The size of omental prolapse increased over the next four hours and about 3 cm length of omentum was protruding outside the parietal wall (Image 1a). Abdomen remained soft and omentum appeared viable with pinkish hue and reddish sub mucosal capillary striae. Surgical specialty consultation was sought and the surgical team recommended surgical reduction of prolapsed omentum under general anaesthesia with fascial closure. Considering the delay and complexity associated with general anaesthesia and surgery, percutaneous reduction of prolapsed omentum was attempted. Under intravenous sedation and local anesthesia the distal part of the omentum was held with a non toothed forceps and the proximal part of the omentum emerging from the skin was gradually pushed millimetre by millimetre back into the peritoneal cavity using the tip of a disposable syringe. The last trace of omentum was pushed deep into the abdomen by inserting the entire length of the tip of the syringe into the puncture site. Abdomen after reduction of prolapsed omentum is shown in Image 1b.Skin and fascia were closed with one through stitch. The procedure was performed at the bed side and took 20 minutes for completion. Child was prescribed antibiotics. Results: A week later the child appeared well, abdomen was soft and there was no incisional hernia. Conclusions: Omental prolapse is a rare complication following peritoneal dialysis. Percutaneous reduction is a simple yet effective way of treating omental prolapse. For successful outcome it is crucial to intervene early before occurrence of omental incarceration and infection.

Introduction: Distal renal tubular acidosis (RTA) is easily recognized in patients with hypokalemia and normal anion gap acidosis. Other concurrent electrolyte abnormalities could change the diagnosis. We describe a newly diagnosed distal RTA complicated with severe hypernatremia and hypophosphatemia while admitted to the intensive care unit. Case report: A 12-year-old girl presented with worsening paralysis. Initial investigations revealed low serum potassium of 1.8mmol/L, pH 7.2mmol/L, bicarbonate 12mmol/L and high urine pH (8.0) suggesting distal RTA. She required mechanical ventilation due to severe metabolic acidosis and hypokalemia. Resuscitation strategies initially focussed on intravenous hydration with 0.9% normal saline and potassium repletion. Delayed correction of acidosis with sodium bicarbonate led to severe hypernatremia (180mmol/L) and slow recovery of serum potassium level. Hypernatremia was also contributed by concurrent nephrogenic diabetes insipidus. Interestingly, her serum phosphate was persistently low (0.4mmol/L) leading to more workup to investigate proximal tubulopathy. It persisted till resolution of hypernatremia and acidosis. Meanwhile she developed sepsis with multiple thromboses attributed to disseminated tuberculosis. Screening for connective tissue diseases were negative. She recovered well and was discharged with anti-tuberculosis drugs, anticoagulation and potassium supplements. Conclusion: In conclusion, correction of acidosis in distal RTA should be prioritised to avoid prolonged hypokalemia and significant increase in serum sodium. Hypophosphatemia in a critically ill patient should be interpreted with caution, correlating with serum sodium and arterial blood gas to avoid incorrect diagnoses.

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