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 high^2,³ 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 benefits^4,⁵ 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 intensivist^10,¹¹ (‘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) aneurysms ²⁰ 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 aneurysms ²³ 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 tenderness in 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).

Table 39.1 Some complications of a ruptured aortic aneurysm

Major bleeding

Renal failure

Myocardial infarction

Acalculous cholcystitis

Increased abdominal pressure – compartment syndrome

Rapid ventilator weaning and extubation are recommended, perhaps with thoracic epidural anaesthesia ³³ 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 dissection ³⁹ 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 source ⁴⁴ 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.

In the critically ill patient with intra-abdominal sepsis, effective source control usually involves surgery, although occasionally interventional procedures may suffice. Laparotomy without delay or further investigation is recommended for most patients presenting acutely with shock and clinical evidence of peritonitis. Diagnostic peritoneal aspiration or lavage, abdominal CT scanning or laparoscopy may have limited applicability in unusual circumstances that do not mandate immediate laparotomy.

Common syndromes include:

• faecal peritonitis

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