CYTOKINE RELEASE SYNDROME–LIKE AKI POST COSMETIC SURGERY

Adipose tissue is now recognized as a metabolically active endocrine organ, secreting a wide range of cytokines and adipokines including IL-6, TNF-α, IL-1β, leptin, and adiponectin. These mediators regulate systemic inflammation and energy metabolism.

Surgical trauma, particularly procedures involving extensive adipose manipulation such as liposuction and abdominoplasty, can cause adipose tissue necrosis and cytokine release. While mild inflammatory responses are expected, severe systemic inflammatory response syndrome (SIRS) or cytokine release syndrome (CRS)–like phenomena are extremely rare.

We describe a case of severe postoperative inflammation following abdominoplasty, presenting with sterile SIRS and AKI, which resolved after debridement of necrotic adipose tissue, suggesting a cytokine-mediated mechanism.

Case Presentation:

A 39-year-old female with a background history of bariatric surgery underwent elective abdominoplasty with liposuction at a private surgical center.

She was discharged home in stable condition, but one week later, she presented to the emergency department with fever, mild abdominal pain, and fatigue.

On examination: Temperature: 38.4°C, Heart rate: 118 bpm, Respiratory rate: 22/min, Blood pressure: 104/68 mmHg, Oxygen saturation: 98% on room air. Abdominal examination: mild tenderness over the surgical site without discharge or redness. Rest of examination was unremarkable. Laboratory results revealed WBC 37× 10⁹/L (with left shift), CRP 343 mg/L, hemoglobin 92 g/L, and rising creatinine from 84 µmol/L on admission to a peak of 321 µmol/L. Peak WBC reached to 58 × 10⁹/L. Urinalysis was negative for protein, RBCs, or leukocyte esterase. Blood, urine, and wound cultures were sterile. Renal ultrasound was normal with preserved cortical echogenicity and no obstruction. CT abdomen showed postoperative changes without fluid collection or abscess.

The patient received broad-spectrum antibiotics empirically; however, no infectious focus was identified.

Given the progressive rise in inflammatory markers and the appearance of indurated, discolored tissue around the surgical site, the plastic surgery team was consulted. Surgical exploration revealed necrotic adipose tissue, which was extensively debrided. Histopathology confirmed fat necrosis with inflammatory infiltration.

After debridement, the patient’s fever subsided, WBC and CRP normalized within days, and serum creatinine gradually decreased to baseline. No additional renal support or dialysis was required.

Diagnosis:

Cytokine-mediated systemic inflammatory response syndrome secondary to fat necrosis, complicated by acute kidney injury.

Discussion:

1. Pathophysiologic Mechanism

This case demonstrates a cytokine release syndrome–like phenomenon following liposuction-induced fat necrosis.

Adipocytes undergoing necrosis release large amounts of proinflammatory cytokines, particularly IL-6, IL-1β, TNF-α, and chemokines that activate macrophages and endothelial cells. This cytokine surge can:

              •            Increase vascular permeability and promote capillary leak

              •            Induce systemic vasodilation and relative hypovolemia

              •            Cause direct tubular injury via oxidative stress and inflammatory signaling

These mechanisms collectively contribute to hemodynamically mediated AKI without primary renal parenchymal disease, explaining the bland urinalysis and reversible nature of renal dysfunction.

2. Differential Diagnosis

Generally, in postoperative patients, AKI is typically multifactorial— which can be contributed  to sepsis, hemodynamic instability, hypovolemia, nephrotoxic drugs, or rhabdomyolysis.

However, in this patient the following facts were present:

              •            Cultures remained negative.

              •            There was no drop in blood pressure readings, evidence of rhabdomyolysis (Creatine kinase was unremarkable), or exposure to nephrotoxic agents.

              •            Urinalysis was unremarkable, which is not going with glomerular or interstitial nephritis.

Thus, inflammatory cytokine-mediated renal injury was the most possible explanation.

3. Comparison with Literature:

Only a few cases have reported systemic inflammatory response syndrome (SIRS) after liposuction-abdominoplasty. In one report (Buis et al., Plast Reconstr Surg Glob Open, 2021), a patient developed postoperative hypotension and tachycardia without infection, attributed to disproportionate inflammatory response.

However, renal involvement has not been described in previous literature.

The present case expands this observation by showing AKI as a consequence of systemic cytokine release from necrotic fat. It shares the same mechanism of cytokine release syndrome, which is prevalent in diseases including hemophagocytic lymphohistiocytosis, severe sepsis, and CAR-T treatment and causes multiorgan failure due to cytokine surge.

4. Therapeutic and Clinical Implications

Source control, which was the surgical excision of necrotic fat tissue, marked a crucial moment in this patient's journey.
The causal association was confirmed when renal function restored, and inflammatory markers started to trend down remarkably after debridement.
Such cases should be managed with an emphasis on the following points:

Early detection of noninfectious SIRS, refraining from overusing antibiotics once infectious causes been ruled out; The importance of resuscitation with volume expansion and Prompt surgical source control to halt the release of cytokines

This case illustrates, cytokine-mediated mechanism of acute kidney injury following abdominoplasty-induced fat necrosis. It emphasizes the importance of considering noninfectious systemic inflammation in the differential diagnosis of postoperative AKI.

Prompt recognition and surgical source control can lead to complete recovery and prevent unnecessary prolonged antimicrobial therapy. This report broadens the understanding of adipose-driven inflammatory kidney injury and highlights one of the possible complication of cosmetic surgery.