Keywords

Introduction

Compartment syndrome , first identified in the context of extremity perfusion, was described in the early 1800s. Inadequate tissue perfusion due to narrowing of the gap between perfusion pressure/flow and tissue pressure was recognized as a threat to limb perfusion and viability. This same principle can be applied to the abdomen and its visceral contents, and it was the recognition of this analogy that eventually led to the recognition of IAH and subsequent ACS as life-threatening entities. The relationship of increased abdominal pressures and its effects on the respiratory system were first described in the late 1800s. Emerson’s work in the 1900s examined the true relationship of intra-abdominal pressures and the cardiovascular system in dogs [1]. The interest in IAH was reinvigorated in the 1980s with multiple publications, initially through the work of Kron et al., who described the effects of IAH and the effects of re-exploration on renal function [2, 3]. Ultimately, the World Society of the Abdominal Compartment Syndrome (WSACS), now termed the Abdominal Compartment Society, was formed in 2004 and exists to promote research and education as it relates to ACS [4, 5].

The pathophysiology of compartment syndrome is simply defined as intra-abdominal hypertension resulting in end-organ failure. The effects of intra-abdominal hypertension have vast implications including cardiac, pulmonary, renal, and even neurological function. Patients with intra-abdominal catastrophes as well as those who have undergone aggressive resuscitation in the context of dysregulated systemic inflammation are patient populations at increased risk for ACS. Once recognized, immediate attention should be directed toward relieving the IAH through consideration of both invasive and noninvasive maneuvers aimed toward decreasing abdominal pressure. These maneuvers, though beneficial in the context of decreasing abdominal pressure, often carry with them their own set of problems and issues, such as acute or chronic open abdominal wounds and challenges that come along with these wounds. Fortunately, experience has led to the creation of multiple short- and long-term options to deal with these issues.

Furthermore, as the understanding of the pathophysiology driving IAH and ACS increases, options aimed upstream of decompression are being described as being important in preventing IAH to begin with. Earlier recognition of uncompensated shock and systemic inflammation, improved fluid resuscitation strategies, and the evolution of lower tidal volume strategies for the management of respiratory failure all represent relatively recent developments in management of critically ill patients that have contributed to a decrease in the incidence and prevalence of IAH and ACS.

Definitions

Standard definitions and taxonomy have been an important focus of recent work by the WSACS . The most recent definitions, published in 2013, define IAH as intra-abdominal pressure (IAP) ≥ 12 mmHg. The various grades of IAP are listed in Table 37.1. ACS is defined as IAH > 20 mmHg that is associated with new organ dysfunction/failure [4]. It is important to recognize that IAH and ACS are not equivalent terms; IAH is a spectrum and ACS only occurs when there is concurrent organ dysfunction. It should be noted that the value of “normal” IAP needs to be better established in various populations including children, the obese, and pregnant women. One other important distinction made by the WSACS is primary versus secondary ACS. Primary ACS is associated with a condition, injury, or disease within the abdominopelvic region, whereas secondary ACS refers to conditions not originating in the abdominopelvic region [4].

Table 37.1 Intra-abdominal hypertension (IAH) grading scheme
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Pathophysiology

Intra-abdominal pressure is normally atmospheric or subatmospheric. In critically ill patients, the IAP is normally 5–7 mmHg [4]. When the IAP rises to a point where organ dysfunction occurs, the diagnosis of ACS can be made. The organ dysfunction arising from ACS can affect multiple systems including cardiovascular, pulmonary, renal, gastrointestinal, and even the central nervous system.

Traditionally, it was thought that ACS occurs when the abdominal perfusion pressure (mean arterial pressure – intra-abdominal pressure) becomes inadequate. However, recent studies suggest this may not be so straight forward. Olofsson and colleagues demonstrated that the mucosal blood flow of small bowel was less affected than other areas of microcirculation during stepwise increases in intra-abdominal pressure (IAP) in a swine model, suggesting a component of autoregulation. As cardiac output decreased, so did microcirculation; however, the small bowel mucosa was less affected relative to the seromuscular layers. This study also found that changes occur at grade 1 and 2 IAH , suggesting even mild IAH is not a benign process [6].

Primary ACS occurs when there is a direct source of increased IAP within the abdomen (trauma, pancreatitis, infection, etc.). Secondary ACS, however, occurs as a result of factors not directly related to the abdominal cavity. Examples of secondary ACS include bowel or retroperitoneal edema due to large-volume resuscitation associated with a non-abdominal source of inflammation, ACS due to massive ascites in the absence of an abdominal operation, and right heart failure associated with visceral edema. Activation of the immune system triggers cytokine release and subsequent capillary leak. This impacts the cellular function of the organ itself, along with the effects of fluid accumulation in the extravascular space. As emphasized by Malbrain, this is well recognized in the pathophysiology of acute respiratory distress syndrome, but clinicians have been slow to adopt the same physiologic blueprint to the gastrointestinal tract [7]. For these reasons, the terms acute bowel injury and acute intestinal distress syndrome were introduced by Malbrain and colleagues.

Acute bowel injury is the result of capillary leak and subsequent edema. In the so-called “two-hit” process , a first hit occurs when an insult results in neutrophil activation and cytokine release. This is followed by a second physiologic insult where capillary leak ensues resulting in persistent and worsening tissue edema and subsequent IAH . As this process continues, IAH will continue to worsen, and eventually acute intestinal distress syndrome and ACS occur. The initial insult simply opens the door to additional IAH which in and of itself will lead to decreased perfusion of the GI tract. The authors compare this to the acute lung injury progression to ARDS pathway. Inherent in this pathway is that ischemia-reperfusion likely plays a substantial role in the pathophysiology of ACS [7].

In addition to global capillary leak, ACS also has profound effects on the cardiovascular, pulmonary, genitourinary, gastrointestinal, and neurological systems. As demonstrated in multiple studies, cardiac output is negatively affected by increases in IAP [6, 8]. Decreases in global cardiovascular performance are usually a result of decreased venous return and diastolic filling (preload) combined with increases in ventricular afterload. Increases in afterload may result from both direct compression of the pulmonary artery, aorta, and their branches and sympathetic vasoconstriction secondary to metabolic stress. Continued fluid administration may be temporarily beneficial; however, ongoing fluid resuscitation without addressing the primary source and abdominal hypertension may be deleterious, as fluid cannot overcome the factors affecting low cardiac output. Fluid administration in patients with ACS has been found to increase pulmonary capillary wedge pressure (PCWP) without any concomitant increase in cardiac index (CI) [9, 10]. Fluid administration can become a viscous cycle of more fluid followed by worsening capillary leak followed by even more fluid. The lack of a systemic response to additional fluid has been appropriately termed the “futile crystalloid preloading cycle.” [10] Furthermore, careful attention should be paid to how preload is being assessed in these patients, as errors in interpreting pressure-derived estimates of preload may lead to conclusions being drawn about intravascular volume status that in fact have little relationship to actual volume status. There is a positive correlation between IAH and PCWP and CVP, but this increase does not result in an increase in cardiac output as one may expect [11]. Thus, hemodynamic monitoring values should be interpreted with caution in patients with IAH.

An increase in IAP invariably leads to increased thoracic pressures and a decrease in functional residual capacity. The decrease in lung compliance is particularly noticeable in the ventilated critically ill patient. Ventilated patients on volume-limited modes will see an increase in peak inspiratory pressure, whereas those on pressure-limited modes of ventilation will have lower tidal volumes. Resultant pulmonary edema secondary to fluid administration and capillary leak results in increased PEEP requirements which then exacerbate the cardiovascular effects mentioned above. It is clear that ACS is a risk factor for the development of acute respiratory distress syndrome (ARDS), which itself is a morbid and mortal syndrome, and its development is likely multifactorial [12]. Appropriate ventilator management with lung protective strategies is crucial when managing the ACS patient.

Oliguria and subsequent renal failure were among the earliest effects of ACS noted in the surgical literature. Renal dysfunction associated with IAH is due to factors both extrinsic to the kidneys themselves and direct effects of IAH on the kidneys. Inadequate global cardiovascular function leads to relative hypotension, decreased cardiac output, and subsequent renal hypoperfusion [2]. Several investigators in the past have looked at the renal subsystem itself very carefully, focusing on both the kidneys, and the renal collecting system. Although ureteral compression was once thought to play a role, renal vein compression (outflow obstruction) along with direct compression of the renal cortex is the most plausible etiology of renal dysfunction [13].

Decompression plays a central role in the management of renal impairment associated with IAH and ACS and, if performed early in the course of the ACS, usually results in improvement in both intrinsic renal function and urine output. However, delays in recognition are often associated with either transient or no improvement in renal function at the time of decompression. Keys to early decompression center around an increased awareness of the risk of IAH in these metabolically stressed patients and definitive decision-making to move forward with decompressive maneuvers once diagnosed.

The gastrointestinal system is also vulnerable to the effects of IAH . This is likely related to the decreased perfusion secondary to the local increased pressures and the changes in the circulatory system described above. Diebel and colleagues have clearly demonstrated the profound negative effect of IAH on mesenteric perfusion using an animal model and measuring the decreases in mesenteric blood flow and mucosal pH with incremental increases in IAP [14]. Further, Chang and colleagues demonstrated a significant improvement in gut mucosal pH, indicating an improvement in intestinal perfusion, after decompression of the abdomen, which supports this concept [11].

Lastly, IAH can have a deleterious effect on the central nervous system by impairing cerebral venous outflow and thus increasing intracranial pressures (ICP). This phenomenon was first recognized with laparoscopy, and it was identified that abdominal insufflation increases ICP [15]. This can have many downstream effects including exacerbating head injury and potentially contributing to altered mental status in the critically ill patient [16]. To further demonstrate this, it has also been suggested that decompressive laparotomy can be used as an adjunctive therapy in lowering ICPs that are refractory to traditional treatments [17].

ACS affects multiple critical physiologic systems concurrently. The effect on each system can adversely potentiate the effect on another bodily system. It is the interrelation of the effects that leads to the ultimate organ failure and potential fatal consequences.

Diagnosis

IAH and ACS can result after a wide range of both anatomic and physiologic insults. The bedside clinician must be vigilant in the ICU to assess at-risk patients for IAH . It is important to always recognize that IAH is distinct from ACS. The vigilant clinician can recognize IAH and intervene, potentially preventing ACS and its significant consequences. In a meta-analysis, large-volume crystalloid resuscitation, the respiratory status of the patient, and shock/hypotension were all risk factors for ACS; obesity, sepsis, abdominal surgery, ileus, and large-volume fluid resuscitation were notable risk factors for IAH [18]. Primary and secondary ACS vary in their presentation and course. As described by Reintam and colleagues, secondary IAH often presents late and may be characterized by a prolonged course where IAP increases over a period of days. Compared with primary IAH , secondary IAH is associated with increased mortality [19].

Early recognition of both IAH and ACS requires both a heightened suspicion of their presence in patients at risk and careful interpretation of bedside monitoring and physiologic information across all potentially affected subsystems. Changes to the respiratory status (increased peak/plateau inspiratory pressures, decreased compliance) may be among the first signs of IAH in the ventilated patient. Decreasing urine output, rising creatinine, abdominal distention, and hypotension are among other signs of IAH and impending ACS. Clinical exam alone is often not reliable in recognizing and diagnosing IAH [20].

When a concern exists for IAH or ACS, direct measurement of intra-abdominal pressure is the gold standard for diagnosis. Multiple techniques have been used to measure the pressures within the abdominal compartment. The most accepted technique involves the measurement of bladder pressure, first described by Kron et al. in 1984. Fundamentally, the bladder is filled with a specified volume of saline solution with the urinary drainage catheter clamped to maintain bladder volume. The wall of the bladder then acts as a passive diaphragm, and transduction of intravesicular pressure, done by attaching a pressure transducer to the catheter, allows a reasonable estimation of intra-abdominal pressure. Optimal volumes of bladder distention with saline have been correlated with direct measurements of intra-abdominal pressure at laparoscopy, and volumes of 25–50 cc provide the most accurate measurements [3]. The most recent recommendations of the WSACS advise to instill no more than 25 cc of saline into the bladder [4]. A schematic of the setup to measure bladder pressures at the bedside is depicted below (Fig. 37.1). Other techniques using pressures within the vasculature, rectum, and stomach have also been described, but bladder pressure is the current standard. [2] This methodology has been validated by comparing bladder pressures to true intra-abdominal pressure during laparoscopy [21]. Optimally, bladder pressure measurements should be measured with the patient in the supine position [22]. If the patient is active or has tense abdominal muscles, the pressure may be interpreted as falsely high. In such patients, consideration should be given to sedation and potential paralysis to obtain an accurate IAP . Space-occupying materials in the pelvis, such as packs, masses, or a pelvic hematoma, may also confound bladder pressure measurements by extrinsically decreasing function bladder wall compliance, leading to elevated bladder pressures independent of increases in intra-abdominal pressure.

Fig. 37.1
figure 1

Bedside setup for measurement of bladder pressure

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Ultimately, a well-defined protocol employing consistent techniques within an institution is essential to obtaining accurate and consistent bladder pressure measurements.

Management

The gold standard treatment of ACS is emergent abdominal decompression. In considering the treatment, however, one must also emphasize that prevention is the best treatment. The WSACS has proposed a treatment algorithm which is detailed in Fig. 37.2. Once IAH is identified, steps can be taken to prevent progression to ACS, directed at both the primary physiologic insult and the secondary insult resulting from the deranged physiology due to the primary problem. Primary ACS can often not be avoided by the clinician, as the patient often has a direct insult to the abdominopelvic cavity. However, leaving the abdomen open after damage control surgery or in cases where the viscera cannot be reduced for abdominal closure has been a hallmark in preventing ACS and is unequivocally the reason there has been a decrease in ACS [12]. Secondary ACS may be also be preventable by intervening upon the inflammatory cascade and being judicious with fluid (particularly crystalloid) administration, with the goal being to achieve and maintain a euvolemic state.

Fig. 37.2
figure 2

Management algorithm for ACS. (Reprinted with permission from Kirkpatrick et al. [4])

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When IAH is recognized, steps should be taken promptly to reduce IAP to prevent progression to ACS. This includes primarily medical management and close observation. Proper pain control and sedation of the patient are essential and may reduce IAP . As alluded to earlier, neuromuscular blockade may reduce IAP . At the very least, paralytics will allow for accurate IAP measurements. Although evidence is lacking, placement of enteric tubes to reduce gastric and colonic distention may be helpful [4]. As mentioned above, fluid balance plays a critical role in the development of ACS (particularly secondary ACS) and should be optimized. Just as optimizing fluid balance has been shown to be favorable in ARDS , the same is likely true for ACS. Increased crystalloid volumes are associated with an increased incidence of ACS, so achieving appropriate fluid balance, which may involve strict management of fluid administration, and sometime diuresis, is critical [23]. In cases of trauma, balanced blood product resuscitation should be pursued, as this has been related to a decrease in the incidence of ACS in this population [24].

Minimally invasive strategies have been proposed to decrease IAP . This includes percutaneous drainage of fluid collections within the abdominal cavity and, in the case of severe pancreatitis, the retroperitoneum. Reports of percutaneous drainage allow for avoidance of the morbidity associated with a laparotomy and the subsequent open abdomen [25,26,27]. Among trauma patients with large resuscitations, percutaneous drainage was found to offer significant reduction in IAP , increase in abdominal perfusion pressure, improved pulmonary compliance, and increase in mean arterial pressure [28]. This procedure is best suited for patients with abdominal fluid after significant resuscitation with crystalloid (severe pancreatitis, sepsis) or after blunt solid organ trauma. Cheatham and colleagues demonstrated 81% treatment efficacy of this modality. These authors suggested that drainage of less than 1000 mL and a decrease in IAP of less than 9 mmHg in the first 4 h are predictive of failure [29]. Subcutaneous fasciotomy of the abdominal wall fascia has also been described in small series [30]. Leppaniemi describes a technique where the linea alba is opened through small skin incisions. This results in a hernia that must be repaired in the long term but avoids the morbidity of an open abdomen [31, 32]. Although the results are promising, this technique has only been studied in small numbers.

In light of these strategies, surgical abdominal decompression via laparotomy remains the standard. This is the most rapid and definitive method to decompress ACS. Prompt decompression results in improved preload, pulmonary function, and visceral perfusion [11]. The treatment phase of ACS not only includes this initial decompression but also includes care of the open abdomen and the subsequent closure and abdominal wall reconstruction. Appropriate management of the open abdomen and the prevention of complications are essential. Once an abdomen is opened, a negative pressure dressing should be used as a temporary closure device [4]. The open abdomen is then treated in a staged approach. This approach is very similar to the open abdomen after damage control surgery in trauma, as described by Rotundo et al. [33] After the initial operation, a temporary closure is placed over the abdominal viscera, and the patient is taken to the intensive care unit for resuscitation and optimization. The patient is then returned to the operating room for re-exploration and definitive closure as early as possible. Potential complications of the open abdomen are inability to close, hernia, enterocutaneous fistula, infection, and even recurrent ACS. Various methods have been described for temporary abdominal closure to maximize fascial closure and minimize hernia. Bowel edema and fascial retraction often make primary abdominal wall closure difficult or impossible.

Temporary Abdominal Closure

The evolution and development of current techniques employed to manage open abdominal wounds is a relatively recent development in surgery. Before the description of the staged celiotomy [34], standard general surgical teaching was that all operations should be completed at the initial operation. In fact, failure to close the abdominal wound was considered a marker of surgical inadequacy. Advances in the understanding of IAH and ACS have driven a significant change in attitudes over the four decades, and the increased understanding of IAH and ACS has carried with it significant advances in the techniques used to safely manage temporary open abdominal wounds. Early techniques, such as skin closure with towel clips, wet dressings over open wounds, and artificial mesh sewn to the skin, are fraught with complications and have largely been abandoned. A silo-type dressing, commonly referred to as “Bogota bag,” involves the placement of a sterilized IV fluid bag over the viscera and sewn to the skin edges [35, 36]. This technique is quick, simple, and inexpensive and provides a true “window” into the abdomen. The drawback to this technique is that it does not provide any tension on the fascial edges, allowing for retraction of the abdominal wall laterally.

In theory, any device or method used for temporary abdominal closure should meet certain minimum criteria. The dressing should protect the viscera, prevent spillage of ascites (with associated heat loss), allow for patient mobility, and minimize metabolic stress. Optimally, the dressing would facilitate measuring and controlling peritoneal drainage, would be flexible enough to expand should visceral edema worsen, and would not involve damage to the fascia, in anticipation of eventual delayed fascial closure.

Vacuum-assisted fascial closure (VAFC) meets most, if not all, of these criteria and has become a popular method of managing temporary open abdominal wounds. This technique involves placing a standard vacuum pack (as described by Barker et al.) to the abdomen at the index operation if the abdomen is not going to be closed [37]. If the abdomen is not able to be closed at the time of reoperation, the VAFC method is employed. Described in detail by Miller et al., this includes placement of a perforated polyethylene sheet over the viscera. A black sponge is then placed on the sheet and sutured to the skin edges with a running nylon stitch (Figs. 37.3, 37.4, and 37.5). Employing this technique allows for an abdominal closure rate of 88%. Interestingly, 48% of the patients in this study were able to be closed after 9 days, suggesting that attempts should continue to be made to close the abdomen even after 1 week or more [38]. The Denver group has described a novel vacuum technique where white sponges are placed on the viscera, followed by fascial tension with PDS sutures, followed by a traditional sponge in the subcutaneous space. By changing this every 2 days, they claim a 100% fascial approximation rate [39]. The ABThera VAC (KCI, San Antonio, TX) is a commercially available device that accomplishes the same principles as the techniques above and has favorable abdominal closure rates. The Wittmann Patch (Starsurgical, Burlington, WI) is a Velcro device that can be sutured to fascial edges and serially tightened until abdominal closure is adequate. Using this device has been shown to facilitate definitive abdominal closure [40, 41]. There are multiple techniques and devices that are available to maintain abdominal domain while the abdomen is open, and each individual provider must choose their preferred method. Whichever technique is employed, it is critical that the clinician recognizes that ACS can occur with a temporary abdominal dressing in place [42].

Fig. 37.3
figure 3

Placement of polyethylene sheet

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Fig. 37.4
figure 4

Black sponge with nylon suture and adhesive dressing

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Fig. 37.5
figure 5

Abdominal closure on postoperative day 21

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Definitive Abdominal Closure

As soon as the abdomen is initially decompressed, planning for definitive abdominal closure should begin. While the abdomen is open, appropriate fluid balance, depending on the patient’s physiologic state, should be maintained. Balanced blood product resuscitation decreases the incidence of ACS and is also related to improved rates of abdominal fascial closure [43]. Enteral nutrition with adequate protein and total caloric intake should begin as soon as feasible in patients with an open abdomen, as this has been shown to improve fascial closure rates [44]. It is important to carefully monitor the protein-rich effluent from the open abdomen, as this affects both the patient’s fluid balance and their nutritional status given the abdominal effluent may have 10–15 g of albumin per liter.

Management of the open abdomen can be broadly divided into three phases: phase 1 is the time after the index operation when a TAC technique is used; phase 2 is the attempted closure of the abdominal wall during the acute phase; and phase 3 is the later (6–12 months) abdominal wall reconstruction in those whom primary closures were not possible during phase 2 [45]. Primary fascial closure is by far the most desired outcome after open abdomen and can be achieved in well over half of patients, as far out as 1 month after injury [46]. In the event that primary fascial closure is unable to be attained, acute mesh repair and component separation are techniques that may be employed to achieve abdominal closure early. Acute component separation and mesh placement, while allowing for early abdominal closure, are associated with a high complication and hernia rate, respectively [45]. When abdominal closure is not accomplished during the acute phase, planned ventral hernia with a staged approach is also an option with future definitive reconstruction.

With planned ventral hernia, the viscera must be covered in some fashion. If a visceral block has formed, the skin may be closed over the viscera with a running suture. If this skin cannot be closed, our preference is to cover the viscera with a skin graft. If a nice bed of granulation exists on the viscera, the graft may be placed directly onto it. In the more common scenario where there is not sufficient granulation or the bowel is not adhered as a block, a polyglactin mesh is sutured to the fascial edges circumferentially. This should not be placed under significant tension, as the mesh can tear; the goal of the procedure is visceral coverage, not fascial tension. Next, negative pressure wound therapy is applied until adequate granulation tissue is present, at which time a split-thickness skin graft is performed. Acellular dermal matrices are another option when closing the abdomen and can be placed to bridge the fascial defect. While this may decrease the incidence of fistula formation, it has a high rate of recurrent hernias and should be approached as a planned hernia [47]. Again, the goal of this procedure is to cover the viscera to decrease the risk of infection and fistula [48]. Many months later, often a year or more, when the skin graft heals and easily pinches away from the underlying bowel, a definitive hernia repair can be performed. Excess skin and the hernia sac are excised and primary fascial closure is attempted. There are various techniques to augment the possibility of fascial closure including external oblique release, posterior rectus release, transversus abdominis release, and Botox injections, to name just a few. Placement of mesh at the time of hernia repair significantly decreases the risk of recurrence [49]. While the techniques of abdominal hernia repair are incredibly important for long-term outcomes, they are beyond the scope of this chapter.

Conclusion

Intra-abdominal hypertension and resultant abdominal compartment syndrome are often markers of severe metabolic and physiologic stress, and patients with these conditions can be the most challenging surgical patients to manage from both a critical care and operative perspective. The decrease in incidence of abdominal compartment syndrome can be credited to the research and subsequent education that has been dedicated to this syndrome in the preceding decades, but it has been associated with a dramatic increase in the incidence of the open abdomen. The astute clinician should be familiar with the prompt recognition, diagnosis, and treatment of ACS to avoid its morbid and mortal consequences. Moreover, management of the open abdomen requires careful planning and oversight to optimize patient outcomes.