Intra-abdominal hypertension and the abdominal compartment syndrome


  • J. D. Hunter,

    1.  Consultant Anaesthetist, Department of Anaesthetics and Intensive Care, Macclesfield District General Hospital, Macclesfield, UK
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  • Z. Damani

    1.  Specialist Registrar, Royal Liverpool and Broadgreen University Hospitals, Royal Liverpool University Hospital, Prescot Street, Liverpool, UK
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Dr J. D. Hunter


The pressure within the abdominal cavity is normally little more than atmospheric pressure. However, even small increases in intra-abdominal pressure can have adverse effects on renal function, cardiac output, hepatic blood flow, respiratory mechanics, splanchnic perfusion and intracranial pressure. Although intra-abdominal pressure can be measured directly, this is invasive and bedside measurement of intra-abdominal pressure is usually achieved via the urinary bladder. This cheap, easy approach has been shown to produce results that correlate closely with directly measured abdominal pressures. Significant increases in intra-abdominal pressure are seen in a wide variety of conditions commonly encountered in the intensive care unit, such as ruptured aortic aneurysm, abdominal trauma and acute pancreatitis. Abdominal compartment syndrome describes the combination of increased intra-abdominal pressure and end-organ dysfunction. This syndrome has a high mortality, most deaths resulting from sepsis and multi-organ failure. Detection of abdominal compartment syndrome requires close surveillance of intra-abdominal pressure in patients thought to be at risk of developing intra-abdominal hypertension. The only available treatment for established abdominal compartment syndrome is decompressive laparotomy. Prevention of abdominal compartment syndrome after laparotomy by adoption of an open abdomen approach may be preferable in the patient at significant risk of developing intra-abdominal hypertension, but this has not been demonstrated in any large trials. Most surgeons prefer to adopt a ‘wait and see’ policy, only intervening when clinical deterioration is associated with a significant increase in intra-abdominal pressure.

The adverse effects of intra-abdominal hypertension were first described in the late 19th Century when the association between intra-abdominal hypertension and oliguria was first reported [1]. Further papers detailing the adverse effects of intra-abdominal hypertension on cardiovascular, renal and pulmonary function followed in the first half of the 20th Century [2,3]. Interestingly, it was an anaesthetist from Dublin who first suggested that postoperative intra-abdominal hypertension might be associated with an adverse outcome. Baggot described the deleterious effects of forcing distended bowel back into the abdominal cavity and attempting abdominal wound closure under tension after a dehiscence or ‘abdominal blow-out’[4]. Despite these early reports detailing the adverse effects of intra-abdominal hypertension, it was not until the 1980s that clinicians began fully to appreciate the significance of increased abdominal pressures. Kron et al. were the first to measure intra-abdominal pressure after surgery, and to use this as a criterion for abdominal decompression [5]. They reported 11 patients with postoperative oliguria associated with an intra-abdominal pressure > 25 mmHg. Decompressive laparotomy was attempted in seven of the patients, and resulted in an immediate improvement, whereas non-surgical intervention in the remaining four patients was associated with the development of acute renal failure and death. This prompted the authors to suggest that if intra-abdominal pressure exceeds 25 mmHg in the postoperative period and is associated with renal dysfunction despite adequate cardiac output and circulating blood volume, then decompression of the abdomen should be considered. The authors coined the term abdominal compartment syndrome to describe this combination of increased intra-abdominal pressure and organ dysfunction.

Patients with abdominal compartment syndrome are not infrequently managed in the intensive care unit, and typically present with a tense distended abdomen, increased peak inspiratory airway pressures, severe hypercapnia, hypotension and oliguria. Measurement of intra-abdominal pressure via the intravesical route is easily achieved and confirms the diagnosis.

Intra-abdominal hypertension

The intra-abdominal pressure in a normal individual ranges from slightly subatmospheric to approximately 6.5 mmHg, and varies with the respiratory cycle [6]. Patients whose lungs are being mechanically patients show a slight increase in intra-abdominal pressure due to transmission of pleural pressures across the diaphragm [7]. The exact value of intra-abdominal pressure that defines intra-abdominal hypertension has not yet been defined. Although an intra-abdominal pressure of > 20 mmHg is clinically significant in nearly all patients, recent studies demonstrate that even at the relatively low intra-abdominal pressure of 10–15 mmHg significant alterations in organ function can be seen [8–11].

Since the contents of the abdomen are relatively non-compressible and contained within the confined space of the abdominal cavity, any increase in the volume of the retroperitoneal or abdominal contents will result in an increase in intra-abdominal pressure. Clinically significant intra-abdominal hypertension is therefore observed in a large number of conditions that are commonly encountered in the intensive care unit (Table 1). The incidence of intra-abdominal hypertension varies with the casemix studied and the cut-off pressure used to define intra-abdominal hypertension. The majority of studies suggest that the highest incidence of intra-abdominal hypertension is observed in patients who have undergone emergency laparotomy for abdominal trauma, and that massive fluid resuscitation is as a major contributory factor [12].

Table 1.  Common causes of increased intra-abdominal pressure.
Abdominal trauma
 use of abdominal packs
 postresuscitation visceral oedema
 pelvic or retroperitoneal bleeding
 intraperitoneal bleeding
Tense ascites
Liver transplantation
Postoperative intra-abdominal haemorrhage
Acute pancreatitis
Intestinal obstruction
Laparoscopy with pneumoperitoneum
Ruptured abdominal aortic aneurysm

Measurement of intra-abdominal pressure

Measurement of intra-abdominal pressure can be performed using several different techniques. Inserting a catheter directly into the peritoneal cavity and attaching it to a pressure transducer gives a direct pressure measurement [2]. Direct intra-abdominal pressures can also be obtained during laparoscopy [13]. These methods are invasive, risk the introduction of infection and are not appropriate for use in the critically ill patient. Intra-abdominal pressure is usually measured indirectly. Pressures recorded from the urinary bladder, the inferior vena cava and the femoral vein give an accurate reflection of intra-abdominal pressure [14]. Kron et al. first described the intravesical route of pressure measurement in 1984, and this is the most practical and straightforward route for everyday measurement in the intensive care unit [5]. Since the bladder is an intra-abdominal structure with a very compliant wall, instillation of the bladder with 50–100 ml of fluid allows the bladder to act as a passive reservoir. Changes in intravesical pressure therefore reflect changes in intra-abdominal pressure. Iberti et al. demonstrated a close correlation between bladder pressure measurements obtained from a transurethral catheter and direct intraperitoneal pressure monitoring [15]. More recently, the relationship between intra-abdominal pressure and intravesical pressure was studied using laparoscopy to measure intra-abdominal pressure directly. This study demonstrated that although intravesicular pressure closely approximated the intra-abdominal pressure using bladder volumes up to 200 ml, the closest correlation between intra-abdominal pressure and intravesical pressure was obtained when 50 ml of fluid was injected into the bladder [16]. It may be that overdistension of the bladder stimulates detrusor muscle activity and thereby leads to inaccuracies.

It is relatively straightforward, quick and cheap to record the pressure in the urinary bladder using equipment commonly available in the intensive care unit (Fig. 1). A 1 l bag of normal saline is used to provide fluid for bladder instillation. This is connected to two three-way taps, a pressure transducer and a 50 ml Luer-lock syringe via a standard giving set. A plastic cannula or needle is then inserted into the specimen collecting port of the urinary catheter, and connected to the giving set assembly using arterial pressure tubing. After flushing with saline, the pressure transducer is zeroed to atmospheric pressure using the level of the symphysis pubis as the reference point. The urinary catheter is then clamped immediately distal to the specimen collecting port. Using the three-way taps to direct flow in the appropriate direction, saline 50 ml is drawn from the infusion bag using the syringe and is then injected into the bladder. The taps are then turned to ensure a continuous column of fluid exists between the bladder and the pressure transducer. After allowing time for equilibration, the patient's intra-abdominal pressure can then be displayed on the bedside monitor. This method allows repeated estimation of intra-abdominal pressure without risk of introduction of infection. If no pressure transducer is available, pressures can be measured using a simple, widely available water manometer [17].

Figure 1.

Modification of the Kron method for the intravesical measurement of intra-abdominal pressure [5].

When the intravesical route of pressure measurement is not appropriate, as in the presence of a tense pelvic haematoma or bladder trauma, the intragastric route can be used. Good reproducibility has been demonstrated when intra-abdominal pressure is measured via the bladder, the balloon of a gastric tonometer and a nasogastric tube [18,19].

Pathophysiology of increased intra-abdominal pressure

Intra-abdominal hypertension causes significant dysfunction of almost all organ systems. These physiological derangements become more pronounced and clinically significant when abdominal pressure is greater than 20 mmHg.


An intra-abdominal pressure > 20 mmHg has a profound influence on the cardiovascular system [20]. Haemodynamic compromise is due to complex alterations in preload, afterload and intrathoracic pressure. A decrease in cardiac output is observed due to an increase in afterload, in turn due to mechanical compression of the abdominal vascular beds, and a decrease in preload due to direct compression of the inferior vena cava and portal vein. Increased intra-abdominal pressure causes elevation of the diaphragm, which causes an increase in pleural and hence intrathoracic pressure [13,20]. The decrease in preload is exacerbated by this increase in intrathoracic pressure, which not only hinders venous return but also causes cardiac compression, leading to a decrease in ventricular end-diastolic volume [21]. A compensatory tachycardia is usually observed in response to the decrease in stroke volume.

Due to the increased intrathoracic pressure, indirect measures of cardiac filling such as central venous pressure and pulmonary artery occlusion pressure give inaccurate results and can be increased despite profound intravascular volume depletion [9]. This is normally seen when intra-abdominal pressures are > 30 mmHg. This paradox was demonstrated by Cullen et al., who studied the cardiovascular effects of massively increased intra-abdominal pressure (mean [SD] = 51 [7] cmH2O). Despite very high left and right atrial pressures, radionucleotide-gated pool scans and echocardiography showed an adequate ejection fraction averaging 55%, and ventricular volumes that were small or normal. The authors suggested that this discrepancy between filling pressures and end-diastolic volume was due to either the measured pressures not being transmural, i.e. respiratory pressures being transmitted, or a decrease in ventricular compliance [22].

The decrease in cardiac output caused by intra-abdominal hypertension is therefore exacerbated by hypovolaemia. Volume resuscitation leads to an improvement in cardiac output and stroke volume [9]. Studies suggest that right ventricular end-diastolic volume as measured with a modified pulmonary artery catheter gives a better indication of preload and cardiac filling than pulmonary artery occlusion pressure [23]. By decreasing venous return, intra-abdominal hypertension may cause venous pooling and stasis, which predisposes to venous thrombo-embolic disease. Appropriate mechanical and pharmacological measures must be taken to decrease the risks of pulmonary embolism [24].


Increased intra-abdominal pressure can lead to respiratory failure. Cephalad deviation of the diaphragm leads to a decline in lung and chest wall compliance, and a decrease in functional residual capacity, total lung capacity and residual volume [5,9]. The resultant increase in ventilation-perfusion mismatch and pulmonary deadspace leads to hypoxia, hypercapnia and the need for mechanical lung ventilation. Because of the changes in compliance of the lungs and chest wall, high peak airway and plateau pressures are often generated. The ensuing increase in intrathoracic pressure and hypoxic pulmonary vasoconstriction can lead to pulmonary hypertension [22,25,26].


Renal dysfunction secondary to increased intra-abdominal pressure is well described in the literature [27]. Sugrue et al. prospectively studied all patients admitted to an intensive care unit after abdominal surgery. A total of 263 patients were studied, and 107 (40.7%) were found to have intra-abdominal hypertension (intra-abdominal pressure > 18 mmHg). Thirty-five (32.7%) of the 107 patients with intra-abdominal hypertension developed renal impairment, compared with 22 (14.1%) of the patients with a normal intra-abdominal pressure (p = 0.004) [28]. Oliguria is observed at intra-abdominal pressures between 15 and 20 mmHg, which can progress to anuria when pressures exceed 30 mmHg. The pathophysiology of this renal dysfunction is likely to be multifactorial, and restoration of the cardiac output to normal does not appear to prevent it reliably [29–31]. However, decompression of the abdomen with a decrease in intra-abdominal pressure usually results in a diuresis [22,32,33].

Changes in cardiac output, direct compression of the renal vessels or renal parenchyma with diminished renal blood flow, an increase in renal vascular resistance and a redistribution of blood from the renal cortex to the medulla are some of the postulated mechanisms of renal dysfunction, and all result in a decrease in glomerular filtration rate [3,30,31]. An increase in both plasma renin levels and aldosterone levels have been reported in animals with experimentally increased intra-abdominal pressure. Plasma renin activity and aldosterone levels were both significantly decreased by intravascular volume expansion and decompression of the abdomen [34]. Compression of the ureters is not thought to contribute to renal dysfunction, as the insertion of ureteric stents does not result in an improvement in urine output [30].


Increased intra-abdominal pressure has an adverse effect on splanchnic haemodynamics, with decreased blood flow, microcirculatory abnormalities, decreased perfusion and, ultimately, tissue hypoxia [35]. Animal experiments using radioactive microspheres to measure intra-abdominal organ blood flow demonstrate a decrease in blood flow to all intra-abdominal organs, with the exception of the adrenal glands, when the intra-abdominal pressure is increased to > 20 mmHg [36].

The effect of increased intra-abdominal pressure on intestinal blood flow has been studied in anaesthetised pigs [37]. Intra-abdominal pressure was increased in a stepwise fashion by infusing crystalloid solution into the peritoneal cavity to a maximum pressure of 40 mmHg. Mesenteric artery blood flow and intestinal mucosal blood flow were assessed using an ultrasonic flow probe and a laser Doppler flow probe. A significant decrease in mesenteric arterial and mucosal blood flow was observed at an intra-abdominal pressure of 20 mmHg despite minimal changes in cardiac output. Mesenteric blood flow became progressively worse as the intra-abdominal pressure was increased. Similar experiments using Doppler flow probes to assess hepatic perfusion demonstrate a significant decrease in hepatic arterial blood flow and portal venous blood flow when the intra-abdominal pressure is as low as 10 mmHg [38]. Significant decreases in bowel tissue oxygenation have been demonstrated in animals with intra-abdominal hypertension [10].

Increasing gut mucosal acidosis and ischaemia as measured by gastric tonometry has been demonstrated with increasing intra-abdominal pressure [39]. A prospective study of 73 patients undergoing major abdominal surgery examined the relationship between increased intra-abdominal pressure and gastric intramucosal pH (pHi). Intra-abdominal pressure and pHi were measured thrice daily, and an intra-abdominal pressure ≥ 20 mmHg and a pHi≤7.32 were considered abnormal. The authors were able to demonstrate a significant association between increased intra-abdominal pressure and abnormal pHi, an abnormal pHi being more than 11 times more likely if intra-abdominal pressure was increased to > 20 mmHg [40]. An improvement in pHi has been demonstrated after abdominal decompression [41].

No human data exist to suggest that mucosal ischaemia secondary to increased intra-abdominal pressure leads to the translocation of bacteria across the gut mucosa. However, data from animal work suggests that this is a possibility, and may be a contributory factor in the development of sepsis and multi-organ dysfunction syndrome in patients with the abdominal compartment syndrome [42,43].

Abdominal wall

Wound complications such as dehiscence and infection are common in patients with intra-abdominal hypertension. This may be due in part to a decrease in abdominal wall blood flow leading to fascial ischaemia. The effects of intra-abdominal hypertension on abdominal wall blood flow were studied in a porcine model. Rectus sheath blood flow was measured using a laser flow probe, and intra-abdominal pressure was increased by instilling crystalloid into the peritoneum. A significant decrease in rectus sheath blood flow was demonstrated when intra-abdominal pressure was increased [44].


In addition to the adverse effects of intra-abdominal hypertension on systemic haemodynamics and oxygenation, it seems that intra-abdominal hypertension is an independent risk factor for the development of secondary brain injury after traumatic brain injury. The observation that increases in intra-abdominal pressure in a patient with a closed head injury and abdominal compartment syndrome was mirrored by an increase in intracranial pressure prompted further investigation of the relationship between intracranial and intra-abdominal pressures [45,46]. Animal experiments in which intra-abdominal pressure was artificially increased confirmed that acutely increased intra-abdominal pressure causes a significant increase in intracranial pressure [47]. Subsequent sternotomy and pleuro-pericardotomy to decrease pleural pressures led to an immediate decrease in intracranial pressure, suggesting that the intracranial hypertension was secondary to obstruction of cerebral venous outflow due to increased intrathoracic and central venous pressures. Human studies have since confirmed this relationship. A prospective, non-randomised study was performed on 15 patients with moderate to severe closed head injury. Measurements of intracranial pressure and intra-abdominal pressure were performed before and 20 min after a 15 l bag of water was placed on the patient's abdomen to increase intra-abdominal pressure. A significant increase in intracranial pressure was observed, accompanied by a rapid increase in central venous and internal jugular pressures, suggesting that the increase in intracranial pressure was as a result of a functional obstruction to cerebral venous outflow [48].

Although volume expansion in the patient with intra-abdominal hypertension and a closed head injury may increase intracranial pressure, there is a beneficial increase in cerebral perfusion pressure because of an improvement in systemic haemodynamics that may be advantageous [49].

Abdominal compartment syndrome

Abdominal compartment syndrome describes the combination of increased intra-abdominal pressure and organ dysfunction [50–52]. The term was first used nearly two decades ago to describe the deleterious effects of intra-abdominal hypertension after abdominal aortic aneurysm surgery [5]. The exact level of abdominal pressure that defines abdominal compartment syndrome has not been agreed, but it is generally accepted that the following criteria must be present to make a diagnosis of abdominal compartment syndrome:

  • • Intra-abdominal pressure > 25 mmHg
  • • Adverse effects on organ function such as a decrease in cardiac output, oliguria, hypoxia, hypercapnia and acidosis.

The incidence of abdominal compartment syndrome is influenced by the casemix studied and the criteria used to define the syndrome. Few prospective data examining its incidence in the general intensive care setting exists, and the majority of published data relate to patients with abdominal trauma. A prospective study by Meldrum et al. reported an incidence of abdominal compartment syndrome of 14% in patients who suffered severe abdominal trauma (Injury Severity Score > 15) [53]. Abdominal compartment syndrome was defined as an intra-abdominal pressure > 20 mmHg complicated by one of the following: peak airway pressure > 40 cmH2O, oxygen delivery index < 600 ml.min−1.m−2 and urine output <0.5−1.h−1. A more recent study investigated the incidence of abdominal compartment syndrome in 311 patients admitted to the intensive care unit after sustaining severe abdominal and/or pelvic trauma. Abdominal compartment syndrome was defined as an intra-abdominal pressure > 25 mmHg, with significant respiratory compromise, renal dysfunction, haemodynamic instability necessitating inotropic support, and a rigid or tense abdomen. A total of 17 patients (5.5%) developed abdominal compartment syndrome. This was caused by persistent intra-abdominal or retroperitoneal bleeding (n = 12, 70.6%), or visceral oedema (n = 5, 29.4%) [54]. Morris et al. reported that abdominal compartment syndrome occurred in 15% of more than 1175 patients requiring a laparotomy for abdominal trauma [55].

Prevention and management of abdominal compartment syndrome

The opportunity to prevent abdominal compartment syndrome in the at-risk patient usually presents after laparotomy. However, there is disagreement between surgeons as to whether it is more beneficial to prevent abdominal compartment syndrome by performing some method of temporary abdominal closure or whether one should perform primary fascial closure and adopt a ‘wait and see’ approach, only intervening when signs of abdominal compartment syndrome develop. Most surgeons appear to favour a more cautious approach, and current opinion does not support liberal use of an open abdomen technique to prevent abdominal compartment syndrome [51,56,57].

Patients identified as being at risk of developing intra-abdominal hypertension and abdominal compartment syndrome should therefore undergo close monitoring of intra-abdominal pressure, usually via the urinary bladder. As the development of intra-abdominal hypertension is usually gradual, measurement of intra-abdominal pressure every 8 h is generally adequate unless there is major intra-abdominal haemorrhage, when more frequent measurement is warranted [58].

Damage-control surgery

The development of abdominal compartment syndrome is a particular risk in those with severe abdominal trauma, especially when staged or ‘damage-control’ laparotomy is performed [59]. The theory behind this concept is that focused surgery with a short operating time minimises the vicious cycle of hypothermia, coagulopathy and acidosis. Surgical bleeding is rapidly controlled, non-surgical bleeding treated by intra-abdominal packing, and the minimal necessary bowel resection is performed to prevent gross contamination. If surgery is followed by primary fascial closure, the likelihood of developing intra-abdominal hypertension and abdominal compartment syndrome is extremely high. Continued intra-abdominal bleeding, bowel oedema secondary to massive crystalloid and colloid resuscitation, and bowel ileus all conspire to increase intra-abdominal pressure. In one series, 100% of patients who underwent damage-control laparotomy and primary fascial closure for severe abdominal trauma developed severe intra-abdominal hypertension after surgery [33]. These patients must therefore undergo close monitoring of intra-abdominal pressure, employing a low threshold for re-exploration and decompression of the abdomen if abdominal compartment syndrome is suspected.

Temporary abdominal closure

When there are risk factors for the development of postoperative intra-abdominal hypertension, such as massive bowel oedema, extensive retroperitoneal haemorrhage, gross abdominal contamination, etc., it is likely that primary fascial closure will result in tamponade of the intra-abdominal contents and the development of intra-abdominal hypertension and abdominal compartment syndrome. Many methods of temporary abdominal closure have therefore been described that allow definitive closure of the abdominal wall to be deferred until the factors responsible for the development of intra-abdominal hypertension have resolved [60].

Temporary closure of the abdominal wall should provide a tension-free and watertight coverage of the abdominal contents to prevent fluid losses and evisceration. Standard towel clips have been used for this purpose, a postoperative increase in intra-abdominal pressure prompting release of several of the clips [61]. Another inexpensive, popular method is to fashion a covering from a sterilised 3 l genitourinary irrigation bag – the so-called ‘Bogota bag’, named after its first description by Londoni in Bogota, Columbia [53]. This provides a watertight seal that has the advantage of being transparent, thus allowing inspection of the underlying viscera. Others advocate the use of non-absorbable prosthetic mesh, e.g. a Gore-Tex patch (W.L. Gore & Associates (UK) Ltd, Livingstone, Scotland). When this technique was used in 18 patients after emergency repair of ruptured abdominal aortic aneurysm or massive abdominopelvic trauma, only one patient subsequently developed abdominal compartment syndrome [60]. Another study examining the incidence of abdominal compartment syndrome after laparotomy for life-threatening penetrating abdominal trauma reported a significant decrease in the occurrence of intra-abdominal hypertension (> 25 cmH2O) in those patients who had mesh closure as prophylaxis for intra-abdominal hypertension [41]. Zipper techniques have also been described that facilitate re-exploration of the abdomen [62,63].

Postoperative monitoring of intra-abdominal pressure can be used to determine the optimal time for definitive abdominal closure. Good systemic oxygenation, euvolaemia and correction of coagulopathy are all necessary prerequisites. Unfortunately, fascial closure may not always be possible, especially if there is a prolonged delay in operation, and various surgical techniques, which are outside the scope of this review, have been described to overcome this problem.

Decompressive laparotomy

A favourable outcome for patients with established abdominal compartment syndrome requires timely recognition and treatment, as many of the adverse effects of intra-abdominal hypertension are reversible if the intra-abdominal pressure is promptly decreased [5]. However, the timing, indications and threshold for surgical decompression are controversial, with very few large trials available to give firm guidance [58]. Burch proposed a grading system (Table 2) based simply on intravesical measurement of intra-abdominal pressure to aid decision making, and recommended abdominal decompression when intra-abdominal pressure was > 35 cmH2O (25 mmHg), as abdominal pressures in excess of this are invariably accompanied by severe physiological dysfunction and clinical deterioration [50]. Most others advocate using markers of physiological deterioration such as oliguria, hypotension and acidosis in conjunction with abdominal pressure > 25 mmHg to determine the optimal time for intervention [51,56]. Worsening hypercapnia, deteriorating pulmonary compliance and excessively increased airway pressures often warrant surgical decompression. Persistent splanchnic hypoperfusion as measured by gastric tonometry may also be a useful aid in the decision making process [35]. Best management of these complex patients therefore requires very close cooperation between surgeon and intensivist. Packs should be removed, ascites drained and any haematoma evacuated. This is usually followed by temporary abdominal closure. Providing anaesthesia for the critically ill patient with abdominal compartment syndrome undergoing decompressive laparotomy is extremely challenging. Transporting a patient whose lungs are difficult to ventilate to the operating theatre may be very hazardous, and consideration should be given to performing the laparotomy in the intensive care unit. The patient should be well resuscitated before the abdomen is opened, and there should be full resuscitation facilities available. Adverse cardiovascular events including malignant arrhythmias and asystole have been described on abdominal decompression, and are presumed to be secondary to reperfusion of the abdominal viscera, resulting in a sudden increase in the blood levels of products associated with anaerobic metabolism [35]. An increase in pulmonary and chest wall compliance can result in hyperventilation if appropriate measures are not taken. Decompression commonly results in a decrease in central venous pressure, pulmonary artery occlusion pressure, mean arterial pressure and systemic vascular resistance. An increase in cardiac output is observed if the intravascular volume is optimised. A brisk diuresis usually follows successful decompression [64].

Table 2.  Burch grading system for intra-abdominal hypertension and abdominal compartment syndrome [50].
GradeBladder pressure; cmH2ORecommendation
I10–15Maintain adequate intravascular volume
II16–25Maintain adequate intravascular volume and closely monitor
III26–35Consider decompression
IV>35Perform surgical decompression


Although the adverse effects of increased intra-abdominal pressure have been recognised for many years, it is only recently that intra-abdominal hypertension has been recognised as a significant clinical problem. An increase in intra-abdominal pressure causes a graded derangement in physiology, with pulmonary, cardiovascular, renal, splanchnic and neurological dysfunction all being reported. Higher levels of intra-abdominal pressure are associated with clinical deterioration, and this combination of intra-abdominal hypertension and multiorgan dysfunction constitutes abdominal compartment syndrome. Abdominal compartment syndrome is associated with a high mortality, with potentially hazardous decompressive laparotomy the only recognised treatment. Identification of the patient at risk and timely intervention requires regular measurement of intra-abdominal pressure, which should be performed routinely in patients thought to be at risk of developing intra-abdominal hypertension. Consideration should be given to temporary abdominal closure after laparotomy in those patients with multiple risk factors for intra-abdominal hypertension.