Acute Mesenteric Insufficiency
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 embolism, followed by arterial thrombosis, low-flow states, and mesenteric venous occlusion.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 30–40%. 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 braches. 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. 13-9 and 13-10). 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, 3F and 4F 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 1–3 mg of tissue plasminogen activator (TPA) in 50-cc 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 promote laparotomy. Best results are seen when symptoms show some resolution within 1 hour.18
Angiogram of superior mesenteric artery (SMA) embolus demonstrating an abrupt cutoff distal to a branch point.
CT Scan of superior mesenteric artery (SMA) embolus showing patent SMA (right) with more distal thrombosis (left).
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 unusual. 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. 13-11).14
CT scan of superior mesenteric artery (SMA) thrombosis at the origin of the vessel. This is usually due to underlying atherosclerosis. Emboli lodge at the origin of the SMA in about 30% or fewer of cases.
The operative approach to acute mesenteric ischemia from thrombosis 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. 13-12). 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 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 a wire is passed 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.
Retrograde bypass of superior mesenteric artery (SMA) occlusion. This can originate from the aorta or the right iliac artery. The “lazy C” loop reduces the chance of graft kinking. The SMA anastomosis is on the posterolateral aspect of the vessel.
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 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. 13-13). 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 rarely indicated. 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.
CT scan demonstrating thrombus in the superior mesenteric vein. CT scan is the most accurate diagnostic study in this condition.
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, as 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 resected or excluded immediately to prevent contamination during vascular reconstruction. Evaluation of the remainder of the small bowel is done after blood flow to the intestine is restored. The bowel is usually observed for 15–20 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 appropriate. 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 18–24 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
Vascular injuries occur in 10–15% of cases of blunt and penetrating trauma.34–38 Associated nonvascular injuries are seen in over 90% of patients with vascular trauma, most commonly small bowel, colon, and liver.37 Vascular injuries can be highly lethal when they occur and remain the most common cause of death following penetrating abdominal trauma. Arterial and venous injuries occur with equal frequency. The pattern of injury differs between blunt and penetrating injuries. In penetrating injuries, the most commonly injured vessels are the vena cava, followed by the aorta, iliac arteries and veins, and the SMA, and vein and multiple vascular injuries are common.10 Vessels of the mesentery are the most commonly involved in blunt trauma. This section provides principles for management of injuries to the major arteries and veins of the abdomen and retroperitoneum. The reader is referred to the prior sections on vascular exposure for a description of how to obtain control of these vessels. The discussion here centers on management of specific injuries.
Overall, principles of trauma management including initial resuscitation of the patient, rapid evaluation and triage, and expeditious operation when indicated should prevail. Stable patients, particularly those with blunt trauma, may undergo one or more diagnostic tests, including peritoneal lavage, “FAST” ultrasound examination, and, with increasing frequency, CT scan.39 Many patients with penetrating trauma are taken directly to the operating room without further diagnostic evaluation. Consequently, in a significant proportion of cases, the extent of vascular trauma is not known preoperatively and must be assessed by the surgeon in the operating room.
Intraperitoneal hemorrhage is easily recognized and should be expeditiously controlled, by application of external pressure, vascular clamps, or intravascular balloon occlusion catheters. Once active hemorrhage is controlled, any visceral perforation is controlled by exclusion to prevent ongoing peritoneal contamination and any remaining solid-organ injuries (ie, liver, spleen, and pancreas) should be stabilized by packing. Definitive treatment of the vascular injuries should then receive priority over definitive visceral repair. The adaptation of a “damage control” approach to abdominal trauma has improved outcomes in abdominal trauma.40,41 Vascular “damage control” involves the control of major venous injuries by ligation or packing and placement of temporary shunts to restore arterial continuity when arterial ligation will not be tolerated.42,43 Shunts are most often used to temporarily restore flow to the extremities but are used less often in management of visceral injuries. In general, visceral vessels are either repaired or ligated during the initial operation. The end organ will either tolerate ligation because of collateral circulation or be sacrificed. The “damage control” concept combined with endovascular techniques may be of particular use when open vascular repair is exceedingly complex and associated with significant morality. This is particularly true of contained retroperitoneal or hepatic injuries. Definitive treatment can be deferred at initial laparotomy in these cases and attempted in an imaging suite using endovascular techniques after the patient is stabilized. Examples of this include embolization of intrahepatic arterial injury and treatment of some contained retroperitoneal hematomas. This approach is in evolution and holds significant promise.
There are a number of situations in which the surgeon must make a decision about whether to explore a contained hematoma. In these cases, the risk of missing a major vascular injury is balanced against the morbidity of operative exploration. Classic trauma training requires exploration of all contained hematomas that result from penetrating injury. In the case of blunt trauma, central hematomas (zone 1) are explored because of the risk of injury to the aorta or vena cava, while lateral and pelvic hematomas are explored only if there is active bleeding or expansion under observation.36 If exploration occurs, it is important to obtain proximal and, whenever possible distal, arterial control outside the area of hematoma before proceeding. Venous control above and below the area of injury is desirable but may not always be obtainable. Approaches to vascular control, including endovascular techniques in various locations, have already been described. Intravascular occlusion catheters should be readily available for additional control as needed. Only after every attempt to control the arterial and venous ingress and egress to the hematoma has been made should it be entered.
The advent of endovascular techniques may be changing the classic paradigm of managing contained hematoma from either blunt or penetrating cause. The rationale for exploring nonexpanding hematomas of any type was based on the concern for occult vascular or visceral injury. The advent of CT angiography and the existence of sophisticated intravascular imagining in the operating room can facilitate evaluation of nonexpanding hematomas from both penetrating and blunt trauma without the need for operative exposure and its attendant blood loss. Furthermore, endovascular techniques such as covered stents or coil embolization will allow treatment of many vascular injuries from remote access with reduced risk of blood loss.44,45 Such treatments are in fact preferred for trauma to branch vessels in the visceral, renal, or pelvic circulations. This potential change in paradigm suggests that the surgeon consider a form of vascular “damage control” in the case of contained hemorrhage, by considering an “endovascular first” approach for diagnosis and treatment of contained hematomas regardless of location. This area is currently evolving, and there is no consensus on the role endovascular techniques should and will eventually play. With these general comments in mind, a discussion of specific vascular injuries and their management follows.
Injuries to the Suprarenal Aorta and Vena Cava
These injuries as a group are highly lethal and management is difficult. They should be suspected in any patient with a central hematoma from either blunt or penetrating trauma. In the stable patient, CT scan with intravenous contrast can help to identify the area of injury. If CT scan is not possible preoperatively, a clear plan of exposure and management is crucial before commencing any attempt at repair. Because of the advances made in endovascular techniques, patients should be treated in an operating room that has the capability of intraoperative fluoroscopic imaging and angiography whenever possible. If an injury to the aorta or vena cava is suspected and the patient is not exsanguinating, the surgeon should consider intraoperative angiography through the femoral artery or vein as appropriate to evaluate the location and extent of vascular injury and consider intravascular control. Following this, proximal and distal control should be established. Open exposure of the aorta at the diaphragmatic hiatus or endoluminal balloon control,3,4 both described previously, can be performed. Injuries to the vena cava can initially be controlled by balloon tamponade, although this may reduce venous return to the right side of the heart. Open control of the vena cava is described in the following text.
Open Repair of the Suprarenal Aorta
The visceral aorta is exposed by a left medial visceral rotation described previously. If access to the posterior aspect of the aorta is required, the left kidney should be elevated along with the other viscera; if access to the anterior aorta is needed, the kidney is left in its bed. Direct suture repair is undertaken whenever possible. Direct repair that does not narrow the lumen of the aorta more than 50% or impinge on a visceral vessel is well tolerated. Larger defects may require patch angioplasty using prosthetic material, arterial autograft, or arterial homograft. In the absence of significant contamination, prosthetic material provides a readily available, strong, and durable material for repair. In the presence of gross fecal contamination, biologic materials should be used if possible. Arterial homograft provides the most expeditious alternative both for size and durability, if available. Saphenous vein is inappropriate in this circumstance due to concerns about strength and durability; deep veins of the leg have proven reliable substitutes for in situ aortic reconstruction in infected fields.46 If appropriate, the aortic repair can be buttressed by an apron of omentum of some paraspinous muscle, to separate the suture line from any visceral vessels. This should be done in the presence of associated visceral injury, particularly injury to the pancreas. Drainage is established as needed. If the damage involves the origins of one or more of the visceral vessels, these are ligated. Revascularization of these vessels can be performed as described in the following text. Damage control of the suprarenal aorta is not possible because of the mesenteric ischemia that would attend any such attempt.
Endovascular Repair of the Aorta
This emerging alternative should be considered in selected circumstances. In a stable patient with a contained injury, placement of a suitable covered stent can be combined with extra-anatomic debranching of one or two visceral vessels, as has been described for treatment of thoracoabdominal aneurysms.47 This is most suitable when a single mesenteric vessel is involved, because the bowel will tolerate more prolonged ischemia than the kidney. Modification of the stent graft (“fenestrations”), to allow continued visceral perfusion, is possible.48 This is most feasible when the aortic defect is posterior and relatively remote from the visceral orifices. More precise fenestrations, as required in suprarenal aortic repair, are currently beyond the capability of most surgeons in an acute setting. If a stent graft is selected, its diameter should be 110–115% of the normal aorta to allow for secure fixation. A variety of off-the-shelf aortic cuffs are available and their successful use has been reported in conjunction with thoracic aortic transection.
Open Repair of the Suprarenal Inferior Vena Cava
Open repair of injuries to the suprarenal vena cava is one of the most difficult of all abdominal vascular operations. Exposure of the infrahepatic suprarenal IVC is achieved by an extended Kocher maneuver and right medial visceral rotation. One cannot overemphasize the utility of intravascular balloon control in these cases to avoid hemorrhage. Balloon control can be combined with external pressure and the application of partial occlusion clamps to provide hemostasis. Fine Allis clamps are useful in coapting and controlling the cut ends of the IVC and are preferable to more traumatic attempts at control. Wounds of the infrahepatic suprarenal IVC are usually managed by lateral venorrhaphy with running vascular suture. Narrowing the IVC 50–60% is often acceptable. If lateral venorrhaphy is not possible, patch repair using prosthetic or biologic material is acceptable. The use of anticoagulation in these circumstances is unsettled and is likely to remain individualized. Ligation of the suprarenal IVC should be avoided. Injuries to the retrohepatic vena cava, especially those that accompany blunt trauma, usually involve avulsion of the hepatic veins. Such injuries are highly lethal. Exposure of the retrohepatic IVC involves mobilization of the liver and anterior medial rotation of the right lobe.49–51 Repair of retrohepatic venous injuries may require hepatic isolation (control of the aorta at the hiatus as well as the vena cava above and below the injury and occlusion of the portal triad), placement of an intraluminal shunt between the right atrium and infrarenal IVC or veno venous bypass with hepatic isolation. These techniques are only used in desperate circumstances when bleeding persists despite adequate perihepatic packing. In general, injuries in this area should initially be treated by packing, nonexpanding hematomas should not be opened, and the extent of injury should be defined and definitive repair planned after the patient has been stabilized.
Endovascular Techniques in the Suprarenal IVC
At this point, any endovascular approach would be considered experimental. The complexities of and poor results with open surgery in this area make an endovascular approach to suprarenal IVC injuries an attractive potential alternative. Remote access and control, facilitating exposure, along with limited occlusion of the IVC, are all points in favor of an endovascular approach. The size and distensibility of the IVC complicate the selection of an appropriate diameter endovascular graft. Patients with caval injury are often in shock and there may be external pressure on the vessel, both factors that cloud the estimation of caval diameter. No stent grafts have been made for caval use, and it is likely that aortic cuffs or short segment of grafts used for thoracic aortic repair would be most useful. Inadvertent coverage of the renal or hepatic veins represents a further potential complicating factor. There have been no reports of endovascular treatment of hepatic vein injuries. Nonetheless, the potential treatment of these injuries by remote rather than direct access is appealing enough that it will undoubtedly be investigated in the future.
Repair of the Infrarenal Aorta and Iliac Arteries
Injuries to the infrarenal aorta and iliac arteries can be managed by a combination of open and endovascular techniques. Use of an endovascular balloon to achieve proximal arterial control, described for ruptured aortic aneurysm, should be considered as a part of management. These techniques require access to intraoperative fluoroscopy and familiarity with endovascular techniques. The balloon should be placed in the operating room before celiotomy if possible, either through the femoral artery with a supporting sheath or the left brachial artery, as previously described.3,4 The balloon does not need to be inflated if the patient remains stable. Because concurrent visceral injury is common, laparotomy is almost universally required. After “damage control” of any gross intestinal spillage, attention is turned to the arterial injuries. Exposure of the aorta and iliac arteries has been described. When there is minimal enteric spillage, irrigation and repair with an in situ prosthetic bypass of appropriate diameter is the most expeditious approach. The repair should be wrapped in omentum if possible to separate it from the viscera. In the presence of significant contamination, the infrarenal aorta and/or iliac vessels should either be repaired primarily, ligated, or a temporary shunt inserted as part of a “damage control “strategy.”42 If ligation is required, extra-anatomic (eg, axillofemoral or femoral) bypass with prosthetic material can be used to restore perfusion to the lower extremities. If the aortic bifurcation is preserved, a unifemoral bypass is possible. In cases where the aortic bifurcation is not salvageable, primary end-to-end anastomosis of the proximal ends of the common iliac arteries can be performed, followed by axillo-unifemoral bypass. If this is not possible, axillo-bifemoral bypass may be required.
Unilateral common iliac artery injuries may be ligated with subsequent cross femoral reconstruction using a prosthetic graft. Isolated external iliac artery injuries can be repaired in most cases with saphenous vein interposition. Internal iliac artery injuries should be ligated. In the absence of significant contamination, interposition graft replacement of the damaged vessel with a prosthetic graft is preferred. There are advocates of in situ prosthetic bypass, even in the face of more significant contamination.52 We prefer not to do this unless the situation is life threatening and prefer temporary placement of a shunt.
Endovascular repair of injured aorta and iliac vessels can be performed using techniques applied for repair of endovascular infrarenal aortic aneurysm repair. One must remember, however, that many of these patients are young and the durability of these repairs is unknown. In addition most patients will require laparotomy for associated injuries. These two factors suggest a limited role for stent grafts in the treatment of traumatic lesions of the aortoiliac system. Endovascular repair has been used in treatment of traumatic dissection of the aorta or iliac arteries.53 As previously noted, endovascular balloon tamponade is a valuable technique and endovascular coil embolization of difficult-to-access hypogastric artery branches can be employed with great success.
Infrarenal IVC and Iliac Vein
The principles of controlling venous injuries, including use of balloon tamponade and external pressure, have been previously described. The infrarenal IVC, iliac confluence, and right iliac vein are exposed through a right medial visceral rotation (see Fig. 13-7). The confluence of the iliac veins is obscured by the aortic bifurcation and right common iliac artery. If the aortic bifurcation cannot be sufficiently mobilized to provide exposure, the right common iliac artery should be mobilized or even transected for additional exposure. This is often required in any event because concomitant arterial injury is common. The more distal left iliac vein is approached on either side of the descending/sigmoid colon depending on the location of the injury.
As with the suprarenal IVC, lateral venorrhaphy is the preferred approach, with autogenous vein patch or ligation as alternatives. If needed, the infrarenal IVC and iliac veins can be ligated, due to the rather extensive collateral network that can develop within hours. While this may cause fluid sequestration in the lower legs, it is usually tolerated in the short term and is preferable to an attempt at repair in an unstable patient. In the rare case that ligation results in extreme distal venous hypertension, a bypass graft is indicated. In patients who have been stabilized, we prefer venous repair, either with a vein patch or, when an interposition graft is required, a ringed prosthetic conduit. Successful venous repair must use a conduit of equal or slightly greater diameter than the native vein and should avoid any tension. Saphenous vein is of insufficient diameter for replacement of the iliac vessels and must be modified to be useful (“panel” grafts”). We find such panel grafts excessively time consuming to construct in these critically ill patients and prefer externally supported PTFE of suitable diameter and length. This is usually done in situ but may be performed using an extra anatomic route. When short segments of prosthesis are used in the presence of distal venous hypertension, flow is usually sufficient to maintain patency without the need for anticoagulation or an adjunctive fistula. In our experience, when thrombosis of a prosthetic vein graft does occur, adequate collateral venous flow has been invariably present. The indication for caval filters in patients with venous injury is not clearly established and remains a manner of individual clinical judgment.
Treatment of Traumatic Arteriovenous Fistula
Fistula between the major arteries and veins can occur at any level, because the vessels are in close proximity throughout their course. It is important to realize that, while this may occur acutely, such a fistula rarely represents a true vascular emergency. Exsanguinating hemorrhage does not occur, because the arterial blood is decompressed into the venous system. Most of these patients present months to years after their initial injury. These patients may present with a continuous bruit, signs of lower extremity edema, and high-output cardiac failure.54 Management depends on an accurate history of trauma, including prior surgery (particularly lumbar disc surgery) or endovascular manipulation. Detailed vascular imaging is essential. These patients are rarely in extremis, and an effort to delineate the problem and develop a careful plan of correction is time well spent. Repair can usually be delayed until the patient is stabilized and other acute problems are corrected.
Treatment is directed at repair of both the arterial and venous defect.54,55 This is most often done by primary suture closure, although patch closure is sometimes required. Proximal and distal arterial control is essential and is obtained using open or endovascular techniques as described previously. Proximal and distal venous control should be obtained when possible before opening the fistula. This can be done by external dissection, compression, or an intraluminal balloon. Central venous occlusion is important to prevent air embolization when the vein is opened. We generally avoid extensive venous dissection in close proximity to the fistula. On occasion, venous control can be obtained by placing a balloon catheter through the fistula from within the artery and then closing the communication with interrupted or running sutures (Fig. 13-14). In the acute circumstance, the artery and vein may be separated, but this is more difficult in the case of a more chronic fistula and closure of the communication, by primary suture or patch, can be done from within the vessel. If this approach is chosen, it is important to be sure that the communication has been completely interrupted at the end of the procedure by use of intraoperative ultrasound or angiography. Appropriate flushing of both the arterial and venous sides is important to avoid embolization of debris or air into the central venous circulation.
Control of the aorta by finger dissection. The aortic neck can be elevated off the spine and a clamp applied.
Arterial-venous communications can also be approached endovascularly using covered stents.56 The stent can be placed only on the arterial side of the defect if the site of injury is in a main artery and can be accurately identified. However, it is important to remember that the arterial injury may be in a branch of one of the iliac vessels, in which case placement of a stent graft in the main artery will not correct the abnormality. Detailed description of repair of these branch fistulae is complex and beyond the scope of this chapter. Suffice it to say that coil embolization can be particularly dangerous in these cases due to the high flow in the venous system and chance of central venous embolization. A variety of techniques can be employed to reduce this possibility. Endovascular treatment of these lesions should only be undertaken by those with significant experience in endovascular techniques. As with open repair, it is important to be sure that complete interruption of the fistulous communications has occurred using completion angiography.
Trauma to the Mesenteric Arteries and Veins
The origin of the celiac axis is exposed through the gastrohepatic ligament or by a left medical visceral rotation as described earlier. While a short bypass from the aorta to the bifurcation of the splenic and hepatic arteries can be performed, the origin of the celiac artery can be ligated safely, if necessary, in most cases. This is preferable to attempting repair in a relatively confined space in an unstable patient. Collaterals through the pancreaticoduodenal and gastroduodenal are usually sufficient to preserve foregut flow. If there is any doubt, a bypass can be performed from the aorta to the common hepatic artery. The splenic artery can be ligated, as can the splenic vein. In the case of proximal injuries to these vessels, the short gastric vessels provide adequate collateral flow. When the splenic vessels are injured close to the hilum, a splenectomy is usually the best approach. Injuries to the common hepatic artery may be ligated because of collateral circulation, while injuries to the proper hepatic artery are more likely to require repair. In order of preference, techniques are primary repair, interposition vein graft, and aortomesenteric graft using either saphenous vein or prosthetic. Two-thirds or more of hepatic flow is supplied by the portal vein, and, if this is intact, proper hepatic artery ligation is an acceptable option. Intrahepatic arterial lesions are generally treated with angiographically directed coil embolization unless massive exsanguination requires resection of the damaged area of the liver.
Injuries to the main trunk of the SMA should be repaired because significant loss of small bowel may result from sacrifice of the vessel. Ligation of proximal SMA aneurysms can be performed with acceptable results, due to the presence of collaterals from the celiac and inferior mesenteric arteries. However, in the trauma setting, integrity of collateral pathways from the pancreaticoduodenal and middle colic vessels is not easily ascertained and repair should be performed. Lesions at the origin of the vessel are best exposed by left medial visceral rotation and repaired with a short bypass originating from the aorta. More distal lesions are exposed through the base of the small bowel mesentery and can be repaired by patch angioplasty, interposition graft using saphenous vein, or proximal ligation and distal bypass arising from the aorta. In the trauma setting, the infrarenal aorta is preferred as inflow for the more distal SMA because supraceliac exposure and control is best avoided in patients who may be unstable and have multiple injuries. Saphenous vein is the preferred conduit. The details of SMA bypass have been described, including the need for proper length and orientation to prevent kinking. Trauma to the branches of the SMA is usually treated by vessel ligation and any nonviable bowel is resected. Attempts to repair distal arterial and venous injuries in the mesentery are not rewarding. Mesenteric hematomas that are not expanding and are not associated with compromised bowel should be observed initially with angiography as necessary to identify vascular lesions. Attempts to explore stable mesenteric hematomas can lead to excessive blood loss and vascular compromise, resulting in more bowel ischemia.
Injuries to the splenic vein are treated by ligation, with or without splenectomy. There is often an accompanying injury to the splenic artery. In the rare instance of isolated splenic vein injury, consideration should be given to concomitant splenic artery ligation or splenectomy. Acute ligation of the splenic vein alone may result in sequestration of significant amounts of blood within the spleen and left-sided portal hypertension. This can be ameliorated by ligating the main arterial inflow to the spleen. Injuries to the main trunk of superior mesenteric vein should be repaired to avoid bowel ischemia secondary to mesenteric venous obstruction. If the vein cannot be repaired using a patch angioplasty or short interposition graft, a bypass from the superior mesenteric vein to the portal vein should be performed. This probably will require a large (6- to 8-mm) conduit of either reinforced PTFE or deep vein (jugular or femoral). Injuries to the portal vein should be repaired if possible, by lateral venorrhaphy, patch angioplasty, or interposition grafting, if the patient is stable enough to undergo repair. The retropancreatic portal vein is best exposed by transection of the pancreas (Fig. 13-15). Isolated injuries of the portal vein, with an intact hepatic artery, may be ligated if necessary to save the life of the patient, although significant hepatic dysfunction and acute massive bowel edema can be anticipated. This leads to significant fluid sequestration and may even result in bowel necrosis. Lesions of the hepatic artery and portal vein that are not immediately lethal should be repaired if possible.
Exposure of the retropancreatic portal vein by division of the pancreas.
Injuries to the inferior mesenteric artery can usually be ligated, because adequate collaterals will exist from the arc of Riolan, the marginal artery of Drummond, and the hemorrhoidal vessels. If it appears that ligation will not be tolerated, reimplantation or a short bypass with saphenous vein is indicated.
Injuries to the Renal Artery and Vein
Management of renal artery lesions is dictated by the overall status of the patient, duration of ischemia, and presence or absence of a contralateral kidney. It is important to remember that after 60 minutes of warm ischemia time, most of the kidney's excretory function is lost. While some authors advocate renal vascular repair within the first 3–6 hours after injury, preservation of long-term renal function in these cases has been poor.57,58 Therefore, situations in which there is nonvisualization of one kidney on a preoperative CTA or intravenous pyelogram (IVP) suggests that renal function will not be salvaged by revascularization. In most cases of arterial transection, ligation with nephrectomy is indicated. In cases of blunt trauma observation is usually indicated. In circumstances where the status of the kidney is unknown or when there is not a contralateral kidney, attempts at revascularization should be undertaken. The most expeditious approach is aortorenal bypass for lesions of the main renal artery, using saphenous vein with PTFE as a second choice. Lesions of the more distal renal artery, at or beyond branch points, are best ligated in the acute situation, unless they can be repaired with a simple vein patch, or if the injury is to a solitary functioning kidney. If there is doubt about contralateral renal function, the ipsilateral (damaged kidney) ureter can be clamped and indigo carmine administered intravenously. Appearance of dye in the urine confirms contralateral kidney function. Renal artery thrombosis due to blunt trauma, diagnosed as lack of perfusion on CT scan, can be treated by endovascular placement of a stent59 if the patient is otherwise stable. However, salvage of a renal vessel in a patient with a contralateral functioning kidney remains a secondary priority in the trauma patient's overall management.
Lesions of the proximal renal veins may be ligated, as long as collateral flow through the gonadal, adrenal, and hypogastric veins is preserved. This works best on the left side. While it is known that some transitory renal dysfunction will occur after renal vein ligation, it is generally well tolerated. If inadequate venous collaterals exist or have been damaged during the course of the injury, a short bypass between the renal vein and the vena cava with 8- to 10-mm PTFE can be performed, although ligation and nephrectomy is appropriate if the patient is unstable. Under rare circumstances of injuries to the renal hilum, for example with a solitary kidney, nephrectomy with ex vivo repair and autotransplantation may be indicated. This extensive reconstructive surgery, however, is unwise in an unstable patient with a contralateral functioning kidney.