Chapter 39 Abdominal surgical catastrophes
Intra-abdominal surgical catastrophes are common conditions in intensive care units (ICUs)1 and typically occur in elderly patients with comorbidity and reduced physiological reserve. They are often associated with sepsis, either primarily or secondarily, and with subsequent multiple-organ failure. Overall mortality is high2,3 and those who do survive usually require a long period in intensive care. The long-term health outcomes of patients with these conditions may be poor, particularly if severe comorbidity and functional impairment were present before the catastrophe. These factors inevitably lead treating clinicians to consider carefully the costs and benefits4,5 of various treatment strategies during an illness which often has many of the characteristics of a tragic saga.6 The clinical issues alone are complex and decision-making is often hampered by the lack of controlled trials of various strategic approaches. These many difficulties create the potential for conflict to arise between intensivists and other involved clinicians, particularly surgeons, who inhabit different moral economies6 and often have differing opinions of what are realistic goals and reasonable strategies,7 particularly for patients who are near the end of life.8,9 It is in the care of these patients that the particular day-to-day work skills of the intensivist10,11 (‘seeing the big picture’, providing meticulous bedside care, and negotiating and maintaining consensus, good communication and teamwork between various clinicians and the family) are tested to the limits. In this chapter, vascular catastrophes, intra-abdominal sepsis and a few serious abdominal complications are discussed. Gastrointestinal bleeding and pancreatitis are covered elsewhere (Chapters 36 and 37).
VASCULAR CATASTROPHES
ABDOMINAL AORTIC ANEURYSM (AAA)
AAA is a disease of the elderly, which is up to six times more common in men than women.12 Rupture of an AAA is the most common vascular catastrophe seen in ICUs and accounts for 2% of all deaths in men over 60 years of age.13 The prevalence of AAA (defined as infrarenal aortic diameter of 30 mm or more), as detected by screening in men, rises from less than 1% at age 50 to around 4% at aged 60, between 5 and 10% at age 70 and around 10% at age 80. Ultrasound screening of elderly men for AAA reduces mortality and is probably cost-effective.14 Aortic diameter is the strongest predictor of the risk of rupture, which is below 1% per year with aortic diameter < 5 cm and about 17% per year with aortic diameter of 6 cm or more.13 The risk of rupture is higher in women (who have faster aneurysm growth rates than men15) and is increased by current smoking and hypertension. Aortic aneurysm expansion is around 0.3 cm/year for aneurysms smaller than 5 cm and around 0.5 cm/year for those larger than 5 cm and this rate may be able to be reduced by a short course of macrolide or by stopping smoking. Perioperative mortality for open elective aneurysm repair is ∼5% – somewhat higher when there is significant preoperative respiratory or renal dysfunction.16 Increasingly endovascular repair is performed because of lower perioperative mortality (∼1.5%), although 2-year survival is the same (∼90%) after either open or endovascular repair.17 A higher proportion of patients treated endovascularly will experience long-term complications (predominantly endoleaks, rupture and graft thrombosis), with associated increase in cost.18 Endovascular repair does not improve survival in patients judged medically unfit for open repair.19
Operative mortality is increased to around 15% in urgently repaired (non-ruptured) aneurysms20 and around 50% in ruptured aneurysms repaired as an emergency.20 Ruptured aneurysm may lead to death before hospital admission in around 30% of cases,21 is almost always lethal without repair22 and not all patients are offered repair. Vascular surgeons are less selective (∼10% non-operative) than general surgeons (∼60% non-operative), without an increase in mortality in operated patients.22
These results have led to recommendations for population screening by ultrasound at age 65, continued surveillance for small aneurysms23 and elective open (or endovascular) repair in patients without severe comorbidity when aneurysm diameter exceeds 5 or 6 cm.24
RUPTURE OF AN ABDOMINAL AORTIC (OR ILIAC ARTERY) ANEURYSM
The clinical features of rupture include the sudden onset of shock and back pain or abdominal pain or tendernessin a patient typically over the age of 70. Most ruptures are, initially at least, retroperitoneal with intraperitoneal rupture resulting in greater physiological disturbance and much higher subsequent operative mortality.25 The correct clinical diagnosis is often not made by the first attending doctor26 as a pulsatile abdominal mass is commonly not detectable25 and many patients do not have shock when first seen. Although immediate bedside ultrasound may sometimes be able to confirm the clinical diagnosis without increasing delay, others have found that this investigation commonly delayed vascular surgical referral and subsequent operation without diagnostic benefit.27 The diagnosis of ruptured aneurysm is confirmed (by computed tomography (CT) angiography) in only half of the patients in whom it is suspected28 but CT carries a significant risk of sudden deterioration outside the operating room. It may sometimes be inappropriate to proceed to operation (very severe comorbidity, poor quality of life) and this decision should be very carefully considered.29 Lack of physiological reserve (often associated with advanced age) predicts high operative mortality and long periods of intensive care and hospitalisation in survivors. Open repair remains the current treatment of choice but successful endovascular repair (sometimes with subsequent laparotomy for evacuation of haematoma30) is also possible in some of these aneurysms31 and is the subject of an ongoing randomised controlled trial.28 A very small number of patients with aortic aneurysm have infection of the aneurysm, usually with Staphylococcus or Salmonella, which is often diagnosed at rupture.32 A period of postoperative intensive care is appropriate for most patients. During this time common physiological abnormalities (e.g. hypothermia, dilutional coagulopathy, minor bleeding, circulatory shock, renal tubular dysfunction) can be corrected and serious complications can be sought and if possible treated (Table 39.1).
| Major bleeding |
| Renal failure |
| Myocardial infarction |
| Acute lung injury |
| Peripheral ischaemia |
| Stroke |
| Pulmonary embolism |
| Persistent ileus |
| Mesenteric ischaemia |
| Pancreatitis |
| Acalculous cholcystitis |
| Increased abdominal pressure – compartment syndrome |
Rapid ventilator weaning and extubation are recommended, perhaps with thoracic epidural anaesthesia33 if coagulation allows. Abdominal decompression in these particular patients may not be helpful.34 Finally, an assessment of overall progress should be made after 24–48 hours. Severe or progressive multiple-organ failure35 or major visceral or limb infarction should lead to a reappraisal of the appropriateness of continued intensive therapies. Persistent renal failure occurs more commonly after acute renal failure in this context than in other intensive care patients. Massive upper gastrointestinal haemorrhage (usually aortoduodenal) is a rare complication, usually resulting from infection of a previous aortic repair and less commonly from primary infection in an aortic aneurysm. Some of these patients can be rescued surgically.
ACUTE AORTIC OCCLUSION
This is an uncommon syndrome, usually due to thrombotic occlusion (of a stenotic or aneursymal aorta) or to saddle embolism. Presentation is with painful lower-limb paraparesis or paraplegia and absent distal circulation. Minimising delay to emergency revascularisation is of the essence but mortality and multisystem morbidity remain high.36
MESENTERIC INFARCTION
This uncommon syndrome presents with an acute abdomen, may develop in critically ill patients and is commonly due to non-occlusive arterial ischaemia, arterial embolism or atherosclerotic arterial thrombosis and less often to venous occlusion, low-flow or hypercoagulable states.37 Despite surgery (usually including gut resection), mortality is high. Successful endovascular revascularisation has been reported.38
AORTIC DISSECTION
Aortic dissection39 has an incidence of 5–30 per million per year. The typical patient is elderly, has a history of hypertension40 and presents with pain in a distribution corresponding to the site of dissection. Cases have been reported in young people and after circumstances suggesting acute situational hypertension. Pericardial tamponade, haemothorax, myocardial infarction, stroke, paraplegia due to spinal cord ischaemia, anuria or an acute abdomen may be present. Most aortic dissections originate in the ascending thoracic aorta. Some dissections extend to involve the abdominal aorta but spontaneous dissection of the abdominal aorta alone is rare. Mortality remains high but is falling in association with earlier diagnosis and treatment.39
SPONTANEOUS RETROPERITONEAL HAEMORRHAGE
Excluding rupture of an aortic aneurysm, spontaneous retroperitoneal haemorrhage is uncommon. It is usually associated with vascular or malignant disease of the kidney or adrenal gland and, less commonly, with spontaneous rupture of the retroperitoneal veins or with anticoagulant therapy, including warfarin, unfractionated heparin and low-molecular-weight heparin. The presentation is most often with acute abdominal pain, shock and a palpable abdominal or groin mass and CT will confirm the diagnosis.41 Correction of coagulopathy and interventionalradiologic embolisation may control some situations but surgery may be required in others, either to stop bleeding or to relieve associated intra-abdominal hypertension.
INTRA-ABDOMINAL SEPSIS
OVERVIEW
Intra-abdominal sepsis is very common in the ICU. In our own experience the abdomen (including continuous ambulatory peritoneal dialysis (CAPD) peritonitis) was the most common septic site in patients admitted to ICU with severe sepsis and accounted for 583 (35.9%) of the 1624 such admissions over the 17 years from 1984 to 2000.42 The incidence of sepsis in ICUs is reported to be increasing43 and our experience reflects this. The mortality of intensive care patients with severe intra-abdominal infections is variously reported between 25 and 80% but varies greatly depending on the extent of comorbidity43 and the severity of the acute illness.
The general principles of the treatment of severe sepsis are to support oxygen transport as required, if possible to remove the septic source44 and to give appropriate antimicrobial therapy. Sepsis should be thought of as a time-critical condition45 wherein delay in the execution of these principles is likely to worsen outcome. The place of other therapies remains controversial.46,47 The issue of severe sepsis in general is covered in Chapter 61.
SURGICAL SOURCE CONTROL
Surgical source control should involve definitive control of the septic site at the first (‘damage control’) operation but definitive surgical therapy for the underlying disease may not always be feasible or desirable at this time. Initial surgery44 involves:
The abdomen may be left open (with a temporary fascial closure) if required for intra-abdominal hypertension or to facilitate repeat laparotomy. Successful primary colonic anastomosis (even left-sided) after resection in the presence of sepsis is supported by several case series.44
Failure of the sepsis syndrome to settle (‘failure to thrive’) after apparently definitive surgical source control should suggest ongoing contamination or ischaemia or the development of abscess. Repeat laparotomy on clinical grounds is recommended when early postoperative progress is unsatisfactory,3 whereas CT scanning followed by either directed laparotomy48 or interventional radiologic drainage are more successful strategies for late abscess formation.
INTESTINAL-SOURCE PERITONITIS
Peritonitis secondary to contamination by intestinal contents usually results in mixed aerobic and anaerobic infection and recommended antibiotic regimens,42,49 therefore usually involve either combination therapy with an aminoglycoside (or aztreonam) and metronidazole (or clindamycin) or alternatively monotherapy with a carbapenem. Similar antibiotic regimens are appropriate in sepsis following intestinal infarction without perforation. An agent active against Staphylococcus aureus50 should probably be included in patients with peritonitis following gastric or duodenal perforation.
ACALCULOUS CHOLECYSTITIS
Acalculous cholecystitis is a rare but serious condition in ICUs. A small number of patients with the syndrome of acute cholecystitis will have acalculous cholecystitis but these patients have low mortality and do not present to ICUs. Of greater concern are the perhaps half of all cases of acalculous cholecystitis that develop insidiously in intensive care patients who are already critically ill for another reason (e.g. recent trauma or surgery) and can therefore go unrecognised until gangrene, perforation or abscess develops. The gallbladder histology in such patients usually includesprominent ischaemia and arteriosclerosis and low cardiac output may predispose to the condition. A high index of suspicion should be had in an intensive care patient who develops new abdominal pain or clinical signs of sepsis. Although a variety of investigations, including scintigraphy, CT scanning, ultrasound and laparoscopy, have been used to help establish the diagnosis, none performs reliably51 and many surgeons advocate a low threshold to exploratory laparotomy on clinical grounds where suspicion exists. Percutaneous cholecystostomy44 has been used successfully whereas early cholecystectomy is advocated by others52 as infarction or perforation of the gallbladder is commonly found at laparotomy.
TOXIC MEGACOLON
Toxic megacolon53 is now a rare indication for intensive care admission. It is characterised by systemic toxicity accompanying a dilated, inflamed colon and is usually due to inflammatory bowel disease. Infection by Clostridium difficile, cytomegalovirus (in patients with human immunodeficiency virus (HIV) disease or immunosuppression) or rarely other organisms may also precipitate toxic megacolon. The diagnosis should be considered in patients with diarrhoea and abdominal distension. Limited colonoscopy (despite the risk of perforation) and biopsy may both yield important microbiological information and help in the decision to operate. Supportive therapy in an ICU is usually recommended and includes both antibiotics as for colonic perforation and steroids (equivalent of ∼300 mg/day of hydrocortisone). Other immunosuppression (tacrolimus or anti-tumour necrosis factor (anti-TNF) monoclonal antibody) has also been used. Frequent surgical reassessment and abdominal X-rays are used to monitor progress. Intravenous nutrition may help to reduce the activity of Crohn’s disease but does not reduce hospital stay or the need for surgery in ulcerative colitis. A period of several days of careful observation may be reasonable to assess the response to medical treatment but urgent surgery (subtotal colectomy with end-ileostomy) is indicated for increasing colonic dilatation, perforation, bleeding or progressive systemic toxicity.54 Parenteral metronidazole may be effective in severe pseudomembranous colitis without megacolon (but early surgery is often recommended if megacolon develops).
SPONTANEOUS BACTERIAL PERITONITIS
SBP is usually a monomicrobial infection (usually with Escherichia coli, Klebsiella pneumoniae, pneumococci or enterococci and rarely with anaerobes).42 The development of SBP in patients with end-stage liver disease is a grave prognostic sign – hepatic decompensation and multiple-organ failure commonly develop and the median survival in such patients (without liver transplantation) is short. Early albumin supplementation has been shown to reduce both renal failure and mortality in SBP associated with end-stage liver disease.55 Treatment with a broad-spectrum beta-lactam antibiotic should be followed by secondary oral antibiotic prophylaxis.
CAPD-ASSOCIATED PERITONITIS
Peritonitis is not uncommon in CAPD patients but is rarely a cause of intensive care admission. The development of (extrarenal) organ failure is an ominous sign and usually reflects delay in effective treatment, abscess formation, the presence of unusual organisms (including a variety of fungi), or an unrecognised gastrointestinal septic source.56
TERTIARY PERITONITIS
Tertiary peritonitis – ‘peritonitis in the critically ill patient that persists or recurs at least 48 hours after the apparently adequate management of primary or secondary peritonitis’57– occurs occasionally in severely ill patients with prior laparotomy. It is commonly due to Staphylococcus epidermidis, enterococci, Enterobacter, Pseudomonas or Candida albicans42,57 and initial empiric treatment should include amoxicillin, gentamicin and metronidazole until culture results are available. When infection is due to Candida spp. other antimicrobial agents should be discontinued, any foreign bodies removed if possible, and treatment with amphotericin B given for at least 4 weeks.58
COMPLICATIONS
INTRA-ABDOMINAL HYPERTENSION AND THE ABDOMINAL COMPARTMENT SYNDROME
These phenomena occur uncommonly in critically ill patients, particularly after surgery for trauma or sepsis and in association with excessive crystalloid fluid administration. A recent consensus conference has defined intra-abdominal hypertension as intra-abdominal pressure (IAP) >12 mmHg and abdominal compartment syndrome as IAP > 20 mmHg with associated organ dysfunction.59 IAP can be conveniently and easily measured via intravesical pressure,34,59 is normally 5–7 mmHg in critically ill adults and is increased in patients with increased body mass index. Physiological impairment (including cardiorespiratory, renal, splanchnic and neurological) can occur with acute increases in IAP to levels above 12 mmHg. However, in the absence of evidence from randomised controlled trials, expert opinion60 suggests that the development of the abdominalcompartment syndrome (IAP > 20 mmHg with associated organ dysfunction) should prompt a search for decompressive measures. Traditionally this has involved urgent decompressive laparotomy and temporary fascial closure; however other measures include:
Diuresis or ultrafiltration or percutaneous drainage of intraperitoneal fluid or gas may be effective in some patients and should also be considered.60 Despite abdominal decompression, mortality for such patients remains high (∼50%).34
THE OPEN ABDOMEN AND STAGED ABDOMINAL REPAIR
The use of synthetic materials to provide temporary fascial closure has facilitated the care of the patient with an open abdomen and allowed repeat laparotomy and staged abdominal repair to proceed in a timely and unhurried manner. Our own practice34 has been to use polypropylene mesh alone for this purpose if the period of open abdomen is likely to be short (less than a week) and the mesh can be removed before significant adhesion occurs. Two or more drains on moderate suction are laid over the mesh and then covered with a clear plastic adhesive dressing to provide a sterile waterproof seal and allow continual removal of ascites. If a longer period is required with an open abdomen, then a non-adherent plastic material should be used either under or instead of the mesh to prevent adherence and minimise the risk of gut perforation and fistula during removal of the material and fascial closure. The management of fistulation in the open abdomen remains problematic as proximal defunctioning is often impossible and control of wound contamination is not ideal with soft-catheter intubation of the small bowel via the fistulous tract.
ENTEROCUTANEOUS FISTULAS – INTESTINAL, BILIARY AND PANCREATIC
These are rare complications in intensive care patients but they usually present formidable problems because of their common associations with serious gastrointestinal comorbidity, e.g. inflammatory bowel disease, intestinal malignancy and pancreatitis as well as concurrent severe sepsis. In addition complex fistulation with multiple collections, fistulation through an open abdomen, inability to proximally defunction or distal obstruction are commonly present. A standard approach to fistula management should apply.61
Although somatostatin analogues have been shown to reduce high-output small-bowel fistula losses and they and H2-blockers are commonly recommended in fistulas of intestinal or pancreatic origin, their efficacy in achieving closure is less clear.62 Parenteral nutrition is usually recommended for proximal small-bowel fistulas but more distal intestinal, biliary or pancreatic fistulas can probably be safely treated with a trial of enteral nutrition. Treatment with an anti-TNF antibody has been shown to be effective in chronic enterocutaneous fistulas in (non-ICU) patients with Crohn’s disease.63 Persistent high-output fistula should lead to investigation of possible causes, including complete disruption of the gut lumen, distal obstruction or persistent intra-abdominal sepsis. Definitive operative treatment for fistulas that do not close should await clinical recovery and, if possible, nutritional repletion.
COLONIC PSEUDO-OBSTRUCTION
Colonic pseudo-obstruction (Ogilvie’s syndrome, a severe form of colonic ileus) is not uncommon in critically ill patients. The syndrome may contribute to ventilatory difficulty, intra-abdominal hypertension and failure of enteral feeding. It carries a small risk of spontaneous perforation with high resultant mortality. Conventional conservative treatment includes nasogastric drainage, intravenous fluid replacement and avoidance of opioids and anticholinergic agents. Treatment with neostigmine has been found to be highly effective64 but may cause symptomatic bradycardia. Colonoscopy or surgery may be required if these measures fail.65
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