Q J Med 2002; 95: 37-40
© 2002 Association of Physicians
Acute renal failure and metabolic disturbances in the short bowel syndrome
From the Department of Renal Medicine, Lister Hospital, Stevenage, UK
Received 31 August 2001 and in revised form 26 October 2001
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Summary |
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Background: Short bowel syndrome (SBS) describes a malabsorptive state caused by extensive loss of small intestinal length.
Aim: To improve understanding of the metabolic complications of SBS.
Design: Observational study of five patients with SBS who presented with acute renal failure.
Results: Acute renal failure in our patients was predominantly due to salt and fluid depletion, and sepsis. Electrolyte imbalance was a major cause of morbidity. Metabolic acidosis was seen in three patients, and may arise from excessive gastrointestinal bicarbonate loss, compounded by impaired renal homeostasis. Our patients also manifested disturbances of calcium and magnesium homeostasis.
Discussion: Patients with SBS are at high risk of renal failure. Prevention of this complication requires close monitoring and the maintenance of sodium homeostasis through increased intake and measures to reduce loss (e.g. anti-motility agents and large bowel re-anastomosis), and calcium, magnesium and vitamin D supplementation.
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Introduction |
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Short bowel syndrome (SBS), defined as intestinal failure with a small bowel remnant length of less than
150 cm,1 describes a malabsorptive state caused by extensive loss of small intestinal length. The usual causes are listed in Table 1
. With advances in medical and intensive care, the numbers of patients surviving these procedures are likely to increase. The chronic nephrological consequences of the short bowel syndrome, in patients with jejuno-ileal bypass procedures, have been recently comprehensively reviewed in this journal.2
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We now complete the spectrum of nephropathies by reporting the case histories of a series of patients presenting to our service with acute renal failure caused by the SBS, describing the range of metabolic disturbances associated with the condition, and making recommendations for treatment.
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Case histories |
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Patient 1: a 59-year-old woman
Following a total abdominal hysterectomy for endometrial carcinoma in 1989 and two subsequent bowel resections for local recurrence, she presented in 2000 with her first episode of acute renal failure, precipitated by sepsis, ureteric obstruction and dehydration. Subsequent laparotomy revealed a fistula between the small bowel, bladder and vagina, necessitating an ileocolic resection and distal anastomosis; the transverse colon being used as a colonic urinary conduit. Her renal function improved and she was discharged home.
She was re-admitted 2 months later with a more severe acute renal failure (serum urea of 20 mmol/l and creatinine of 328 µmol/l) and a marked metabolic acidosis (arterial pH 7.07 and bicarbonate of 3.5 mmol/l, but only a slightly raised anion gap of 19.3). She was mildly hypocalcaemic (corrected calcium 2.1 mmol/l) and significantly hypomagnesaemic (0.39 mmol/l), with a raised alkaline phosphatase (282 IU). She was clinically dehydrated, and subsequently was found to have a methicillin-resistant staphylococcal septicaemia.
She was treated with intravenous fluids and antibiotics, oral sodium bicarbonate, anti-motility agents, magnesium supplements and vitamin D. She was stabilized and discharged with a serum creatinine of 240 µmol/l, equating to a creatinine clearance of 21 ml/min. She was also found to be mildly deficient in vitamin B12 and folic acid, which were corrected with intramuscular and oral supplements, respectively.
Patient 2: a 42-year-old woman
In 1990, she presented with recurrent episodes of urinary retention. Following investigation, and an unsuccessful trial of a suprapubic catheter, an ileal conduit was fashioned. This leaked shortly after creation, and in 1991 the ureters were divided and anastomosed into the rectum. Several episodes of large bowel obstruction ensued, necessitating repeated resections and complicated by a series of faecal fistulas. During this time, a diagnosis of Hirschsprung's disease was established. Eventually a total colectomy was undertaken, with creation of an ileostomy and a second ileal conduit.
The following years were marred by a series of admissions for intestinal obstruction, fistulae, repeated abdominal abscesses and septicaemias. She became malnourished, being fed initially with a naso-gastric tube and subsequently a percutaneous gastrostomy.
She was admitted in August 2000 with dehydration and acute renal failure (serum urea 46 mmol/l, serum creatinine 200 µmol/l and serum potassium 6.5 mmol/l); she was rehydrated and discharged with normal serum urea and creatinine.
In January 2001 she again presented to the renal service with hyperkalaemia (6.3 mmol/l), acute renal impairment (serum urea 16 mmol/l and creatinine of 116 µmol/l) and dehydration. She was mildly hypocalcaemic (2.14 mmol/l) and significantly hypomagnesaemic (0.52 mmol/l).
She was rehydrated with intravenous fluids, and her calcium and magnesium deficiency corrected with supplements. Despite antimotility agents, her salt and fluid losses and malnutrition necessitated insertion of a Hickman line for intravenous total parenteral nutrition and saline supplementation. A trial of octreotide improved the gastrointestinal losses, but not enough to stop the intravenous supplementation. On several occasions following this she has suffered line-related septicaemic episodes, and her Hickman line has had to be replaced
Patient 3: a 42-year-old woman
At the age of 5 years she had presented with severe constipation (details and diagnoses uncertain) and underwent an ileostomy. Repeated episodes of abdominal pain resulted in a series of small bowel resections. In 1982, she was hysterectomized for pelvic inflammatory disease, and in 1994 underwent a cholecystectomy. In 1994 her stoma prolapsed, and was repaired. At this time a Hickman line was inserted and her intake has been supplemented by total parenteral nutrition.
In 1995, she was noted to have renal impairment, renal biopsy revealing tubulointerstitial scarring. In January 2001 she was admitted with acute-on-chronic renal failure (serum urea of 33 mmol/l and creatinine was 534 µmol/l), secondary to dehydration and a presumed Hickman line sepsis. Blood cultures subsequently grew Pseudomonas. She was hypokalaemic (3.2 mmol/l) with a normal calcium (2.28 mmol/l) and normal bicarbonate (30 mmol/l). She was rehydrated, treated with antibiotics and discharged with a serum urea of 13.2 µmol/l and serum creatinine of 187 mmol/l.
Patient 4: a 39-year-old man
He suffered from Crohn's disease, and in 1981 underwent a panproctocolectomy and ileostomy, which was refashioned in 1985. Long-term lithium treatment for depression had caused nephrogenic diabetes insipidus, and he was noted to have stable moderately impaired renal function (serum creatinine 149 µmol/l).
In 1997 he was admitted for small bowel obstruction, which required laparotomy, ileal resection and refashioning of ileostomy. Two weeks later, further resections of a segment of necrotic ileum and a small bowel fistula were required.
At one day before the operation, he had developed acute renal impairment (serum urea 31.7 mmol/l, serum creatinine 357 µmol/l). He was hypokalaemic (2.7 mmol/l), hypomagnesaemic (0.43 mmol/l), had a low/normal calcium (2.18 mmol/l) and demonstrated a metabolic acidosis (serum bicarbonate 15 mmol/l). He was clinically dehydrated and septicaemic with coagulase-negative Staphylococcus grown from blood cultures.
He was resuscitated with antibiotics and intravenous fluids. Subcutaneous octreotide brought his stoma output to manageable proportions. His renal function remains stable, most recently 147 µmol/l.
Patient 5: a 54-year-old man
Since 1985 he had suffered Crohn's disease, controlled on mesalazine. In July 2000, he developed a pericolic abscess and vesico-colic fistula treated by colectomy, division of strictures/ileal resection and ileostomy. Post-operatively he rapidly improved, but then gradually his condition worsened, characterized by weight loss, anorexia, thirst and large losses from his ileostomy.
In February 2001, he presented with hypocalcaemia (total calcium 1.38 mmol/l), hypomagnesaemia (0.19 mmol/l) tetanic spasms and acute renal failure (serum urea 36 mmol/l, serum creatinine 220 µmol/l) with a mild metabolic acidosis (serum bicarbonate 21 mmol/l).
He was rehydrated, the calcium and magnesium deficits were corrected, initially intravenously and subsequently orally (including vitamin D supplementation), and anti-motility agents were initiated. This improved but did not resolve the large ileal losses, and therefore the ileostomy was reversed. His condition has gradually improved back to normal, and his serum urea and creatinine currently stand at 8.8 mmol/l and 143 µmol/l, respectively.
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Discussion |
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Some 40–50% of small intestine can usually be lost without major metabolic or nutritional sequelae,3 however if more than 75% is lost, maintenance of nutritional status, at least initially, usually requires parenteral nutrition. Adaptive mechanisms, including intestinal dilatation and increases in crypt depth and villus height4 can lead to progressive recovery of the remaining bowel. The pattern of presentation of the SBS also depends on the site of intestinal resection (jejunal or ileal resection), the loss or preservation of the ileocaecal valve and large bowel and co-existent small intestinal, liver or pancreatic disease.4
The major problems following established SBS are related to fluid/electrolyte imbalance, deficiencies in calcium, magnesium, zinc and vitamins A, D, E, K and B12, hypergastrinaemia, bile salt depletion, protein-calorie malnutrition, pancreatic maldigestion and oxalate nephrolithiasis.
Acute renal failure in our patients was predominantly due to salt and fluid depletion, and sepsis, particularly central catheter-related sepsis in those receiving parenteral nutrition.
Electrolyte imbalance is a major cause of morbidity in the SBS. Patients with ileal resection and ileostomies lose large amounts of faecal sodium (85–180 mmol/24 h), inevitably resulting in degrees of chronic sodium depletion, dehydration and hyperaldosteronism.5 Judicious supplementation of salt and fluids will help correct sodium homeostasis. Intravenous replacement is invariably required initially, but in the long term oral sodium supplements (tablets or solutions) usually suffice. In some cases long term parenteral therapy is required. Anti-motility agents will help reduce faecal losses. Loperamide and codeine are commonly used, and in extreme cases subcutaneous octreotide has proven helpful. Preservation of at least half the large bowel often allows patients to maintain sodium balance (but at the expense of oxalate nephrolithiasis).6
Chronic deposition of oxalate crystals in the tubules and interstitium leading to hyalinization and interstitial fibrosis poses a longer-term threat to renal function.2,7 Patients 3, 4 and 5 all exhibited varying degrees of chronic renal impairment, probably due to this cause. In one report of 18 patients with SBS, eight had interstitial changes consistent with an oxalate induced interstitial nephritis.7 It was noted that as little as 20–30 cm ileal resections could lead to hyperoxaluria, although presumably more extensive resection is required to lead to the interstitial changes observed. In these patients, an intact colon may result in increased absorption of oxalates as calcium precipitates with fatty acids in the colon8 or from increased colonic permeability to oxalates caused by unabsorbed bile salts and fatty acids in the lumen.9 It is likely that these chronic interstitial changes could antagonize electrolyte disturbances, particularly if they lead to salt-losing nephropathies. Renal biopsies also occasionally show deposition of complement (C3) and immunoglobulins (IgM) in capillary walls, postulated to be caused by antigenic stimulation from bacterial breakdown products in the gut.
Metabolic acidosis may arise from excessive gastrointestinal bicarbonate loss (normal anion gap or hyperchloraemic metabolic acidosis) and is compounded by impaired renal homeostasis caused by profound salt and water depletion. Some patients suffer D-lactic metabolic acidosis (a raised anion gap metabolic acidosis), caused by carbohydrate that escapes small intestinal absorption and is thereafter fermented to the D and L isomers of lactic acid. L-lactic acid can be metabolized further by L-lactate dehydrogenase, but no such pathway exists for D-lactic acid, which accumulates.
Calcium homeostasis is maintained by the interplay of vitamin D, parathyroid hormone, phosphate and magnesium. In SBS, several of these factors may be deranged, leading to severe states of hypocalcaemia. Calcium and magnesium absorption usually occurs actively and passively in the proximal short bowel, but also to degrees in more distal segments. Malabsorption of vitamin D in the proximal small bowel, and impaired vitamin D metabolism in those patients with chronic renal interstitial disease will worsen the calcium and magnesium malabsorption. Hypomagnesaemia also impairs PTH function and further exacerbates hypocalcaemia.10
Of our five patients, four exhibited derangements in these divalent cations. Management involves replacement, initially intravenously, and subsequently oral supplementation. The recommended daily allowance of calcium in healthy adults is 800 mg, but patients with states of malabsorption may require some 2–4 g,11 and over 1000 times the recommended daily allowance of vitamin D may be required.12
It is likely that with advances in medical care, the number of patients with SBS will increase, and inevitably these patients will be at risk of renal and metabolic complications. The most important metabolic consequences of the short bowel syndrome are listed in Table 2.
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Surgeons and gastroenterologists will be best placed to identify at-risk patients. They should then be referred for close monitoring, and preventative treatment, specifically maintenance of sodium homeostasis through increased intake and measures to reduce loss (e.g. anti-motility agents and large bowel re-anastomosis), and calcium, magnesium and vitamin D supplementation.
Further studies into the chronic interstitial deterioration2,7 and possible preventative measures to limit the hyperoxaluria, also need to be undertaken.
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Notes |
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Address correspondence to Dr P. Warwicker, Lister Hospital, Coreys Mill Lane, Stevenage, Hertfordshire SG1 4AB. e-mail: p.warwicker{at}doctors.org.uk
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References |
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