Jeremy Nightingale, St Mark’s Hospital, Harrow
Presented at ACPGBI Liverpool 2013, 1 July
16% of patients with a small bowel stoma have problems of HOS (more than 2L stomal output/day) in the first 3 weeks of surgery, 73% of these resolve and need no further treatment, 20% need long-term treatment and 7% parenteral fluids (Baker et al).
Subclinical sodium depletion is common in patients with an ileostomy and can be associated with low bone mineral density (Ng et al). The assessment the sodium and water balance in a patient with a high output stoma starts with asking about thirst, looking for rapid weight change, postural hypotension, oliguria, raised urea/creatinine, low serum magnesium and low urine sodium concentration. Following this the cause of the HOS is sought. A short remaining length of small intestine (less than 2 metres from duodeno-jejunal flexure) is the most common reason. Intermittent obstruction is common and may result in episodic admissions to hospital for intravenous saline and magnesium. A low fibre diet may prevent this occurring. Other causes include prokinetic drugs (e.g. metoclopramide), opiate withdrawal (e.g. codeine phosphate), low cortisol, abdominal sepsis, enteritis (Cl difficile), small bowel diverticulae, recurrent disease, internal fistula or Coeliac disease. For this reason a contrast follow through that measures bowel length is useful, and may also show an obstructing point or an entero-enteric fistula. Stomal output is cultured for clostridium and coeliac serology and morning cortisol measured (Nightingale and Woodward).
While Gastric acid hypersecretion, increased gut transit, loss of normal daily secretions may contribute to a HOS, the most important factor is thirst which results in much hypotonic fluid being drunk and this further increases the stomal output. The concentration of sodium in small bowel stomal fluid is always about 100 mmol/l and so more sodium is also lost as the stomal output increases and this causes even more thirst. Hypomagnesaemia is common and may result from secondary hyperaldosteronism, removal of ileum/colon and unabsorbed free fatty acids binding magnesium in the bowel lumen.
After other causes have been excluded and the HOS is considered to be due to a short or dysfunctional remaining small bowel, oral hypotonic fluid is restricted to less than 1L daily, a glucose-saline solution (1-2 L containing 90-120 mmol/l sodium) is sipped, an oral magnesium supplement is given. Occasionally drugs such as loperamide before meals are needed. If the gut length is less than 1 metre a proton pump inhibitor will reduce the gastric secretion volume and thus stomal output (Nightingale). If patients are malnourished, a liquid feed supplements