Journal of Pediatric Critical Care

P - ISSN : 2349-6592    |    E - ISSN : 2455-7099

Year : 2016 | Volume : 3 | Issue : 4 | Page : 63-72

An Update on Intra-abdominal Hypertension and Abdominal Compartment Syndrome in children

Veena Raghunathan*, Maninder Singh Dhaliwal**, Praveen Khilnani***, Yatin Mehta****

* Consultant, Pediatric Intensive Care unit, Medanta, the Medicity, Gurgaon
** Senior Consultant, Pediatric Intensive Care unit, Medanta, the Medicity, Gurgaon
***Director, Pediatric Intensive Care Unit, BLK Hospital, Delhi
**** Chairman, Institute of Critical Care and Anaesthesia, Medanta, the Medicity, Gurgaon.

Correspondence Address:

Veena Raghunathan
Consultant, Pediatric Intensive Care unit, ICU 5, Medanta, the Medicity, Gurgaon – 122001, Phone number +91-9871221112, email id:
Received: 09-Oct-16/Accepted: 24-Oct-16/Published online: 22-Nov-16

Source of Funding:None Conflict of Interest:None


The concept of intra-abdominal hypertension and abdominal compartment syndrome is relatively new, but increasing awareness and evolving management strategies have been instrumental in reducing mortality by nearly half in critically ill patients with this condition. The thresholds for intraabdominal hypertension and abdominal compartment syndrome in children are different from adults. When intraabdominal pressure increases, it affects both abdominal and extra-abdominal organs. This needs to be recognised, the vicious cycle of poor perfusion and increasing intraabdominal pressure which ultimately leads to ischemic cellular necrosis. Focus has gradually shifted from treatment to prevention of progress of intraabdominal hypertension. Various non invasive methods can be used effectively to decrease intra-abdominal pressure, but surgical decompression is essential when organ dysfunction and abdominal compartment syndrome set in. This review describes the definitions, risk factors, pathophysiology and management strategies for increased intra-abdominal pressure in children.

Key words: intra-abdominal hypertension, abdominal compartment syndrome,children

The abdominal cavity has limited capacity to expand and hence is subject to increased pressure similar to other closed compartments in the body. Increased intra-abdominal pressure is common in critically ill patients and leads to organ dysfunction both within and outside the abdomen, resulting in increased morbidity and mortality. Kron et al coined the term abdominal compartment syndrome (ACS) in 1989 for the condition when increased intra-abdominal pressure leads to new/progressive organ dysfunction, and showed that mortality in ACS approaches 100% when untreated1. Increased awareness of the deleterious effects of increased intra-abdominal pressure lead to the formation of the World Society of the Abdominal Compartment Syndrome (WSACS) in 2004. In 2007, the society gave its first guidelines for diagnosis and management of this condition2. These guidelines were updated in 2013, and included specific pediatric definitions and considerations as laid out by a dedicated subcommittee 3. The following review is based on the updated guidelines.

Definitions and Concepts:
1. Intra-abdominal pressure (IAP): it is the steady state pressure present inside the abdominal cavity in supine position at end expiration. In the spontaneous breathing healthy child it is around 0 mm Hg. In a large prospective observational study in mechanically ventilated children, IAP was found to be 7 ± 3 mm Hg, irrespective of weight of the child4.
2. Abdominal perfusion pressure (APP) = Mean Arterial pressure (MAP)-IAP Similar to other organ perfusion indicators, [e.g.: cerebral perfusion pressure (Mean Arterial Pressure –Intra-cranial Pressure)], APP is thought to be a more accurate indicator of status of visceral perfusion in abdomen. It is hence probably a better parameter to be targeted than IAP alone. In adults a goal of APP = 60 mm Hg is generally considered to be adequate. In children however, there is lack of studies regarding APP affecting pediatric outcomes. Hence no guidelines on APP are available, but practically it seems beneficial to aim for IAP < 10 mm Hg, and to keep APP ≥ 35 mm Hg in infants and ≥ 50 mm Hg in children5.
3. Intraabdominal Hypertension (IAH): refers to a sustained elevation of intra-abdominal pressure without evidence of organ dysfunction IAP in critically ill children is approximately 4-10 mm Hg. A sustained pressure> 10 mm Hg has been proposed to define pediatric IAH.
4. Abdominal Compartment syndrome (ACS): In children, it is considered when sustained IAP > 10 mm Hg is associated with new / progressive organ dysfunction that can be attributed to elevated IAP. In adults on the other hand, the pressure cut offs that define IAH/ ACS are higher. IAH is defined as sustained IAP >=12 mm Hg in adults. It is further graded as follows: Grade I: IAP 12-15 mm Hg, Grade II: IAP 16-20 mm Hg, Grade III: IAP 21-25 mm Hg, Grade IV: IAP > 25 mm Hg. ACS is defined as sustained IAP > 20 mm Hg associated with new organ dysfunction/failure.
5. Polycompartment syndrome: is said to occur when ≥ 2 anatomical compartments have elevated compartmental pressures.

Types of IAH/ ACS
Primary IAH /ACS: It is a condition associated with injury or disease in the abdominopelvic region Secondary IAH/ACS: It is a condition that does not originate from the abdominopelvic region Recurrent/ Tertiary IAH/ACS: It is a condition in which IAH/ ACS redevelops after previous surgical or medical treatment of primary or secondary ACS.

Risk Factors for IAH/ACS6-8
Table 1 enumerates the various risk factors for development of IAH/ACS in critically ill children. The WSACS has recommended that intra-abdominal pressure measurement is indicated if a patient has any risk factor for development of IAH/ACS3.

Pathophysiology Effects of IAH/ACS
Abdominal compliance (Cabd) is defined as change in intra-abdominal volume (IAV) divided by change in intra-abdominal pressure. i.e Cabd =Δ IAV/Δ IAP. It depends mainly on the abdominal wall and to a lesser extent on the diaphragm. The abdominal compartment is a compliant structure under normal physiological conditions. As the intra-abdominal volume increase, intra-abdominal pressure is only minimally affected, until till critical volume is reached. Thereafter small changes in volume result in markedly increased pressures9. The relation of intra-abdominal volume and pressure is thus curvilinear (Figure 1). Decrease in abdominal wall compliance (in case of abdominal wall edema, tight abdominal closure, burn eschars or tight dressings) also leads to larger increase in intra-abdominal pressure change for small rise in volume. Conditions in which intra-abdominal volume increases or compliance decreases (or a combination of both) predispose to the development of IAH/ACS.

Physiological Effects of IAP
Blood flow to organs and tissues in normal conditions occurs along a pressure gradient from the heart to the capillaries in the organ/tissue. This flow is opposed by venous and interstitial pressures which are normally very low and do not exceed the perfusion pressure to the organ, thus allowing for adequate blood flow. As pressure increases in the abdominal compartment, it is transmitted to the interstitial spaces and microvasculature, thus hampering the perfusion to the intra abdominal organs. Inadequate perfusion leads to ischemia of the organs and consequently congestion and swelling. This swelling in the already compromised intra-abdominal space is further detrimental as it leads to increased compromise of vascular supply to organs and thus a vicious cycle of worsening perfusion and organ dysfunction leading to cellular necrosis and death10. Elevated pressure in the intra-abdominal compartment can adversely affect intra-abdominal organs and additionally lead to secondary multisystemic effects.

Intra-abdominal Structures
1. Vascular compression: Elevated pressures lead to compression of Inferior vena cava thus decreasing venous return and consequently cardiac output. This leads to increased levels of catecholamines and angiotensin II which in turn lead to increased systemic vascular resistance and vasoconstriction, thus hampering abdominal organ perfusion and further decreasing cardiac output.
2. Renal dysfunction: Decreased cardiac output as discussed above leads to decreased renal blood flow. Renal dysfunction occurs as a result of renal vein compression and cortical arteriolar compression, which leads to decreased glomerular filtration rate11. The above renal perfusion changes lead to increased levels of angiotensin II and aldosterone. This further excaberates renal hypoperfusion and results in decreased GFR, oliguria and fluid retention that are responsible for worsening ACS12.
3. Hepatic dysfunction: Even small increases in IAP can lead to compromised blood flow to liver and hepatobiliary dysfunction13. This causes increased lactate levels and consequent metabolic acidosis.
4. Gut ischemia: Decreased perfusion leads to intestinal ischemia that may lead to bacterial translocation14. This leads to sepsis with SIRS and/or shock resulting in third spacing of fluid that further compounds ACS.

Respiratory System
Increased abdominal pressure is transmitted easily to the chest, by virtue of its proximity. Also the diaphragm is pushed upward, leading to decreased volume and increased pressure in the intrathoracic space15,16. This leads to atelectasis of the lower lobes of the lung, intrapulmonary shunting, increased dead space and thus ventilation- perfusion mismatch. Thus a patient with IAH/ACS will develop hypoxia and hypercarbia. Increased intrathoracic pressure is transmitted to the smaller airways and results in increased airway pressures. It may also contribute to impaired pulmonary venous return and increased extravascular lung water, thereby worsening ARDS. In a ventilated child, the effect of increased IAP manifests as increased peak inspiratory, plateau and mean airway pressures17. Also, higher level of PEEP may be required to prevent lung atelectasis and preserve alveolar recruitment; some studies suggest setting PEEP equal to IAP18.

Cardiovascular System
Increased IAP leads to 2 main effects on hemodynamics i.e. decreased preload and increased afterload, which in turn lead to decreased cardiac output. Decreased preload occurs as a result of increased intrathoracic pressure which impedes venous return. Paradoxically the central venous pressure (CVP) may be elevated which may falsely suggest euvolemia, when in fact patient has intravascular depletion19. Increased IAP and consequently increased intrathoracic pressure both contribute to increased systemic vascular resistance and increased afterload20. Also direct compression and elevated intrathoracic pressure lead to decrease in ventricular compliance and Right ventricular end diastolic volume20. These changes collectively lead to decreased cardiac output, which may initially show improvement with fluid administration; however, eventually this will lead to further worsening of IAH/ACS. Volumetric indices may be more accurate than barometric indices in the hemodynamic monitoring of such patients21.

Intracranial pressure (ICP)
Increase in IAP leads to increase in ICP. This is because increase in IAP is transmitted to the chest as increased intrathoracic pressure and artificially increased CVP which impede cerebral venous outflow. This along with decreased cardiac output contribute to creation of a functional obstruction22,23. This results in increased ICP ,along with other contributing factors like reduced systemic blood pressure and increased permeability of blood brain barrier (due to release of interleukins induced by ACS). It has been observed that ICP substantially reduces in patients of ACS who undergo decompressive laparotomy24.

Polycompartment syndrome
Compartment refers to an enclosed anatomic space in which increase in pressure may lead to compromise in viability of the tissues within leading to compartment syndrome2. The four important compartments in the body include: head, chest, abdomen, and extremities. Scalea et al in 2007 suggested that different compartments in the body are not isolated but closely connected and pressure changes in one get transmitted to the others25. This gave rise to the term, polycompartment syndrome2. This is of 2 types: primary and secondary. Primary polycompartment syndrome is when initial insult is the increase pressure in any of the compartment due to physical tissue/organ injury with consequential involvement of other compartments. Secondary polycompartment syndrome occurs when there is no primary insult/injury in any particular compartment, but pressure changes are transmitted to multiple compartments26. A combination of both can also occur. The conditions which can lead to polycompartment syndrome include massive fluid resuscitation, prolonged shock and severe burns.

Diagnosis and Measurement of IAP
It is very important have a high degree of suspicion and understanding of the pathophysiology to be able to suspect and diagnose IAH before it progresses to ACS. IAH/ACS is usually seen in a sick child on mechanical ventilation with presence of one or more of the risk factors as discussed above. It is rarely seen in the awake, nonventilated patient where the cause may be a large abdominal space occupying lesion. Symptoms in such a case include enlarged/ tense abdomen, respiratory distress and abdominal pain in an older child. Clinical examination of the abdomen may suggest presence of IAH, however it is inaccurate and unreliable to detect and quantify IAH. Observational studies of intensivists’ ability to detect raised increased IAP clinically have shown a sensitivity of around 60% or less27. Hence IAP must be objectively measured and this is can be done either directly by placing a pressure transducer in the peritoneal cavity) or by various indirect methods. Although direct method is very accurate, it is invasive and involves insertion of catheter into peritoneal cavity. Hence it is neither considered to be feasible nor is the preferred method to monitor IAP in critically ill children. Various less invasive (indirect) techniques have been devised to measure IAP- these include measurement of intravascular (bladder), intragastric and intracolonic pressure. Amongst these WSACS has advocated the use of the bladder method as standard2,28. This is due to its several advantages including good accuracy, low cost, simplicity and feasibility to monitor continuous/ serial IAP. IAP can be measured by bladder technique in the following ways:

1. Intermittent method: This is done by filling bladder with 1 mL/kg of sterile saline as an instillation volume, (Minimum: 3 ml, maximum 25 ml) and thereafter measuring the pressure in the bladder via a transducer in mm Hg29. The transducer is zeroed in the mid-axillary line at the level of the iliac crest. As room temperature saline may cause initial detrusor contraction leading to falsely high IAP, hence IAP is determined 30-60 seconds after instillation of saline to allow adequate time for bladder detrusor muscle relaxation
2. Foley Manometer method: This is a practical method, useful in smaller centres as it does not require any expensive monitoring equipment. Instead of a transducer, it uses the patients’ urine as medium for measurement of IAP28. Like in the above method 1 ml/kg saline is instilled in the bladder, 30-60 seconds after which height of column above mid axillary line is noted in saline filled tubing. This reflects IAP in cm H2O which is converted to mm Hg (1 mm Hg= 1.34 cm H2O).
3. Continuous bladder pressure method: This is done using a 3- way urethral catheter. Commercial kits are available- AbViser kit with AutoValve used in adults, however lack of availability of small 3-way urethral catheter sizes precludes its use in children30. Also due to its stiff nature and large size, hematuria may occur. It may be adapted for children by the use of feeding tube with adaptor as an improvised urinary catheter.

Some important points worth noting about IAP measurement include:
1. Reference zeroing: The level universally accepted to be the reference zero level for the transducer is the mid axillary line at the iliac crest. The pubis symphysis was used earlier as the reference mark, but is no longer recommended.
2. Patient position: Patient should be in supine position during IAP measurement. Elevation of head of bed may lead to falsely higher values.
3. Other causes of false values:
-Ideal IAP measurement should be done at end expiration. However this is difficult in young children who have fast breathing rates and especially when respiratory distress is present. This may lead to inaccurate IAP values. In case patient is ventilated, sedation and paralysis will improve accuracy of readings.
- Abdominal muscle contraction (for instance during crying or after abdominal surgeries) or forced expiration (in obstructive lung) can lead to falsely high values31
-Overdistension of the bladder (excessive instillation volumes) lead to false high values
- Presence of pelvic masses/ hematoma or hematoma in rectus abdominas/ iliopsoas may compress on bladder leading to false high values.
- The manometer method utilises the patient’s urine as a medium for measurement. When this method is used in patients with acute kidney injury and oliguria, it may lead to falsely low IAP values.
- The temperature of the instilled fluid, presence of air bubbles in tubing, improper position of transducer are some of the other factors which lead to false readings32.
4. Monitoring IAP by the Foley manometer or transducer method does not increase risk of urinary tract infections in critically ill patients33.

The onset and progress of IAH/ACS has many deleterious effects as described above. It is thus imperative to prevent progress and treat IAH/ACS at the earliest. Surgical abdominal decompression has been considered to be the ultimate treatment of ACS (especially primary ACS) and was earlier the only known option, although it was not found to improve clinical outcomes 34. Over the years, various non invasive strategies have evolved. Also, the emphasis has shifted from treatment of established ACS to early recognition and institution of prompt measures to prevent progression of IAH.

Non invasive methods/ Medical management of increased IAP:
There are various non invasive strategies which are effective in decreasing/ preventing progress of IAH which will be discussed below. It is needs to be strongly emphasized here that clinical assessment of the critically ill patient is important, as severity of increased IAP does not depend solely on the measured value but its effects show individual variation depending on the clinical scenario. So, although many conservative strategies exist, in case of established ACS with severe organ dysfunction, there should be no hesitation to perform surgical abdominal decompression, as it can be life-saving in such cases35.

Specific abdominal measures:
1. Improving abdominal wall compliance
a. Sedation, analgesia and neuromuscular blockade: If a patient on ventilator exhibits restlessness or agitation, both the resultant asynchrony and abdominal wall muscle contraction will contribute to increase in IAP36. This underlines the role of adequate sedation and analgesia to prevent rise in IAP. Neuromuscular blockade has been demonstrated to significantly decrease IAP and can be used as a temporary measure to decrease IAP37. It is however unclear if these measures alter outcomes in patients with IAH/ACS3.
b. Removal of constrictive dressings if present also aids to improve abdominal wall compliance.

2. Evacuation of intraluminal contents:
a. Nasogastric tube insertion: Ileus is common in critically ill children and distension of stomach and intestines can contribute to marked increases in IAP38. While routine post-operative use of nasogastric tubes is not necessary, all sick patients with IAH must have the nasogastric tube placed followed by decompression of intraluminal contents.
b. Pharmacological promotility agents: Neostigmine has been shown to help in decompression in cases of colonic ileus/colonic pseudoobstruction39. However it is not known if this translates to decreased IAP or whether outcomes are altered by use of promotility agents.
c. Colonic decompression, use of rectal tubes and enemas: These may be used if no contraindications exist in cases of colonic ileus.

3. Evacuation of intraabdominal fluid collections:
Large collections of fluid or blood in the abdominal cavity can contribute to increase IAP. This can be seen in conditions like abdominal trauma, chronic liver disease and burns. It appears that drainage of this fluid does help to decrease IAP and avoid need for surgical decompression40. The pediatric subcommittee of WSACS has advocated use of percutaneous catheter drainage of fluid in those with IAH/ACS when this is technically possible as it may obviate need for more invasive surgical decompression3. However drawbacks include:
-Recurrence of ACS as fluid may re-accumulate on continued monitoring for IAP 41
-Ineffectiveness in cases of trauma/post volume resuscitation (where bowel edema rather than free fluid may be the main contributor)
- Difficulty in accessing loculated collections for drainage

General measures-Optimal fluid and hemodynamic management:
The essential principles of resuscitation in critically ill patients to avoid progress of IAH/ACS include:
1. Avoid excessive crystalloids: It has been clearly demonstrated that resuscitation with excessive crystalloids leads to IAH/ACS42. Two successful strategies have been developed to overcome this in the last decade. First is the use of massive transfusion protocol in cases of severe hemorrhagic shock i.e. resuscitation with 1:1 ratio of blood and plasma along with lesser use of crystalloids. The 1:1 blood: plasma ratio reduces volumes of resuscitation products needed (due to more effective bleeding control). Also patients who receive crystalloid to packed RBC ratio of >1.5:1 have been shown to have a 2 fold higher risk of developing ACS than those who receive lesser crystalloid compared to blood 43. Second is the use of colloids over crystalloids. This has been especially studied in burn patients, where administration of colloid/plasma decreases crystalloid requirement and keeps IAP lower44.

2. Goal directed measures in management of shock
Random fluid boluses or fluid challenge should be avoided in patients with IAH/ACS as they may improve BP (albeit transiently) but at the cost of increasing bowel edema and worsening IAH/ACS. The amount of fluid resuscitation required must be carefully planned, utilising various hemodynamic indices. While managing shock, it must be kept in mind that increased IAP does influence some of the hemodynamic indices which may lead to misinterpretation. Central venous pressure (CVP) will be excessively elevated in these cases due to abdominothoracic transmission of IAP. Adjustment for this is made as follows: transmural CVP= measured CVP – ½ IAP (assuming average 50% transmission of IAP)45. As IAH leads to increased intrathoracic pressures, it may lead to increases in stroke volume variation and pulse pressure variation, thus mimicking a fluid responsive state. On the other hand, IAH can lead to a false negative passive leg raising test46. Hence above considerations must be taken into account while interpreting results of these various tests and indices in the setting of IAH/ACS. Volumetric indices like right ventricular end diastolic volume index (RVEDI), left ventricular end diastolic area index (LVEDAI), global end diastolic volume index (GEDVI) are more accurate in presence of IAH/ACS21. Apart from this base deficit and lactate are reliable end points for resuscitation.

3. Correction of positive fluid balance
After acute aggressive resuscitation, it is quite common to find a high cumulative fluid balance in a critically ill patient who then develops IAH/ACS. Gradual removal of this fluid will be beneficial in such circumstances. However this is not easily done, as third spaced fluid needs to be removed gradually, without causing intravascular volume depletion or hypotension. Diuretics with/without albumin is commonly used for this purpose, but may not be tolerated well in a sick patient whose hemodynamics have just stabilised. Also, it is not known if their use alters outcomes in patients with IAH/ACS. Early fluid removal by continuous renal replacement therapies may be appropriate in these cases and is being increasingly used47.

Invasive management of treatment of ACS:
Although various non-invasive methods to alleviate increased IAP exist, when progressive ACS sets in, the definitive and most effective method is decompressive laparotomy. It can dramatically reduce IAP and improve organ function, however is associated with many complications leading to mortality in around 50% cases34. When delayed, morbidity increases further and mortality of upto 88% has been noted34.
Decompressive laparotomy is performed by taking a midline incision through a midline incision from xiphoid to symphysis or performing linea alba fasciotomy . This allows for reduction in IAP and gives room for further expansion of vital abdominal organs during ongoing resuscitation. Following this, the abdomen is left ‘open’ i.e. skin and fascia are not approximated, but abdomen is closed by use of temporary closure methods till reversal of the primary condition leading to ACS. The same principle is being used in severe trauma patients, where after damage control laparotomy, primary closure of abdomen is not done, but temporary methods are used in order to reduce/ prevent progression of ACS48. The disadvantages of open abdomen are: heat and fluid losses, increased catabolic state, risk of sepsis, visceral adhesions to the fascial edges and formation of enteric fistula48. These are reduced/ prevented by the use of temporary closure methods.
For temporary closure, moist gauze was used earlier, but became unpopular due to high risk of enteric fistulas. ‘Bogota bag’ is a clear plastic sheet covering sutured to the skin/fascia45. It allows for easy visualisation and access to the underlying abdominal contents, but managing fluid losses becomes cumbersome. Negative pressure wound therapy (NPWT) is a newer technique that involves application of a gentle continuous negative suction via a NPWT dressing49. This helps to prevent visceral adhesions, allows easy quantification of fluid losses and may also remove pro inflammatory cytokines, thus reducing third spacing and progress of ACS50. Bioprosthetic mesh closures should not be used routinely for early closure of open abdomen. Thus a comprehensive approach of medical management along with optimal timing of abdominal decompression, prophylactic use of open abdomen and negative pressure wound therapy are all important components of the management of progressive IAH/ACS which are essential for better outcomes and improved survival. In fact timely recognition and appropriate management strategies have been instrumental for reducing mortality in ACS by almost half (from 60% to 34-37%) in the last decade51. The key components of monitoring and management strategy in children have been summarised in Figure 3.

Key messages:
Key messages:
• IAH and ACS in children occur when IAP > 10 mm Hg, with absence and presence of organ dysfunction respectively.
• It is important to have a high index of suspicion and understanding of pathophysiology and risk factors to diagnose IAH early.
• Clinical examination is not sensitive to detect IAH; objective measurement of IAP is essential. The bladder method is universally accepted standard for measurement of IAP.
• Children in PICU with any of the known risk factors must undergo IAP monitoring
• The emphasis has shifted from treatment to early detection and prevention of progression of IAH/ ACS to decrease mortality
• Non invasive methods (including specific abdominal measures and optimal fluid and hemodynamic management) along with optimal timing of surgical decompression are the key elements in management.
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