Muscle cell membrane damage by very low serum sodium

Varghese, Joye; Balakrishnan, Vallath; Sadasivan, Shine; Nair, Prakash; Narayanan, V. A.

doi:10.4314/pamj.v3i1.52453

Cited by 3 publications

(4 citation statements)

References 11 publications

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“…It is accepted that low sodium levels lead to dysfunction of the sodium/calcium pump, which can activate intracellular proteases and lipases that are responsible for lysis of rhabdomyocytes 4. Of note, rhabdomyolysis significantly improved within 48 hours following correction of hyponatremia.…”

Section: Discussionmentioning

confidence: 99%

Adenoma mimicking hyponatremia of SIAD

Ilaiwy¹,

Thompson

Waheed

2018

BMJ Case Reports

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Hyponatremia is a common electrolyte disorder, with prevalence as high as 20% in inpatient settings. It is classified based on volume status, urine sodium and osmolality results. While this approach might help narrow down the differential diagnoses, it can leave other diagnoses unentertained. In this case, we report recurrent and refractory hyponatremia secondary to hypocortisolism due to non-functioning pituitary macroadenoma. Interestingly, urine studies mimicked syndrome of inappropriate antidiuresis, but exclusively responded to hydrocortisone replacement. Hospital course was also complicated by hyponatremia-induced rhabdomyolysis, which is a rare complication of severe hyponatremia. We also discuss the role of anchoring heuristics and how they influence the physician’s decision leading to possible diagnostic errors. One way to minimise the effect of anchoring bias on physicians is their cognitive awareness of such bias. In addition, discussing complicated cases with all members of medical team can highlight the clinician’s thought processes, share uncertainty and help broaden differential diagnoses.

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Section: Discussionmentioning

confidence: 99%

Adenoma mimicking hyponatremia of SIAD

Ilaiwy¹,

Thompson

Waheed

2018

BMJ Case Reports

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“…Another theory is that in acute hyponatremia, due to lower osmolality of extracellular fluid, cells start to swell and in order to maintain cell membrane integrity, intracellular potassium is extruded for hours, which in turn lowers the transmembrane potential. If the hyponatremia state is not corrected, the stressed cells release creatine kinase and myoglobin with cell injury [ 6 , 7 , 14 ]. The serum creatine kinase may elevate after 48 to 96 hours of hyponatremia either due to the lowered sodium level itself or the rapid correction of hyponatremia [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Craniopharyngioma presenting with severe hyponatremia, hyponatremia-induced myopathy, and panhypopituitarism: a case report

et al. 2017

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BackgroundCraniopharyngiomas are rare intracranial tumors commonly presenting with neurological symptoms. Reports of severe hyponatremia as a presenting manifestation of a craniopharyngioma and hyponatremia-induced myopathy are rare. We report the case of a patient with craniopharyngioma presenting with severe hyponatremia, panhypopituitarism, and hyponatremia-induced myopathy.Case presentationA 52-year-old Sri Lankan man presented with anorexia, nausea, fatigue, generalized muscle weakness, and cramps for 1 week. The onset of his illness had been preceded by vomiting and diarrhea for 1 day which he attributed to food poisoning. On examination, he had an apathetic disposition with a generalized “sallow complexion.” He was not dehydrated. Apart from reduced muscle power (4/5) and hyporeflexia, the neurological examination was normal. His serum sodium was 102 mmol/l; potassium 4.1 mmol/l; chloride 63 mmol/l; plasma osmolality 272 mosm/KgH2O; urine osmolality 642 mosm/KgH2O; and urine sodium 79 mmol/l. His creatine phosphokinase was 12,400 U/l, lactate dehydrogenase 628 U/l, aspartate aminotransferase 360 U/l, and alanine aminotransferase 64 U/l. His hormone profile revealed panhypopituitarism. An electromyogram showed nonspecific abnormalities while a muscle biopsy did not show any pathology. Magnetic resonance imaging of his brain demonstrated a well-defined craniopharyngioma with suprasellar extension. His pituitary gland was compressed and the pituitary stalk was displaced by the tumor. He had marked improvement in muscle power and rapid reduction of serum creatine phosphokinase levels paralleling the correction of severe hyponatremia, even before the initiation of hormone replacement.ConclusionsThis case illustrates the rare presentation of severe hyponatremia and hyponatremia-induced myopathy in patients with craniopharyngioma, awareness of which would facilitate early appropriate investigations and treatment.

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“…This situation seems to be more common in patients under the effect of various medications, especially thiazide diuretics, proton pump inhibitors and trimethoprim-sulfamethoxazole. ( 6 )…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism by which hyponatremia induces rhabdomyolysis seems to be dysfunction of the sodium/calcium pump, which leads to the activation of the proteases and lipases that are responsible for cell lysis. ( 4 , 6 ) There is another theory arguing that the decrease in the osmolarity of the extracellular fluid leads to the outflow of potassium from the cells, resulting in its consequent depletion and cell destruction. ( 7 ) This last mechanism, reflecting the inability of regulating cell volume, suggests an explanation for the occurrence of rhabdomyolysis, both in hyponatremia and in its correction, which is another situation that has been recently identified.…”

Section: Discussionmentioning

confidence: 99%

Recurrent rhabdomyolysis secondary to hyponatremia in a patient with primary psychogenic polydipsia

Aguiar¹,

Monteiro²,

Coutinho³

2015

Revista Brasileira De Terapia Intensiva

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Rhabdomyolysis is characterized by the destruction of skeletal muscle tissue, and its main causes are trauma, toxic substances and electrolyte disturbances. Among the latter is hyponatremia-induced rhabdomyolysis, a rare condition that occurs mainly in patients with psychogenic polydipsia. Psycogenic polydipsia mostly affects patients with schizophrenia, coursing with hyponatremia in almost 25% of the cases. It is also in this context that rhabdomyolysis secondary to hyponatremia occurs most often. In this article, the case of a 49-year-old male with a history of schizophrenia, medicated with clozapine, and brought to the emergency room in a state of coma and seizures is described. Severe hypoosmolar hyponatremia with cerebral edema was found on a computed tomography examination, and a subsequent diagnosis of hyponatremia secondary to psychogenic polydipsia was made. Hyponatremia correction therapy was started, and the patient was admitted to the intensive care unit. After the hyponatremia correction, the patient presented with analytical worsening, showing marked rhabdomyolysis with a creatine phosphokinase level of 44.058UI/L on day 3 of hospitalization. The condition showed a subsequent progressive improvement with therapy, with no occurrence of kidney damage. This case stresses the need for monitoring rhabdomyolysis markers in severe hyponatremia, illustrating the condition of rhabdomyolysis secondary to hyponatremia induced by psychogenic polydipsia, which should be considered in patients undergoing treatment with neuroleptics.

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Muscle cell membrane damage by very low serum sodium

Cited by 3 publications

References 11 publications

Adenoma mimicking hyponatremia of SIAD

Adenoma mimicking hyponatremia of SIAD

Craniopharyngioma presenting with severe hyponatremia, hyponatremia-induced myopathy, and panhypopituitarism: a case report

Recurrent rhabdomyolysis secondary to hyponatremia in a patient with primary psychogenic polydipsia

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