Abdominal compartment syndrome: effects on organ function
M. Stamatakos, S. Tsaknaki, R. Iannescu, A. Stathellis, P. Safioleas, N. Rompoti, M. SafioleasReferate generale, no. 6, 2007
* 2nd Department of Propaedeutic Surgery
Characteristics
The abdominal area consists of a closed cavity of rigid
structures (spine, pelvis, costal arch), as well as elastic
segments (abdominal wall, viscera and diaphragm), governed by Pascal's hydrostatic laws (1). Thus, any increase in intra-abdominal volume causes a parallel rise in the pressure of this compartment (2). Although the abdomen is partially flexible and capable to expand, the case of a compartment syndrome development under special circumstances is remarkably
possible.
Intra-abdominal pressure
This is defined as the pressure within the abdominal cavity under normal circumstances. Intra-abdominal pressure (IAP) is characterized by a small fluctuation following the aspiratory movements, meaning an inspiratory increase caused by the contraction of the diaphragm and an expiratory decrease
during diaphragm relaxation. According to recent studies
normal IAP seems to have a mean value of 6.5 mm Hg, which appears dependent to body mass index and sagittal abdominal diameter. In mechanically ventilated patients intraabdominal pressure up to 10 mm Hg can be considered as normal under the prerequisite that a positive IAP is produced during mechanical ventilation (2-4).
The volume of the viscera and the quantity of fluid
contained inside the abdominal cavity are mainly responsible for the value of IAP. Intrabdominal pressure presents a
limited value fluctuation respectively to great changes of
volume in the abdominal cavity, as observed in laparoscopy, where infusion of approximately 5 L of gas inside the
abdominal cavity has no significant effect on IAP. A previous study suggested that a gas volume of 8.8 L is required for IAP to rise up to 20 mm Hg (5).
Intraabdominal hypertension (5)
This condition is characterized by either (1) a continuing increase of intrabdominal pressure, valued >12 mm Hg, measured at least three times with a time interval of 4-6 hours, or (2) abdominal blood perfusion pressure (APP) valued <60 mm Hg, measured at least three times, with a time interval of 1-6 hours. (table 1)
Abdominal Compartment Syndrome
A variety of pathological conditions can be causative
factors to this syndrome. Syndromes commonly invade a prodromal stage with atypical symptoms and signs; it so happens with ACS, with its respective preceding stage being intraabdominal hypertension.
The abdominal compartment syndrome includes intra-abdominal hypertension detected by a minimum of three measurements of intraabdominal pressure which demonstrate values of >20 mm Hg, conducted 1-6 hours apart, as well as the presence of initiating single or multiple organ system
failure (4-5).
Considering that ACS consists of a main factor of
multiple organ failure among critically ill patients, its
distinction regarding the underlying pathology could be helpful in the management of these patients:
Hyperacute IAH
Hyperacute IAH: a sudden rise of intraabdominal pressure, presenting duration of only few seconds or minutes, usually appear in normal activities, such as laughing, straining, coughing, sneezing, defecation or physical exercise.
Acute IAH
It develops within hours, usually caused by trauma or intra-abdominal haemorrage of any cause (rupture of abdominal aortic aneurysm).
Subacute IAH
It takes place within days, induced by most medical causes (e.g. fluid resuscitation and capillary leak).
Chronic IAH
It occurs within months or years, due to morbid obesity, intraabdominal tumor, chronic ascites or pregnancy.
Primary ACS
This form appears either after trauma or disease of the abdominopelvic area serious enough to demand surgical or angioradiological management, or after an operation in the abdominal cavity (e.g. severe acute pancreatitis, spleen
rupture, massive retroperitoneal hematoma, secondary
peritonitis).
Secondary ACS
It is associated with pathology initiating from other systems than those related to the abdomen, such as pneumonia with sepsis and capillary leak, major burns or other conditions requiring massive fluid administration.
Tertiary or recurrent ACS
This term is used for cases in which ACS proves to be inevitable, despite the application of preventive methods or surgical and medical management of primary or secondary ACS. This condition may present as persistence of ACS after decompressive laparotomy or as recurrence of ACS despite a hermetic closure of the abdominal wall (4-6).
An increase of IAP is usually caused by:
1. Trauma and intraabdominal hemorrhage;
2. Abdominal surgery;
3. Retroperitoneal hemorrhage;
4. Peritonitis, usually secondary or tertiary (pancreatitis, recurrent abscess);
5. Laparoscopy and pneumoperitoneum;
6. Repair of large incisional hernia;
7. Abdominal banding with postoperative Velcro belt to prevent incisional hernia;
8. Ileus (paralytic, mechanical or pseudoobstructive) (2, 3, 5, 7, 8).
Incidence of ACS
Efforts conducted in order to estimate the prevalence of ACS have led to controversial results. This is due to the use of
different parameters for the definition of the syndrome, the variability of the patient populations studied, as well as a
variety of diagnostic and therapeutical methods application. All these factors, including the inexistence of continuous
statistical analysis, result in inadequate knowledge of the risk for the development of ACS (4, 5).
Balogh et al mention that of 188 patients with multiple injury undergoing a standardized management, 6% developed primary ACS and 8% secondary ACS (9). 97 patients were enrolled in a recently published multicenter prospective study. The prevalence of IAH was 50.5% and 8.2% developed ACS (1). However, independent of the incidence of ACS which varies among different studies, the mortality rate of ACS remains between 29 and 100%.
Diagnosis
The measurement of intraabdominal pressure, is indispensable in the diagnosis of abdominal compartment syndrome and should be conducted in all postoperative intensive care unit patients after emergency abdominal operation, complex
elective abdominal cases, in patients undergoing massive fluid administration and extensive burns (8, 10). In contrast, the clinical examination in these groups of patients does not seem to offer much in posing the suspicion of ACS development.
A variety of methods have been applied for the measurement of IAP, with the gold standard for an intermittent
indirect measurement being the use of an intravesical catheter (2, 4, 5, 10, 11). The bladder, being a compliant intra-abdominal organ, easily accessible, presents pressure changes, which directly reflect respective changes of the intraabdominal pressure. However, a previously operated bladder, an intravesical tumor or even functional (neurological)
impairment of the bladder may lead to incorrect measurement (7). Other methods suggested, though not adequately
evaluated yet, are the use of a nasogastric tube, manometry with probes through the inferior vena cava, the rectum and the uterus (3, 4).
The ideal for a direct estimation of the intraabdominal pressure is placement of a transperitoneal catheter connected to a saline manometer or pressure transducer during
peritoneal dialysis or laparoscopy (3, 5, 7, 11). In order to provide a continuous indirect measurement of intraabdominal pressure, a balloon-tipped catheter within the stomach or continuous bladder irrigation, are the methods of choice (4, 5).
Body position during measurement is also important. The patient should be placed in a supine position and IAP should be measured at end-expiration, in order to avoid interference with ventilatory pressures, and after confirming abdominal muscle relaxation, with the transducer zeroed at the level of mid-axillary line. The value of IAP should be expressed in mm Hg (4, 5, 11, 12). It is necessary to be aware of changes of the IAP within hours, thus repeated measurements with a time interval of 8 hours should be conducted. In higher risk patients, such as emergency operated patients after abdominal injury, IAP should be undertaken every 2-4 hours (10).
The indications for IAP measurement are the following:
1. Abdominal surgery (aortic surgery, laparoscopy, liver transplantation).
2. Patients with blunt or open abdominal trauma, who have undergone emergency laparotomy.
3. ICU patients under mechanical ventilation with other organ dysfunction (especially with signs of liver failure)
4. Patients presenting the following clinical manifestations: tensely distented abdomen, rising peak ventilatory pressure, elevated central venous pressure, decreased CO, hypoxia, hypercapnia, oliguria.
5. Cases of burns, massive fluid resuscitation.
6. Abdominal pathology: acute pancreatitis, hemoperitoneum, ileus, intraabdominal sepsis.
Effects of intraabdominal hypertension
on organ failure
Effects on central nervous system
Multiple recent studies on animal models as well as humans, have shown a high correlation between IAP and intracranial pressure (ICP). In both animals and humans a rise of IAP was combined with increase of ICP as well as a limitation of cerebral perfusion pressure (CPP) (13-16). It has been hypothesized that the increase of IAP in the critical patient leads to an upward displacement of the diaphragm; thus an increase of intrathoracic pressure, elevation of jugular venous pressure impairment of cerebral venous return and intracranial
congestion, which is responsible for the following decrease of CPP (7, 13-16). Subsequent sternotomy or pleuro-pericardiotomy (16) or abdominal decompression (13, 15), according to various studies, are followed by an obvious decrease of intracranial pressure or even prevention of its rise, confirming the previously suggested mechanism.
The cranial cavity consists of osseous structures, vascular structures, cerebrospinal fluid and the cerebral parenchyma. Normally, the pressure enclosed within this compartment can remain relatively stable with small increases of volume until a certain value of volume after which small volume increase results in a large rise of intracranial pressure (4). This characteristic should be kept in mind in cases where abdominal compartment syndrome is associated with intracranial lesions or severe cerebral trauma, already causing an intracranial
volume increase (e.g. hematoma, edema, intracranial tumors). In such conditions even a minor rise of IAP may result in extremely high ICP, particularly low CPP, with deleterious consequences especially in patients with hypotension or hypovolemia, due to progressive cerebral ischemia (13).
This evidence verifies, to a certain degree, the causes of idiopathic intracranial hypertension or pseudotumor cerebri development in the morbidly obese, as well as central nervous system deterioration which is observed in patients with severe abdominal trauma without cranial injury (3, 7, 12).
Effects on the cardiovascular system
Increased intraabdominal pressure pushes the diaphragm
superiorly and raises intrathoracic pressure, leading to a decrease of venous return, as well as a cardiac output limitation, due to increased superior and inferior vena caval pressure (3, 5, 8, 17-19). Usually IAP higher than 20 mm Hg is required for the appearance of the effects mentioned above (2,3). Cardiac compression caused by high intrathoracic
pressure is demonstrated by a decrease of cardiac index. Associated reduction of right and left heart end-diastolic ventricular volumes is observed, explained by low compliance and motion of ventricular walls (2, 4, 19).
Meanwhile, systemic and pulmonary vascular resistance is increased; the heart rate remains stable or may increase, and mean arterial pressure initially increases but afterwards decreases, and pulmonary arterial pressure increases (7, 18). The consequences of raised IAP are particularly more obvious in hypovolemic patients, leading to greater deterioration of cardiac function and aggravated clinical condition at equal IAP levels (2, 8, 18).
The significant cardiopulmonary disorders demonstrated in patients with IAH can affect the accuracy of PAOP and CVP measurements as estimates of intravascular volume
status (20). As both the central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) are often quite elevated, the physician may be misled to the wrong conclusion that the patient has an adequate intravascular volume, whereas in reality the patient is relatively hypovolemic (2, 4, 17, 19).
It seems that continued fluid resuscitation usually improves cardiac output and organ perfusion in patients with even significantly elevated PAOP and CVP values (12). Moreover, in a porcine model it was shown that the presence of IAH causes significant intravascular volume depletion, not related with the CVP values. A 30mmHg increase in IAP from normal level resulted in a 55% and 67% reduction in intrathoracic blood volume and total circulating blood
volume respectively. Meanwhile, a 27% decrease in cardiac output was observed, along with increased CVP (12, 19). In conclusion, intravascular pressures are not reflective of intravascular volumes. On the contrary, intrathoracic blood volume (ITBV) and right ventricular end-diastolic volume index (RVEDVI), as well as echocardiography, proved to
provide valid estimates of cardiac preload, even at high intrathoracic pressures, as is the case with IAH and ACS (4, 8, 19, 22).
Finally, there is an increased risk for peripheral edema and venous thrombosis, especially in obese patients, due to the increased femoral vein pressures and the reduced venous blood flow and the resulting rise in venous hydrostatic
pressure. This may lead to fatal pulmonary embolism on decompression (4, 12). Appropriate mechanical and pharmacological measures must be taken to decrease the risks of
pulmonary embolism.
These aforementioned deleterious effects on cardiac function may be aggravated by preexisting impairment of myocardial function (12).
Effects on respiratory system
The total compliance of the respiratory system is determined by the chest wall compliance and the lung compliance. The chest wall includes the anterior and posterior thoracic cage and the diaphragm, which is in direct contact with the abdomen, thus influenced by intraabdominal pressures. The expanding force of the lung is the transpulmonary pressure (alveolar minus pleural pressure), defined by the pressure applied to the airways and the relationship between lung and chest wall compliance. Consequently, in low chest wall
compliance values the same airway pressure may lead to
significantly lower transpulmonary pressure, greater pleural pressure, decreased lung distention, and thus severe hemo-dynamic effects.
In patients with IAP the upward movement of the diaphragm causes reduction of chest wall and lung
compliance, increasing intrapleural pressure, decrease of
ventilation and increase of pulmonary vascular resistance (2, 7, 8, 19, 23).
The main respiratory problem in ACS patients is the development of compression atelectasis of the lung parenchyma, mainly in the caudal parts, caused by the elevation of the diaphragm. This results to alveolar collapse, creating a shunt of unoxygenated blood, plus the appearance of ARDS due to increased alveolar permeability and edema development (12, 19, 20, 24, 25). Thus ventilation-perfusion mismatch appears, with obvious clinical hypoxia, hypercapnia and acidosis (3, 6, 8, 25). In addition, all static and dynamic lung volumes
(functional residual capacity, total lung capacity, residual
volume) are decreased, mimicking a restrictive pulmonary
disease (5, 7, 24). Adequate ventilation can be achieved only with increased airway pressure. Adequate oxygenation and ventilation is possible through mechanical ventilation with high positive end-expiratory pressure (PEEP) (6, 26) but poor compliance develops secondary to high airway pressures. Hence, the elevated peak airway pressure accompanies ACS. The problem is manifested by a marked increase in peak
inspiratory pressure (PIP) and decreased dynamic and static lung compliance, while the patient is difficult to ventilate (10, 20, 25, 26). Extreme caution is required for the possibility of acute lung injury development due to overinflation during management of hypoxygenation by mechanical ventilation. Efforts towards ventilation improvement through abdominal decompression (4, 24), appropriate body position or even weight application on the upper chest, in order to balance the compression of the basal regions, are considered more
effective and less perilous (5).
Respiratory problems caused by increased intraabdominal pressure may complicate the clinical condition of patients under non-invasive positive pressure ventilation. NIPPV is a commonly applied management of acute respiratory failure and it decreases the risk of intubation. However, this method may present variable complications, including gastric
distention due to aerophagia, leading to high IAP and
manifestation of ACS (5, 11). This complication is responsible for the appearance of increased parasympathetic tone, thus bradycardia or even asystole. Moreover, abdominal distention may evolve to the point of compressing the thoracic cavity, resulting to reduced lung volumes, impaired gas exchange and high ventilatory pressures, enhancing the risk of barotraumas as well (4). The development of compression atelectasis induces activation of lung neutrophils, leading to pulmonary inflammatory infiltration and alveolar edema, increasing in this way the risk of infection, already high due to mechanical ventilation (27). Cardiovascular and respiratory problems in patients under NIPPV automatically improve after the insertion of a nasogastric tube (26). In conclusion, the development of ACS in these patients should be highly suspected and repeated abdominal clinical examination should be
conducted. If IAH is suspected IAP should be measured, and in pressures greater than 10 mm Hg the introduction of a nasogastric tube is considered indispensable. This is especially important in hypovolemic patients, who present greater
sensitivity in the complications of IAH and in obese patients when placed in the upright position (11, 25).
Effects on renal system
Renal impairment in patients with IAH is demonstrated by profound oliguria and in late stages, by anuria. It has now bean suggested that an IAP value of 10 to 15 mm Hg is required for oliguria to develop, while IAP of more than 30 mm Hg is responsible for anuria (6, 12, 28-30).
Reduction of cardiac output, directly applied pressure on renal vein and renal parenchyma, as well as compression of the abdominal aorta and renal arteries, lead to decrease of renal arterial blood flow and perfusion pressure, thus reduction of pressure gradient across the glomerular membrane and thereby the glomerular filtration rate (GFR) (7, 9, 31). A large increase in renal vascular resistance also occurs, resulting in blood redistribution between the cortex and the medulla and creation of corticomedullary shunting of renal plasma flow, reducing effective renal plasma flow (3, 7, 30).
These evident changes in renal and systemic haemo-dynamics enhance the secretion of renin, followed by increased levels of circulating angiotensin II and aldosterone, along with an associated increased secretion of anti-diuretic hormone, all responsible for further renal vascular resistance elevation, reduction of renal blood flow and GFR (8, 30, 31). Elevated aldosterone levels produce sodium and water retention, contributing to oliguria.
The role of direct ureter compression as an additional
factor for renal impairment in patients with IAH has been excluded because it has been demonstrated that the insertion of ureteric stents or catheters presented no improvement of diuresis (4,8). Moreover, it is obvious that improvement of
cardiac output or efforts towards renal function improvement by administration of dopaminergic agonists or diuretics have no significant positive impact (3, 30).
It seems that IAH is an independent factor for acute renal failure development among postoperative patients (12, 32). It is not clear however if a certain degree of preoperative renal derangement is already present in such cases (5). Multiple studies conducted upon the effects and the prognostic factors of acute renal failure caused by ACS suggested abdominal or renal perfusion pressure (MAP minus IAP) and filtration
gradient (MAP minus 2IAP) as useful prognostic parameters (4, 32). The situation is completely reversible with the
appearance of diuresis by performing abdominal decompression and reduction of IAH (3, 30 32, 33).
Effects on gastrointestinal system
Splanchnic ischemia
Splanchnic blood flow seems to be decreased in cases of IAH with several factors and mechanisms contributing to this haemodynamic effect. Compression of the portal vein, reduced chylus flow via the thoracic duct, direct pressure on mesenteric arteries lead to limitation of arterial blood
perfusion (2-4). Impaired blood and oxygen perfusion is demonstrated in mesenteric arterial, hepatic arterial, intestinal mucosal and portal venous circulation (3, 34, 35). Moreover, it has been shown in multiple experimental
animal models that an IAP>20 mm Hg correlates with reduced blood flow, apart from the intestine, to the
pancreas, spleen, kidney, though with paradoxically increased blood perfusion to the adrenal glands (8, 30). It has also been postulated that vasoconstriction agents such as catecholamines, angiotensin, and vasopressin secreted in reaction to IAH, are related to the actual mesenteric
vasoconstriction observed in ACS patients (7, 36, 37).
Hypoperfused mucosal tissue demonstrates a reduction of tissue O2 tension, anaerobic cell metabolism, acidosis, free radical generation, marked by low pH values (3, 38). It has been suggested that intramucosal pH measured by
gastric tonometry, is a sensitive clinical indicator of gut ischemia in the ACS patients (7, 38-40).
Intestine ischemia along with portal venous resistance
elevation, thus decreased venous outflow, cause abdominal visceral edema, which further aggravates IAH (36, 39). Gut ischemia caused by IAH may even lead to intestinal infarctions, an effect described during prolonged laparoscopy, although general haemodynamics and renal function may remain normal (7).
Bacterial translocation
Blood perfusion derangement related to the intestine is a causative factor for mucosal barrier impairment and increased intestine parietal permeability. Thus, elevation of IAH may lead to bacterial translocation through the
visceral wall, towards the mesenteric lymph nodes, the liver and the spleen (39, 41-43).
Moreover, although MOF frequently follows IAH, it has been difficult to suggest bacterial translocation as a pathogenic factor (42).
Multiple Organ Failure
As mentioned above, IAH and ACS have been related to a higher risk of MOF development and death (3, 6, 12), an argument enhanced by the study of Balogh et al, which demonstrated the higher incidence of MOF among major trauma patients managed by massive fluid resuscitation (44). The release of proinflammatory cytokines, induced by IAH, has been considered as a possible responsible factor, as has been shown in several recent studies on animal models (27). It seems that an IAP level of 20 mm Hg causes such an increased level of TNFa, IL-6 and IL-1b, even more obvious in cases of ischemia-reperfusion, fluid resuscitation after hemorrhagic such as shock (45). Splanchnic ischemia and bacterial translocation have also been related to MOF after IAH (41, 43) among patients with intestinal hypoperfusion, mucosal hypoxia, either through inducing the secretion of proinflammatory cytokines or by septicemia or endotoxemia alone. More research is required in order to clarify the
relationship between IAH and MOF and the potential provocative mechanisms.
Hepatic Effects
Hepatic blood flow
Animal experiments have demonstrated an obvious reduction of hepatic blood perfusion in IAH cases, marked by an IAP greater than 10 mm Hg (36, 46). This effect is due to a decrease in portal venous flow and a limitation of hepatic arterial flow as well, the second observed in higher levels of IAP (20 mm Hg) (46, 47). This parallels the impairment of hepatic microcirculation and mitochondrial dysfunction (43), appearing with affected laboratory findings concerning the liver enzymes and bilirubin level, as well as paracentral necrosis in histological examination. The release of endotoxin in portal circulation caused by intestinal ischemia may further aggravate parenchymal dysfunction (48).
Cirrhosis and esophageal varices
Among patients with pre-existing cirrhosis and esophageal varices, an elevation of intra-abdominal pressure leads to increased variceal pressure, wall tension, radius and volume. This data summarizes the conclusion of a recent study of Spanish investigators who observed the effects of IAH on bleeding esophageal varices after increasing the IAP by 10 mm Hg using an inflatable girdle in 14 patients (49). The rise of variceal pressure contributes to a progressive dilatation of these vessels that precedes rupture of varices in portal hypertension. Such patients should take extreme caution to avoid rising of IAP during physical activity, e.g. weight lifting, while constipation and recurrence of ascites should be prevented.
It should be mentioned that recently a significant but poor correlation between IAP and plasma disappearance rate of indocyanine green (PDR-ICG) was found (50). Injected ICG binds immediately to plasma proteins and is absolutely cleared by the liver, deviating enterohepatic microcirculation. A low rate of ICG clearance is a poor prognostic factor for an IAH patient.
Effects on extremity perfusion
Increased intra-abdominal pressure prevents venous reflux from the extremities as well, demonstrated by an elevated femoral venous pressure, although increasing peripheral
vascular resistance, thus leading to a reduction of femoral artery blood flow of as much as 65% (51).
Effects on abdominal wall
The compliance of the abdominal wall is primarily affected by a rising of IAP and in fact the abdominal wall pressure-volume curve is not linear. Progressively smaller increases in volume are required in order to cause a stable rate of IAP increase, creating a rising stiffness of the abdominal wall (7). The general circulation impairment induced by IAH further compromises the abdominal wall, producing a vicious circle of increased edema, hypoxygenation, thus limitation of abdominal wall compliance, back to increasing IAP (16, 52). A
progressive increase of IAP from 10 to 40 mm Hg in a pig model led to reduction of abdominal wall blood flow to 20% of baseline and fascial ischemia. The consequences may be delayed or incomplete abdominal wall wound healing, with complications of dehiscence and infection (2, 8, 53).
Management of ACS in ICU patients
Prevention is always better than cure. Early identification of the patients at risk for ACS development is the key to avoid its deleterious consequences. However, active detection of ACS is not a common practice in many ICUs and clinical examination alone is not reliable to pose the suspicion at these patients. Several statistical studies have demonstrated independent predictive factors for ACS. Balogh Z. et al (6) suggested a distinction between primary and secondary ACS, with hypothermia, low haemoglobin concentration and high base deficit being statistically significant
predictive factors of the primary type. On the other hand, large crystalloid fluid infusion volume and impaired renal function were revealed as secondary ACS predictors. Mc Nelis J et al (29) identified increased 24-hour fluid balance and increased peak airway pressure (PAP) as the factors
predictive of ACS formation.
Decompressive laparotomy remains the gold standard method of management for patients developing ACS (4, 6, 10, 18, 53-55). There lies the problem of decision upon its application. The value of Urine Bladder Pressure (UBP) is widely accepted as a satisfactory indicator for decompression (3). It has recently been suggested that follow-up of IAP through the UBP should be indispensably performed in all patients after damage control laparotomy and under
consideration in those with complex abdominal pathology, massive fluid resuscitation and burns (3, 10). Moreover,
checking of urine output, peak airway pressure, gastric
tonometry and liver function could provide early diagnosis and treatment in case of deterioration of these parameters (3, 7, 8, 53). Suggested indicative conditions for decompressive surgery are a UBP > 25 mm Hg associated with oliguria or the presence of IAP > 20 mm Hg and any significant
physiological abnormality, such as elevated PAP (> 45 cm H2O) or oliguria (urine output < 0,5 ml/kg/h) (7, 33, 56, 57). Thus, patients with IAP values between 15 and 20 mm Hg should be considered individually and managed according to the progression of organ dysfunction. Other studies suggest aggressive management in even lower values of IAP in case of intestinal ischemia and mucosal acidosis demonstrated by gastric tonometry (58, 59). In case of intestinal ischemia, not responding to optimization of oxygen delivery or intracranial hypertension, decompressive laparotomy is also indicated in IAP lower than 20 mm Hg (3, 15).
During decompressive laparotomy the abdomen should be thoroughly explored for sources of bleeding, hemorrhage should be controlled and the abdominal wall should be closed only if intra-abdominal volume is diminished (7, 60). In cases of intestinal edema temporary abdominal closure by the use of towel clips or sutures on the skin may be required. The choice between definitive fascial closure and temporary abdominal closure is based upon the IAP values and the possibility of developing ACS (60). Temporary abdominal closure may be even applied in patients at risk for the development of ACS in order to provide prevention of ACS and minimize fluid loss, produced in the case of an open abdomen (7), or even facilitate a second-look laparotomy, if required (5). Definitive abdominal closure may be conducted only if no further laparotomy is required and the patient presents a steady cardiovascular condition, with adequate oxygenation (7).
In any case, decompressive surgery is associated with reduced airway pressures, improvement of cardiac output and stabilization of urine output (8, 61). However, abdominal decompression itself is not a method free of complications. Patients may become hemodynamically unstable, sudden
respiratory alkalosis or hypokalemia may develop and cardiac arrhythmias or asystolic arrest may occur, possibly due to an ischemia-reperfusion syndrome (59). Considering the
additional risks of bleeding or infection, and the hernia complications, it is preferable that decompression is conducted in a controlled setting in the operating room (2, 8).
Some possible general supporting measures applied in patients with an IAP < 20 mm Hg with mild organ
dysfunction are paracentesis, gastric suctioning, rectal
enemas, gastroprokinetics, furosemide, continuous aggressive veno-venous hemofiltration application of negative abdominal pressure. Curarization and body-positioning may also be helpful (4, 5).
Conclusion
Elevation of IAP leads to a progressive deterioration of
physiological functions. Intra-abdominal hypertension affects negatively all systems including pulmonary, cardiovascular, renal, gut and neurological impairment, producing the abdominal compartment syndrome. Awareness of clinicians upon the identification of patients presenting predisposing and predictive factors for development of ASC is crucial for primitive management, thus limitation of morbidity and
mortality due to ACS. Such patients should undergo
continuous estimation by UBP measurement, checking of urine output, cardiac and respiratory function, as well as
gastric tonometry. Decompressive laparotomy is recognized as the only potential treatment, and if performed early, it
provides a higher possibility of survival.
Further research upon this entity will hopefully lead to an earlier recognition and more effective management of ACS.
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