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Year : 2019  |  Volume : 22  |  Issue : 8  |  Page : 1166-1168

Osmotic demyelination syndrome following acute kidney injury with hypernatremia

Department of Medicine, Abubakar Tafawa Balewa University Teaching Hospital, PMB 0117, Bauchi, Bauchi State, Nigeria

Date of Acceptance18-Feb-2019
Date of Web Publication14-Aug-2019

Correspondence Address:
Dr. N H Alkali
Department of Medicine, Abubakar Tafawa Balewa University Teaching Hospital, PMB 0117, Bauchi, Bauchi State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njcp.njcp_542_18

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Osmotic demyelination syndrome (ODS) is a life-threatening neurological condition often associated with rapid correction of hyponatremia. While ODS is thought to be rare, with prevalence rates of not more than 0.5% in autopsy series, mortality rates are as high as 90% in some studies. Thus, timely diagnosis and life-saving treatment rest on a high index of suspicion among clinicians. In this report, we discuss the case and literature review of a 45-year-old female with sepsis, acute kidney injury, and spontaneous hypernatremia who developed ODS but responded to therapy with high dose steroids, antibiotics, and supportive care.

Keywords: Acute kidney injury, hypernatremia, osmotic demyelination syndrome, pneumonia, sepsis, steroids

How to cite this article:
Alkali N H, Jibrin Y B, Dunga J A, Abdu A. Osmotic demyelination syndrome following acute kidney injury with hypernatremia. Niger J Clin Pract 2019;22:1166-8

How to cite this URL:
Alkali N H, Jibrin Y B, Dunga J A, Abdu A. Osmotic demyelination syndrome following acute kidney injury with hypernatremia. Niger J Clin Pract [serial online] 2019 [cited 2023 Jan 29];22:1166-8. Available from:

   Introduction Top

Osmotic demyelination syndrome (ODS) is a life-threatening neurological disorder associated with rapid correction of hyponatremia.[1] However, it is also found in other medical conditions.[2] While ODS is thought to be rare, the prevalence rate is as high as 0.5% in some autopsy series, and mortality rates range widely between 6% and 90%.[3] Thus, timely diagnosis and management of affected patients are essential to medical practice. We herein report the case of a female patient with acute kidney injury (AKI) and hypernatremia who developed ODS but responded to treatment. We then reviewed the relevant literature.

   Case Report Top

A 45-year-old female Caucasian presented to the hospital with 1 month of cough, fever, and weight loss. Chest x-ray revealed right lobar pneumonia with consolidation. She improved after 2 days of intravenous (IV) co-amoxiclav and was discharged on oral treatment. She received no IV fluids and had normal serum electrolytes, urea, and creatinine.

Three days later, she was found unconscious at home. Past medical history revealed she was not epileptic, diabetic, or hypertensive, and she never smoked or drank alcohol. She had no history of jaundice or kidney disease. Drug history revealed no record of penicillin allergy and she had not been on any medication recently.

At the second admission, she had a temperature of 38.9°C, a pulse of 112 beats per minute, blood pressure 122/70 mm Hg, and generalized petechiae with ecchymosis. Respiratory rate was 28 cycles per minute, with coarse crepitations heard over both lungs. Glasgow Coma Scale was 9/15 (eye opening 2; best motor response 4; best verbal response 3), with normal, reactive pupils. There was global hypotonia, exaggerated deep tendon reflexes, and bilateral extensor plantar responses. We diagnosed sepsis with disseminated intravascular coagulation to keep in view Lassa fever, which was locally endemic.

Investigations revealed a normal clotting profile, hematocrit of 14%, platelet count of 80,000, and normal white blood cell (WBC) counts. Serial blood cultures yielded no growth. HIV screening and polymerase chain reaction (PCR) test for Lassa fever virus infection were negative. Urine was positive for blood and protein, but abdominal ultrasound and electrocardiography (ECG) were normal. Serum glucose, glycated hemoglobin, and liver enzymes were normal, but electrolytes, urea, creatinine, and serum osmolarity were all elevated at presentation and persisted for 2 weeks [Table 1].
Table 1: Serum electrolytes, urea, creatinine, glucose, and osmolarity in a patient with osmotic demyelination syndrome

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Brain magnetic resonance imaging (MRI) showed multiple lesions in the pons, thalamus, and basal ganglia that were hypointense on T1 and hyperintense on FLAIR and T2-weighted sequences [Figure 1]. The radiologist suggested lacunar infarcts or multiple sclerosis, but we favored ODS in view of the clinical scenario and high serum osmolarity. Lumbar puncture yielded normal cerebrospinal fluid on microscopy and chemistry with no bacterial growth on culture.
Figure 1: Brain magnetic resonance imaging in (a) axial FLAIR and (b) sagittal T2-weighted sequences showing hyperintense lesions in the pons, midbrain, and thalamus (arrows) consistent with osmotic demyelination syndrome

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She received intramuscular dexamethasone 8 mg q8-hourly for 5 days followed by oral prednisolone 30 mg daily for 10 days, which was then tapered off. She also received IV ceftriaxone 2 g twice daily for 10 days, 5% dextrose water, and supportive care. Four weeks after admission, she regained consciousness but had impaired speech and muscle power which improved gradually. Repeat chest x-rays showed resolution of lung consolidation. She was discharged home 2 months later with muscle power of Grades 3-4/5 in all limbs.

   Discussion Top

In its classic form, ODS, also called central pontine myelinolysis, presents with encephalopathy and seizures due to hyponatremia, which improve with rapid correction of serum sodium. However, patients soon deteriorate in the second phase when demyelination of corticospinal and corticobulbar tracts at the level of the pons give rise to dysarthria and quadriparesis.[3]

This predilection for the pons explains the old terminology, but other parts of the brain are also affected. Indeed, ODS spares the pons in extra-pontine myelinolysis.[4] When lesions involve the cerebral hemispheres, midbrain, medulla, or pontine tegmentum, clinical features may include aphasia, ataxia, dysphagia, dystonia,  Parkinsonism More Details, cranial nerve palsies, seizures, coma, and the locked-in syndrome.[3],[5]

ODS is also seen in patients with normonatremia or hypernatremia, especially among those with diabetes mellitus, chronic alcoholism, malnutrition, liver transplantation, pituitary surgery, lithium toxicity, hypokalemia, hypophosphatemia, and chronic kidney disease.[2],[6]

The pathologic hallmark is brain demyelination in areas, such as the pons, with abundant grey and white matter interface.[2] The exact mechanism is not known, but evidence implicates a reduced adaptive capacity of neuroglia to large shifts in serum osmolarity, activation of microglia, and disruption of the blood-brain barrier with the release of endothelial cell cytokines and neutral proteases. These processes are all thought to cause damage to myelin and oligodendrocytes.[2],[7]

Diagnosis is mainly clinical, supported by findings of symmetric, demyelinating lesions on brain MRI. Lesions often appear triangular on axial images and “bat-wing” or “butterfly” shaped on coronal views.[3],[7] However, MRI findings may be normal or delayed for up to 4 weeks. Brain computed tomography (CT) scans may also reveal lesions but are less sensitive than MRI.

Treatment involves the use of high-dose steroids and correction of hypernatremia with desmopressin or 5% dextrose in water.[1],[7] Other treatments that have been tried with varying degrees of success include plasma exchange, IV immunoglobulin, and minocycline.[8],[9],[10]

Our patient initially had pneumonia, which was treated with co-amoxiclav. She soon returned with high serum osmolarity, AKI, and hypernatremia suggestive of ODS. Tests were negative for diabetes mellitus and chronic liver disease, suggesting AKI and hypernatremia were the major risk factors for ODS. She subsequently responded to therapy with IV fluids, steroids, and antibiotics, though she remains limited in speech and muscle function.

Sepsis was the likely cause of AKI, in view of septicemia at her second admission. She had normal blood pressure and no history of excess fluid loss recently, which made hypovolemia an unlikely cause. However, we could not totally exclude drug-induced nephritis as a contributing factor even with the negative history of penicillin allergy.

This report highlights the need for internists, neurologists, and nephrologists to consider ODS in the differential diagnosis of unconscious patients with AKI. While hypernatremia associated with ODS often arises from rapid correction of hyponatremia, it may also occur de-novo due to AKI, as seen in this patient. A brain MRI helps to support the diagnosis of ODS, while prompt therapy with steroids and supportive care may improve survival.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Pearce JMS. Central pontine myelinosis. Eur Neurol 2009;61:59-62.  Back to cited text no. 1
Jha AA, Behera V, Jairam A, Baliga KV. Osmotic demyelination syndrome in a normonatremic patient of chronic kidney disease. Ind J Crit Care Med2014;18:609-11.  Back to cited text no. 2
Rao PB, Azim A, Singh N, Baronia AK, Kumar A, Poddar B. Osmotic demyelination syndrome in intensive care unit. Ind J Crit Care Med 2015;19:166-9.  Back to cited text no. 3
Zunga PM, Farooq O, Dar MI, Dar IH, Rashid S, Rather AQ, et al. Extrapontine demyelination syndrome. Ann Neusosci 2015;22:51-3.  Back to cited text no. 4
Feng XM, Zhao T, Zhou CK, Liu JY. Psychiatric symptoms and limb tremors associated with central pontine myelinosis: A case of alcoholism without hyponatremia. Exp Ther Med2016;12:3485-7.  Back to cited text no. 5
Hirosawa T, Shimizu T. Osmotic demyelination syndrome due to hyperosmolar hyperglycemia. Clev Clin J Med 2018;85:511-3.  Back to cited text no. 6
Dagur G, Khan SA. Current concepts in pontine myelinosis: Review of literature. Transl Biomed 2015:6:38.  Back to cited text no. 7
Kumon S, Usui R, Kuzuhara S, Nitta K, Koike M. The improvement of the outcome of osmotic demyelination syndrome by plasma exchange. Intern Med 2017;56:733-6.  Back to cited text no. 8
Thirunavukarasu S, Biswas A, Furruqh F, Gnanavelan A. Response to IV immunoglobulin in a case of osmotic demyelination syndrome. BMJ Case Rep 2015. doi: 10.1136/bcr-2015-212985.  Back to cited text no. 9
Tagaki H, Sugimura Y, Suzuki H, Iwama S, Izumida H, Fujisawa H, et al. Minocycline prevents osmotic demyelination associated with aquaresis. Kidney Int 2014;86:954-64.  Back to cited text no. 10


  [Figure 1]

  [Table 1]


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