Postoperative Complications

Fig. 16.1
Intraoperative photo demonstrating full-thickness serosal changes in ischemic colitis

The causes of ischemic colitis are numerous, though the exact etiology of the initial insult is often difficult to pinpoint—especially in elderly, debilitated patients with multiple contributing comorbidities. In addition, the differential diagnosis remains vast, with inflammatory and infectious colitis heading the list and often with similar presentations. Regardless of its etiology, patient outcome depends markedly on the severity and extent of the ischemic insult and is largely influenced by the clinician’s ability to make a prompt diagnosis and initiate appropriate management.

Historically, ischemic colitis following vascular surgery was associated with mortality rates approaching 45–67 % [4]. Unfortunately, even more recent reports have demonstrated only modest improvements. Currently, ischemic colitis is the most common form of gastrointestinal ischemia, accounting for 50–60 % of all cases, translating to ~1 in 2000 hospital admissions [5]. The incidence of colonic ischemia specifically following repair of a ruptured AAA (rAAA) is 4–5 times higher than an elective repair, increasing from ~1–6 % to ~17–35 % [6]. Not surprisingly, the outcomes are significantly worse in patients that have a delayed diagnosis or present with a more advanced state of ischemic colitis, such as those patients with a concomitant perforation. In these cases, mortality rates have been reported to be >90 % [7]. In one retrospective study of 222 patients after a rAAA repair, ischemic colitis was the most common cause of death, even above multi-organ system failure and myocardial infarction [8]. It is easy to then understand why early diagnosis is of chief importance. Unfortunately, clinical parameters to identify patients with colonic ischemia lack specificity, which is even more limited in the rAAA population. In this chapter, we will review the pathophysiology, risk factors, diagnostics, and treatment options for patients who suffer ischemic colitis after a rAAA.


Regardless of the underlying etiology, the pathophysiology of ischemic colitis revolves around an inadequate blood supply to the colon. In patients suffering from a rAAA, there are numerous potential etiologies of this decreased blood flow including perioperative hemorrhage resulting in a loss of overall blood volume, prolonged hypotension, splanchnic vasoconstriction due to shock and vasopressors, and cross clamping or balloon occlusion of the aorta. The surgical repair itself, for both the open and endovascular (EVAR) approaches, occludes blood flow (at least temporarily) through the inferior mesenteric artery (IMA), which directly supplies the left colon. In addition, embolization of debris (thrombus and plaque) may occur from opening the aneurysmal sac or manipulation of the graft and wires inside the sac. These embolic phenomena can cause a less predictable variation of ischemic colitis, with numerous reports of right-sided colonic and even small bowel ischemia [9].

However, there is an intrinsic protective mechanism already in place. Although the colon derives its blood supply from branches of the major vessels [i.e., superior mesenteric artery (SMA) and inferior mesenteric artery (IMA)], it is the extensive collateral circulation that allows this ischemic process to be avoided in many cases. The two main collateral routes are via the marginal artery of Drummond that parallels the colon and gives rise to the vasa recta, and the meandering mesenteric artery (or arc of Riolan) which, while not always present, can represent another potential connection between the SMA and IMA systems. In addition, the IMA and internal iliac arteries communicate via the superior and middle hemorrhoidal arteries, while the left colic branch of the IMA contributes to overlap of the transverse colon that is supplied mostly by branches of the SMA. In an otherwise healthy patient, the vast vascular network would prevent any significant degree of colonic ischemia after ligation of the IMA. Yet, patients who suffer a rAAA generally have severe vascular comorbidities and are often in physiologic extremis, which explains why there is such a higher rate of colonic ischemia despite this collateral circulation. Certain parts of the colon are more prone to fluctuations in blood flow, leading to the all-too-common “rounds” question with answers consisting of the splenic flexure (i.e., Sudeck’s) and rectosigmoid junction (i.e., Griffiths). It is felt that these are the most vulnerable segments given that there is incomplete anastomosis of the marginal artery in these two locations. The next most common area affected is the cecum, likely secondary to low blood flow in the terminal branches of the ileocolic artery combined with varying presence and competency of the right colic artery [1012].

Ischemic colitis is not an all or nothing process. The earliest manifestations are witnessed at the mucosal level, those furthest away from the vasa recta [10, 13] (Fig. 16.2). As such, there is a progression in the stages of ischemic colitis: (a) Grade I, transient mucosal ischemia; (b) Grade II, mucosal and muscularis involvement that may result in healing with fibrosis and stricture formation; and (c) Grade III, transmural ischemia and infarction which results in gangrene and perforation [14] (Fig. 16.3). Importantly, sepsis can occur in the absence of transmural ischemia, as an ischemic mucosa loses its barrier function and allows bacterial translocation to occur, which may result in sepsis.


Fig. 16.2
Mucosal changes with ischemic colitis


Fig. 16.3
Full-thickness changes with gangrenous ischemic colitis

Risk Factors for the Development of Ischemic Colitis

There are certain risk factors that clearly put a patient with an AAA at higher risk of suffering ischemic colitis. The greatest risk factor is the focus of this chapter; a patient with a rAAA has a two- to fourfold increased risk for ischemic colitis. Interestingly, those underdoing surgery with a symptomatic aneurysm (even in the absence of rupture) have higher rates of ischemic colitis than elective repair based on size criteria alone in the absence of symptoms. Other independent risk factors for colonic ischemia include renal insufficiency, open versus endovascular repair, operative time >4 h, prolonged cross clamp, preoperative hypotension, aorto-bifemoral graft placement, and postoperative acidosis [15, 16].

Many of these make intuitive sense. Others have second- or third-order ramifications that promote the onset of ischemic colitis. For example, renal insufficiency itself results in a decreased ability to handle changes in volume, clear toxins, and recovery from any physiological insult. Yet, in addition, it is thought to be a marker of systemic atherosclerotic disease, which would be reflected in the mesenteric vessels that directly supply the colon, therefore decreasing the colon’s tolerance to hypotension. Worsening of renal insufficiency following repair may also represent a reflection of the severity of hypotension the patient endured perioperatively.

While the exact operative time that correlates with the onset of ischemic colitis is likely more variable, when the length of surgery is over 4 h, studies have shown a four- to sixfold increase in incidence [16]. This is likely related both to the technical difficulty of the surgery and associated hypotension and blood requirement needed during the operation. Open repair is another independent risk factor for colonic ischemia, as demonstrated in one large national database review that showed that open elective AAA repair had a rate of 2.2 % versus 0.5 % with elective EVAR repair [4]. A small randomized trial comparing open and endovascular repair in patients with rAAA found half the rate of colonic ischemia (8 % vs. 4 %) when using EVAR, but it was underpowered to reach significance [17]. However, it is remarkable to witness the drastic drop in onset with the use of endovascular approaches, even in the setting of rupture.

Some surgeons have recommended reimplanting the IMA to allow restoration of direct “forward flow” from the aorta to the left colon. While controversial, IMA reimplantation with an open repair has multiple studies, including a randomized controlled trial, that have failed to show a decreased rate of colonic ischemia with IMA reimplantation when compared with ligation of the IMA and maintenance of normothermia and normal blood pressures. On the other hand, common vascular surgery dogma is to do whatever possible to prevent pelvic ischemia because once it occurs, it is likely not reversible and is associated with high morbidity rates [18]. With this in mind, many surgeons will reimplant based on intraoperative findings such as poor backflow from the IMA (<40 mmHg) or decreased antimesenteric vasculature Doppler signals [16, 19]. An additional tool used in the past was laser Doppler flowmetry, which measures the erythrocyte flux to bowel segments and has been specifically shown to be a successful tool to determine the necessity of reimplanting the IMA [20]. More recent advances, such as the intraoperative availability of indocyanine green [21, 22] that can demonstrate real-time perfusion, may soon find its way into this intraoperative algorithm for evaluating colonic ischemia—even though it still not applicable to EVAR cases. Other more traditional operative tools such as Doppler or Wood’s lamp with fluorescent dyes can only be used in open surgery to help determine bowel viability. In contrast, there is a device available that can be used in open and endovascular aneurysm repairs that utilizes a probe placed in the rectum and measures tissue oxygen saturation. It has been shown to be sensitive in predicting colonic ischemia if the saturation drops below fifty percent of baseline. This tool can provide objective evidence to allow the opportunity to revascularize the IMA or the hypogastrics [23]. While promising, the current data is limited, and ultimately only longer-term data with a wider experience will determine its role in the evaluation and treatment of ischemic colitis.

The importance of hypogastric preservation also appears to be predicated highly on the method of repair—endovascular versus open. In open surgery, there are higher rates of colonic ischemia when hypogastric aneurysms are present or if both hypogastrics are ligated [24]. With endovascular repair, there is literature that states there are only minimal complications associated with embolization of the hypogastrics [2527] and other series reporting increased risk of colonic ischemia if they are not preserved [28, 29]. In the setting of rAAA, there is only anecdotal evidence when discussing preserving hypogastrics, but given the extremis that patients are often in, it is likely prudent to preserve any potential collaterals to the colon, if possible. Yet, the surgeon must take into account the stability of the patient and weigh any downside that may occur with the additional operative time that another procedure would require.

Additional risk factors for the development of ischemic colitis that have no randomized data, but have been reported in small retrospective studies, include previous colonic surgery and pelvic irradiation. This should also make sense, as patients who have had previous colonic surgery have likely had the collaterals between the SMA and IMA disrupted. While there was a substantial rate of colonic ischemia in this subset of patients, these reports have been largely underpowered [16]. Yet, even a patent meandering marginal artery (arc of Riolan) has been shown to have some protective effects against ischemic colitis [30].

Finally, pelvic irradiation leads to obliteration of the microvasculature to the sigmoid and rectum, creating conditions ripe for small vessel ischemic changes. Furthermore, these radiation effects are cumulative and progressive, a fact often overlooked. Although it has not been widely studied, this appears to be a real association with patients at a higher risk of developing ischemic colitis [31]. Furthermore, this may be a precipitating factor not only in early disease but helps to explain the underlying disorder that leads to chronic changes such as colonic stricture.


The key to diagnosing ischemic colitis first and foremost involves a high degree of suspicion by the treating provider, especially given the drastic improvements in outcomes for patients that are recognized and treated promptly. Unfortunately, the signs and symptoms vary drastically and are remarkably inconsistent from patient to patient. Occasionally, ischemic colitis is recognized intraoperatively; however, that tends to be way too late. Despite a somewhat “textbook” presentation for more severe forms, the mean time to diagnosis remains ~5.5 days [14].

This delay is secondary to the wide-ranging spectrum of disease—from mild mucosal sloughing to severe (perforation and sepsis). In some cases, the majority of symptoms are often self-limited and nonspecific. The most common symptoms encountered are left lower quadrant pain, bloating, and diarrhea. The diarrhea is a consequence of mucosal sloughing which causes colonic peristalsis. Depending on the extent and severity of the ischemia, patients can present with melena, hematochezia, watery diarrhea, or even no diarrhea at all. The abdominal pain may be limited to the hypogastrium or left lower quadrant or in more severe cases present with frank peritonitis and diffuse pain. Similar to the symptomology, the imaging and laboratory studies are generally nonspecific. Plain films may show colonic dilatation and/or fluid levels. More advanced cases may have pneumatosis, portal venous gas, or pneumoperitoneum.

Historically, barium enemas were used, often showing mucosal edema suggested by thumbprinting or colonic strictures with more chronic disease. In general, barium should be avoided in this setting. Water-soluble enemas may demonstrate similar findings but are much less commonly used. The workhorse of radiology tests remains the CT scan. Although they are not initially as sensitive, later in the course, they can be more helpful showing colonic wall thickening and an inflamed edematous mesentery/fat stranding. CT also provides the ability to evaluate the bowel as well as the surrounding tissue. In this light, mucosal enhancement, intramural air, bowel dilatation, or even more ominous signs such as portal venous gas can be visualized. It can also be a very useful test in ruling out other diagnoses [32]. In general, angiography does not help in patients with acute ischemic changes and is rarely used for vessel patency (embolic/thrombotic) or to rule out other sources.

Laboratory examinations are similarly nonspecific for ischemic colitis, and no marker exists to date that is specific in identifying colonic ischemia. For more advanced cases, a leukocytosis and metabolic acidosis may be present. Occasionally, electrolyte and renal abnormalities (i.e., hypokalemia, rising BUN/Cr) may be present due to severe diarrhea combined with a lack of oral intake. Serum lactate levels may be elevated, though generalized systemic hypoperfusion or tissue hypoxia may also cause this, and is therefore not a specific marker. Unfortunately, many of these concerning lab values such as lactate, creatinine, acidosis, or leukocytosis are all commonly seen postoperatively after a rAAA. A small prospective study of 12 patients who underwent open AAA repair reported an elevated d-lactate (uncommon isomer of more common L-lactate) could be detected within 2 h postoperatively in patients with ischemic colitis compared to patients without ischemic colitis [13]. Yet, this has yet to achieve widespread clinical use.

Colonoscopy remains the most sensitive and specific study available for diagnosis of ischemic colitis (Fig. 16.4). Some suggest that any concern for colonic ischemia warrants an endoscopic evaluation and even argue routine endoscopy after rAAA using a flexible sigmoidoscopy should be performed within 24 h of the surgery. Endoscopy has a diagnostic accuracy of 78–98 % for ischemic colitis [33], in part due to the wide extent of changes and characteristics ischemia has when viewed endoscopically. In the acute phase, the bowel will demonstrate hyperemia, edema, friable mucosa, ulcerations, and petechial hemorrhages. As the ischemia progresses, evidence of submucosal edema and hemorrhage may appear as bluish-black blebs or nodules protruding into the lumen of the bowel [34]. When full-thickness transmural ischemia occurs, the mucosa typically appears gray or black, indicating gangrene. If the ischemia is more chronic, changes such as strictures and fibrosis would be endoscopy also allows the examiner to sample the colonic mucosa for pathologic assessment to help differentiate inflammatory, infectious (e.g., C. difficile), and ischemic etiologies. In reality, biopsy (Fig. 16.5) is rarely useful and is more likely to demonstrate either nonspecific ischemic or inflammatory changes and rarely shows the ghost cells that are classic for ischemia [11]. It is important to recognize that endoscopy is not without its own potential hazards. Air insufflation may result in distention of the bowel, diminishing colonic blood flow and may actually worsen the colonic ischemia [9]. In addition, the ischemic wall of the colon is fragile and at an increased risk of perforation. Chronically, endoscopy will demonstrate a smooth stricture without an associated mass, consisted with the fibrotic process that occurs over time [35].


Fig. 16.4
Ischemic colitis seen on colonoscopy


Fig. 16.5
Histology of ischemic colitis demonstrating sloughing of the mucosa and inflammatory cells

Endoscopic Surveillance Following rAAA

There have been two prospective studies that have evaluated the effectiveness of routine colonoscopic screening in all patients who survive after the initial repair of a rAAA (Figs. 16.6 and 16.7). The first study by Megalopoulas et al. [36] identified preoperative risk factors (hypotension, temperature, pH, > 6 units PRBCs, fluid sequestration >5 L) that correlated with the presence of ischemic colitis. The authors concluded that when less than four were present, they were unlikely to develop colonic ischemia and therefore did not need routine endoscopic screening. One criticism of this study was that it is difficult to extrapolate to outside hospitals, as many of the parameters depend on the overall management of the patient apart from the use of endoscopy. To address this deficiency, Tottrup and colleagues prospectively screened 41 patients who survived a rAAA with colonoscopy in the first 24 h following surgery. Only nine of their patients developed colonic ischemia, and there were no perioperative or intraoperative clinical or biochemical parameters that were sufficiently reliable to distinguish patients with colonic ischemia versus those without [6]. Their conclusion was that the worse outcomes associated with a delayed diagnosis of colonic ischemia after rAAA warrant all patients to undergo routine endoscopic surveillance [37].


Fig. 16.6
Mild changes seen on colonoscopy with early ischemic colitis


Fig. 16.7
Gangrenous changes seen on colonoscopy

Conversely, routine surveillance has been questioned by those who feel colonoscopy does not necessarily change the management of patients and can even exacerbate the problem by placing a scope in a friable segment of bowel and filling it with pressurized air. They argue that if a patient has suggestive symptoms along with radiologic and examination findings concerning for severe ischemic colitis, they should undergo an exploration. On the other hand, if a patient has clinical signs of ischemic colitis but lacks peritoneal signs or sepsis, they should undergo supportive therapy alone. This argument is supported by a study that showed that clinicians are unable to differentiate mucosal versus transmural necrosis reliably with colonoscopic evaluation [38].

Treatment Options

Once ischemic colitis is identified, treatment falls into two categories depending on the degree of injury: supportive therapy and colectomy. As most patients present with only mucosal ischemia, their clinical course is often relatively benign and warrant supportive therapy alone. Supportive therapy consists primarily of fluid resuscitation, blood pressure support, bowel rest, and antibiotics. Broad-spectrum antibiotics should typically be started due to risk for bacterial and endotoxin translocation following disruption of the mucosal membrane. Vasopressors should be used cautiously and only in septic patients. Alpha agonists are likely to worsen colonic ischemia by further reducing splanchnic blood flow. Beta-adrenergics can be considered as a first-line option if fluid therapy is inadequate to maintain blood pressure. However, pressor requirement should prompt the physician to consider if an abdominal exploration is warranted. The majority of these patients have a poor nutritional status at baseline and a high metabolic demand and will likely have a prolonged time that they will be NPO; therefore, early parenteral nutrition is often required.

Serial abdominal exams, laboratory testing, and plain film labs should be performed to monitor for worsening in their condition. Approximately 10 % of patients will fail supportive therapy and ultimately require a colectomy. Failure of supportive therapy can be obvious with signs of peritonitis, or it can be more insidious. There are patients that will continue to have persistent pain, leukocytosis, low-grade fevers, tachycardia, tender abdominal exam, but not frank peritonitis. After ruling out other sources of sepsis, abdominal exploration with colectomy is often undertaken, as the devitalized colon serves as the source for persistent problems. Decisions on when to repeat flexible endoscopy vary, but likely should be repeated if there are no resolution in symptoms, an acute change in symptoms, or prior to beginning an oral diet.

When Grade III or transmural/gangrene is identified, emergent colectomy is almost always indicated. This subset of patients, even with colectomy, have mortality rates >50 %. Patients who suffer a rAAA, compared to an elective AAA repair, and develop colonic ischemia are more likely to undergo a colectomy [4]. This is due to the larger physiologic insult that occurs with rupture. Interestingly, one study found patients undergoing colectomy for ischemic colitis after elective EVAR had significantly higher mortality than patients undergoing colectomy for rAAA or open AAA repair. This should not be misinterpreted; however, as EVAR is generally much safer and associated with lower rates of ischemic colitis. More likely, this finding reflects the delay in diagnosis, as suspicion is generally lower after elective EVAR, or the differing mechanism of the ischemic insult (i.e., cardiac) [4].

With rare exceptions, all patients with evidence of bowel infarction or perforation require surgical exploration. The greatest challenge associated with abdominal exploration is determining which portion of bowel is salvageable and which is nonviable. When evaluating the bowel intra-abdominally, it is important to remember that the serosa may appear healthy, even when there is actually full-thickness mucosal and muscularis necrosis. It is often helpful to combine an endoscopic evaluation to help determine the level of bowel viability (even despite its relative lack of accuracy). Laser Doppler flowmetry and spectrophotometry are all techniques that can assist clinical judgment in deciding bowel viability and what requires resection and what can be salvaged. Furthermore, palpation of mesenteric pulses, detecting Doppler signals on the antimesenteric portion of the bowel wall, and Wood’s lamp evaluation of the bowel wall following administration of fluorescein dye intravenously are all described techniques to help separate perfused from non-perfused bowel. Some surgeons will routinely perform a second look operation in 24–48 h, whereas others will perform it selectively when there is higher concern for intestinal viability (see Algorithm).


Operative therapy must consider both the need for bowel resection and vascular reconstruction. The surgeon must balance the need to avoid leaving behind necrotic bowel with the potential morbidity of overzealous resection leading to short bowel syndrome, although the intraoperative judgment of the well-trained surgeon remains one of the most important factors. In most cases, surgical resection involves a total abdominal colectomy with end ileostomy (Fig. 16.8). Although primary anastomosis after a subtotal or partial colectomy (Fig. 16.9) with a proximal diversion may be considered in isolated hemodynamically stable patients with healthy bowel margins, this is often a poor choice [34]. Regardless of the approach, the need for an exploration and bowel resection in the acute setting has been associated with mortality rates as high as 40 %, particularly when the patients has multiple underlying comorbidities [39].


Fig. 16.8
Total abdominal colectomy for colonic ischemia


Fig. 16.9
Segmental resection for demonstrating colonic ischemia

Finally, vascular repair involves first determining the patency of the vessel supplying the at risk portion of the colon. In addition, determining whether there is antegrade flow to the iliac vessels that may provide potential pelvic collaterals is crucial. While the technical aspects of vascular reconstruction are beyond the scope of this chapter, options for dealing with the inferior mesenteric artery or other major visceral vessels include resection of the base of the vessel along with a small cuff of aortic wall (Carrel patch) and reimplanting it in the aorta or graft, patch angioplasty of the stenotic opening, bypass grafting, or endarterectomy of the atherosclerotic plaque [4042]. In either light, embarking on a complex vascular reconstruction should not be undertaken lightly and again needs to be weighed against the potential downside of prolonged operative time, excess blood loss, and failure of the repair.


Ischemic colitis is the leading cause of death after repair of a rAAA. With few operative or clinical parameters that are sensitive or specific for colonic ischemia, suspicion must remain high in the postoperative period. Early identification and treatment of this feared complication is the only clear way to help reduce morbidity and mortality.

Abdominal Compartment Syndrome Following Ruptured Abdominal Aortic Aneurysm

Martin Björck10   and Anders Wanhainen10

Department of Surgical Sciences, Section of Vascular Surgery, Uppsala University, Uppsala, Sweden



Martin Björck


The knowledge that a tense abdomen is a life-threatening condition is very old, with observations from ancient Greece and during the Middle Ages. The twentieth century was a golden age of understanding human physiology, including the importance of intra-abdominal hypertension (IAH) and the abdominal compartment syndrome (ACS). It is often a consequence of aggressive resuscitation after major bleeding, thus partly an iatrogenic condition [43, 44]. In the first paper naming the condition, the vascular surgeon Irving Kron described it following ruptured abdominal aortic aneurysm (rAAA) [45]. The association between IAH/ACS and colonic ischemia following rAAA repair was demonstrated in multiple investigations [4651]. Survival can be improved if the hypoperfusion of the abdominal organs created by IAH/ACS is prevented or reversed timely [46, 50, 51]. The purpose of this chapter is to offer guidance how that can be accomplished.

Definition of IAH/ACS

“IAH is defined by a sustained or repeated pathological elevation in intra-abdominal pressure (IAP) >12 mmHg.” This is the definition of IAH, as first stated in the 2005 Consensus document [43], and unaltered in the 2013 Updated Consensus Definitions and Clinical Practice Guidelines [52]. It was shown in basic research, and in clinical studies, that an IAP above 12 mmHg affects organ function negatively. In particular renal function is affected at this relatively low pressure. Please note the words “sustained or repeated.” A single elevated value, maybe the result of the patient being in pain, is not sufficient. This threshold for negative effects on organ function is important to consider in patients operated on for rAAA, since multiple prospective clinical studies have shown that it is uncommon that the IAP is less than 12 mmHg in the early postoperative period after open surgery [49, 50, 53, 54]. The situation after EVAR for rAAA is less well studied [55], but if hemodynamically instable patients are treated with EVAR, there is no reason to believe the situation to be different [51]. Although the evidence-based approach used in the revision of the guidelines did not find support for a subdefinition of low abdominal perfusion pressure (APP = MAP-IAP <60 mmHg), it is a clinical observation that hypotensive patients are more sensitive to IAH.

ACS is defined as a sustained IAP >20 mmHg (with or without an APP <60 mmHg) that is associated with new organ dysfunction/failure [52]. Again, the exact wording is important: “a sustained IAP >20 mmHg” means that the measurement has to be repeated at least once, and it needs to be associated with a “new organ dysfunction/failure,” with a timely deterioration of vital organ function. ACS is never defined as a mere measurement of IAP but the combination of this high IAP and its effect on vital organ function!

There are many ways to measure IAP. Almost everyone measures IAP in the bladder, intermittently or continuously. For details, please consult the guidelines [44, 52]. Our preferred method is the Foley manometer method, with the advantage that it can easily be applied outside of the ICU, which is a great advantage after EVAR for rAAA, since those patients seldom need to stay in the ICU after surgery.

How Common Is IAH/ACS After rAAA Repair?

One of the problems in answering this question is the fact that prior to 2005 [43], there was not a consensus definition of ACS, and even after 2005, some investigators have continued to use “homemade” definitions of ACS. The incidence will depend on several factors. The routines for resuscitation are of paramount importance. Balogh et al. showed that the administration of crystalloids is an independent risk factor for ACS in abdominal trauma patients [56]. We have reasons to believe that this is true in any bleeding patient. A policy of preoperative permissive hypotension may decrease the risk of IAH/ACS.

Mell et al. showed that patients who received less than one unit of plasma for every two units of red blood cells during rAAA repair had a four times higher mortality than those given more plasma [57], highlighting the importance of a massive transfusion protocol. Massive transfusion protocols, which are discussed in another chapter of this book, do not only reduce mortality, they also reduce the risk of fluid overload and risk of ACS.

The introduction of endovascular aneurysm repair (EVAR) [58, 59] by Volodos in 1985 transformed aortic surgery. The application of EVAR on patients with rAAA was first described by Veith in 2000 [60]. Although it has not been possible to show an advantage in survival of this technique in randomized trials, it is natural that the surgical technique used for elective surgery that surgeons feel comfortable with will also be used in emergencies. How the use of EVAR on patients with rAAA affects the incidence of IAH/ACS is controversial, however.

If measured consistently, IAP >20 mmHg occurs in about half of the patients after open repair (OR) of a rAAA, and 20 % develop ACS [53, 54]. In many series on patients operated on for rAAA with EVAR, a selection of more circulatory stable patients took place, however, resulting in a lower incidence of IAH/ACS [55]. The Zürich group that treats virtually all ruptured patients with EVAR and monitors IAP on a regular basis reported a higher incidence of ACS, however: 20 % (20/102) [51], similar to the results after OR. In a prospective cohort study in four Swedish hospitals, the risk to require treatment with open abdomen (OA) was similar after EVAR (3/86, 3.4 %) and OR (14/115, 2.5 %) [61].

In a nationwide, population-based study during 2008–2013 in Sweden, 6612 aortic repairs were studied, 1341 (20.3 %) of them for rupture and 28 % of them with EVAR. [62] ACS was registered prospectively in the national vascular registry (Swedvasc) and developed in 6.8 % after OR and in 6.9 % after EVAR, p = 1.0. Among those with ACS, decompression laparotomy (DL) was performed in 77.3 % after OR and in 84.6 % after EVAR, p = 0.433. Interestingly, the abdomen was not closed at OR in 10.7 %. Adding these figures approximately 15 % were treated with OA, one in seven patients. In conclusion, IAH/ACS is a common problem after rAAA repair, irrespective of which surgical technique used.

Risk Factors for ACS After rAAA Repair

Although most patients develop IAH after surgery for rAAA, the risk to develop the ACS increases when one or multiple of the risk factors given in Table 16.1 are present. These factors were either identified as general risk factors for ACS, described in the Guidelines from the World Society of the Abdominal Compartment Syndrome [44, 52] (www.​wsacs.​org), or they were identified in the already mentioned nationwide, population-based study [62].

Table 16.1
Risk factors for ACS after rAAA repair

Preoperative risk factors

Intraoperative risk factors

Postoperative risk factors



Massive fluid resuscitation (>5 L)

No permissive hypotension

Preoperative intubation

Morbid obesity (BMI > 35)

Massive transfusion (>10U/24 h)


No massive transfusion protocol

Hypothermia (<33o C)

Acidosis (pH < 7.2)

Intraoperative bleeding >5 L

Prolonged operation

Prolonged cross clamping

Need of occlusion balloon (EVAR)

Continued need of transfusions

Continued bleeding (e.g. through endoleakage after EVAR)

Fluid overload (capillary leakage)

Renal failure

Respiratory failure (especially if elevated intrathoracic pressure)

Intestinal failure/Ileus

Liver failure/ascites

These risk factors were identified in the references [44] (general risk factors for ACS) and [62] (a large population-based cohort study)

Can ACS Be Prevented? Medical Management?

Being aware of the risk factors (Table 16.1), and if possible avoiding them, is an obvious preventive strategy. It is also possible to treat IAH in a proactive way, preventing further deterioration of the patient and development of ACS. This treatment is sometimes referred to as “medical management,” or “conservative management,” which is not an appropriate label since it can be quite aggressive.

The therapeutic alternatives are described in Table 16.2. There are two mechanisms through which the IAP can be reduced. One mechanism is volume reduction of the intra-abdominal cavity. Evacuation of the retroperitoneal hematoma after EVAR for rAAA has been attempted using surgical approach through the lateral/dorsal part of the abdominal wall. Another alternative was described by Hörer et al. who inserted tissue plasminogen activator (tPA) through a 20 F catheter placed in the hematoma with CT guidance, in 13 patients [63]. None of these techniques are truly minimally invasive, and major bleeding was reported. Although we lack personal experience of these techniques, decompression laparotomy seems both safer and more effective.

Table 16.2
Nonsurgical treatment of intra-abdominal hypertension

Reducing intra-abdominal volume

Improving compliance of the abdominal wall

Evacuating the retroperitoneal hematoma:

 (a) Lumbectomy

 (b) tPA-assisted hematoma evacuation

Drainage of free intra-abdominal fluid

Drainage of intragastric contents

Enema, drainage of fecal contents

Reducing fluid overload

Pain relief

 (a) Avoid opioids, if possible

 (b) Epidural analgesia

Neuromuscular blockade

Reducing fluid overload

Drainage of gastric content is important, but early enteral nutrition should not be halted [64], since bowel movements are of strategic importance. We initiate enteral feeding the first postoperative day, even in the presence of IAH, but the gastric contents are drained twice daily to avoid accumulation. Enemas and other activities to stimulate the fecal flow are seldom effective after rAAA repair. Early enteral nutrition and avoiding opioids are more effective. It is common that the IAP increases hours before the first bowel emptying, when bowel movements start, after which the IAP drops substantially. Free drainable fluid in the abdominal cavity is uncommon, but may occur if there is hepatic or pancreatic pathology.

Abdominal compliance (AC) measures the ease of abdominal expansion, expressed as a change (delta = Δ) in intra-abdominal volume (IAV) per change in intra-abdominal pressure (IAP): AC = ΔIAV/ΔIAP. This is a dynamic variable dependent on baseline IAV and IAP, as well as on reshaping and stretching capacity of the abdominal wall. The first phenomenon is that the abdomen transforms from an oval into a circular shape (reshaping, see Fig. 16.10), followed by stretching and finally followed by a rapid increase in IAP. In a recent review of AC the most important conclusion was that patients with high IAP have a reduced AC, making the IAP very sensitive to small changes in IAV. [65] A critically ill patient with IAH may have a reshaped and quite rigid abdominal wall, where a small increase of IAV results in ACS. Inversely, a small decrease in IAV may result in a substantial decrease of IAP.


Fig. 16.10
A 70-year-old man was treated with EVAR electively despite an unfavorable anatomy because of obesity (110 kg) and chronic obstructive pulmonary disease. There was an acute rupture of the aneurysm, secondary to a distal type I endoleak. There was a long transport with helicopter to Uppsala. The patient was treated with an extension of the endograft covering the internal iliac artery, with a good result, but had increased his body weight to 125 kg. He had a MAP of 70 and an IAP of 18 and developed anuria. Despite not fulfilling the criteria of ACS, a DL was performed, resulting in improved renal function, with urinary outputs of 300 ml/h, the first hours post DL. This picture was taken during the first redressing, when a VACM was applied. Despite unfavorable conditions, the patient survived and the abdomen was closed with delayed primary fascial closure after 30 days. No incisional hernia developed

One of the most effective ways of decreasing the IAP is pain relief, but it is also strategically important to avoid opioids. During rAAA repair, there is seldom time to apply an epidural catheter prior to surgery, and after surgery, the patient often has coagulopathy. We routinely discuss with the anesthesiologists, postpone LMWH medication, give thrombocytes if necessary, and then apply epidural analgesia whenever possible.

Neuromuscular blockade (NMB) is an effective way of immediately reducing IAP when the patient is on the ventilator, which is often the case after rAAA repair with massive bleeding and transfusion, even if EVAR was used. It reduces IAP by 30–50 %, which is often sufficient to improve renal function, reduce fluid overload, and reverse the situation of increasing IAP before ACS develops. In a study on 191 trauma patients undergoing damage control laparotomy, 92 who were on NMB the first 24 h had higher primary fascial closure rate [66]. A large randomized French trial showed that NMB during 48 h was safe and improved survival in patients with acute respiratory failure, in 340 mixed ICU patients [67]. There are no published specific data on rAAA patients, but in our experience, it works well.

Reducing the fluid overload acts through both mechanisms, reducing intra-abdominal volume and making the abdominal wall more compliant, as the edema decreases. How this shall be best achieved is probably worth a special chapter, written by an intensivist. This issue is highly controversial, however. Many argue that colloids are beneficial in this situation, others that they only leak into the extracellular space, adding further to the fluid overload and affecting renal function negatively. We tend to use plasma in the first postoperative phase, when the patient often is coagulopathic, and hypertonic 20 % albumin combined with furosemide or renal replacement therapy later. If the patient is on the ventilator, an increased PEEP may help to recruit fluid from the lungs.

The fluid overload is often more iatrogenic than what is recognized. The Uppsala protocol is very restrictive with the administration of crystalloids from early resuscitation. Not all are aware of the fact that when we give fractionated blood products (erythrocytes, plasma, and thrombocytes, 1:1:1), to compensate for one liter of blood loss, 4–500 ml of saline solution is also added. Thus, even if only blood products are given, the transfusion to compensate for 10 l of blood loss will automatically result in a fluid overload of 4–5 l, making further administration of crystalloids dangerous.

Decompression Laparotomy (DL)

When ACS is incipient, or even manifest, the only effective treatment is DL. It should preferably be performed in the midline, from the costal arch to the symphysis pubis. If the primary laparotomy was a transverse incision, which fortunately is very rare after rAAA repair, that may need to be used again, but it will be less effective. To not open the entire abdomen is a classical beginner’s mistake, less effective, and more difficult to close.

The timing of DL is important but a difficult subject to discuss. Ideally, the two strategies of early or delayed DL should be compared in a randomized design. It does not make sense to await severe organ dysfunction/failure before DL, but OA treatment is a morbid procedure associated with both morbidity and mortality.

When a decision to perform DL has been taken, often in the middle of the night, there may be a waiting list for OR. Other patients may have high priorities, in which case NMB can reduce the ischemic injury to the abdominal organs during waiting. It is important to inform the anesthesiologist that the patient needs to have an extra bolus of fluids prior to DL, to avoid hypotension, which is common during DL.

The effect of DL is often dramatic, reducing IAP, and improving oxygenation and urinary output. Effects on multiple organ failure scores (SOFA, APACHE) are not as quick, however, since multiple organ failure is not reversed quickly. In a recent multicentre study on 33 patients undergoing DL for overt ACS, with different pathologies including rAAA, the IAP decreased from 23 mmHg (range 21–27) to 12 mmHg (9–15) after 2 h [68].

Prophylactic Open Abdomen Treatment

Is it best to leave all patients open as a routine after OR of a rAAA, or is it better to close most patients (who do not have a very tense abdomen) and follow them closely in the postoperative period? This issue should ideally be investigated in a randomized study, but that has not taken place. The Mayo Clinic reported having left 19 % open after AAA repair (43/223) [69], and a similar experience was reported from Zürich [51].

Based on a systematic EBM review of the literature, the updated consensus document favors primary closure and IAP measuring [52]. They recommend “measuring IAP when any known risk factor for IAH/ACS is present in a critically ill or injured patient” and “use of protocolized monitoring and management of IAP versus not.” Furthermore, “we could make no recommendation regarding the prophylactic use of the open abdomen”.

The policy in Uppsala is to leave the patient open primarily after OR of a rAAA only if the abdomen is tense and difficult to close, in approximately 5–10 %. Most patients with rAAA are treated with EVAR. We monitor IAP every 4 h in all patients, more frequently the first hours and when IAH, early medical treatment and DL on demand. An algorithm was published [70]. In the largest study ever on ACS after rAAA repair, 1341 operations were studied. Among the 72 % operated on with OR, 10.7 % were left open [63].

Management of the Patient with Open Abdomen (OA)

Managing a patient with OA after rAAA repair is a vast topic; many review articles have been written on this subject [7072]. The first issue is how to optimize the management of the open abdomen itself. It is important to maintain a sterile environment, to keep the intestines moist and protected from injury, and to protect the abdominal wall. A classification system of the open abdomen was developed, in order to facilitate training and research [73]. Preventing and controlling contamination, as well as lateralization of the abdominal wall, are key elements to enable to close the abdomen as soon as possible [52, 73, 74].

The importance of closing the abdomen as soon as possible was illustrated by the results of a recent publication from Helsinki, Finland [75]. They used a temporary abdominal closure (TAC) device including continuous negative pressure (the VACM method, see below), yet the open abdomen of their patients was progressively colonized so that 80 % of the patients had positive bacterial cultures after 2 weeks of OA treatment.

The choice of TAC has attracted much attention, and multiple solutions were developed [76]. The first to treat patients with OA were the pediatric surgeons, who started to repair omphalocele in the 1940s, using silastic coverage of the intestines. A similar system was later popularized in trauma surgery by the Colombian invention of the Bogotá bag, using the plastic bag from a drip that is sutured to the skin or the fascia. This system works well for a few days, but during a more prolonged treatment (which is necessary after rAAA repair), three major problems develop. Two of those were solved by the later development of the vacuum pack technique, developed in 1995 by Barker in Philadelphia, USA [77]: the active suction prevented leakage of fluids from the OA, and the surgical towels covered with plastic prevented adhesions to form between the intestines and the abdominal wall. This system was further refined by a commercially available ready-made system (V.A.C.® Abdominal Dressing System; KCI, San Antonio, Texas, USA).

A third problem, the lateralization of the abdominal wall, remained however, making it difficult to close patients who had been treated with OA >5 days. This was the reason why we developed a novel combination in Uppsala and Malmö, Sweden, the vacuum-assisted wound closure and mesh-mediated fascial traction (VACM) method, published in 2007 [78]. This is a combination of the commercially available VAC system with a prolene mesh that is sutured to the fascial edges to permit an active traction toward the midline. A multicenter study with this technique (including only patients with a need of OA during >4 days) showed an 89 % primary delayed fascial closure rate after a median time of 15 days with OA [79], and in a subgroup analysis of those treated for aortic disease, this figure was 100 % [61]. These results have been repeated independently at other major centers [80, 81] and is now the preferred TAC method in many centers worldwide.

The problem of lateralization was defined in the updated consensus document [52]: “Lateralization of the abdominal wall is the phenomenon where the musculature and fascia of the abdominal wall, most exemplified by the rectus abdominis muscles and their enveloping fascia, move laterally away from the midline with time.” It is also included in the classification system of OA [73].

The Uppsala algorithm summarizing the management of patients after rAAA repair, regarding preventing and treating ACS, is summarized in Fig. 16.11.


Fig. 16.11
The Uppsala algorithm to prevent and treat ACS


The overall mortality in the aforementioned international multicenter study on decompression laparotomy for ACS (including but not exclusively rAAA patients) was 28 % at 28 days and 55 % at 1 year; non-survivors were older (63 vs. 53 years) [69]. The large population-based cohort study from Sweden, including 1341 rAAA repairs, showed the great impact that ACS has on the prognosis after rAAA [62]. Thirty-day mortality rate was 42.4 % with ACS versus 23.5 % without ACS, p < 0.001, at 1 year 50.7 % versus 31.8 %, p < 0.001. Furthermore, all registered complications, such as myocardial infarction, renal failure, multiple organ failure, ICU care >5 days, intestinal ischemia, bowel resection, and reoperation for bleeding, were all four to six times more common among the 94 patients who developed ACS after rAAA repair. Those results are actually rather encouraging, since untreated ACS has a mortality approaching 100 %, and maybe the fact that ACS has been recognized and treated for many years in Sweden is one of the explanations why survival after rAAA has increased over time [82].

Spinal Cord Protection in Emergency Aortic Surgery

Anthony M. Roche11, Hernando Olivar11 and Koichiro Nandate11

Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA



Spinal cord ischemia during endovascular repair of aortic aneurysms can lead to devastating neurological deficits including complete paraplegia. Depending on the type of aortic surgery, it has a quoted incidence of 2.5–13 % [83]. This variation differs based on extent of surgery, elective or emergency surgery, open versus endovascular techniques, as well as perioperative management. The available literature implicates an overall spinal cord injury (SCI) rate of 6–13 % [83] for open procedures, with thoracic endovascular aneurysm repairs (TEVAR) having an associated rate of 3–4 %. In a systematic review of SCI associated with TEVAR and cerebrospinal fluid drainage, Wong et al. found 46 eligible studies totaling 4936 patients. They discovered an overall SCI rate of 3.89 % [84]. There is a paucity of literature on SCI in emergency aortic surgery, and no studies specifically relating to SCI in emergency EVAR surgery. Since there is such a paucity of literature specifically on SCI in emergency endovascular aortic repairs, we present our institutional approach to spinal cord protection based on current literature with emphasis on overall patient safety.

Pathogenesis and Risk Factors

The pathogenesis of SCI is multifactorial; however, most injuries are the result of ischemia or ischemia–reperfusion injury. Spinal cord perfusion is a dynamic process, which is dependent on major segmental arteries and vast networks of collateral blood flow. In most circumstances of open or endovascular abdominal aortic aneurysm surgery, there is usually limited to no occlusion of major segmental arteries. The picture changes somewhat when a thoracic repair is indicated. In such scenarios, segmental arteries are usually implicated, especially with longer grafts or previous aortic procedures. This results in the spinal cord perfusion being increasingly dependent on the vulnerable and often inadequate collateral circulation. Hemodynamic disturbances and fluctuations inevitably lead to a reduction in collateral circulation flow.

Part of patient preparation for surgery, be it elective or emergency, should include some form of risk stratification for adverse perioperative outcomes. As is the case for adverse cardiac outcome risk assessment and subsequent stratified management bundles, it is prudent to assess the risk for SCI in aortic surgery. This enables the surgical team to better quantify the risk of SCI, improve patient counseling, and plan stepwise spinal cord protection strategies [85, 86].

Known risk factors for SCI in TEVAR include the following: previous aortic interventions; long aortic coverage, especially if the left subclavian and/or hypogastric arteries are covered; renal insufficiency (with creatinine levels greater than 1.5 mg/dL); and prolonged periods of hypotension (mean arterial pressures less than 65–70 mmHg) [87]. Furthermore, age, comorbidities (e.g., hypertension, hyperlipidemia, diabetes mellitus), and increasing number of aortic stents may also increase risk of SCI [83, 85, 88, 89]. Symptomatic disease or rupture has also been implicated, especially in open thoracic aortic surgery.

Spinal Cord Protection

As described above, an important first step is recognizing the risk of SCI. Based on that risk assessment, a stepwise approach can be employed to reducing the risk of spinal cord ischemia.

It is recommended as a minimum that hypotension be avoided during aortic surgery [87]. The basis of spinal cord perfusion rests with the simple equation:SPP = MAP – ITPLegend: SPP is spinal perfusion pressure, MAP is mean arterial pressure, and ITP is intrathecal pressure.

The goal of spinal cord perfusion pressure management is to remain as close to each patient’s baseline as possible [83, 90]. This is less of a problem in mostly abdominal aortic surgery, regardless of open or endovascular technique, where it is less likely that segmental branches to the spinal cord will be covered or ligated. Fastidious control of SPP is especially important in circumstances of longer stents/grafts and in patients determined to be at higher risk of SCI. The underlying principle is to maintain spinal blood flow and oxygenation, thereby reducing the risk of ischemia or ischemia–reperfusion injury.

The avoidance of hypotension, although self-explanatory, can be described especially as reducing duration thereof. Sustained hypotensive periods, with MAPs below 65–70 mmHg for longer than 5–15 min, are associated with higher incidence of SCI. Strict BP management is therefore a crucial first step in reducing SCI [91]. This is a difficult goal to achieve, especially in compromised patients undergoing emergency procedures. One of the most effective measures that we perform at our institution during the initial surgical approach of patients with aortic emergencies is to achieve endovascular control of the aorta. Once the balloon is in place, intravascular accesses and invasive blood pressure monitoring as well as fluid resuscitation are initiated. If the patient does not tolerate light sedation, general anesthesia is induced. Permissive hypertension is described as a potential management strategy for patients with symptomatic SCI [91].

Our center uses the following algorithm for blood pressure management:

  • Maintain intraoperative MAP >80 mmHg.

  • Increase MAP to greater than 80–90 mmHg at the moment of graft deployment.

  • Maintain the MAP greater than 80–90 mmHg postoperatively for 24–48 h.

  • If neurologic symptoms are present at any time point, increase MAP to greater than 100 mmHg using vasopressors and/or inotropes.

  • Lumbar CSF drainage (description to follow)

Although controversial, lumbar CSF drainage has been shown to be effective in the prevention and management of SCI during TEVAR and open thoracoabdominal aneurysm repair [90, 9295]. As a result, it has been recommended as part of spinal cord protection algorithms. The rationale is, like MAP management, to improve spinal cord blood flow and oxygenation. In addition to increasing MAP, reducing CSF pressure (ITP) increases SPP. Lumbar CSF drains should be placed preoperatively, following existing national guidelines for neuraxial block placement and anticoagulants/patient coagulation status (see Table 16.3). Reasonable ITP pressure goals are be as follows:

Table 16.3
University of Washington neuraxial access and anticoagulation protocol




Catheter placement

While catheter in place

Catheter removal

Reinitiation of anticoagulation


Activate plasminogen

Alteplase, Urokinase, Streptokinase


Avoid lumbar puncture/catheter placement



If fibrinolytics are required, check if neuraxial technique/catheter was placed within 10 days. If yes, medication is contraindicated


Direct thrombin (IIa) inhibition

Bivalirudin (Angiomax), desirudin (Iprivask), argatroban (no trade name), dabigatran (Pradaxa)


Insufficient data; avoid lumbar puncture/catheter placement



Not addressed, insufficient data
Indirect thrombin (IIa) inhibition via AT III

Unfractioned heparin (UFH)

5 K U SQ BID—no restrictions on placement

>10 K. Catheter placement 4 h after last dose. Check PTT and platelet before puncture

*Check Plts if on heparin >4d

Ok if dose less than 10 K units (QD, BiD)

TID doses or >10 K units. Contraindicated

Remove after 4 h of discontinuation

Reinitiate 4 h after catheter removal
Indirect Xa inhibition via AT III

LMWH: dalteparin (Fragmin), enoxaparin (Lovenox)


Dalteparin, enoxaparin. Catheter placement after 12 h of QD doses. 24 h for higher doses.

Fondaparinux: contraindicated

LMWH QD doses ok. Avoid BID doses

Fondaparinux is contraindicated

Remove after 12 h of discontinuation

Reinitiate after 6 h of catheter removal
Direct Xa inhibition

Apixaban (Eliquis), rivaroxaban (Xarelto)

No specific recommendations. Weigh risks. Recommend to stop 48 h before puncture

No specific recommendations. Weigh risks. Not recommended

No specific recommendations. Weigh risks. Not recommended

No specific recommendations. Weigh risks. Xarelto manufacturer recommends reinitiate after 6 h of removal
Vit K epoxide reductase inhibition (II, VII, IX, X)

Warfarin (coumadin)

Stop 5 days before, bridge to UFH or LMWH and follow recommendations.

INR <1.4


INR <1.5: remove + monitor x 24 h

Timing according to patient’s risk of thromboembolic events and risk of surgical bleeding

INR 1.5–3.0: remove w/caution; monitor until INR is normal

INR >3.0: reduce dose or hold; no definitive removal recs.


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Nov 11, 2017 | Posted by in ABDOMINAL MEDICINE | Comments Off on Postoperative Complications
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