Among the many acute abdominal conditions that confront the general surgeon, disorders involving the vascular system are in the minority. Yet these conditions are often highly lethal if undiagnosed or inappropriately treated. Because operations involving vascular exposure, control, and repair are uncommon in the practice of most abdominal surgeons, a straightforward plan to identify and manage these conditions is required for optimal success. This chapter concerns itself with the general diagnosis of acute vascular abdominal conditions, principles of vascular control and repair, and a discussion of the management of the 3 most common types of vascular emergency: mesenteric ischemia, ruptured abdominal aneurysm, and abdominal vascular trauma. Whenever possible, emphasis is placed on general principles that can be applied to a variety of conditions. Acute pathology of the gastrointestinal tract that results in hemorrhage (eg, bleeding ulcer, esophageal varices, bleeding diverticula) is not considered within this chapter.

Acute vascular conditions can be divided into those associated with hemorrhage and those accompanied by vascular thrombosis. The presentation within each of these 2 broad categories is generally distinct. Conditions associated with hemorrhage present with evidence of blood loss including shock. Hemodynamic alterations, for example hypotension and tachycardia, predominate over physical findings. Signs of an “acute abdomen,” specifically peritoneal irritation, are often absent. While abdominal pain is usually present, it is often focal and may be associated with a palpable abdominal mass. Signs of shock in the absence of generalized peritonitis or visceral perforation should prompt the consideration of a vascular emergency. In contrast, vascular thrombosis leads to intestinal ischemia and perforation. The clinical presentation of vascular thrombosis is often identical to that of other acute nonvascular abdominal conditions that cause an acute abdomen. Stigmata of cardiovascular disease, for example peripheral vascular occlusions, history of cardiac disease, atrial fibrillation, vascular bruits, and advanced age, should all increase the clinical suspicion of a vascular event as the underlying cause of symptoms. Nevertheless, thrombotic vascular complications often remain undiagnosed until the time of laparotomy.

While physical examination may help to identify patients with intra-abdominal or retroperitoneal bleeding (signs of hemorrhagic shock, absence of peritonitis), routine laboratory evaluations are less helpful. Acute hemorrhage may not result in changes in hemoglobin in its early stages. Laboratory studies are generally useful in excluding other acute inflammatory states, such as pancreatitis, and acute processes of the biliary tree or intestine. Plain films of the abdomen may reveal vascular calcifications or suggest hemorrhage (loss of psoas shadow) but are often nondiagnostic. Computed tomography (CT) scanning, when available, is the most useful preoperative diagnostic study (Fig. 20-1). With the addition of intravenous contrast, CT angiography (CTA) can identify vascular calcifications, aneurysms, and pseudoaneurysms; localize and quantify blood loss; and often identify thrombosis of major arterial and venous structures. Refinements in CTA, such as 3-dimensional (3D) reconstructions, have markedly reduced the need for diagnostic angiography and streamlined the evaluation of all patients with acute abdominal problems. In addition to visualizing vascular structures, nonvascular findings on CT scan may raise the suspicion of an acute vascular emergency.^1,2 Thickening of the bowel wall and pneumatosis intestinalis may be present without an identifiable lesion in the mesenteric arterial or venous system. Evidence of visceral embolization, particularly in the spleen or liver, should suggest a proximal embolic source, most often from endocarditis. Evidence of a shrunken kidney is a sign of visceral atherosclerosis and, while a nonspecific finding, should increase suspicion of disease in other visceral beds.

CT scanning cannot identify all acute vascular conditions, particularly when intravenous contrast is not administered, and scans may not be performed before laparotomy in a number of emergent cases. Under these circumstances, the diagnosis of an acute vascular emergency is made at the time of laparotomy. Most often this diagnosis is obvious on clinical grounds, identification of a mesenteric or retroperitoneal hematoma, presence of free blood in the abdomen, or the presence of infarcted bowel without evidence of internal hernia.

Expeditious vascular exposure and control is essential for optimal management of vascular emergencies. The principles of operative vascular control are well established: proximal and distal control in a relatively normal area of the vessel. Proximal control should always be established before the lesion is addressed. When attempts to establish distal control would result in excessive dissection or cause damage to adjacent tissues and organs, the vessel is opened after proximal control is established and distal control established intraluminally by placing balloon catheters to control back bleeding. Increasingly, intraluminal techniques are being used for establishing proximal arterial control from remote access sites. Antegrade intravascular balloon control can be established without concern for balloon migration from arterial pulsation. A good example of this is placement of an arterial occlusion balloon in the suprarenal abdominal aorta through the arm vessels.³ When the balloon catheter is placed from a site distal to the artery (retrograde control), the balloon must be buttressed to avoid migration as a result of the repetitive force of arterial pressure.⁴ This can be done by supporting the catheter and balloon by a rigid sheath on which the balloon can rest. Balloon catheters can be used to tamponade proximal collateral bleeding if the main arterial inflow has otherwise been controlled. The most common example of this is the combination of supraceliac clamping coupled with placement of a Foley catheter to control collateral visceral back bleeding during repair of a ruptured aortic aneurysm.

In cases of active hemorrhage or when dissection is difficult, initial venous control is usually obtained by external pressure. Extensive venous dissection is usually avoided to reduce iatrogenic venous damage. Circumferential venous dissection must be meticulous because of the many venous tributaries and the fragility of the vein wall. Intraluminal balloons can be combined with external compression for both proximal and distal control in cases of venous injury, because this is a low-pressure system and catheter dislodgement is not a problem.

Endovascular techniques have been applied across all aspects of vascular surgery, and management of abdominal vascular emergencies is no exception. However, the application of most of these techniques requires angiographic capabilities in the operating room and significant endovascular experience. In routine practice, the most expeditious way to achieve control remains open exposure. Endovascular techniques remain most useful when they replace extensive or dangerous open dissection. While endovascular options will be discussed within the context of each disease process, these approaches will not be described in detail within this chapter. What follows is a description of the open surgical approach to control of the major abdominal vessels.

Exposure of the Aorta

SUPRACELIAC EXPOSURE

Expeditious supraceliac control of the abdominal aorta is the most important and versatile technique in the management of abdominal vascular emergencies. While suprarenal, intrarenal, and occasionally supramesenteric controls of the aorta are all possible, there is no evidence that these prove superior to supraceliac aortic control as long as visceral ischemia is limited to 45 minutes or less. Supraceliac aortic control can be achieved rapidly with very little risk of damage to adjacent organs such as the intestines, pancreas, or vena cava or the visceral vessels. Finally, the supraceliac aorta is most likely to be free of either aneurysmal or atherosclerotic vascular disease. For this reason, exposure and control of the aorta at that level is easier and safer than control between the visceral vessels.⁵ Supraceliac control of the aorta through a left retroperitoneal approach has been well described⁶ but is not germane in this situation, because it precludes evaluation of the abdominal viscera. Therefore, only the transabdominal exposure of the supraceliac aorta is described.

The supraceliac aorta is approached through the gastrohepatic ligament, which is divided between clamps (Fig. 20-2A). The left lobe of the liver is mobilized by dividing its diaphragmatic attachments if necessary. Division of the gastrohepatic ligament brings one directly down on to the esophagus and aorta as they course through the diaphragmatic hiatus. The aorta lies to the right of the esophagus and should be easily palpable. In the event that the 2 organs are not easily distinguishable, a nasogastric or orogastric tube may be placed in the esophagus to aid in distinguishing, but this is rarely required in our experience. Once the aorta has been identified, the key to obtaining control is complete division of the fibers of the left crus of the diaphragm as they cross the anterior aspect of the aorta (Fig. 20-2B). This can be done by placing either the index finger or a large-angled clamp between the aorta and the crural fibers as they cross over its anterior aspect. The fibers are divided, slightly to the left of the midline (“2 o’clock” position) to avoid bleeding, either with scissors or electrocautery. The phrenic arteries are identified and either clipped or, preferentially, spared. One cannot overemphasize the importance of completely dividing these fibers and clearing the anterior, medial, and lateral aspects of the aorta prior to applying the vascular clamp. If this is not done, any aortic clamp will slip anteriorly, resulting in loss of aortic control with disastrous results. Once the crura are divided, the aorta is encircled between the thumb and index finger of the operating surgeon’s right hand (Fig. 20-2C). The aorta is then lifted gently off the spine to be sure that it has been completely mobilized. A clamp can then be reliably placed across the aorta. More extensive dissection of the aorta is not required, and we avoid passing angled clamps and loops under the aorta to minimize damage to intercostal vessels. Use of the index finger and a straight aortic clamp are all that is required.

EXPOSURE OF THE VISCERAL AORTA

This area of the aorta will rarely need to be exposed for acute vascular emergencies. Transperitoneal control of the visceral aorta requires a left medial visceral rotation.⁷ The left colon is mobilized along Toldt’s line (Fig. 20-3A), the retroperitoneal and phrenic attachments of the spleen are divided, and the spleen, colon, and tail of the pancreas are reflected medially, leaving the left kidney down (Fig. 20-3B). This results in exposure of the anterior aspect of the aorta, and the origins of the renal, celiac, and superior mesenteric arteries (SMAs). If exposure of the posterior aspect of the aorta is required, the left kidney is elevated with the other viscera (Fig. 20-3C). Exposure of the visceral vessels more distally is described as follows.

INFRARENAL AORTIC EXPOSURE

This technique is familiar to most surgeons and involves incision of the ligament of Treitz and mobilization of the fourth portion of the duodenum superiorly and to the right (Fig. 20-4). When encountered, the inferior mesenteric vein may be divided between clamps. This sometimes improves exposure and is preferable to leaving an intact vein under tension with the risk of avulsion. The left renal vein serves as a reference to identify the superior extent of dissection. This vein almost never requires division. Should additional mobilization be required, the gonadal and lumbar veins can be divided for superior mobility and the adrenal vein is divided if the vein is to be retracted inferiorly. If these collaterals are divided and the renal vein is subsequently sacrificed, it should be repaired, either primarily or with an interposition graft. If the left renal vein is not encountered during this dissection, one must consider the possibility of an aberrant renal vein coursing posterior to the aorta, which occurs in 1% of patients.⁸ In that case, the vein is at risk for damage during aortic cross clamping and particular care should be taken during the posterior dissection of the aorta.

Lymphatic and areolar tissue anterior to the aorta is cauterized or divided and ligated between clamps. It is better to ligate large lymphatics to prevent chyle leak postoperatively. As with the suprarenal aorta, the vessel is encircled using the thumb and index finger and lumbar vessels usually do not require division. We are more inclined to place a tape around the aorta in the infrarenal location, because visualization is optimal, but this is not required. As described previously, the aorta is circumferentially mobilized digitally, raised off the spine, and an aortic cross clamp is placed under direct vision (Fig. 20-5).

Exposure of the Iliac Arteries

The common and external iliac arteries are controlled after entering the retroperitoneum. For proximal iliac control, the small bowel mesentery is reflected to the right and the aortic bifurcation is exposed. For more distal control, particularly of the external iliac arteries, the right or left colon is mobilized along Toldt’s line and reflected toward the midline (Fig. 20-6). It is important to be mindful of the ureter as it crosses over the iliac bifurcation. Control of the iliac arteries at the aortic bifurcation can be dangerous because of the confluence of the iliac veins behind the right iliac artery. This is one of the most common sites of iatrogenic vascular injury during aortoiliac surgery. The venous structures are gently separated from the arteries by use of blunt dissection (sponge on stick, kitner dissector, or digital dissection). We avoid use of clamps to dissect around the iliac vessels whenever possible. Once the vessels are separated from the adjacent venous structures, they can be encircled with vessel loops and clamped. Relatively blind clamping of the iliac arteries without dissection away from surrounding veins is discouraged as venous injury may result with disastrous consequences.

The hypogastric arteries and distal external iliac arteries can be difficult to expose, particularly in a deep pelvis. The hypogastric artery in particular may present challenges with the risk of injury to deep pelvic veins. This artery can usually be controlled by retrograde balloon tamponade and oversewn. The very distal external iliac artery can be controlled with an intravascular balloon and, if necessary, oversewn. Vascular continuity can be restored by a bypass to the common femoral artery.

EXPOSURE OF THE CELIAC ARTERY AND ITS BRANCHES

Exposure of the proximal celiac artery can be obtained through the gastrohepatic ligament, as described for the suprarenal aorta, or by left medial visceral rotation. We prefer the former approach whenever possible. The celiac artery is identified as it originates from the aorta at the diaphragmatic hiatus. Division of diaphragmatic fibers facilitates proximal exposure. More distal control is achieved by careful dissection along the anterior aspect of the vessel with caudal traction on the stomach and superior border of the pancreas. The tissue surrounding the vessel is carefully divided and ligated.

By opening the gastrohepatic ligament along the lesser curvature of the stomach, one can trace and isolate the common hepatic artery superior to the pancreas. The proper hepatic artery courses in the portal triad anterior and medial to the portal vein. The standard techniques for exposure of the porta hepatis will serve to identify and isolate this structure. The splenic artery is exposed by entering the lesser sac and reflecting the pancreas inferiorly and anteriorly. The multiple branches of this vessel that supply the pancreas must be ligated for adequate exposure. The distal splenic artery is best exposed by mobilizing the spleen as for splenectomy.

EXPOSURE OF THE SUPERIOR MESENTERIC ARTERY

Transabdominal control of the superior mesenteric artery (SMA) at its origin requires medial visceral rotation of the left colon, spleen, and tail of the pancreas.⁷ Exposure of the more distal SMA can be done through the base of the small bowel mesentery or by approaching the vessel on its posteromedial aspect after reflecting the small bowel mesentery to the right (as in standard aortic exposure). In the former approach, the transverse colon is elevated and the middle colic vessel is traced down to the SMA in the small bowel mesentery (Fig. 20-7). The anterior aspect of the vessel is cleared, taking care not to injure the adjacent vein. In the latter approach, the vessel is palpated in the root of the small bowel mesentery and dissection proceeds on the lateral aspect of the vessel (see Fig. 20-4A). In either case, dissection requires meticulous division and ligature of small venous, arterial and lymphatic branches, and the preservation of as many major arterial and venous branches as possible.

EXPOSURE OF THE RENAL ARTERIES

Transperitoneal control of the renal arteries can be achieved in a variety of ways, depending on the area of the artery to be controlled. The left renal artery is exposed in the same manner as the infrarenal aorta. The artery is usually superior and posterior to the left renal vein. The renal vein may require mobilization, including division of its lumbar, gonadal, or adrenal tributaries. Occasionally, the retroperitoneal attachments at the inferior border of the pancreas must be incised so the pancreas can be retracted in a cephalad fashion. The renal artery can be traced distally from its origin at the aorta. If the distal renal artery, near the hilum of the kidney, requires exposure, this is most easily done by mobilizing the left colon toward the midline. This may require mobilization of the splenic flexure and occasionally the tail of the pancreas, although this is not always the case. The proximal right renal artery can be exposed for a short segment between the aorta and inferior vena cava (IVC). The first part of the exposure is similar to that for the infrarenal aorta. Because the right renal artery runs behind the IVC, significant proximal exposure of this vessel requires mobilization of the vena cava and retracting it to the right. This requires careful division of 1 and often 2 sets of lumbar veins. Even with this maneuver, only the most proximal portion of the renal artery is exposed. As a result, the right renal artery is most often exposed by an extended Kocher maneuver; which reflects the duodenum, ascending colon and hepatic flexure toward the midline.⁹ The artery again lies posterior and inferior to the renal vein, which often requires mobilization.

EXPOSURE OF THE VENOUS STRUCTURES

The visceral veins are exposed by the same approaches as their corresponding arteries. Exposure of the vena cava and iliac veins requires some discussion. In general, these vessels are not involved in acute abdominal vascular emergencies outside the trauma setting. However, the vena cava is the vascular structure most commonly involved in penetrating abdominal trauma.¹⁰ The IVC and confluence of the iliac veins are generally exposed by a right medial visceral rotation (Fig. 20-8). This involves mobilization of the right colon along with an extended Kocher maneuver rotating the duodenum and head of the pancreas when more proximal venous exposure is required. When exposing venous structures, one must be exceedingly cautious of the fragility of the vessel and, in particular, disrupting small, posterior, lumbar vessels. As a consequence and because the venous system is a “low-pressure” system, compression plays a greater role in control of the vena cava and iliac veins than it does in exposure and control of the corresponding arterial segments. Circumferential mobilization of the veins is avoided if possible, as is the application of clamps. The use of blunt instruments such as sponge sticks can usually provide adequate hemostasis (Fig. 20-9). Fine clamps, such as Allis clamps, can be used to coapt cut ends of vessels and facilitate either suture or control by applying partial occlusion clamps. Whenever possible, only the anterior segments of the vein are exposed to avoid dissection around the lumbar vessels. Exposure of isolated posterior injuries involves significant mobilization and rotation of the vena cava and often requires ligation of multiple tributaries. Ligation is liberally applied in cases of extensive venous injury.

Several factors dictate the approach to emergency arterial repair, including the extent of contamination, size of the arterial defect, and the adequacy of collateral circulation. The following are principles that should guide the choice of procedure:

1. 
   

   When possible, primary repair is indicated. While most circumstances do not lend themselves to this approach, lateral repair or primary end-to-end anastomosis, or even arterial reimplantation, is associated with good long-term results and avoids use of a conduit.

   
   
2. 
   

   When adequate collateral circulation exists, ligation without repair is an appropriate option. This is the case with most splenic artery aneurysms and selected aneurysms of the hepatic and superior mesenteric arteries.

   
   
3. 
   

   In the absence of contamination, prosthetic conduits provide the best choice for bypass of major intra-abdominal arteries. The high flow in the aorta and major visceral arteries along with their relatively large diameters is associated with good long-term patency of prosthetic bypass. Prosthetic conduits have the advantage of adequate diameter and ready availability, which makes them preferable to saphenous vein in the absence of any contraindication. Occasionally when reconstruction of a small to medium diameter (<6 mm) vessel is required, saphenous vein may be the preferred conduit.

   
   
4. 
   

   In the presence of anything in excess of minor contamination, autogenous material should be used when vascular reconstruction is required. The risk of prosthetic graft infection with rupture argues against its routine use. For small- to medium-sized vessels (<6 mm), or when a patch closure is feasible, saphenous vein is usually adequate. For larger vessels, deep veins (femoral, popliteal, or jugular) should be considered. Short segment arterial repairs (eg, visceral and renal vessels) can be performed with hypogastric artery. Aortoiliac repair in the face of contamination should be performed with either deep leg veins, or more often arterial ligation and extra-anatomic bypass to restore perfusion. In the patient in extremis in whom obtaining autogenous conduit expeditiously is not an option, antibiotic-soaked prosthetic material can be used to salvage the situation, accepting an increased risk of infection and secondary surgery.

Acute Mesenteric Insufficiency

PRESENTATION

Patients with acute mesenteric insufficiency generally present with abdominal pain out of proportion to their physical findings. However, if undiagnosed, acute ischemia will progress to intestinal infarction with the attendant signs of peritonitis. Laboratory investigations include complete blood count, electrolytes, lactic acid, liver panel, amylase, and lipase. In general, findings are nonspecific early in the course of the disease and consist of a leukocytosis and perhaps some evidence of hemoconcentration. Liver panel, amylase, and lipase are most useful to exclude other acute abdominal conditions. Elevated lactic acid is usually a late sign and associated with a poor prognosis. Plain radiographs are nonspecific. An ileus may be present and occasionally edema of the bowel wall (“thumb printing”) may be present. CT, with intravenous contrast, has emerged as the most useful imaging modality. CT scans can identify abrupt arterial cutoffs, particularly when 3D reconstructions are available. In addition, late-phase CT angiography is the most reliable means to identify mesenteric vein thrombosis. Occasionally, angiography may be required, particularly when nonocclusive mesenteric ischemia (NOMI) is suspected. In these cases, angiography may be both diagnostic and therapeutic.

Mesenteric ischemia results from a variety of conditions; the most common is arterial thrombosis, followed by arterial embolism, low-flow states, and mesenteric venous thrombosis.^11–15 Mortality is highest in low-flow (nonocclusive) ischemia and lowest in mesenteric venous thrombosis. Mortality of ischemia resulting from acute arterial occlusion remains 30% to 40%. Diagnosis is delayed in up to two-thirds of patients with mesenteric ischemia. Outcomes in acute mesenteric ischemia are related to the time to diagnosis,^11,15 and therefore effective treatment relies on prompt diagnosis and initiation of therapy before extensive bowel infarction occurs. This is dependent on a high index of suspicion. Prompt effective fluid resuscitation is important in all cases of mesenteric ischemia, along with the initiation of broad-spectrum antibiotics. Patients with signs of an acute abdomen should be taken to the operating room as soon as they have been adequately resuscitated. Beyond this, however, the specific management of each type of mesenteric ischemia differs somewhat according to the etiology. Therefore, they are discussed separately.

Acute mesenteric embolization presents with the sudden onset of severe abdominal pain in the setting of a relatively normal abdominal examination. Most emboli are of cardiac origin and the patient may have an irregular pulse, cardiac murmur, or a history of prior myocardial infarction. Many patients may have a history of atrial fibrillation and/or prior embolic events. Because of the flow characteristics of the visceral vessels, most emboli preferentially go to the SMA. While some emboli lodge at the origin of this vessel, most end up distal to the first jejunal branches. An abrupt cutoff of flow in the SMA distal to the first jejunal branches on catheter angiography or CT angiogram is diagnostic of this condition (Figs. 20-10 and 20-11). Treatment is generally laparotomy and embolectomy. Characteristically, the most proximal jejunum is viable in the case of SMA embolus, because the occlusion occurs distal to the first jejunal branches. This is a helpful, but not foolproof, way to differentiate mesenteric embolization from mesenteric thrombosis.

As described earlier in this chapter, the SMA is exposed. The artery is usually soft and the site of the embolus is readily apparent. While a transverse arteriotomy with primary repair can be done, we prefer a longitudinal arteriotomy, and patch closure in most circumstances. The longitudinal arteriotomy can be extended if necessary and will allow thorough examination of the vessel and meticulous closure. It also facilitates bypass should this be required. Once the artery is opened, 3-F and 4-Fr embolectomy catheters are passed both proximally and distally to reestablish flow. If necessary, papaverine, 1 mg/kg, or 100 μg of nitroglycerine can be instilled in the distal vessels to reduce vasospasm. When there is concern about residual distal thrombus, 250 mg of urokinase or 1 to 3 mg of tissue plasminogen activator (TPA) in 50 mL saline can be instilled in the distal vascular bed.¹⁶ If there is clinical evidence of atherosclerosis in the artery, a longitudinal arteriotomy and patch closure are mandatory. If bowel resection is required, proximal saphenous vein should be used for arterial reconstruction.

In unusual circumstances, catheter-directed thrombolysis can be used as an alternative to open embolectomy.¹⁷ The patient should have no signs of peritonitis and angiography should demonstrate distal emboli (not easily retrieved by an embolectomy catheter) or a partially occluding proximal embolus that permits distal flow to continue during thrombolysis. In these rare circumstances, an infusion of TPA directly into the SMA can be attempted. Mechanical thrombolysis should not be attempted because of the danger of distal embolization. The patient must be observed carefully during lysis for signs of deterioration and any concern over bowel viability will prompt laparotomy. Best results are seen when symptoms show some resolution within 1 hour.¹⁸

The clinical signs of acute mesenteric thrombosis are indistinguishable from those of acute embolic occlusion; however, there are often differences in the history and some physical findings. History of arterial occlusive disease (stroke, claudication, myocardial infarction) is common, and atrial fibrillation or prior embolic episodes are less frequent. Careful questioning may elicit a history of chronic postprandial pain and weight loss, characteristics of chronic mesenteric ischemia. Physical examination often reveals stigmata of atherosclerosis, for example absent pulses and vascular bruits. Angiographic findings usually reveal diffuse atherosclerosis of the aorta and visceral vessels with multivessel involvement. When vascular occlusion occurs, it is usually at the origin of the mesenteric vessels (Fig. 20-12).¹⁴

The operative approach to acute thrombotic mesenteric ischemia differs from that of embolic occlusion. Mesenteric flow cannot be restored by a simple embolectomy and alternatives are required. The most common procedure required is bypass of the SMA usually from the infrarenal aorta or from one of the iliac arteries. While suprarenal bypass is preferred in elective surgery for chronic ischemia, an infrarenal origin of the bypass is more expeditious in the acutely ischemic patient and avoids the acute hemodynamic consequences of suprarenal clamping in a patient already acutely ill and often hemodynamically compromised. Because bowel resection is usually required, autogenous saphenous vein is the preferred conduit and should be harvested from the proximal thigh. When the bypass is performed, there should be sufficient redundancy to allow a “lazy C” loop, traveling from right to left in the abdomen to avoid sharp kinking (Fig. 20-13). The bypass is usually performed on the lateral side of the SMA slightly posterior, so that it can lie without compromise when the viscera are returned to the abdomen. While it is tempting to use very short bypasses, these may be prone to kinking and perioperative thrombosis. In the acute setting, revascularization is usually restricted to the SMA alone.

When there is no suggestion of intestinal necrosis and angiography reveals high-grade stenosis rather than vascular occlusion, an endovascular approach may be attempted.^19,20 Although an endovascular approach has been favored by many in patients with chronic mesenteric ischemia, it is more problematic in the acute setting. Endovascular recanalization is more dangerous when vessels are completely occluded because of the possibility of causing distal embolization. While the target lesion remains the SMA, it is reasonable to perform angioplasty of multiple visceral arteries if the patient remains stable. The visceral vessels may be engaged either transfemorally or more often via a transbrachial approach. The latter facilitates access to the origin of the vessel and passage of angioplasty balloons and stents as required. If there is any indication of intravascular thrombus, lytic infusion should be performed prior to any attempt at angioplasty to avoid the possibility of distal embolization. Once the possibility of thrombus is excluded, angioplasty with the placement of a balloon expandable nitinol stent is then performed. Use of a short (15-20 mm) 5- to 6-mm–diameter balloon–expandable stent allows precise deployment. The stent should completely traverse the area of narrowing and extend a few mms out into the aorta. This is important because the lesion in this case usually has its origin in the aorta. Selecting an endovascular approach does not mean that laparotomy is avoided, because bowel ischemia may be present. Any signs of peritonitis require prompt laparotomy and inspection of the bowel for viability.

Retrograde endovascular recanalization of a proximal SMA lesion has been reported at the time of celiotomy.²¹ This technique involves a longitudinal arteriotomy made in the SMA and passing a wire retrograde into the aorta under fluoroscopic guidance. Balloon angioplasty of the proximal lesion is performed as an alternative to bypass, and the arteriotomy is closed with a patch. While reports are anecdotal, this procedure is of interest because it avoids the possibility of distal embolization and may be performed more expeditiously than a vein bypass.

Nonocclusive mesenteric ischemia (NOMI) may occur as the result of low flow, without evidence of acute arterial thrombosis or embolization. In one form of this condition, the colon, in whole or in part, is involved. The arterial supply of the colon is less robust than that of the small bowel and, in elderly patients particularly, the inferior mesenteric artery (IMA) may be diseased or occluded. Systemic illness with reduced visceral blood flow, or abrupt interruption of the IMA, such as with aortic resection, may precipitate infarction of marginally perfused areas of the colon. This is most common in the sigmoid colon and the splenic flexure. The rectum is often spared in this process, because of its dual supply through the hemorrhoidal vessels. The small bowel is also usually spared. In these situations, resection of the infarcted colon, with exteriorization and diversion as necessary, is all that is required. The SMA and celiac arteries are usually normal, and no attempt at revascularization of the IMA is indicated.

Mesenteric ischemia without an underlying visceral lesion may also involve the SMA and celiac distribution. This has been called “nonocclusive mesenteric ischemia” (NOMI) and is associated with severe systemic illness, hypotension, and spasm of the mesenteric vessels without evidence of an obstructive lesion.²² Patients with NOMI are often already in an intensive care unit (ICU) and have had a cardiac event requiring vasoactive drug infusions. Some patients may have been on digitalis preparations that themselves are known to reduce visceral blood flow. There have been some recent reports of NOMI following dialysis in patients with end-stage renal disease.²³ Angiography, when performed, shows “pruning” of the mesenteric vessels without discrete obstruction. Management of these patients is directed at overall cardiovascular support, treatment of the underlying acute condition(s), and broad-spectrum antibiotics. Intra-arterial papaverine may be administered to relieve vascular spasm, although this is not always effective and may be complicated by systemic hypotension. NOMI usually portends a bad outcome in general, which is related as much to the underlying illness as to mesenteric compromise. Laparotomy should be reserved for patients in whom intestinal infarction is suspected and who are deemed otherwise salvageable since it often will not influence the outcome in this disease.

Mesenteric venous thrombosis may result in acute intestinal ischemia, although this accounts for only about 5% of all cases. Patients are a distinct subgroup, being younger (30-50 years) and predominantly female.^24–27 Associated hypercoagulable state can be identified in more than three-quarters of patients and a history of prior venous thrombosis is not uncommon. Common inherited states include deficiencies of protein C, protein S, and antithrombin III; activated protein C resistance; factor V Leiden mutation; and methylenetetrahydrofolate mutations.²⁷ Acquired prothrombotic states include profound dehydration, polycythemia, cancer, pelvic or abdominal inflammation, and hormone use. Mesenteric venous occlusion is most readily diagnosed by venous-phase CT angiography, which can demonstrate thrombus in the superior mesenteric vein and portal system (Fig. 20-14). Early diagnosis, and therefore a high clinical index of suspicion, and prompt initiation of systemic anticoagulation are critical to success. Operative findings suggestive of this condition are edematous beefy red bowel with thrombus in veins of the mesentery. The primary mode of therapy is anticoagulation; operative intervention is reserved for situations when bowel necrosis is suspected and resection is required. In those situations, limiting resection with a “second-look” laparotomy, along with ongoing anticoagulation, is the appropriate course. Most patients can be managed supportively, although significant volume resuscitation may be required. There are anecdotal reports of mesenteric and portal vein thrombectomy and thrombolysis,^28–30 but these do not reflect the standard of care for most patients.

DETERMINING INTESTINAL VIABILITY: THE ROLE OF “SECOND-LOOK” SURGERY

A major challenge in managing patients with intestinal ischemia is assessing the need for, and extent of, intestinal resection. Preoperatively, colonoscopy can be used to assess the viability of the large intestine in questionable situations. Friable red mucosa suggests viability and a grey mucosa that readily sloughs indicates the need for resection. Viability of the large bowel is difficult to judge from external appearance at the time of laparotomy, and in general, it is preferable to err on the side of resection in questionable circumstances, because maintaining large bowel length is not an absolute requirement for survival. Primary repair should not be undertaken after large bowel resection; diversion with secondary reconstruction is preferred.

When the small intestine is involved, the problem becomes more complex.^31–33 Every effort should be made to preserve as much small bowel as possible. Clearly necrotic segments of bowel and areas of perforation are excluded immediately to prevent contamination during vascular reconstruction and subsequently resected. Evaluation of the remainder of the small bowel is done after blood flow to the intestine is restored. The bowel is usually observed for 15 to 20 minutes after revascularization and warm lap pads are applied to the intestines to reduce any vasospasm. External inspection, with attention to color and peristalsis, is more helpful than in the large bowel. Doppler interrogation of the antimesenteric border for arterial flow is useful when positive. Use of fluorescein (1 ampule given intravenously) followed by inspection with a Wood’s lamp, is the most sensitive means of determining perfusion. Viable bowel will be fluorescent yellow while nonperfused bowel will appear dark purple. When the extent of resection is minimal and the remaining bowel is clearly viable, anastomosis and abdominal closure is reasonable. When there are large areas of questionable bowel that might mandate extensive resection, an alternative approach is undertaken. Under these conditions, marginal segments of bowel are left in situ and their ends are simply closed over and returned to the abdomen. Plans for a second operation are made. Stomas are not performed at this stage to preserve intestinal length. Fluorescein is not used at this time but reserved for the second procedure. The abdomen is temporarily closed using a “Bogotá bag,” polytetrafluoroethylene (PTFE) patch, or other temporary appliance (to minimize the chance of abdominal compartment syndrome) and the patient is returned to the ICU where resuscitation continues. A subsequent laparotomy is performed at 18 to 24 hours, after the patient has been stabilized. At this point fluorescein is injected and nonviable bowel is resected. Intestinal continuity is restored unless it is unsafe to do so. The abdomen often cannot be closed primarily at this point because of the danger of compartmental hypertension, and an “open abdomen” approach with delayed closure may be needed. Any deterioration in the patient’s subsequent hospital course should suggest breakdown of an anastomosis and prompt the appropriate therapy.

Despite increased clinical awareness and advances in diagnostic modalities and perioperative care, management of intestinal ischemia remains a significant challenge to the most experienced surgeon with continued high mortality and morbidity.

Management of Abdominal Vascular Trauma