Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (87 page)
Read Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice Online
Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Intestinal fistulas pose their own particular problems and can greatly complicate patient management. They contribute to sepsis, malnutrition, fluid and electrolyte imbalances, difficulties in wound care, as well as posing an enormous psychological challenge to the patient.
A fistula is defined as an abnormal communication between two epithelial lined surfaces. There are many types and exhaustive description is beyond the remit of this chapter. The great majority of those seen within the context of severe abdominal sepsis follow surgery and result from anastomotic leakage or an inadvertent enterotomy, either overlooked or unsuccessfully repaired.
An intestinal fistula, from somewhere in the intestinal tract to the laparotomy wound, will occur occasionally in every gastrointestinal surgeon's practice, arising most commonly as a result of anastomotic leakage or bowel damage. While a few will show signs of severe sepsis, more often than not there is a period of apparent ileus, wound infection and clinical stagnation. When the wound ruptures or is opened to treat the infection, the enteric or faecal nature of the contents will become apparent. This may not be convincing to begin with as the enteric flow is usually preceded by a volume of pus and blood, as with most postoperative wound infections. Postoperative fistulas may also occur through drains or along recent drain sites, to the vaginal vault (especially in those who have undergone previous hysterectomy) and occasionally to the rectum or other parts of the gut.
However, fistulas are more likely to occur after emergency surgery, usually carried out for another postoperative complication, commonly sepsis, obstruction or bleeding. In these operations, the inherent difficulty of the procedure, brought about by adhesions, bowel distension and softened tissues, makes further bowel damage a real possibility. If that damage is not, or cannot, be repaired effectively, if there is persisting obstruction of the intestine postoperatively, a postoperative phlegmon or an open abdomen, then the likelihood of fistulation escalates considerably. Postoperatively, the combination of small-bowel obstruction and an undrained abscess is also likely to result in a fistula as the obstructed bowel eventually softens and gives way at, or into, the collection. Thus it will be evident that repairing a leaking anastomosis once the patient is septic and local tissues oedematous and friable is all too often doomed to failure. Bowel exposed in an open abdomen will also invariably be subject to some degree of trauma unless the dressings or appliances are handled and changed expertly. Again, if there is distal obstruction, a local and exposed suture line or local trauma, a fistula will often occur. Perhaps 10–20% of ‘laparostomies’ will fistulate and this sometimes happens even with expert care.
A significant number of intestinal fistulas heal spontaneously, although they will cause misery and morbidity while they do so. The factors that contribute to persistence of a fistula are shown in
Box 18.9
.
Box 18.9
Factors contributing to the occurrence and persistence of postoperative fistulas
Occurrence
Repaired anastomosis
Inadvertent enterotomy (repaired or missed)
New anastomosis in unfavourable circumstances
Persisting abscess or phlegmon causing obstruction
Fistulating disease
Open abdomen
Persistence
Distal obstruction (including constipation)
Open abdomen
Disconnected bowel ends
Local abscess
High output from fistula
Complex fistula
Mucocutaneous continuity
The best-known approach to fistula care is that described at the specialist fistula unit in Salford (UK), and known by the acronym SNAP (Sepsis, Nutrition, Anatomy, Procedure). The most pressing effects of a fistula relate to intra-abdominal sepsis. There can also be wound sepsis, usually in the form of cellulitis, although occasionally local necrosis can occur. Once the necessary resuscitation is in hand, an early priority is CT of the abdomen, preferably with both gut and intravenous contrast. The frequency of intra-abdominal abscess formation is high, in the region of 66%,
43
and often these are not evident clinically. Without diagnosis and control of the sepsis, the prognosis is bleak. Management strategies follow the principles outlined above.
An integral part of early management is wound care and control of the fistula effluent. When there is a small fistula orifice in a drain site or through part of a wound, the effluent can be controlled with a stoma bag. At the other extreme, when bowel contents are leaking into a laparostomy, management may be very difficult. Large fistula bags are available; the largest may be needed for a new laparostomy. The author's unit often uses a sandwich dressing initially, as described above, with low-grade suction attached to soft rubber catheters placed near the fistula site. The same suction technique can be placed inside a fistula bag when appropriate in order to reduce the frequency of bag leakage.
Important ancillary techniques include reducing fistula output by avoiding enteral feeding and reducing gastric acid output with proton-pump inhibitors. Codeine and loperamide can subsequently be used to contribute to this control of gut secretions. Octreotide will also reduce gut secretion in some patients but, in the author's experience, its effect is inferior to the steps already described. It is perhaps most useful in pancreatic fistulas and upper small-bowel fistulas.
Immediate fluid management will have been considered as the patient was resuscitated but attention will have to turn rapidly to the optimal means of nutrition. The deleterious effect that enteral nutrition often has on output and wound care, particularly in the early stages, has been noted above. Additionally, enteral feeding may also ‘feed’ the abdominal sepsis, if there is complexity to the fistula with a further unrecognised proximal hole in the bowel. There is often partial obstruction associated with the sepsis and with most fistulas it is often better and more reliable to resort to parenteral nutrition while the patient stabilises and the situations with regard to sepsis, wound care and fistula anatomy each become clearer. Indeed, it is often better to see parenteral nutrition as the ongoing mainstay of nutritional support in intestinal fistulation with abdominal sepsis. In some circumstances, enteral nutrition can take over some, or even all, of the role, but this will usually take time and is only possible in selected patients.
Fistulas can be categorised as high or low output (high > 500 mL per 24 hours). This cut-off represents a level above which the fistula is likely to have a significant effect on fluid balance and nutrition. Some proximal fistulas have outputs of one or more litres per day and fluid balance will be challenging in its own right. Senior surgical staff will need to commit to adequate supervision of the recording of the various inputs and outputs, particularly in the initial unstable and complicated phase of care. Fistula output will often reduce with time and, when possible, some healing begins to occur. A typical anastomotic wound fistula will be a side hole and if there is free distal flow, no sepsis, no bowel disease and no distal obstruction (or constipation), then healing may occur. It is unknown whether restricted oral intake helps, but it is intuitive to minimise the flow through the hole to encourage healing. As healing occurs, usually after 2–4 weeks, oral intake can be increased. If there is no healing by 6 weeks and no apparently reversible factor (e.g. abscess, constipation), then many would assume the fistula will not heal and allow more liberal oral intake.
In the ICU setting, once sepsis is excluded or controlled and the open abdomen, if present, is starting to granulate, oral or enteral feeding can begin cautiously, maintaining a careful watch for recurrent sepsis. The nutritional effect of this will depend on the length and condition of gut available for absorption and it will often take time for enteral feeding to be tolerated. During this phase, combined enteral and parenteral feeding is used.
It will be clear from the above that further surgery is usually only advocated to deal with abdominal sepsis. Further operations at this stage to try and correct the fistula often cause more harm than good through loss of bowel (risking short-bowel syndrome) or the creation of yet more fistulas. If surgery is undertaken then the approach follows that described above for abdominal sepsis. Surgery for fistulas is best deferred until the patient is well physically, nutritionally and emotionally, and only after the anatomy has been defined radiologically. This is often some months later and in complex cases is a highly specialist undertaking.
Intestinal fistulas often settle down and can run a course of chronic abdominal sepsis where there is low-grade inflammation but no organ failure. This can be punctuated with further acute episodes and it may be difficult to be certain if the sepsis comes from the feeding line, urinary catheter, chest, wounds or abdomen. Unusual bacteria or fungi can be involved and occasionally less common sites become infected (e.g. myocardium or heart valves secondary to feeding lines). During this period there is a continuing requirement for close daily monitoring with senior surgical input, often for several months, if the patient is to recover. Ongoing parenteral nutrition is often integral to this and, again, the help of a specialist unit can be invaluable. In these units, the support of specialist nursing staff in maintaining sepsis-free nutrition and providing expert fistula care is fundamental to success. The overall recovery or otherwise of the patient will be indicated by the clinical and biochemical picture combined. A falling white count and C-reactive protein with a steady rise in the serum albumin, together with increasing general well-being, are all good signs. Further surgery should probably be deferred for at least 6 months after the last laparotomy in order to allow the abdomen to become less hostile, and prolapse of stomas or fistulas is a useful indicator that re-peritonealisation has occurred. Restorative surgery is still usually prolonged and difficult, and reconstructing the abdominal wall after laparostomy has its own difficulties, which may benefit from help from a plastic surgeon.
Key points
Abdominal sepsis is a leading cause of death in acute surgical practice and cases still carry a high mortality.
A systematic approach, based on a sound understanding of pathophysiology, is fundamental to successful sepsis management. Adequate resuscitation, safe, timely diagnosis, rapid definitive treatment, and accurate and ongoing reassessment are essential if the progression to organ dysfunction and failure is to be avoided.
Identifying and rapidly treating the underlying cause of sepsis (‘the septic focus’) is fundamental to a successful outcome.
Radiological intervention for localised sepsis is growing in importance.
Indications for laparotomy include generalised peritonitis, necrotic tissue, multifocal abscesses and failure of radiological intervention.
Re-laparotomy is often difficult and advanced techniques may be required.
Intra-abdominal hypertension and abdominal compartment syndrome are probably under-recognised. Medical management has a role, but in refractory cases surgical abdominal decompression will be required.
Intestinal fistulas can occur following any abdominal intervention, but are more common after emergency surgery. Prompt eradication of sepsis and attention to nutrition is key. Definitive surgery to correct the fistula should be deferred until the patient is well and the anatomy has been clearly defined.
Abdominal sepsis often runs a prolonged course in which the surgeon will have to play an ongoing role.
1.
Scottish Audit of Surgical Mortality 2010.
http://www.sasm.org.uk/Publications/SASM_Annual_Report_2010.pdf
2.
Bone, R.C., Toward a theory regarding the pathogenesis of the systemic inflammatory response syndrome: what we do and do not know about cytokine regulation.
Crit Care Med
. 1996;24(1):163–172.
8565523
3.
Hotchkiss, R.S., Karl, I.E., The pathophysiology and treatment of sepsis.
N Engl J Med
. 2003;348(2):138–150.
12519925
4.
Marti-Carvajal, A.J., Sola, I., Lathyris, D., et al. Human recombinant activated protein C for severe sepsis.
Cochrane Database Syst Rev
. 4, 2011. [CD004388].
5.
Remick, D.G., Pathophysiology of sepsis.
Am J Pathol
. 2007;170(5):1435–1444.
17456750
6.
Opal, S.M., DePalo, V.A., Anti-inflammatory cytokines.
Chest
. 2000;117(4):1162–1172.
10767254
7.
O'Sullivan, S.T., Lederer, J.A., Horgan, A.F., et al, Major injury leads to predominance of the T helper-2 lymphocyte phenotype and diminished interleukin-12 production associated with decreased resistance to infection.
Ann Surg
. 1995;222(4):482–492.
7574928
8.
Zimmerman, J.E., Knaus, W.A., Wagner, D.P., et al, A comparison of risks and outcomes for patients with organ system failure: 1982–1990.
Crit Care Med
. 1996;24(10):1633–1641.
8874298
9.
Rangel-Frausto, M.S., Pittet, D., Costigan, M., et al, The natural history of the systemic inflammatory response syndrome (SIRS). A prospective study.
JAMA
. 1995;273(2):117–123.
7799491
This prospective epidemiological study of SIRS and related conditions provides evidence of a clinical progression from SIRS to sepsis to severe sepsis and septic shock.
10.
Pinsky, M.R., Vincent, J.L., Deviere, J., et al, Serum cytokine levels in human septic shock. Relation to multiple-system organ failure and mortality.
Chest
. 1993;103(2):565–575.
8432155
11.
American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference, Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis.
Crit Care Med
. 1992;20(6):864–874.
1597042
12.
McLauchlan, G.J., Anderson, I.D., Grant, I.S., et al, Outcome of patients with abdominal sepsis treated in an intensive care unit.
Br J Surg
. 1995;82(4):524–529.
7613902
13.
Levy, M.M., Fink, M.P., Marshall, J.C., et al, SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference.
Intensive Care Med 2003
. 2001;29(4):530–538.
12664219
14.
The Royal College of Surgeons of England and Department of Health Working Group on Peri-operative Care of the Higher Risk General Surgical Patient.
The higher risk general surgical patient: towards improved care of a forgotten group
. The Royal College of Surgeons of England and Department of Health; 2011.
15.
National Institute for Health and Clinical Excellence, NICE clinical guidline 50: Acutely ill patients in hospital. 2007.
16.
Dellinger, R.P., Levy, M.M., Carlet, J.M., et al, Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008.
Crit Care Med
. 2008;36(1):296–327.
18158437
17.
Levy, M.M., Dellinger, R.P., Townsend, S.R., et al, The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis.
Crit Care Med
. 2010;38(2):367–374.
20035219
Outcome data on 15 022 patients who were managed according to the Surviving Sepsis Campaign initiative. Despite incomplete compliance with every aspect of the care bundles, a significant reduction in hospital mortality was associated with participation in the initiative.
18.
Anderson, I.D. Assessing the critically ill surgical patient. In: Anderson I.D., ed.
Care of the critically ill surgical patient
. London: Arnold; 1999:7–15.
19.
Boermeester, M.A., Surgical approaches to peritonitis.
Br J Surg
. 2007;94(11):1317–1318.
17939137
20.
Goldie, A.S., Fearon, K.C., Ross, J.A., et al, Natural cytokine antagonists and endogenous antiendotoxin core antibodies in sepsis syndrome. The Sepsis Intervention Group.
JAMA
. 1995;274(2):172–177.
7596007
21.
Kumar, A., Zarychanski, R., Light, B., et al, Early combination antibiotic therapy yields improved survival compared with monotherapy in septic shock: a propensity-matched analysis.
Crit Care Med
. 2010;38(9):1773–1785.
20639750
A retrospective multicentre cohort study of 4662 culture positive cases of bacterial septic shock showed that combination antibiotic therapy was associated with significantly decreased 28-day mortality compared to monotherapy.
22.
Go, H.L., Baarslag, H.J., Vermeulen, H., et al, A comparative study to validate the use of ultrasonography and computed tomography in patients with post-operative intra-abdominal sepsis.
Eur J Radiol
. 2005;54(3):383–387.
15899340
23.
Kumar, A., Kazmi, M., Ronald, J., et al. Rapidity of source control implementation following onset of hypotension is a major determinant of survival in human septic shock.
Crit Care Med
. 2004;32(12):A158.
24.
Angus, D.C., Linde-Zwirble, W.T., Lidicker, J., et al, Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care.
Crit Care Med
. 2001;29(7):1303–1310.
11445675
25.
Cinat, M.E., Wilson, S.E., Din, A.M., Determinants for successful percutaneous image-guided drainage of intra-abdominal abscess.
Arch Surg
. 2002;137(7):845–849.
12093344
26.
Akinci, D., Akhan, O., Ozmen, M.N., et al, Percutaneous drainage of 300 intraperitoneal abscesses with long-term follow-up.
Cardiovasc Intervent Radiol
. 2005;28(6):744–750.
16091990
27.
Prytherch, D.R., Whiteley, M.S., Higgins, B., et al, POSSUM and Portsmouth POSSUM for predicting mortality. Physiological and Operative Severity Score for the enUmeration of Mortality and morbidity.
Br J Surg
. 1998;85(9):1217–1220.
9752863
28.
Anderson, I.D., Fearon, K.C., Grant, I.S., Laparotomy for abdominal sepsis in the critically ill.
Br J Surg
. 1996;83(4):535–539.
8665253
29.
van Goor, H. Consequences and complications of peritoneal adhesions.
Colorectal Dis
. 2007;9(Suppl. 2):25–34.
30.
Condon, R.E., Frantzides, C.T., Cowles, V.E., et al, Resolution of postoperative ileus in humans.
Ann Surg
. 1986;203(5):574–581.
3707236
31.
Sajja, S.B., Schein, M., Early postoperative small bowel obstruction.
Br J Surg
. 2004;91(6):683–691.
15164435
32.
Jansen, J.O., Loudon, M.A., Damage control surgery in a non-trauma setting.
Br J Surg
. 2007;94(7):789–790.
17571297
33.
van Ruler, O., Mahler, C.W., Boer, K.R., et al, Comparison of on-demand vs planned relaparotomy strategy in patients with severe peritonitis: a randomized trial.
JAMA
. 2007;298(8):865–872.
17712070
34.
Carlson, G.L., Dark, P., Acute intestinal failure.
Curr Opin Crit Care
. 2010;16(4):347–352.
20489609
35.
Connolly, P.T., Teubner, A., Lees, N.P., et al, Outcome of reconstructive surgery for intestinal fistula in the open abdomen.
Ann Surg
. 2008;247(3):440–444.
18376187
36.
Barker, D.E., Green, J.M., Maxwell, R.A., et al, Experience with vacuum-pack temporary abdominal wound closure in 258 trauma and general and vascular surgical patients.
J Am Coll Surg
. 2007;204(5):784–793.
17481484
37.
Bee, T.K., Croce, M.A., Magnotti, L.J., et al, Temporary abdominal closure techniques: a prospective randomized trial comparing polyglactin 910 mesh and vacuum-assisted closure.
J Trauma
. 2008;65(2):337–344.
18695468
38.
Teubner, A., Anderson, I.D., Scott, N.A., et al, Intra-abdominal hypertension and the abdominal compartment syndrome (Br J Surg 2004; 91:1102–1110).
Br J Surg
. 2004;91(11):1527.
15499642
39.
Moore, A.F., Hargest, R., Martin, M., et al, Intra-abdominal hypertension and the abdominal compartment syndrome.
Br J Surg
. 2004;91(9):1102–1110.
15449260
40.
Hong, J.J., Cohn, S.M., Perez, J.M., et al, Prospective study of the incidence and outcome of intra-abdominal hypertension and the abdominal compartment syndrome.
Br J Surg
. 2002;89(5):591–596.
11972549
41.
Malbrain, M.L., Cheatham, M.L., Kirkpatrick, A., et al, Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions.
Intensive Care Med
. 2006;32(11):1722–1732.
16967294
42.
Cheatham, M.L., Malbrain, M.L., Kirkpatrick, A., et al, Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations.
Intensive Care Med
. 2007;33(6):951–962.
17377769
43.
Harris, C., Nicholson, D.A., Anderson, I.D. Computed tomography: a vital adjunct in the management of complex postoperative sepsis.
Br J Surg
. 1998;85:861–862.
