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Unilateral Acute Anterior Compartment Syndrome from Correction of Psychogenic Polydipsia-Induced Hyponatremia
CLINICAL COMMUNICATION TO THE EDITOR
Unilateral Acute Anterior Compartment Syndrome from Correction of Psychogenic Polydipsia-Induced Hyponatremia
The patient was emergently taken to the operating room, where a fasciotomy was performed. The anterior tibialis extensor, digitorum longus, and extensor hallucis longus muscles appeared ischemic. Four days after surgery the patient’s serum creatine kinase trended down to 1469 U/L.
To the Editor:
DISCUSSION
Acute compartment syndrome from rhabdomyolysis is a rare complication of treating acute hyponatremia from psychogenic polydipsia.1,2 We report the first case of unilateral acute compartment syndrome as a complication of correcting psychogenic polydipsia-induced hyponatremia.
CASE DESCRIPTION A 59-year-old man with a history of syndrome of inappropriate antidiuretic hormone secretion (on salt tablets), psychogenic polydipsia, and coronary artery disease was admitted from prison for altered mentation. After being unable to urinate for a required random urine drug screen, he consumed 30 glasses of water. Upon arrival he had a witnessed seizure in the emergency room; the patient had no prior history of seizures. With a sodium level of 111 mEq/L, serum osmolality of 236 mOsm/kg, and urine osmolality of 577 mOsm/kg, he received 3% normal saline with 1500 mL fluid restriction. On day 3 the patient’s mental status improved, and sodium was 124 mEq/L. He was clinically stable but complained of a new right foot drop with inability to dorsiflex his right ankle. Neurologic examination was unrevealing except for inability to dorsiflex his right foot. A duplex ultrasound examination was negative for deep vein thrombosis. A stat right lower extremity computed tomography scan showed no fracture but raised concern for anterio-tibial compartment edema; serum creatine phosphokinase was 37,096 U/L. General surgery was consulted, who determined an anteriotibial compartment pressure of 14 mm Hg but a high clinical suspicion for anterior acute compartment syndrome.
Although only 2 cases of bilateral anterior acute compartment syndrome have been reported in patients undergoing treatment for psychogenic polydipsia-induced hyponatremia,1,2 unilateral anterior acute compartment syndrome associated with this condition has yet to be described in the literature. Additionally, acute compartment syndrome as a complication of hyponatremia correction from psychogenic polydipsia has never been reported in the United States. We report a patient who developed anterior acute compartment syndrome secondary to rhabdomyolysis during treatment of hyponatremia. The mechanism of hyponatremia-induced muscle injury is unclear. It is hypothesized that acute hyponatremia from water intoxication causes cellular swelling due to lowered osmolality of extracellular fluid. As cellular swelling normalizes within hours from extrusion of intracellular potassium, this lowers the transmembrane potential, leading to rhabdomyolysis with release of muscle creatine kinase and myoglobin.3 Given that hyponatremia from psychogenic polydipsia is common, acute neurologic limb symptoms during sodium correction should instigate a high clinical suspicion for acute compartment syndrome from rhabdomyolysis in these patients. Early diagnosis and treatment can prevent permanent neuromuscular dysfunction and kidney injury from high levels of circulating serum muscle proteins. Muhammad Omer Zaman, MDa Ethan Greenberg, MDa Qalb Abbas Khan, MDa Naveedullah Jan, MDa Sania Bashir, MDa Mohammad Khalid Mojadidi, MDb a
Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a key wrote in writing the manuscript. Requests for reprints should be addressed to Mohammad Khalid Mojadidi, MD, Division of Cardiology, Department of Medicine, University of Florida Health, Shands Hospital, 1600 SW Archer Road, North Tower, M-430, Gainesville, FL 32608. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2016 Elsevier Inc. All rights reserved.
Department of Medicine Crozer Chester Medical Center Upland, Pa b Division of Cardiology Department of Medicine University of Florida College of Medicine Gainesville
http://dx.doi.org/10.1016/j.amjmed.2016.06.026
2
References 1. Maiocchi L, Bernardi E. Acute anterior compartment syndrome associated with psychogenic polydipsia. Australas Psychiatry. 2012;20(2): 159-161.
The American Journal of Medicine, Vol -, No -,
-
2016
2. Dubin I, Gelber M, Schattner A. Rare times rare: the hyponatremia, rhabdomyolysis, anterior compartment syndrome sequence. JRSM Open. 2016;7(5), 2054270416629326. 3. Zaidi AN. Rhabdomyolisis after correction of hyponatremia in psychogenic polydipsia possibly complicated by ziprasidone. Ann Pharmacother. 2005;39:1726-1731.
Unilateral Acute Anterior Compartment Syndrome from Correction of Psychogenic Polydipsia-Induced Hyponatremia
The patient was emergently taken to the operating room, where a fasciotomy was performed. The anterior tibialis extensor, digitorum longus, and extensor hallucis longus muscles appeared ischemic. Four days after surgery the patient’s serum creatine kinase trended down to 1469 U/L.
To the Editor:
DISCUSSION
Acute compartment syndrome from rhabdomyolysis is a rare complication of treating acute hyponatremia from psychogenic polydipsia.1,2 We report the first case of unilateral acute compartment syndrome as a complication of correcting psychogenic polydipsia-induced hyponatremia.
CASE DESCRIPTION A 59-year-old man with a history of syndrome of inappropriate antidiuretic hormone secretion (on salt tablets), psychogenic polydipsia, and coronary artery disease was admitted from prison for altered mentation. After being unable to urinate for a required random urine drug screen, he consumed 30 glasses of water. Upon arrival he had a witnessed seizure in the emergency room; the patient had no prior history of seizures. With a sodium level of 111 mEq/L, serum osmolality of 236 mOsm/kg, and urine osmolality of 577 mOsm/kg, he received 3% normal saline with 1500 mL fluid restriction. On day 3 the patient’s mental status improved, and sodium was 124 mEq/L. He was clinically stable but complained of a new right foot drop with inability to dorsiflex his right ankle. Neurologic examination was unrevealing except for inability to dorsiflex his right foot. A duplex ultrasound examination was negative for deep vein thrombosis. A stat right lower extremity computed tomography scan showed no fracture but raised concern for anterio-tibial compartment edema; serum creatine phosphokinase was 37,096 U/L. General surgery was consulted, who determined an anteriotibial compartment pressure of 14 mm Hg but a high clinical suspicion for anterior acute compartment syndrome.
Although only 2 cases of bilateral anterior acute compartment syndrome have been reported in patients undergoing treatment for psychogenic polydipsia-induced hyponatremia,1,2 unilateral anterior acute compartment syndrome associated with this condition has yet to be described in the literature. Additionally, acute compartment syndrome as a complication of hyponatremia correction from psychogenic polydipsia has never been reported in the United States. We report a patient who developed anterior acute compartment syndrome secondary to rhabdomyolysis during treatment of hyponatremia. The mechanism of hyponatremia-induced muscle injury is unclear. It is hypothesized that acute hyponatremia from water intoxication causes cellular swelling due to lowered osmolality of extracellular fluid. As cellular swelling normalizes within hours from extrusion of intracellular potassium, this lowers the transmembrane potential, leading to rhabdomyolysis with release of muscle creatine kinase and myoglobin.3 Given that hyponatremia from psychogenic polydipsia is common, acute neurologic limb symptoms during sodium correction should instigate a high clinical suspicion for acute compartment syndrome from rhabdomyolysis in these patients. Early diagnosis and treatment can prevent permanent neuromuscular dysfunction and kidney injury from high levels of circulating serum muscle proteins. Muhammad Omer Zaman, MDa Ethan Greenberg, MDa Qalb Abbas Khan, MDa Naveedullah Jan, MDa Sania Bashir, MDa Mohammad Khalid Mojadidi, MDb a
Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a key wrote in writing the manuscript. Requests for reprints should be addressed to Mohammad Khalid Mojadidi, MD, Division of Cardiology, Department of Medicine, University of Florida Health, Shands Hospital, 1600 SW Archer Road, North Tower, M-430, Gainesville, FL 32608. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2016 Elsevier Inc. All rights reserved.
Department of Medicine Crozer Chester Medical Center Upland, Pa b Division of Cardiology Department of Medicine University of Florida College of Medicine Gainesville
http://dx.doi.org/10.1016/j.amjmed.2016.06.026
2
References 1. Maiocchi L, Bernardi E. Acute anterior compartment syndrome associated with psychogenic polydipsia. Australas Psychiatry. 2012;20(2): 159-161.
The American Journal of Medicine, Vol -, No -,
-
2016
2. Dubin I, Gelber M, Schattner A. Rare times rare: the hyponatremia, rhabdomyolysis, anterior compartment syndrome sequence. JRSM Open. 2016;7(5), 2054270416629326. 3. Zaidi AN. Rhabdomyolisis after correction of hyponatremia in psychogenic polydipsia possibly complicated by ziprasidone. Ann Pharmacother. 2005;39:1726-1731.