A compartment syndrome may occur in any body region where “increased pressure within a limited space compromises the circulation and function of tissue within that space”.1 The most commonly recognised is acute compartment syndrome within a limb. It is now appreciated that compartment syndromes may affect other body regions where there is potential for increased pressure, leading to capillary congestion and impaired perfusion, with subsequent inflammatory and ischaemic changes. This may result in either a limb or life-threatening situation that requires urgent recognition and treatment.2 3

Abdominal compartment syndrome (ACS) is not a new concept. It has been recognised for many years that there is a link between increased abdominal pressures and poor urine output. There are also deleterious effects of closing a tight abdomen on recovery from laparotomy, and possible wound dehiscence.4 However, it was not until the last 20 years that recognition of this condition became more widespread, and now there is clearer understanding of the pathophysiology and consequences of ACS when left untreated.

There has been a recent surge in interest concerning ACS, but little has been published in the emergency medicine literature. However, an understanding of ACS and how management in the emergency department (ED) can influence the development of the condition are essential if the effects are to be minimised during the subsequent phase of treatment. A high index of suspicion for ACS in susceptible patients, together with early measurement of intra-abdominal pressure (IAP), and early involvement of surgical and critical care teams, could prevent further complications and reduce mortality.

This paper aims to review the different causes and pathophysiology of ACS, with particular reference to why it should be considered, and how it may be detected and prevented by early intervention in the ED. It also describes the measurement and different treatment options available.

METHODS

A comprehensive search of the literature was carried out, using Medline and Pre-Medline 1966 to November 2006, Embase, and Evidence Based Medicine reviews (including the Cochrane database of systematic reviews and the Cochrane central register of controlled trials). Search terms included intra-abdominal pressure, intra-abdominal hypertension and abdominal compartment syndrome. The reference database from the World Society of the Abdominal Compartment Syndrome (WSACS) was also examined. The bibliographies of relevant papers were examined and cross-referenced. Papers were critically appraised for the quality of evidence presented. Studies were preferred in accordance with the usual hierarchy of evidence, namely controlled clinical trials, prospective studies (including case control studies) and case reports. Review articles were examined for their reference lists.

DEFINITIONS

A compartment syndrome can occur in any area of the body where increased pressure can result in impaired capillary perfusion within the compartment, and subsequently impaired function at a cellular level. Most obvious are those inside the closed fascial space within a limb, but this can be extended to include intra-thoracic conditions such as tension pneumothorax, and intracranial conditions such as a traumatic haematoma and cerebral oedema causing impaired cerebral perfusion. Within the abdomen a similar situation can arise as a result of a rise in IAP, causing intra-abdominal hypertension (IAH) and subsequent ACS.

As with all newly recognised conditions there has been some debate regarding definitions. In December 2004 the first meeting of the World Society of the Abdominal Compartment Syndrome (WSACS) developed a consensus on these definitions which were subsequently ratified and published (table 1).5

When considering the perfusion of intra-abdominal organs at a cellular level, the abdominal perfusion pressure (APP) can be used. This may be a theoretical equation rather than a measurable and real entity, but it gives the clinician an appreciation of the factors contributing to the development of organ dysfunction in ACS. As with many clinical measurements, it should be stressed that in reality trends of values may be far more useful than absolute values.

MEASURING INTRA-ABDOMINAL PRESSURE

The method of measurement of IAP has also been a matter for some debate, with the need to balance accuracy with practicality. Different methods have included direct peritoneal cannulation, rectal, vesical, gastric measurements, and also via the inferior vena cava. It has been demonstrated that clinical examination is not an accurate way to identify those patients with IAH; a study in Australia published in 2002 showed intensive care unit (ICU) physicians had a less than 50% chance of correctly identifying IAH.6 There are advocates of continuous7 8 and intermittent9 monitoring, with no clear consensus.

It would now appear that intravesical pressure monitoring has been adopted as standard practice10^–16 and is the most commonly used to measure IAP within the UK.17 This method is relatively simple and can be performed easily and quickly within any ED. Cheatham and Safcsak describe this method in more detail elsewhere,11 but in summary it is performed by taking an angiocatheter or needle, which is then connected via a length of tubing to two serially connected three-way stopcocks. These are then connected to either a transducer or a manometer. (The authors of the original article suggested an 18 gauge angiocatheter—if a needle is used care should be taken to avoid a needlestick injury). Attached to the stopcock closest to the urinary catheter is a 50 ml syringe and attached to the other tap is a reservoir of a 1 litre bag of normal saline, connected via a giving set.

After priming the system with saline, the needle or catheter is then inserted into the urine aspiration port of the catheter collection system. The bladder is emptied and then the urinary catheter clamped; 25 ml of normal saline is drawn from the reservoir into the syringe and this volume is then infused into the bladder (to ensure the bladder wall is not adherent with the catheter). The three-way taps are then turned to allow the intravesical pressure to be read on the manometer or by the transducer. (It is noted that the original authors suggest using 50 ml of saline; this has been amended in line with the WSACS recommendation that intermittent IAP measurement via the bladder should use a maximum instillation volume of 25 ml of saline.5)

INCIDENCE OF ACS

The incidence of ACS is difficult to define because of inconsistencies in the definitions before 2004.18 No studies have specifically looked at incidence in the ED. One paper suggests an overall incidence of 1% in trauma ICU patients which can be as high as 14% in high risk (multiple injury and shocked) patients.19 Another study looking at 706 patients admitted to a trauma ICU found the incidence to be 1% for ACS and 2% for IAH.20 However, another study which looked at a 1 day snapshot of 13 ICUs in 16 countries8 found that 58.8% had a raised IAP (with IAH >12 mm Hg).

AETIOLOGY OF ACS

There are a large number of causes of ACS, which can be divided into primary, secondary or recurrent.

Primary ACS is associated with injury or disease within the abdominal cavity—for example, abdominal trauma, haemorrhage,21 22 massive ascites (though many patients with ascites can tolerate raised IAP due to what is thought to be an accommodation process over a period of time23), ileus and bowel obstruction, intraperitoneal sepsis, ruptured aortic aneurysm, laparoscopy with pneumoperitoneum, and acute pancreatitis. ACS is a recognised complication of damage control surgery; Offner et al described 52 patients who had damage control surgery, of whom 17 developed ACS.24 These patients were also at a higher risk of developing acute respiratory distress syndrome (ARDS), multi-organ failure, and death.

Secondary ACS refers to conditions that originate outside the abdomen or pelvis. It was first described in the early 1990s after a review of the care of burns patients,25 but the phrase was not coined until 1999.26 The major cause of secondary ACS is massive fluid resuscitation and sequestration of fluid in the extracellular interstitial space within the abdomen. Examples are severe burns27 28 (either early during the resuscitation phase, most especially if large amounts of fluid are used, or later when sepsis evolves), major sepsis, and shock of any cause (cardiogenic, haemorrhagic, septic).29 30 This problem often originates in the ED where large volumes of fluid are necessarily transfused to maintain end organ perfusion. There are also case reports of ACS secondary to non-invasive ventilation,31 tension pneumothorax32 and penetrating chest injury.33 All involve a similar common pathway which leads to ACS.34

Recurrent ACS occurs when primary or secondary ACS has been treated either medically or surgically, but IAH and organ dysfunction persists or worsens.5

Box 1 lists those patients who may present to the ED who should be considered at a higher risk of developing IAH and ACS.

PATHOPHYSIOLOGY

As in limb compartment syndrome, the initial effect is on low pressure vessels (that is, capillaries and veins). The increase in abdominal pressure reduces venous return and leads to an increase in intracapillary pressure. This increases hydrostatic pressure within the vessels, leading to oedema and a deleterious cycle is commenced. The abdominal compartment is relatively large and even considerable intraperitoneal haemorrhage may have little effect on the abdominal pressure. It is the inflammatory response causing oedema within the abdomen which leads to the significant morbidity and mortality associated with ACS.37 A recent study in rats has also shown that IAH provokes the release of proinflammatory cytokines, which it is felt may serve as a secondary insult for the induction of multi-organ failure.38 The increase in interstitial fluid causes the abdominal pressure to increase, affecting systems both within and outside the abdomen.

SYSTEMS AFFECTED BY ACS

Renal system

Oliguria is a recognised sign of IAH and ACS. As early as 1947, Bradley and Bradley39 demonstrated that in the presence of increased IAP there was a reduction in renal plasma flow and glomerular filtration rate (GFR). Work in animal models has confirmed this, and has demonstrated that increased IAP reduces venous return from the kidneys by direct compression, leading to an increase in renal vascular resistance and a subsequent decrease in GFR. This leads to a reduction in urine output and eventually renal failure, which seems to be reversible with timely management.40

Cardiovascular effects

Cardiac output is reduced by a number of mechanisms. Firstly there is reduced venous return to the heart, secondary to compression of the IVC and the hepatic vein.37 ACS causes increased intrathoracic pressure, which reduces left ventricular compliance and therefore cardiac contractility, reducing cardiac output. The increased intrathoracic pressure leads to an apparent increase in central venous pressure (CVP). As CVP is often used as a guide to resuscitating patients, this can result in them being insufficiently fluid loaded. In a study of 16 severe burns patients it was found that using CVP to guide fluid resuscitation was inaccurate as IAP and IAH had such an effect on the CVP.41

Respiratory system

Increased abdominal pressure has an effect on the respiratory system. The increased IAP acts to splint the diaphragm and proportionally increases intrapleural pressure, reducing vital capacity and lung compliance. It also results in an increase in airway pressure.

Patients who reach this stage often require positive pressure ventilation to maintain oxygenation.

Visceral effects

The increased IAP also compresses organs within the abdomen. As already mentioned the kidneys in particular are affected, as are the liver and bowel.42 43 Splanchnic blood flow is reduced secondary to reduced cardiac output and reduced perfusion pressure. This leads to visceral hypoperfusion and bacterial translocation. This has been demonstrated in rat models44 and it has been suggested that bacterial translocation is the “motor” for development of multi-organ dysfunction.45

Ivatury et al have suggested that splanchnic hypoperfusion and gut mucosal acidosis commence at much lower pressures than other clinical markers of ACS and therefore should be treated early (drawing an analogy with limb fasciotomy).2 Balogh et al have suggested that GAPCo2 (gastric mucosal CO₂– end tidal CO₂) may be a useful early marker for ACS using gastric tonometry.19 Kirkpatrick suggests that in primary ACS caused by intraperitoneal haemorrhage, homeostatic responses that reduce gut perfusion (as perfusion to other organs is preserved) increase gut ischaemia and therefore bacterial translocation. Bowel oedema is then worsened by impaired venous return caused by the increase in IAP.46

Cerebral effects

The possibility of a raised IAP causing a rise in intracranial pressure (ICP) (therefore reducing cerebral perfusion pressure) seems to stretch the imagination, but Bloomfield et al have demonstrated exactly this in an animal model.47 The transmission of high IAP to the thorax, causing a rise in CVP and impaired venous return from the brain, is thought to be the cause.

In patients with moderate to severe head injury, Citerio et al have confirmed that by increasing the abdominal pressure (by placing weights on the abdomen), intracranial pressure was seen to rise.48 They felt that IAP should be monitored in patients with head injury as a redeemable cause of increased ICP.

Other sequelae

When ACS is relieved at laparotomy there is often a sudden improvement in both the patient’s respiratory and cardiovascular function. However, a reperfusion effect similar to that seen when limb compartment syndrome is relieved can occur, with release of intracellular contents into the circulation, with the potential to cause cardiac arrhythmias and metabolic acidosis.49 It has been reported that risk of asystolic cardiac arrest can be up to 25% at decompression.50

WHAT CAN WE DO TO PREVENT IT?

Early anticipation and recognition of the problem in the ED has the potential to minimise the effects of this important condition. In particular, early control of haemorrhage in trauma and judicious use of fluid when practical could prevent cases of ACS. For example, the current vogue of early goal directed therapy in the ED and ICU has been shown to improve survival in severe sepsis51 and in severe burns, but patients typically receive large quantities of crystalloid in the first 24 h following injury.52 These regimens include aggressive fluid resuscitation, which may result in secondary ACS.30 46 The question is whether this iatrogenic component to the development of ACS can be averted by using different therapies in patients known to be at risk. Goal directed treatment does have its detractors. There is some evidence that it may worsen outcome in some patients who are at risk of developing ACS. In one study examining 152 trauma ICU patients, goal directed resuscitation to improve cardiac function was ineffective and 15% of patients developed ACS.53

Oda et al have suggested that hypertonic lactate saline (HLS) should be used in burns patients, as it reduces the intravenous fluid load and therefore the risk of ACS.54 In their study, 36 patients with >40% burns were split into two groups, one receiving HLS and the other receiving Ringers lactate. The HLS group needed less fluid to maintain their urine output; 14% of HLS versus 50% of the Ringers lactate group developed IAH.

Biffl et al looked at 14 patients who developed ACS in an attempt to ascertain who should be monitored for ACS. They suggest that any patient receiving more than 10 litres of crystalloid, or 10 units of blood, should have their IAP measured, although this would still have missed two of their 14 patients.29

In trauma patients, management in the ED focuses on control of haemorrhage while maintaining critical perfusion. The potential for development of secondary ACS is even more reason to control haemorrhage early, as this will reduce the requirement for fluid resuscitation and blood transfusion.30 It should be remembered that secondary ACS is a consequence of a difficult compromise between adequate resuscitation and over-resuscitation. Kirkpatrick et al argue that secondary ACS is often iatrogenic but not always avoidable.55

With regard to primary ACS, avoiding primary closure of a tight abdomen in theatre is known to reduce the incidence of IAH and ACS.56 In the presence of visceral oedema or following damage control surgery, the abdomen may be left open (laparostomy). In a series of patients undergoing damage control surgery, Offner et al showed a reduced risk of ACS if primary fascial closure was avoided (necessitating the use of a Bogotá bag or simple skin closure).24

AWARENESS OF THE CONDITION

No published studies have specifically looked at awareness among ED staff. A paper published in 2004 looked at the attitudes of British intensive care doctors to IAP. There was a widespread awareness of IAH and ACS, but 24% of responding units had never measured IAP.17 In another questionnaire study from the UK, 73% of district general hospitals and 97% of teaching hospital ICUs had dealt with ACS. That said, the threshold and method for diagnosing ACS was variable, as were the treatments prescribed.57

A survey of members of the Trauma Association of Canada reported that despite a confidence in understanding ACS, 66% felt that physical examination was a useful diagnostic tool in ACS58 and only a half of responders routinely screened for ACS. There was no consensus regarding definitions of open abdomen, or how ACS should be managed.

TREATMENT OF ACS

If ACS cannot be prevented it at least needs to be anticipated and treated early to prevent complications and reduce morbidity and mortality.2 The treatment options are surgical, with abdominal decompression at laparotomy, and conservative.

Some authors suggest the only treatment for ACS should be abdominal decompression, with the main question being when to undertake the surgery.37 However, other non-operative measures have been utilised in an attempt to reduce the need for surgery (box 2).

CONCLUSION

ACS is now a well recognised problem in critical care patients, and where there are risk factors for ACS, patients should be identified in the ED and early monitoring of IAP should be initiated.

Measures to reduce the incidence of secondary ACS as a result of massive fluid resuscitation include early surgical control of haemorrhage. Permissive hypotension until control of haemorrhage has been achieved will also minimise fluid load. Treatment options include some non-operative measures but often surgical decompression is necessary. There is a need for more class 1 and 2 evidence to support management of this difficult group of patients, and it is hoped that now there is a consensus on definitions and a broader awareness of the condition this will be possible in the future.