|Year : 2019 | Volume
| Issue : 6 | Page : 54-56
Unusual complication of severe hypernatremia - Rhabdomyolysis
Sandip Gupta1, Krishanu Mondal1, Shivakumar Shamarao2, Ashwath Ram Rao2
1 Fellow, Department of Pediatric critical care, Manipal Hospital, Bangalore, Karnataka, India
2 Senior Consultant, Department of Pediatric Critical Care, Manipal Hospital, Bangalore, Karnataka, India
|Date of Submission||10-Aug-2019|
|Date of Acceptance||16-Nov-2019|
|Date of Web Publication||20-Dec-2019|
Department of Pediatric Intensive care, Manipal Hospital, Bangalore- 560017, Karnataka
Source of Support: None, Conflict of Interest: None
Dyselectrolytemia is a common reason for admission to Pediatric Intensive Care Unit (PICU). Both hypo and hypernatremia are very common dyselectrolytemias in PICU. Common complications associated with these electrolyte disturbances happen to be seizures, encephalopathy, raised intracranial pressure and intracranial bleeds. We report our experience with a 10-year-old child with rhabdomyolysis, as a very unusual complication, triggered by acute hypernatremic dehydration, following adeno-tonsillectomy.
Keywords: Hypernatremia, Rhabdomyolysis, PICU
|How to cite this article:|
Gupta S, Mondal K, Shamarao S, Rao AR. Unusual complication of severe hypernatremia - Rhabdomyolysis. J Pediatr Crit Care 2019;6:54-6
|How to cite this URL:|
Gupta S, Mondal K, Shamarao S, Rao AR. Unusual complication of severe hypernatremia - Rhabdomyolysis. J Pediatr Crit Care [serial online] 2019 [cited 2022 Dec 6];6:54-6. Available from: http://www.jpcc.org.in/text.asp?2019/6/6/54/279481
| Case Report|| |
A 10-year-old boy underwent adeno-tonsillectomy on 12/05/2016 in a medical college hospital, for chronic adeno-tonsillitis. After an uneventful surgery and postoperative course, he was discharged home, where he suffered severe dysphagia and odynophagia. He had multiple episodes of altered bloody vomiting and required admission after 7 days of surgery in the same hospital. He had generalized seizure lasting for 2 minutes along with altered sensorium. In addition, he was dehydrated and was in hypotensive shock.
He was managed with normal saline bolus (20ml/ kg), lorazepam and fosphenytoin for seizure control. He was also started on empirical antibiotics. Throat examination revealed operative site having clotted blood without any active bleeding. Initial lab work-up revealed Hemoglobin (Hb)-11gm/dl, Total leucocyte count (TLC)-14650/mm3, C-reactive protein (CRP)- 8 mg/dl, Blood urea nitrogen (BUN)-150mg/dl, creatinine (Cr)-1.4mg/dl , Aspartate Transaminase AST-207 U/L, Alanine Transaminase (ALT) -112U/ L, sodium (Na+)-180 meq/L and potassium(K+)- 3.8meq/L. Blood culture, Leptospira IgM , Malaria Ag test, Weil–felix test and cerebrospinal fluid analysis were negative. Computed Tomography and Magnetic Resonance Imaging of brain were normal. The child was given 0.45% Normal saline (NS) for 48h, 0.3% NS for next 24h, and then 0.2 % NS for hypernatremia, which caused wide fluctuation of sodium level. After 3 days child was referred to our hospital for persistently altered sensorium, progressive deterioration in renal function & refractory hypernatremia.
At our PICU, we started him on NS followed by 0.45NS along with salt free nasogastric tube feeds. Correction of hypernatremia was regulated not to exceed 0.5meq/l/hr. Laboratory work up revealed-Hb-11.2gm/dl, TLC-19680/mm3, platelet count-86 X 103/mm3, Na+-170meq/l, K+-3.6meq/L, BUN-21mg/dl, Cr-0.7mg/dl, AST-2607 U/L, ALT-877U/1, albumin-3.2 g/dl, LDH-4676 mg/dl, serum osmolality - 356mosm/L and urine osmolarity- 980mosm/L. Urine routine examination revealed 4-5 red blood cell in every high power field and urinary protein was 3+. He was passing dark red color urine [Figure 1]. Further analysis of urine was positive for myoglobin. Total Creatine phosphokinase (CPK) level was 192743 U/L. He was started on hyper-hydration therapy with total fluid of 3L/m2/day targeting urine output >2ml/kg/hr. We used 0.45% NS and salt free nasogastric feeds to restore normal sodium. His sodium level and CPK level were normalized in subsequent 5 days as presented in [Table 1] and [Figure 2]. His sensorium gradually improved and at discharge, he was alert and conscious.
| Discussion|| |
Rhabdomyolysis is rare condition characterized by acute destruction of muscle tissue with release of myoglobin in blood. Immediate consequences of muscle destruction include hyperkalemia, hypocalcemia and acute renal failure. In children, it is commonly caused by infection, trauma, anesthetic complications inherited disorders and electrolyte imbalances. ,,
Hypernatremia as a cause of rhabdomyolysis is rarely reported, particularly in children.,,,,,, Hypokalemia, hypophosphatemia, and hyponatremia are more commonly associated with rhabdomyolysis. The mechanism of rhabdomyolysis associated with hypernatremia is not well established; however, one theory implies that it could be associated with inhibition of electrogenic sodium pumps due to hyperosmolar state. This will impair sodium calcium transport. Increased intracellular calcium can damage the myocyte via several pathways including persistent contraction, activation of phospholipase and free radical mediated injury., Tzu yang et al reported rhabdomyolysis in a 12 year old neurologically impaired child with hypernatremia associated with diarrhea and dehydration. Another case of hypernatremia induced rhabdomyolysis was reported in a 5 year old girl with hypodipsia-hypernatremic syndrome associated with holo prosencephaly. Recently a case of rhabdomyolysis associated with severe hypernatremia after an episode of acute gastro-enteritis in an 1 year old girl was reported.
Severe hypernatremia contributes to hyper-osmolality and causes cellular dehydration. It may lead to cerebral demyelination and clinical manifestations ranging from irritability and lethargy to coma apart from the common symptoms like fever, tachypnea high-pitched cry, changes in skin turgor.,, We initially could not explain the elevated LDH and transaminases in our child and subsequently looking at color of urine we considered rhabdomyolysis. Our child had severe hypernatremia, rhabdomyolysis, myoglobinuria and acute kidney injury (AKI). The hypernatremia and circulatory shock was probably secondary to poor oral intake following the surgery due to severe throat pain coupled with repeated vomiting. The AKI was probably a combination of pre-renal and pigment induced renal dysfunction. Around 10-40% of cases of rhabdomyolysis leads to AKI. Kidney injury in rhabdomyolysis is multifactorial including mechanisms like renal vasoconstriction, ischemia, and renal tubular obstruction by cast formation and direct tubular injury by myoglobin. AKI related to myoglobinuria may respond to fluid therapy, alkalinization, and diuretics. However, if conservative therapy fails, hemodialysis is the modality of choice.,,, Our case responded to appropriate fluid and electrolyte management and did not require dialysis. We could not find any cause apart from hypernatremia for rhabdomyolysis in our child.
| Conclusion|| |
Although rare, rhabdomyolysis is a known complication of hypernatremia. It is worthwhile to anticipate this rare complication with hypernatremia and hyperosmolar states because of its life threatening consequences.
Source of Funding: Nil
Conflict of Interest: Nil
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[Figure 1], [Figure 2]