Journal Article

Severe hypernatremia and rhabdomyolysis 30 days after laparoscopic sleeve gastrectomy: a case report

Journal of Surgical Case Reports, Volume 2026, Issue 9, September 2026, rjag859, https://doi.org/10.1093/jscr/rjag859
Published:
28 September 2026
Article history
Received:
30 July 2026
Revision received:
22 August 2026
Accepted:
03 September 2026
Published:
28 September 2026

Abstract

Rhabdomyolysis is an uncommon but potentially life-threatening complication of bariatric surgery, typically occurring in the immediate postoperative period and associated with prolonged operative time, improper positioning, or extreme obesity. We report a 16-year-old female with class III obesity who underwent uneventful laparoscopic sleeve gastrectomy and was discharged on postoperative day 1. Approximately 30 days later, she presented with progressive weakness, myalgia and severe hypernatremia, elevated creatinine and creatine phosphokinase, suggestive of rhabdomyolysis. She was managed with aggressive intravenous hydration and gradual correction of hypernatremia, with full recovery of muscle strength and renal function. This case highlights a delayed presentation of severe hypernatremia and rhabdomyolysis following laparoscopic sleeve gastrectomy in an adolescent patient. Clinicians should maintain a low threshold for checking creatine phosphokinase and electrolytes in post-bariatric patients with myalgia, weakness, or dark-colored urine, regardless of the time elapsed since surgery.

Introduction

Obesity is a chronic, multifactorial disease characterized by abnormal or excessive fat accumulation that adversely affects health [1–3]. Bariatric surgery is an effective treatment for severe obesity but is associated with specific perioperative complications [1–4]. Rhabdomyolysis (RML), defined as skeletal muscle breakdown with release of intracellular contents into the circulation, is a rare but potentially fatal complication in this setting [5, 6]. Myoglobin-mediated injury may lead to acute kidney injury (AKI), which develops in about one-third of patients with RML and carries substantial mortality [6]. Although RML after bariatric surgery is usually reported early after the operation, delayed presentations are uncommon [5, 7, 8]. We report severe hypernatremia and rhabdomyolysis presenting 30 days after laparoscopic sleeve gastrectomy (LSG) in an adolescent patient.

Case presentation

A 16-year-old female with class III obesity underwent elective LSG. Her preoperative weight was 111 kg, height 158 cm, and body mass index 43 kg/m2. The procedure was completed laparoscopically in 90 min without intraoperative complications. She was mobilized early, started a clear liquid diet on postoperative day (POD) 1, and discharged on POD 1 with standard instructions emphasizing hydration.

At follow-up on POD 10, she reported mild nausea without vomiting or abdominal pain. Her diet was adjusted, and the next visit was scheduled for POD 30. During the following weeks, she developed progressive nausea and vomiting and was unable to maintain adequate oral intake. No clear anatomical cause of poor intake was identified. Two days before the second visit, she developed generalized weakness, myalgia, and dark-colored urine. She was evaluated by a family physician, diagnosed with nephrolithiasis, and treated with antiemetics and non-steroidal anti-inflammatory drugs; only complete blood count and urinalysis were obtained, showing hematuria.

When she presented to our clinic, she reported fatigue, dizziness, and progressive weakness impairing tandem gait. Laboratory findings are summarized in Table 1. She had severe hypernatremia, elevated creatine phosphokinase (CPK), AKI, thrombocytopenia, and elevated liver enzymes. Coagulation profile, thyroid function, calcium, albumin, lactate dehydrogenase, and vitamins B6 and B12 were normal. Urinalysis showed concentrated urine with trace protein and blood. A myositis antibody panel was negative except for borderline anti-OJ positivity, and peripheral smear showed no immature cells or schistocytes.

Table 1

Laboratory findings at admission and discharge.

ParameterAt admissionAt discharge
Platelet count (×109/L)87119
Sodium (mmol/l)174141
Blood urea nitrogen (mg/dL)337
Creatinine (mg/dL)2.71.0
Aspartate aminotransferase (AST)182110
Alanine aminotransferase (ALT)265176
Alkaline phosphatase (ALP)341278
Creatine phosphokinase (CPK) (U/L)5740640
Total bilirubin (mg/dL)1.10.7

Non-contrast abdominal computed tomography showed no sleeve twisting or staple-line leak. Abdominal ultrasonography showed no portal vein thrombosis or structural abnormality. Neurological examination revealed Medical Research Council grade 4/5 strength in proximal and distal muscle groups, normal sensation, and impaired heel-to-shin and tandem gait testing. Rhabdomyolysis was considered the leading diagnosis.

She was treated with aggressive intravenous hydration, electrolyte correction, and close nephrology supervision. Hypernatremia was gradually corrected with parallel clinical improvement. The temporal trends in serum sodium, creatinine, CPK, platelet count, fluid intake, and output during the intensive care unit (ICU) stay are presented in Table 2. Her platelet count was 87 × 109/L on admission and recovered to 119 × 109/L by discharge. Abdominal ultrasonography showed no splenomegaly, and no specific cause for the transient thrombocytopenia was identified.

Table 2

Temporal trends of laboratory findings and fluid balance.

Admission dayNa (mmol/L)K (mmol/L)Cr (mg/dL)BUN (mg/dL)CPK (U/L)AST/ALT (U/L)Platelet count (×109/L)Intake (mL)Output (mL)
0174 → 1803.6 → 3.42.7 → 2.433 → 365740—8745001100
1169 → 1663.3 → 3.31.6 → 1.625 → 225649336/31711146002600
21593.51.5206501283/23910841002800
31523.70.9183525—9340002350
41493.91.1132690—10435002500
51504.10.992525203/22013130002500
61463.71.0111106145/215106N/AN/A
71413.61.07646110/176119N/AN/A

Electromyography and nerve conduction studies on hospital day 3 showed moderate myopathic changes with myotonic features. She was discharged on hospital day 7 with normal muscle strength and resolution of dizziness and lightheadedness. At 1-, 3-, and 6-month follow-up, she remained asymptomatic, with normalization of serum creatinine and CPK and no recurrent muscle symptoms.

Discussion

Rhabdomyolysis after bariatric surgery usually occurs within the first few postoperative days and is associated with prolonged operative time, extreme obesity, and positioning-related muscle injury [5, 7, 8]. Our patient lacked these typical perioperative risk factors, with a body mass index of 43 kg/m2 and an operative time of 90 min. Delayed presentation several weeks after surgery is therefore unusual.

Reported incidence of bariatric surgery-related rhabdomyolysis varies widely, reflecting differences in patient selection and diagnostic thresholds. Prolonged operative time, particularly beyond 240 min, is among the strongest recognized risk factors [7]. The markedly delayed onset in our patient suggests that factors other than classic perioperative muscle compression were involved.

Hypernatremia and rhabdomyolysis are known to be associated, and severe hypernatremia has been reported to directly precipitate rhabdomyolysis through cellular dehydration, shrinkage, and muscle membrane instability [6, 9]. The available fluid-balance data during ICU admission are shown in Table 2. Pre-admission oral fluid intake could not be quantified, and she had received no intravenous fluids before admission. The severe hypernatremia was considered most consistent with a substantial volume deficit due to prolonged inadequate oral intake. However, a direct causal relationship between LSG and rhabdomyolysis cannot be established.

The associated AKI was likely multifactorial. Severe volume depletion likely contributed substantially, while concurrent rhabdomyolysis may also have caused pigment-mediated tubular injury. The available data do not permit definitive distinction between these mechanisms. In addition, electromyography demonstrated myotonic features and anti-OJ antibody was borderline positive, raising the possibility of an underlying neuromuscular or inflammatory myopathy. Nevertheless, complete clinical recovery, normalization of renal function and CPK, and absence of recurrent symptoms over 6 months make an underlying chronic myopathy less likely, although it cannot be excluded with certainty.

This case has an important practical message. Postoperative fluid intake may be inadequate in the weeks following LSG, especially in adolescents with nausea or vomiting. In patients presenting after bariatric surgery with myalgia, weakness, or dark urine, clinicians should maintain a low threshold for checking electrolytes and CPK, even when presentation occurs weeks after surgery.

Conflicts of interest

The authors declare that they have no conflicts of interest relevant to this article.

Funding

None declared.

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