Year : 2018 | Volume : 6 | Issue : 4 | Page : 116 - 119  

Case Reports
Post partum hypernatremia with necrotizing myopathy and CSVT

Gopal Poduval*

Department of Neurology & Medicine, Global Hospitals, Hyderabad

*Corresponding author:  



The complications in the post partum period can be varied and sometimes devastating. Venous thrombosis is one of the most common post partum event followed by metabolic abnormalities. Here we discuss a patient with hypernatremia, rhabdomyolysis and CSVT occurring during the post partum period.

Key words: Post partum, hypernatremia, rhabdomyolysis, cerebral sinus venous thrombosis (CSVT)


The post partum state is well known for several complications viz. vascular and metabolic. Occasionally multiple complications may occur at the same time yet patient may recover completely. Vascular complications mostly venous and arterial infarcts are most common and at times can cause significant mortality and morbidity. Electrolyte abnormalities are less common and less life threatening and easier to correct. Dehydration either due to gastrointestinal loss or due to deliberate decreased intake of fluids is common factor for both the vascular and metabolic abnormalities.

Case Report:

24 years old female patient came to the ER on with the complaints of fever with chills, shortness of breath and bilateral upper limb tremors of 20 days duration. Patient was a housewife and had undergone full term normal delivery 20 days back and 2 days after delivery she began having fever with chills. . She was not a known patient of diabetes, hypertension and was euthyroid when last checked. During her earlier pregnancy she had an unremarkable post partum period. For the present symptoms she had received parenteral antibiotics and antimalarials before she was referred here. There was no history of loss of consciousness, altered behavior   , seizures, headache or vomiting.

On admission patient was conscious and oriented. Her temperature was 102 deg F, pulse 96/min regular with all peripheral pulses being felt. Her blood pressure was 110/60 mm Hg and she was maintaining an oxygen saturation of 100% while breathing room air. A random blood sugar done at the time of admission was 115mg%.On neurological examination patient was oriented to time and person. Her speech was normal and there were no cranial nerve deficits. She had 4/5 power equally on all limbs, the deep tendon jerks were diminished symmetrically and plantar reflex showed bilateral normal flexor response. Patient had bilateral upper limb large amplitude action tremors more proximal than distal both postural and aggravated on movement. Evaluation of sensory and cerebellar functions was normal. Optic fundi were normal. Except for a small palpable spleen examination of other systems were unremarkable Her hematological and biochemical parameters on admission were as follows: Blood Hemoglobin 12.4gm%, Total leukocyte count 10,400/cu mm, with polymorphonuclear leucocytosis, platelet count 1.28L/cu mm, total bilirubin 0.4mg%, ALT 126 IU/L, AST 315 IU/L, serum albumin 2.3mg/dl, serum globulin 4.4mg/dl, blood urea 70mg/dl, serum creatinine 2.0 mg/dl, serum lactate dehydrorgenase 2495 IU/L, serum uric acid 4.5mg%, serum sodium 165 mEq/L, serum potassium 3.1 mEq/L and serum calcium 6.7 mEq/L. Over the next three days patient had frequent large volume diarrhea, fever and developed altered sensorium. Her urine had turned dark brown and she became oliguric. Investigations revealed persistent hypernatremia (serum sodium 168 mill Eq/L,), serum creatine phophokinase raised several fold to 1, 11,000 U/L and myogloblinuria. She was managed with half normal saline, free water via nasogastric tube, antibiotics, and prophylactic leveterecetam. An EEG done did not reveal any ongoing seizure activity and a MRI brain done showed acute venous infarct in the left precentral gyrus and  a  magnetic resonance venogram showed a partial filling defect in the mid superior sagital sinus (Fig 1,2). Low molecular weight heparin was started for the same. On the 6th day of her admission patient was fully conscious and oriented and her tremors had decreased substantially. Patient however had severe proximal muscle weakness and was unable to stand with support. A nerve conduction study done of all 4 limbs including femoral nerves showed normal sensory motor conduction and a ENMG showed low amplitudes with normal duration CMAPS suggestive of myopathy. Patient underwent a muscle biopsy which showed evidence of necrotizing myopathy (Fig 3). Gradual sodium correction was continued and with rest and physiotherapy her muscle weakness improved and she was discharged wheel chair bound. She recovered completely and was independent for all activities of daily living after 1 month of discharge from the hospital.


The above case brings out two complications seen in the post partum period; hypernatremia and cerebral sinus venous thrombosis. The common etiological factor for both the conditions in this case was dehydration secondary to diarrhea and decreased fluid intake. The patients altered sensorium; involuntary movements can be attributed to hypernatremia. Acute hypernatremia causes increase in cerebral osmolality due to shift of water from intracellular and interstitial compartments. The intracellular osmolytes so far known are myoinositol, creatine and choline. In patients with hypernatremia on MR spectroscopy the osmolytes were found to be increased within cells (1). Hypernatremia and rhabdomyolysis in the postpartum state have been discussed in a series of cases earlier. However none of these cases in this particular series had CVST though MR venogram was done in some of the patients to rule out the same. 2

Hypernatremia is an important cause of metabolic encephalopathy requiring management in the neurology intensive care unit. The incidence of spontaneous hypernatremia is less than that seen in hospitalized patients. 3 Loss of water via skin, urine, or GI tract is the usual cause for hypernatremia. Impaired thirst and or decreased access to water sustain hypernatremia. The central and peripheral clinical features of hypernatremia include headache, seizures, coma, and muscle cramps. Mortality is higher in acute hypernatremia (75%) while it is less for chronic hypernatremia (10%). 4

Rhabdomyolysis in our patient produced severe proximal muscle weakness, myogloblinuria several fold rise in CPK (1, 11,000U/L). . Rhabdomyolysis is a potential lethal condition more commonly seen in adults than in children. 5 Hypernatremia inhibits the electrogenic sodium pump on the muscle cells impairing sodium –calcium transport which increases the cytoplasmic calcium level. Increased intracellular calcium activates intracellular proteases leading to destruction of muscle and extracellular leakage of CPK and myoglobin. 6, 7 Muscle trauma , excessive muscle activity and hereditary muscle enzyme defects are the most common causes of rhabdomyolysis while less common causes are metabolic, infections and temperature alterations. 8 In our patient gradual restoration of sodium to normal levels reversed her encephalopathy and myopathy.

The CSVT in our patient was almost an incidental finding with the MRI showing an area of restricted diffusion in the left superior frontal lobe. The MRV showed mid level occlusion in the superior sagital sinus. Unlike earlier reports we did not see any bilateral symmetric T2W and FLAIR abnormalities seen with hypernatremia. 8 As is well known, post partum period induces a hypercoagulable state and this compounded by dehydration is the most common cause of CSVT. 9 Fortunately despite all these risk factors her venous infarct was small and she responded well to subcutaneous low molecular weight heparin.


This case highlights the occurrence of three complications; hypernatremia, rhabdomyolysis and CSVT in the post partum period. Infectious diarrhea with dehydration was the probable cause. Sodium correction, antibiotics and low molecular weight heparin reversed all the three conditions. Ensuring adequate hydration during the post partum period remains the cornerstone in preventing such complications.


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Fig 1: MRI DW and ADC images showing acute infarct in the left precentral gyrus


Fig 2:  MR Venogram showing partial obstruction of the mid superior sagital sinus


Fig 3: Muscle Biopsy light microscopy. (A) Maintained fascicular architecture of the muscle without any evidence of inflammation. (B&C) Necrotic fibers (D) Moth eaten fibers on NADH