Robert J. Feezor
Timothy C. Flynn
Patients requiring vascular intervention—whether open surgery or endovascular procedures—are elderly and have comorbidities that make their overall care complicated. To achieve a successful outcome, the perioperative care of the vascular surgery patient requires meticulous attention to detail and knowledge about the possible pitfalls these patients can encounter. Even the most seemingly innocuous clinical symptom must be thoroughly investigated and potentially treated in order to achieve acceptable perioperative outcomes. Despite meticulous attention to detail, vascular patients often fall victim to their comorbidities.
A key element in the care of the vascular patient is the recognition of vascular pathology as a systemic disease and not just a focal anatomic problem regardless of the procedure that brings the patient to the intensive care unit (ICU). The main exception to this is the young patient who sustains vascular injury. The nature of atherosclerosis is that it affects the blood vessels of all circulatory beds: cardiac, peripheral, and cerebral. Thus, patients who present with leg ischemia are at significantly higher risk than the general population for having both myocardial infarctions as well as cerebrovascular accidents. In fact, the average patient with claudication has an estimated mortality rate of 50% at 5 years, with the predominant cause of death being cardiovascular (1). Furthermore, there is progressing evidence that the vascular occlusive process is proinflammatory in nature. These patients have elevated levels of C-reactive protein (CRP), interleukin (IL)-6, and soluble intercellular adhesion molecule-1. Elevated CRP has recently been shown to be a predictor of cardiovascular events among patients with peripheral artery disease (PAD) (2). Up-regulation of inflammatory mediators may contribute to complications in the ICU.
In most series, patients with vascular occlusive disease have a high incidence of chronic obstructive pulmonary disease, occult cardiac disease, diabetes, and renal insufficiency. The adverse pulmonary sequelae of arterial revascularization are frequently related to the ravages of smoking. In most reports of operative repair of peripheral arterial disease, the incidence of tobacco use among patients exceeds 50%, and often approaches 90%. In a study looking at femoral atherosclerosis using duplex ultrasound, smoking was the largest risk factor, more influential than exercise tolerance, hypertension, or hypercholesterolemia (3). We may choose a potentially less durable endovascular therapy for patients based on their condition and ability to tolerate general anesthesia. Although general endotracheal anesthesia (GETA) is still the most common type of anesthesia used in vascular patients, increasing evidence suggests that spinal or epidural anesthesia may be more appropriate. In a review of 14,788 patients in the National Surgical Quality Improvement Program (NSQIP) of the Department of Veterans Affairs, GETA was associated with a higher incidence of cardiac, pulmonary, and graft complications when compared to spinal or epidural anesthesia (4).
Patients with known vascular disease are assumed to have associated coronary artery disease, even though they may be asymptomatic. In a landmark study by Hertzer et al., greater than 90% of patients undergoing peripheral vascular reconstruction had coronary artery disease evident by cardiac catheterization, and nearly one third had multivessel disease (5). The goals of the American Heart Association/American College of Cardiology should be targeted, including a blood pressure less than 140/90 mm Hg, serum low-density lipoprotein (LDL) <100 mg/dL, and hemoglobin A1C less than 7% (6). To achieve these goals, patients should be on an aspirin, a β-blocker dosed to a target heart rate of 70 to 75, an angiotensin-converting enzyme (ACE) inhibitor or other antihypertensive therapy, and probably a statin (independent of baseline cholesterol levels). Despite recent reports questioning the use of β-blockers, judicious use that avoids excessive hypotension or bradycardia may still be reasonable (7).
There is increasing evidence that patients with vascular disease should all be treated with a statin regardless of cholesterol levels (8). Statins have numerous effects other than reduction of cholesterol including anti-inflammatory, immunomodulatory, and anticoagulant effects. Moreover, abrupt discontinuation may lead to a rebound effect and possibly increase cardiovascular complications (9). It is our practice to routinely start patients on a statin preoperatively and continue it throughout the postoperative period. The antiplatelet drug clopidogrel is frequently used in vascular patients. Preoperatively we review the indications for this drug, and if the indications are compelling, such as the patient with a recent coronary stent placement, we will continue the drug through the perioperative period, recognizing that there may be a slightly increased incidence of wound complications. We do not hesitate to start the drug in patients who exhibit cardiac ischemia in the postoperative period.
The electrocardiogram (ECG) should be monitored continuously for any changes suggestive of ischemia. For the diabetic population, angina may present as nausea and must be interpreted as signs of myocardial ischemia until proven otherwise. Lastly, cardiac dysrhythmias are often caused by ischemia, electrolyte disturbances, or fluid shifts in the postoperative period, and patients should be monitored closely for such events.
In order to decrease the risk of perioperative cardiac events in the vascular surgery patient population, much attention has been given to preoperative risk stratification. In the surgical and anesthesia literature, most vascular surgery procedures for occlusive or aneurysmal disease are placed in the “high-risk” category. The question is how to minimize the risk of perioperative cardiac complications. Data from several randomized, multicenter trials have shown that coronary revascularization (percutaneous or open) before elective major vascular surgery does not decrease the overall mortality (10). Nevertheless, many clinicians request preoperative cardiology consultation to help determine existing cardiac function, usually with an ECG, an echocardiogram, or a chemical cardiac stress test.
Even without prior known elevated serum creatinine, many vascular patients have renal insufficiency as determined by creatinine clearance. Nephrotoxic effects of the IV contrast commonly used in revascularization procedures make postoperative renal dysfunction a constant threat. Moreover, perioperative mortality after most vascular procedures is significantly increased in patients with renal failure (11). Strict monitoring of fluid balance, maintenance of serum electrolytes, appropriate dosing of nephrotoxic medications, adequate hydration, and resumption of chronic diuretics will all help to minimize the chance of postoperative renal dysfunction.
A majority of vascular patients have diabetes mellitus and this group is at higher risk for postoperative complications, both vascular and nonvascular. From a vascular perspective, patients with diabetes have a higher rate of postoperative amputations after peripheral bypass surgery for tissue loss (11). Diabetics are also at risk for other postoperative morbidities including postoperative wound infections. They should be maintained euglycemic, even if that requires a constant intravenous infusion of insulin, with a target blood glucose of 80 to 110 mg/dL.
There is a subset of patients with vascular disease with underlying hypercoagulable states. The concern for a hypercoagulable state should be raised with patients with seemingly advanced atherosclerotic disease at a younger age. A careful history can assist with determining these patients, but when identified, they should be started on appropriate anticoagulation. Hematology consultation should be obtained, but may be of somewhat limited value in the setting of the acute thrombotic event.
Vascular Care in the Intensive Care Unit
All patients in an ICU have a propensity for developing venous thromboembolic events. Virchow's triad dictates that patients at risk include those with stasis, endothelial injury, and a hypercoagulable state. In the postsurgical population, venous stasis is inevitable due to the patients' relative immobility. Endothelial injury occurs during the course of the surgical procedure. It is our practice that all patients receive chemical and/or mechanical prophylaxis; we routinely use low-molecular-weight or unfractionated heparin and/or sequential compression devices when there is no existing contraindication. We avoid lower extremity sequential compression devices in patients with severe peripheral arterial occlusive disease, although the data for this practice are anecdotal. The incidence of heparin-induced thrombocytopenia is relatively rare, and when suggested by a decline in platelet count, we promptly cease all systemic or local heparin and transition to purely mechanical prophylaxis.
Stress gastritis is a constant threat in the vascular ICU patient. Patients are routinely placed on either histamine-receptor blockers or proton pump inhibitors, irrespective of any clinically detected gastrointestinal hemorrhage. Opponents of this practice suggest that in doing so, one of the body's natural defense mechanisms (gastric acidity) is altered, but we find that the risk of stress gastritis exceeds the diminution in host defenses.
Ventilator-associated pneumonia has been well documented to increase in-hospital mortality, length of stay, and overall cost of hospitalization. We employ routine suctioning, aggressive bronchoscopy to control secretions, and head elevation for all our intubated patients. Once extubated, activity is encouraged and adequate pain control is important for patients with an abdominal or a thoracic incision.
The routine assessment of the vascular ICU patient includes not only all the usual cardiovascular, pulmonary, and metabolic parameters, but also frequent and detailed physical exams. All incisions should be inspected for signs of early wound complications such as infection, separation, or hematoma. Objective assessment of distal perfusion should be performed regularly, even hourly, in the immediate postoperative period. This assessment includes looking at the extremity for cutaneous signs of malperfusion, assessing motor function, and palpating the major muscle groups for tenseness, which may signify compartment syndrome in patients who are too sedated to relate the classic “pain with passive motion.” The best exam, in our opinion, is to elevate the lower extremity by placing the hand behind the Achilles tendon and palpating the anterior calf compartment with the posterior leg off the bed. A patient should be alert enough to follow commands of simple dorsiflexion, again ensuring that the posterior knee is off the bed. (Dorsiflexing the foot with the heel resting on the bed can be achieved with flexion of the quadriceps muscles, thereby not testing the anterior calf compartment, which is the muscle group of interest.)
Some centers have advocated use of pressure monitoring devices to measure compartment pressures, but it has been our practice that if compartment syndrome is even suspected, it is imperative to perform fasciotomies emergently. This is best accomplished by the two-incision technique with a medial infrageniculate incision releasing the pressure within the deep and posterior compartments, and a lateral incision releasing the anterior and lateral compartments. Fasciotomies can be performed in the ICU setting using Bovie electrocautery and sterile scissors. The underlying muscle should bulge when released, thereby confirming the diagnosis. The wound should be left open and treated with routine dressing changes with subsequent closure in several days to weeks when the swelling abates. The metabolic sequelae of compartment syndrome may consist of cellular lysis with release of potassium and myoglobin that may cause systemic hyperkalemia and possibly acute renal failure. We routinely check urine myoglobin and administer aggressive intravenous fluids to ensure brisk urine output of at least 100 mL/hour. Electrolytes are checked frequently and continuous telemetric cardiac monitoring is employed.
Each extremity should be assessed by checking for palpable pulses; if none is found, Doppler signals must be auscultated to assess the perfusion. Ample quantity of Doppler gel should be used and the Doppler probe should be positioned at 60 degrees from the long axis of blood flow to maximize the signal. Normal Doppler signals are described as triphasic: the initial forward flow of blood is due to left ventricular systolic ejection; the second (reversal) flow is due to the intrinsic resistance of the arterioles in the circulation; the third phase again is forward-directed flow, and is largely attributed to the elasticity of the aorta. Doppler signals distal to an obstruction may be characterized as biphasic or monophasic signals with the latter suggesting significantly diminished blood flow. Sometimes it is difficult to tell if the sound is venous or arterial. If the sound disappears with gentle pressure on the Doppler probe, it is likely a venous sound. Also, if the sound in one of the pedal pulses disappears with gentle compression around the forefoot, it may be a venous and not arterial sound. At the conclusion of any vascular procedure, extremity perfusion is assessed prior to leaving the operating room. The operating surgeon should relay to the ICU team of physicians and nurses the quality and location of each Doppler signal or palpable pulse, as well as the frequency that he or she wants the perfusion assessed. Any change in the exam or inability of the examiner to detect the signal may potentially constitute an emergent trip back to the operating room to restore perfusion. Loss of a palpable pulse even if the pulse remains by Doppler should always be cause for alarm and the operating team should be alerted.
As an objective marker of extremity perfusion, we advocate bedside ankle-brachial index (ABI) measurements. This is done by inflating blood pressure cuffs on each arm and listening to the Doppler signal of the brachial arteries and comparing the values to the Doppler signals auscultated at the dorsalis pedis (DP) and posterior tibial (PT) arteries after inflating the cuff on the calves. The pressure at which arterial perfusion is restored as the cuff deflates is noted in each location. The ABI is the quotient of the pressure in the higher of the DP or PT pressures and the higher of the arm pressures. Each leg has a single ABI. Any change of greater than 0.15 is significant and should be reported, independent of any other clinical event.
All vascular surgery wounds should be examined daily for signs of infection. Of particular difficulty are the incisions made in the groins. The incidence of groin wound complications in the vascular surgery patient has been estimated to be up to 44% in some series (12,13). Although most surgeons try to close groin wounds with several layers of suture, any breakdown of the wound can be a significant complication. Groin wound breakdown is especially common in obese patients and efforts should be directed toward keeping this area dry and covered with sterile gauze. We tend to keep Foley catheters in place in the questionably mobile patient to avoid contamination of the wound, or at the least, maceration of the skin surrounding the surgical site. Most breakdowns can be treated with local therapy, usually routine dressing changes at the bedside.
Although there has been a great deal of interest in new techniques and agents to expedite wound healing, few advances have impacted the overall rate of wound complications, possibly owing to the patient's underlying systemic illnesses that translate into slow healing. The most disastrous complication of groin, or any other wound, breakdown is the exposure of the underlying vascular graft or anastomosis with the devastating potential for anastomotic disruption. When the bypass graft is noted to be exposed, patients should be scheduled for the operating room for exploration and attempted reclosure of the wound, preferably with autogenous tissue such as a sartorius or rectus flap. Until the patient can go back to the operating room (OR), it is imperative that all health care personnel treating the patient be aware of exposed vasculature. We have instituted a “blowout precaution” protocol wherein patients are kept at bedrest and blood typed and crossed. Any bleeding from the wound is a potential emergency. Immediate pressure should be held on the wound, the patient stabilized, and the operating team notified. We have on occasion had to rush back to the operating room with a member of the team holding direct pressure on the wound until the patient is intubated and anesthetized, the surgeon scrubbed in, and the operative field prepped (even if this includes the team member's gloved hand being prepped into the field).
For the vascular patient, meticulous care of the skin is mandatory, and even modest duration of pressure on the heel by the bed mattress can lead to skin breakdown and turn a successful revascularization into an amputation. Since the vast majority of vascular patients have compromised distal perfusion, we try to keep the heels off of the bed by placing the extremity on pillows, which allows the weight of the leg to be borne over a larger surface area. There is no substitute for frequent inspection of all pressure-sensitive areas and this should be part of the physician's and nurse's practice.
Pharmacologic prophylaxis against thromboembolic events is the routine. However, many patients require systemic anticoagulation after vascular surgical procedures (14) such as with distal bypasses when there is compromised outflow or less than ideal conduit. The need for systemic anticoagulation must be balanced with the risk of bleeding complications, and usually we hold off full anticoagulation until postoperative day 2 or 3. In most patients we will give subtherapeutic heparin (400–500 U/hour) in the early postoperative period. Patients are monitored for any decline in platelet counts, and if seen, a heparin antibody panel is sent. If the clinical suspicion is high, we stop all heparin and switch to anticoagulation with other agents. Regardless of the agent chosen, it is imperative that the anticoagulation be monitored closely and is best accomplished with protocol-driven therapy (15).
Acute limb ischemia in the ICU setting can have disastrous consequences. The pathologic differential includes embolic events (usually from cardiac or aortic sources) or in situ thrombosis of pre-existing atherosclerotic lesions that likely is a consequence of plaque instability and the aggregation of platelets, which then occludes the vessel. If identified acutely, there may be a role for intra-arterial thrombolysis, although in the setting of the postsurgical patient, this role is limited due to excessive bleeding risk. When an ischemic extremity is identified, patients should immediately be fully anticoagulated while resources are being mobilized to further evaluate the problem. More aggressive intervention, either catheter-based therapy or open surgical thrombectomy, should be entertained. In general, if the acute arterial occlusion is associated with motor or sensory deficits, then an emergent exploration is indicated. On rare occasions, patients present with acute lower extremity paralysis secondary to acute infrarenal aortic occlusion. There is often a delay in diagnosis owing to an investigation of neurologic causes of the paraplegia. Absence of femoral pulses is a clue to the vascular nature of the paralysis. These patients typically require emergent procedures, and despite operative success, the perioperative mortality rate exceeds 50% (16).
Common ICU causes of arterial occlusion include sequelae of invasive monitoring, usually intra-arterial lines. In a recent review of brachial artery cannulations for cardiac catheterizations, the overall complication rate was an astonishing 36% (17). Not infrequently we are called to assess lack of distal perfusion in an extremity with an indwelling arterial line. The first step is to remove the catheter and to observe for restoration of perfusion. The collateral blood supply should also be assessed (usually the ulnar pulse in the event of radial artery occlusion) as well as the distal perfusion, including motor and sensory assessment. Choices of therapy include observation, systemic anticoagulation, local thrombolysis, and operative thrombectomy with the potential for bypass.
The choice of invasive arterial and venous monitoring can represent a continuous challenge in any ICU patient, but in particular the vascular ICU patient. Lower extremity intravenous and arterial lines are contraindicated in patients with peripheral arterial occlusive disease. Furthermore, patients with dialysis access fistulae should have that extremity kept free of IVs, central venous catheters, invasive arterial lines, and noninvasive blood pressure cuffs. If a patient is identified as likely to require permanent vascular access in the future, duplex ultrasonography should be used to identify a potential arm for future access, and the identified extremity should be preserved.
Various bleeding complications can occur in the postoperative vascular wound. These can range from simple “skin edge” bleeding to frank exsanguination. Skin edge bleeding may be a nuisance, and may be treated with manual compression, application of silver nitrate, or a simple suture. Hematomas are monitored closely. Recurrent blood transfusion requirements, overlying skin or wound compromise, deleterious mass effects, and hemodynamic instability are all indications for operative evacuation of the hematoma. Patients who have had percutaneous interventions (usually through the groin at the common femoral artery) should also be monitored for hematomas, and in these instances, simple manual compression may be adequate. Attempted femoral artery punctures that are aimed more cephalad may in fact be external iliac artery punctures. Compression for hemostasis may be ineffective due to the retroperitoneal location of the arteriotomy. A progressive hematoma in such a location more often requires surgical repair (open or endovascular).
Specific Conditions
Aneurysmal Disease
Infrarenal Abdominal Aortic Aneurysm
Approximately 90% of the extracranial aneurysms found in the human body involve the infrarenal aorta. The natural history of aneurysms of the aorta is to expand and rupture. The tension felt by the thinning aortic wall can be estimated by the Law of Laplace, which describes the relationship between aortic diameter and wall tension. The results of randomized trials and observational studies have led vascular surgeons to recommend operative repair when the diameter of the aorta reaches 5.5 cm in asymptomatic patients (18), but the numeric value varies, especially with female patients. Most aneurysms are asymptomatic and are discovered during radiographic workup of other problems. Patients who have symptomatic aneurysms generally complain of back or abdominal pain. These symptoms should be interpreted as a sign of impending rupture necessitating urgent repair. We no longer place pulmonary artery catheters routinely, but all patients have arterial lines and Foley catheters and most have central lines. All patients get a single dose of preoperative antibiotics, which are not continued postoperatively.
Endovascular Repair
Depending on patient anatomy and institutional expertise, abdominal aortic aneurysm repair can be performed either via an open or endovascular approach. The endovascular approach holds great appeal in terms of reduced physiologic insult to the patient. Typically, both common femoral arteries are accessed either percutaneously or via an open groin exposure, and the device is placed from within the arterial lumen using fluoroscopic guidance. The weakened arterial wall is bolstered from within with stents made of a malleable metal alloy and a woven fabric. These patients rarely require admission to the ICU but are monitored for hematomas and lower extremity pulses. The devices used to deploy endovascular stents can be as large as 26 French, and these are introduced through femoral or external iliac arteries. There is a possibility of local arterial damage or dislodging of plaque that may embolize distally.
Open Repair
Open aneurysms, on the other hand, require surgical ICU monitoring postoperatively. The overall perioperative mortality is approximately 5% (19). Because a prosthetic graft has been sewn to the abdominal aorta, the main concern is bleeding. Furthermore, because the blood supply to the lower extremities is occluded intraoperatively during the aortic repair, it is vital to objectively assess and document lower extremity perfusion. Lower extremity ischemic events after open abdominal aortic aneurysm repairs occur in 2% to 5% of patients (20). Any inability to detect a Doppler signal or palpate a pulse when there previously was one is a potential surgical emergency.
A major complication of open abdominal aortic aneurysm surgery is gastrointestinal problems. A large retrospective study estimated the incidence of postoperative prolonged ileus to be 11% and nonischemic diarrhea to be 7.1% (20). All patients will have a brief period of postoperative ileus that may be shortened by use of a retroperitoneal approach to aneurysmorrhaphy (21). However, the dreaded complication is colonic ischemia with an estimated prevalence of 0.6% (20). Most instances present as bloody stools 3 to 5 days postoperatively but may occur as early as the first 24 hours after surgery and are cause for considerable concern. Warning signs include fever, abdominal pain, thrombocytopenia, unexplained leukocytosis, or lactic acidosis. Any suspicion of colonic ischemia should prompt endoscopic evaluation, with the obvious caveat that endoscopy will only view the mucosal changes, and cannot evaluate for transmural ischemia. However, in the appropriate clinical setting, mucosal ischemia may justify operative exploration with possibly colon resection and end colostomy. These patients require intensive invasive ICU monitoring, as they often progress to multisystem organ failure as a result of their colonic ischemia. Routine broad-spectrum antibiotics to include Gram-negative and anaerobic coverage are used.
Other potential gastrointestinal complications known to occur include cholecystitis and pancreatitis. The latter is probably related to direct surgical trauma during aortic exposure and is usually self-limited. Cholecystitis may be ischemia related or may be a variant of acalculous cholecystitis seen in ICU patients. Treatment options range from percutaneous cholecystostomy to surgical cholecystectomy. Much like the problem of colon ischemia in the setting of an aortic graft, an infected gallbladder should not be overlooked or minimized.
The incidence of postoperative renal dysfunction can be as high as 5.4% after open infrarenal aortic surgery, but dialysis requirement is much less at 0.6% (20). Renal dysfunction is significantly lower in patients who have undergone infrarenal aortic cross-clamp, thereby avoiding the obligate renal ischemia-reperfusion. The exact etiology of the renal dysfunction after infrarenal clamping is largely speculative, but may involve migration of atheroemboli leading to acute tubular necrosis. In the early postoperative period, oliguria is most frequently due to intravascular depletion and not intrinsic renal dysfunction. However, patients with baseline renal insufficiency, those more than 2 days postoperative, or those who do not respond appropriately to intravenous fluid challenges should be investigated for acute tubular necrosis or other intrinsic (nonprerenal) cause of oliguria.
In the absence of other causes (e.g., colon ischemia), patients may experience postoperative thrombocytopenia. Although an inciting event or agent is not always identifiable, there are several likely etiologies. Before occluding the aorta in the operating room, all patients are systemically heparinized, and although our practice is to reverse the anticoagulant effects of heparin toward the end of the case, the drug's side effects may persist. Unless there is evidence of ongoing bleeding, mild thrombocytopenia is usually well tolerated.
The cohort of patients who get abdominal aneurysms may have coronary artery disease and are at risk for postoperative myocardial infarctions, dysrhythmias, and episodes of congestive heart failure. Johnston reported an incidence of myocardial infarctions (5.2%), heart failure (8.9%), and dysrhythmia requiring treatment (10.5%). The overall incidence of any perioperative cardiac event was 15.1% (20). Unless contraindicated, patients undergoing open aneurysm repair should be on a medical regimen consisting of a β-blocker with a target heart rate of 70 to 75, a statin (independent of serum cholesterol levels), and some form of antiplatelet therapy, usually aspirin.
Ruptured Aortic Aneurysms
A meta-analysis found the operative mortality rate of ruptured abdominal aortic aneurysm (AAA) to be 48%, with a small decline in mortality for each decade from the 1950s to the 1990s (22) (much higher than an elective AAA repair of <5% mortality). With ruptured AAA, there are impressive fluid shifts that transpire during such an emergent operation, independent of overt blood loss. These fluid shifts, associated with the hypotension and the physiologic strain of an emergent procedure, contribute to a tenuous postoperative course. The incidence of colonic ischemia is significantly higher after ruptured aneurysm repair compared to elective open aneurysmorrhaphy, and some authors recommend empiric and routine endoscopic evaluation of the colonic mucosa.
Juxtarenal or Suprarenal Aortic Aneurysms
Most aortic aneurysms are infrarenal, meaning that the proximal extent of the dilated segment of aorta is caudal to the lowest renal artery. Therefore, operative repair usually can be performed with infrarenal aortic occlusion in the operating room. If the aneurysm extends to the level of the renal arteries, or involves the para-visceral aorta, the repair becomes technically more challenging. The postoperative complications escalate dramatically due to renal and possibly mesenteric ischemia-reperfusion. Depending on the length of intraoperative ischemia, there is a resultant release of pro- and anti-inflammatory cytokines that drives a systemic inflammatory reaction resulting in multisystem organ failure (23). There is considerable third spacing of fluid in the first 24 hours as edema collects in the interstitial spaces. Attempts to improve mortality and morbidity by a hybrid approach involving multiple visceral bypasses and endovascular repair of the aneurysm have met with mixed results (24).
If the thoracic cavity is violated as a part of the aneurysm repair, the patient will have an even greater risk of pulmonary complications. Routinely a chest tube is placed intraoperatively to drain any pleural fluid that may accumulate. Adequate pain control is key in these patients.
Infected Aortic Graft
One of the more dreaded complications of aortic surgery is infection of the prosthesis. This rarely happens in the early postoperative period, and the majority occurs months to years later with unexplained fevers and a computed tomography (CT) scan that shows fluid around an aortic graft. Other patients present with gastrointestinal bleeding (a manifestation of an aortoenteric fistula) or a draining sinus in the groin. These are serious surgical problems, and patients should be treated aggressively. Broad-spectrum antibiotics (although the causative organism is usually Staphylococcus), IV resuscitation, and close hemodynamic monitoring should be undertaken. Patients should be medically optimized and prepared for a staged procedure. The initial step is usually an extra-anatomic bypass in the form of an axillobifemoral bypass, with subsequent laparotomy and excision of the aortic graft. In patients who are good operative candidates, a single-stage aortic replacement using autogenous tissue (syndactylized bilateral femoral veins) of cadaveric vessels can be entertained. These patients are routinely sent to the ICU since some may become floridly septic after manipulation of the infected retroperitoneum.
Despite the misnomer of a “dissecting aneurysm,” aneurysms do not dissect. Rather, dissections may become aneurysmal. Dissections start as an intimal flap and blood escapes the true lumen and channels down the aorta, shearing apart the layers of the wall. Dissections that involve the ascending aorta (Stanford type A) are cardiac surgical emergencies for fear of retrograde dissection, causing coronary malperfusion or cardiac tamponade. Aortic dissections that do not involve the ascending aorta (Stanford type B) are usually treated medically with aggressive blood pressure control. The four indications for operative intervention are branch vessel malperfusion (usually celiac, superior mesenteric, renal, or iliac), inability to control hypertension, persistent pain related to the dissection, or aneurysmal degeneration. Dissections can be repaired via open techniques or endovascularly. The postoperative implications and precautions are the same as with any thoracic aortic intervention, with the additional caveat that blood pressure control is paramount.
Arterial Occlusive Disease
Many patients experience narrowing or occlusion of their aortoiliac arterial tree. This can be detected by the absence of a palpable femoral pulse and symptoms of lower extremity vascular compromise: claudication, tissue loss, or ischemic rest pain. The specific diagnosis and management of these problems are beyond the scope of this chapter. The most durable surgical solution for aortoiliac occlusive disease is an aortobifemoral (ABF) bypass. This is accomplished using a celiotomy incision as well as two groin incisions. The prosthetic graft (usually Dacron) is sewn to the aorta just below the renal arteries with similar complications as with open aneurysmorrhaphy (i.e., bleeding, postoperative ileus, colonic ischemia, renal dysfunction, lower extremity ischemia, cholecystitis, pancreatitis). The limbs of the bifurcated graft are then tunneled beneath the ureters and sewn into the femoral bifurcation, usually hooded onto the profunda femoris. The groin incisions, similar to those used for infrainguinal bypasses, should be monitored for wound breakdown, infection, and drainage. Peripheral pulses are regularly monitored and any deviation from the immediate postoperative result is a potential emergency as it may represent a graft thrombosis. Another complication is distal embolization with ischemia of the toes (trash foot). Management is expectant and most often this resolves with minimal or no permanent tissue loss.
As endovascular technology evolves, many iliac lesions are treated with angioplasty and possible stent placement. Although better tolerated by patients, the stents may not be as durable as the surgical bypass procedures. The wound is much smaller in stent placement (puncture sites) compared to the larger abdominal and groin incisions seen in ABF. A small subset of patients, namely patients under the age of 55, are believed to have better long-term vascular durability for infrarenal aortic reconstruction with autogenous tissue rather than Dacron (25). Femoral veins can be harvested and syndactylized to be used as aortic replacement. This requires more extensive operations with longer OR times and larger leg incisions, which can be a cause of significant morbidity.
As with any surgical procedure, redo aortic surgery is fraught with intraoperative and postoperative complications. Patients generally require longer recovery periods. If the decision is made to avoid operating in the same surgical field (abdomen and retroperitoneum), extra-anatomic bypasses may be performed, usually axillobifemoral. These procedures are considered to be less invasive but less durable and still require the same vascular monitoring as any other bypass procedures. Although abdominal complications are not seen, patients still require groin and axillary incisions and there is significant subcutaneous tunneling for the graft placement. With rehabilitation, trapeze devices are contraindicated to avoid undue stress on a fresh arterial axillary anastomosis.
Infrainguinal Bypasses
Infrainguinal bypasses are commonly performed to alleviate symptoms of vascular compromise. The principles for vascular surgery are simple: the patient must have adequate inflow (from the femoral artery), adequate outflow (of the popliteal, tibial, peroneal, or pedal arteries), and conduit (“pipe” to perform the bypass). The incisions that are made are significant, and may not only be located on the extremity being reperfused, but also may be on either leg or either arm as a site of vein harvest. We are particularly aggressive about harvesting autogenous tissue for vein conduit as the patency of infrainguinal bypass grafts using autogenous tissue, especially the greater saphenous vein, is clearly superior to that using prosthetic tissue (e.g., polytetrafluoroethylene [PTFE]) (26). The main sources of morbidity from these procedures are arterial occlusion (which can be detected with routine close pulse/Doppler monitoring), bleeding, and wound complications. The mortality from peripheral bypasses is estimated to be between 2% and 8%, and the cause of mortality is primarily cardiac, so aggressive cardiac medical management, judicious use of antiplatelet therapy, and careful fluid status monitoring are essential (27,28).
Any revascularization procedure is associated with a reperfusion syndrome that is usually mild and well tolerated. However, the reperfused extremity should always be monitored for compartment syndrome and acted upon early. Details about the technique of detecting compartment syndrome and fasciotomies have been described above. Electrolytes and cardiac rhythm should be monitored, and the urine assessed for myoglobinuria, even if that means a simple visual inspection of the urine color.
A major complication of any revascularization procedure is graft thrombosis with the highest risk in the immediate postoperative period most likely due to platelet aggregation on a surgically damaged endothelium. Patients with “high-risk” grafts (i.e., multiple segments of vein sewn together as a conduit, small distal target arteries, or poor-quality arteries) are routinely systemically anticoagulated postoperatively with heparin (14). At our institution, there has been a slight increase in the incidence of postoperative wound hematomas, but the fraction that need operative evacuation is small. In addition to full anticoagulation, patients with endovascular stents are routinely placed on clopidogrel to decrease the incidence of in-stent restenosis. All patients should be on aspirin unless otherwise contraindicated.
Carotid Endarterectomy
Carotid endarterectomy has been shown to decrease the chance of a future cerebrovascular accident in certain patients with carotid stenosis. The procedure involves a neck incision along the anterior border of the sternocleidomastoid muscle, and occlusion of the carotid artery to attain vascular control. Once occluded, the operating surgeon then may place a plastic shunt to reroute blood flow and allow distal perfusion while the endarterectomy is being performed. Although there are many intraoperative variables in technique (mode of anesthesia, whether or not to shunt, and type of shunt), the key outcome variable is perioperative stroke related to disruption of cerebral blood flow or embolic event from clamping an atherosclerotic vessel. Aspirin should be continued in the recovery phase, but full anticoagulation is seldom indicated unless carotid occlusion has occurred. Neurologic deficit may manifest itself upon awakening or occur in the early postoperative period. Any change in neurologic function that occurs after awakening with a normal neurologic examination should be reported to the operating team. Opinions vary whether to investigate with imaging or return directly to the operating room depending on whether the deficit is transient or seems to be dense and progressive.
Due to the baroreceptors in the carotid bulb, patients often experience large fluctuation in blood pressures, which should be targeted to the “normal range” of 120 to 140 mm Hg. Additionally, any wound hematoma, because the neck is a relative closed space, can cause carotid compression and resultant bradycardia or potentially airway compression. The operating team should be alerted if hematoma is suspected. Because the field of dissection is intimately associated with the cranial nerves, a detailed head and neck exam is mandatory at regular intervals. Particular attention should be paid to assessing the function of the marginal mandibular nerve and the hypoglossal nerve. Headache and even seizure activity may be a manifestation of cerebral reperfusion syndrome. This is rarely seen in the immediate postoperative period, but may cause readmission for blood pressure control in the weeks after carotid endarterectomy. These patients should also have a CT scan because of the incidence of intracranial bleeding that accompanies these symptoms.
Mesenteric Revascularization
Mesenteric ischemia, whether acute or chronic, can have lethal consequences. The restoration of intestinal perfusion sets in motion a cascade of inflammatory cytokines that frequently progresses to the systemic inflammatory response syndrome, multisystem organ failure, and even death. After restoration of blood flow, patients typically have a period of hemodynamic stability for 24 to 48 hours after the procedure, but then progress to retaining more fluid and show signs of systemic inflammation. Subtle early changes such as a diminution in platelet count should elicit concern. To date, despite numerous anticytokine therapies, the treatment of the systemic inflammation is largely supportive (29). As this response is not uniform, efforts to predict which patient will progress to clinical deterioration have been unsuccessful. As with any other revascularization bypass, the patency of the mesenteric graft should be assessed objectively. Duplex ultrasound is noninvasive and is highly sensitive. Despite all the usual supportive measures, the average postoperative length of stay is over 3 weeks (30).
Vascular Trauma
The care of the trauma patient with vascular injuries shares many of the same principles as care of other vascular surgery patients with the exception that this cohort frequently, but not always, lacks the systemic comorbidities of the typical atherosclerotic vascular patient. Most extremity vascular injuries are associated with orthopedic fractures and dislocations; some injuries are nearly synonymous with vascular injuries, such as a posterior knee dislocation and popliteal artery injury. In the secondary survey as part of the Advanced Trauma Life Support (ATLS) evaluation of the trauma patient, extremity pulses should be assessed and clearly documented. For any patient recovering from an orthopedic procedure, the same attention to distal perfusion is merited. Any change in pulse exam or hard sign of vascular injury mandates radiographic evaluation, usually with an arteriogram, although a CT angiogram is sufficient.
Although most surgeons no longer explore extremities when a penetrating injury is in proximity to a vessel, penetrating trauma associated with hard signs of vascular injury (decreased distal perfusion, active arterial hemorrhage, or a rapidly expanding hematoma) should be evaluated immediately after life-saving measures are undertaken. Often, the area of interest is operatively explored and the vessel visually inspected. If injured, it is either repaired or blood is rerouted around the “blast field” (e.g., an external iliac artery injury in a contaminated field may be repaired with vessel ligation and a femoral-femoral bypass to perfuse the ipsilateral leg). Venous injuries are ligated unless easily repaired. Revascularization of an extremity that has been malperfused for greater than 6 hours increases the likelihood of a reperfusion syndrome and at the least, compartment syndromes should be considered. Most surgeons will perform fasciotomies if there is any question of reperfusion injury.
Naturally, vascular injury to an extremity that has too extensive musculoskeletal damage to be salvageable can be treated with simple ligation and amputation. Lastly, trauma to an artery and adjacent vein can result in a traumatic arteriovenous fistula. This can occur even months after the inciting trauma, and unexplained extremity swelling, distal ischemic symptoms, heart failure, or an audible bruit over an extremity should alert the clinician to the presence of a fistula.
The perceived incidence of aortic trauma is increasing, possibly due to the increased use of CT scans in trauma management. In the abdomen, any central periaortic hematoma should be operatively evaluated. With the resolution of the current scanners we are seeing a number of intimal injuries and short segments of dissection in the infrarenal aorta and iliac vessels that previously were not detected. In the absence of hemodynamic compromise most of these can be observed. Thoracic aortic injuries are increasingly treated with endovascular devices. Initial care is directed toward treating the urgent life-threatening injuries and controlling blood pressure with β-blockers. Open surgical repair is still a viable option, though in most series the morbidity is clearly greater.
Penetrating neck trauma can involve the carotid artery, which can be exposed readily in certain locations (zone 2) or require more extensive operations to expose adequately (zones 3 and 1). Our current management of neck trauma in the stable patient with a zone 2 injury is to cover the wound in the trauma bay, perform the global assessment of the patient including abdominal sonography and intravenous resuscitation, and then take the patient to the OR for exploration. Only then is the injury exposed since unroofing a clot and losing hemostasis is best done with good exposure in the OR. For more proximal or distal injuries, angiography (standard contrast angiography or CT angiography) plays a vital role in both diagnosing and planning either open or endovascular treatment.
Blunt trauma to the head can result in injury to the carotid or vertebral arteries. Because these injuries are relatively rare (<1% of blunt trauma patients), controversy remains about the best way to diagnose and treat these patients. The Eastern Association for the Surgery of Trauma (EAST) has recently published practice management guidelines on blunt cerebrovascular injury (31). They recommended screening, preferably with angiography, for blunt trauma patients who present with or develop an unexplained neurologic deficit or who have cervical spine fractures, LeFort II or III fractures, petrous bone fracture, or fracture through the foramen transversum, and for those with a Glasgow coma scale score <8 or diffuse axonal injury. While CT angiography has been reportedly used as screening, some have questioned its sensitivity, although it is likely that the newest generation of devices may eventually be accurate enough for diagnosis in this situation (32). The most common lesion discovered is a dissection or intramural hematoma. The general consensus is that these lesions should be treated with either full anticoagulation or an antiplatelet agent that should continue for 3 to 6 months. Occasionally pseudoaneurysms are seen and endovascular repair seems to be the evolving treatment modality for this lesion. Morbidity from this lesion remains high since many patients present with a deficit. In one large series there was a 26% mortality and only 31% of patients were discharged to home. However, in the asymptomatic group that was treated with either anticoagulation or antiplatelet therapy, the failure rate was only 9% (33).
Traumatic amputations, although grossly impressive, typically are not life threatening. Traumatic amputations of a major extremity (digits not included) should be wrapped with warm gauze, and manual pressure applied while the protocol-driven trauma evaluation proceeds. Once other life-threatening injuries have been evaluated, the amputated stump may be examined. The treatment priority should be hemostasis and local debridement to remove large debris. Patients should be given tetanus toxoid if there are no other contraindications. Dressing changes should be initiated, and when stabilized, a formal, closed amputation can be undertaken, with an emphasis on leaving a functional stump for the patient to use.
Hemodialysis
Although the annual mortality of patients on hemodialysis approaches 25%, many patients in the ICU are on chronic hemodialysis with functional fistulae. The extremity with the fistula should be preserved from invasive and noninvasive monitoring devices, and all IVs and central lines should be placed away from that extremity unless there are no other options. Because of the presence of the fistula, the extremity distal to it is at risk of ischemic events, and should be monitored closely. Additionally, tunneled catheters already in place should not be routinely used as a convenient intravenous line except in dire circumstances. These lines can often be a source of infection, and limiting their use to their intended purpose will decrease the chance of infection. When they are accessed for dialysis purposes, it is routine practice to “lock” the catheter with concentrated heparin to minimize the chance of a mechanical catheter complication. Flushing this heparin “lock” will systemically anticoagulate the patient, even if transiently.
Summary
The care of the vascular patient in the ICU setting can be complex and challenging; it requires not only meticulous attention to detail, but also comprehensive knowledge of cardiovascular anatomy and physiology. As vascular disease is a systemic process, the patients typically have comorbidities that are symptomatic before surgery or unmasked with the stress of a surgical intervention. Regular and careful assessment of the patient can minimize, but not eliminate, the risks of perioperative complications.
Pearls
· Peripheral vascular disease is one manifestation of a systemic process that is proinflammatory in nature and affects the coronary, cerebral, and peripheral vasculature.
· Ninety-three percent of patients undergoing the most common vascular procedures (AAA repair, carotid endarterectomy, peripheral bypass) have documented coronary artery disease; all patients should be managed accordingly.
· Patients with diabetes can manifest angina as nausea, diaphoresis, or “indigestion.”
· Any objective change in the assessment of distal perfusion—either by palpation of pulses or auscultation of Doppler signals—is a potential surgical emergency.
· All patients with obstructive or aneurysmal vascular disease should be placed on a β-blocker, an aspirin, and a statin, unless otherwise contraindicated.
· Compartment syndrome may be subtle, especially in the sedated ICU patient. The disappearance of pulses is a late finding. Clinicians should have a low threshold to perform fasciotomies.
· Colon ischemia after aortic surgery may present as hematochezia or melena, or may be more insidious: leukocytosis, thrombocytopenia, or fevers.
References
1. Muluk SC, Muluk VS, Kelley ME, et al. Outcome events in patients with claudication: a 15-year study in 2,777 patients. J Vasc Surg. 2001;33:251–257; discussion 7–8.
2. Rossi E, Biasucci LM, Citterio F, et al. Risk of myocardial infarction and angina in patients with severe peripheral vascular disease: predictive role of C-reactive protein. Circulation. 2002;105:800–803.
3. Leng GC, Papacosta O, Whincup P, et al. Femoral atherosclerosis in an older British population: prevalence and risk factors. Atherosclerosis. 2000;152:167–174.
4. Singh N, Sidawy AN, Dezee K, et al. The effects of the type of anesthesia on outcomes of lower extremity infrainguinal bypass. J Vasc Surg. 2006;44:964–968; discussion 8–70.
5. Hertzer NR, Beven EG, Young JR, et al. Coronary artery disease in peripheral vascular patients. A classification of 1,000 coronary angiograms and results of surgical management. Ann Surg. 1984;199:223–233.
6. Smith SC Jr, Allen J, Blair SN, et al. AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update: endorsed by the National Heart, Lung, and Blood Institute. Circulation. 2006;113:2363–2372.
7. Perioperative Ischemia Evaluation (POISE). http://www.cardiosource.com/clinicaltrials/trial.asp?trialID=1629. Accessed December 4, 2007.
8. Durazzo AE, Machado FS, Ikeoka DT, et al. Reduction in cardiovascular events after vascular surgery with atorvastatin: a randomized trial. J Vasc Surg. 2004;39:967–975; discussion 75–76.
9. Weant KA, Cook AM. Potential roles for statins in critically ill patients. Pharmacotherapy. 2007;27:1279–1296.
10. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med. 2004;351:2795–2804.
11. Seeger JM, Pretus HA, Carlton LC, et al. Potential predictors of outcome in patients with tissue loss who undergo infrainguinal vein bypass grafting. J Vasc Surg. 1999;30:427–435.
12. Kent KC, Bartek S, Kuntz KM, et al. Prospective study of wound complications in continuous infrainguinal incisions after lower limb arterial reconstruction: incidence, risk factors, and cost. Surgery. 1996;119:378–383.
13. Wengrovitz M, Atnip RG, Gifford RR, et al. Wound complications of autogenous subcutaneous infrainguinal arterial bypass surgery: predisposing factors and management. J Vasc Surg. 1990;11:156–161; discussion 61–63.
14. Sarac TP, Huber TS, Back MR, et al. Warfarin improves the outcome of infrainguinal vein bypass grafting at high risk for failure. J Vasc Surg. 1998;28:446–457.
15. Baird RW. Quality improvement efforts in the intensive care unit: development of a new heparin protocol. Proc (Bayl Univ Med Cent). 2001;14:294–296; discussion 6–8.
16. Babu SC, Shah PM, Nitahara J. Acute aortic occlusion–factors that influence outcome. J Vasc Surg. 1995;21:567–572; discussion 73–75.
17. Hildick-Smith DJ, Khan ZI, Shapiro LM, et al. Occasional-operator percutaneous brachial coronary angiography: first, do no arm. Catheter Cardiovasc Interv. 2002;57:161–165; discussion 6.
18. Lederle FA, Wilson SE, Johnson GR, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med. 2002;346:1437–1444.
19. Johnston KW, Scobie TK. Multicenter prospective study of nonruptured abdominal aortic aneurysms. I. Population and operative management. J Vasc Surg. 1988;7:69–81.
20. Johnston KW. Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. J Vasc Surg. 1989;9:437–447.
21. Cinar B, Goksel O, Kut S, et al. Abdominal aortic aneurysm surgery: retroperitoneal or transperitoneal approach? J Cardiovasc Surg (Torino). 2006;47:637–641.
22. Bown MJ, Sutton AJ, Bell PR, et al. A meta-analysis of 50 years of ruptured abdominal aortic aneurysm repair. Br J Surg. 2002;89:714–730.
23. Welborn MB, Oldenburg HS, Hess PJ, et al. The relationship between visceral ischemia, proinflammatory cytokines, and organ injury in patients undergoing thoracoabdominal aortic aneurysm repair. Crit Care Med. 2000;28:3191–3197.
24. Lee WA, Brown MP, Martin TD, et al. Early results after staged hybrid repair of thoracoabdominal aortic aneurysms. J Am Coll Surg. 2007;205:420–431.
25. Jackson MR, Ali AT, Bell C, et al. Aortofemoral bypass in young patients with premature atherosclerosis: is superficial femoral vein superior to Dacron? J Vasc Surg. 2004;40:17–23.
26. Gentile AT, Lee RW, Moneta GL, et al. Results of bypass to the popliteal and tibial arteries with alternative sources of autogenous vein. J Vasc Surg. 1996;23:272–279; discussion 9–80.
27. Abou-Zamzam AM Jr, Lee RW, Moneta GL, et al. Functional outcome after infrainguinal bypass for limb salvage. J Vasc Surg. 1997;25:287–295; discussion 95–97.
28. Nicoloff AD, Taylor LM Jr, McLafferty RB, et al. Patient recovery after infrainguinal bypass grafting for limb salvage. J Vasc Surg. 1998;27:256–263; discussion 64–66.
29. Huber TS, Gaines GC, Welborn MB 3rd, et al. Anticytokine therapies for acute inflammation and the systemic inflammatory response syndrome: IL-10 and ischemia/reperfusion injury as a new paradigm. Shock. 2000;13:425–434.
30. Rectenwald JE, Huber TS, Martin TD, et al. Functional outcome after thoracoabdominal aortic aneurysm repair. J Vasc Surg. 2002;35:640–647.
31. Blunt Cerebrovascular Injury Practice Management Guidelines. http://www.east.org/tpg/archive/html/BluntCVInjury.html. Accessed December 4, 2007.
32. Malhotra AK, Camacho M, Ivatury RR, et al. Computed tomographic angiography for the diagnosis of blunt carotid/vertebral artery injury: a note of caution. Ann Surg. 2007;246:632–642; discussion 42–43.
33. Edwards NM, Fabian TC, Claridge JA, et al. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid injuries: results from longterm followup. J Am Coll Surg. 2007;204:1007–1013; discussion 14–15.