatric patients with water intoxication (3). Water intoxication resulting in hyponatremia and cerebral edema could be seen as an inability to reach maximal water diuresis, caused by an altered “osmostat” setting working at a lower osmolality, or decreased sensitivity of the central nervous system to hyponatremia. Differences from the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which has also been suggested to play a role in MDMA-associated hyponatremia, are increased urine osmolality and urine sodium in SIADH vs. normal to decreased urine osmolality and normal urine sodium in psychogenic polydipsia (which appears to be the case in the patient described by Ghatol and Kazory). Therapeutic options that have been proven to be effective in mild cases of polydipsia resulting in hyponatremia are fluid restriction and behavioral approaches limiting polydipsia (4). The initial treatment advised in current literature for patients with marked neurologic symptoms is hypertonic saline. If osmotic diuresis, as suggested by the authors, can improve the prognosis of severe cases, it has yet to be proven. Jack J. Ligtenberg, MD, PHD Tycho J. Olgers, MD Evelien K. van de Meeberg, MD Jan C. ter Maaten, MD, PHD Emergency Medicine University Medical Center Groningen Groningen, The Netherlands http://dx.doi.org/10.1016/j.jemermed.2013.08.148 REFERENCES 1. Ghatol A, Kazory A. Ecstasy-associated acute severe hyponatremia and cerebral edema: a role for osmotic diuresis? J Emerg Med 2012;42:e137–40. 2. Ligtenberg JJM, Wymenga ANM, Tulleken JE, van der Werf TS, Zijlstra JG. A lethal complication of psychogenic polydipsia: cerebral edema and herniation. Int Care Med 1998;24:644–5. 3. Goldman MB, Luchins DJ, Robertson GL. Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia. N Engl J Med 1988;318:397–403. 4. Vieweg WV, Karp BI. Treatment strategies in the polydipsiahyponatremia syndrome. J Clin Psychiatry 1994;55:154–60.

, ACUTE CYANIDE INTOXICATION DUE TO APRICOT SEEDS: IS “EVIDENCE” COUNTABLE? , To the Editor: We read the letter to the editor by Akıl et al. with great interest (1). However, we have serious doubts about assigning cyanide as the poisoning agent. This letter also has raised some concerns about the diagnostic, clinical, and therapeutic aspects of the case reported. The child did not exhibit the classic symptoms of cyanide poisoning, for example, high anion gap metabolic acidosis. In addition, the authors did not mention the child’s lactate level, which can be used as a surrogate marker for cyanide intoxication when the blood cyanide level cannot be measured due to technical limitations (2). It has been shown that in acute cyanide poisoning, a lactate level > 8 mmol/L is highly specific for cyanide intoxication (3). Simple bedside clues, such as the presence of bright red venous blood or impaired oxygen extraction reflected as increased peripheral venous partial pressure of oxygen (>40 mm Hg) or decreased SaO2-SVO2, were not utilized in this case to reinforce the diagnosis (4). The child could have accidentally ingested another chemical, material, or medicine; toxic screening in urine or blood was not done to rule out these substances. In addition, the authors did not mention other conditions, such as hypoglycemia or hyponatremia, which could have contributed to altered sensorium. Yam bean seed poisoning can mimic acute cyanide intoxication from a cyanogenic glycoside-containing plant, or many other plants could have contributed to this poisoning, yet a discussion of the differential diagnosis is not provided (5). There was no evidence anywhere in the report that this child was intubated despite the Glasgow Coma Scale score (pediatric version) of 6. It was extremely imprudent to administer activated charcoal to this child without protecting the airway, as she was unconscious and likely to have a seizure in the near future. In addition, activated charcoal might not be effective in countering acute cyanide poisoning because of the high potency of cyanide, the rapid onset of poisoning, and the small size of cyanide molecules. Not only that, but the dose administrated was not correct. Above all, use of a Cyanokit in this case needs reconsideration for want of more evidence, as this report does not provide evidence to substantiate that the child was intoxicated by cyanide. Hydroxocobalamin has the ability to scavenge nitric oxide effects, from which the child’s blood pressure would have increased; this has been demonstrated even in healthy volunteers. This report