Anaesthesiology Intensive Therapy, 2010,XLII,2; 96-101

Measurement of intra-abdominal pressure in clinical practice

*Dariusz Onichimowski1,2, Iwona Podlińska1, Sebastian Sobiech1, Robert Ropiak3


1Department of Anaesthesiology and Intensive Therapy, Regional Specialist Hospital in Olsztyn


2Chair of Basic Medical Sciences, University of Warmia and Mazury in Olsztyn


3Department of Medical Emergency, University of Warmia and Mazury in Olsztyn

  • Fig.1 Algorithm of management in intra-abdominal hypertension and abdominal compartment syndrome [according to 7]

In recent years, significant interest has been observed in intra-abdominal hypertension and abdominal compartment syndromes.

Intra-abdominal pressure (IAP) has been defined as a static pressure between organs in the abdominal cavity. Continuous or recurrent increase in the IAP above 12 mm Hg (1.6 kPa) is regarded as abdominal hypertension (IAH). Among the most common causes of IAH are massive fluid resuscitation after major injuries or burns, and ischemia of intestines after major vascular surgery.

Abdominal compartment syndrome has been defined as a continuous intra-abdominal pressure above 20 mm Hg (2.67 kPa) with coexisting organ dysfunction or failure. The mortality of patients with recognized abdominal compartment syndrome may be as high as 42%.

Diagnosis of intra-abdominal hypertension is based on the measurement of IAP only. The World Society of the Abdominal Compartment Syndrome (WSACS) has been advising screenings of IAP in all patients admitted to intensive care units with certain risk factors. As a standard measurement of IAP, the pressure in the bladder filled maximally with 25 mL of sterile normal saline is accepted. IAP should be measured at the end-expiratory phase, in the flat supine position, after relaxation of abdominal muscles and referred to the median axillary line as a zero-level. In confirmed cases of IAH and/or ACS, immediate action should be taken. It consists of evacuation of gastric and bowel contents, maintenance of adequate blood pressure, diuretics and/or ultrafiltration, and ultimately deeper sedation and/or muscle relaxation. Surgical percutaneous evacuation of the fluid or a decompression laparotomy may be considered.

In the last decade, widespread interest was observed in intra-abdominal hypertension and abdominal compartment syndrome as the causes of increased mortality amongst critically ill patients treated in surgical wards and ITUs. The questionnaire survey (about 2000 respondents) carried out by the European Society of Intensive Care Medicine has shown that in over 85% of European ITUs intra-abdominal pressure is measured and considered as a potential source of negative effects on organ functions [1]. In Poland, the frequency of such measurements is substantially lower.

In 2006, the World Society of Abdominal Compartment Syndrome (WSACS) published the definitions associated with intra-abdominal hypertension and abdominal compartment syndrome [2]:

  • definition 1 – intra-abdominal pressure (IAP) – a static pressure between organs in the abdominal cavity,
  • definition 2 – abdominal perfusion pressure (APP) – the difference between mean arterial and intra-abdominal pressure (APP = MAP – IAP),
  • definition 3 – filtration gradient (FG) – the difference between glomerular filtration pressure (GFP) and proximal tubular pressure (PTP). GFP may be defined based on abdominal perfusion pressure and equals the difference between mean arterial pressure and doubled intra-abdominal pressure (FG = GFP – PTP = MAP – 2xIAP),
  • definition 4 – intra-abdominal pressure should be expressed in mm Hg and measured at the end- expiratory phase, in the flat supine position, after relaxation of  abdominal muscles and referred to the median axillary line as a zero level,
  • definition 5 – a standard for intermittent measurements is the pressure in the bladder filled maximally with 25 mL of sterile 0.9% NaCL,
  • definition 6 – normal intra-abdominal pressure in critically ill adults ranges from 5  to 7 mm Hg (0.6-0.9 kPa),
  • definition 7 – intra-abdominal hypertension (IAH) is a continuous or recurrent increase in IAP >12 mm Hg (>1.6 kPa),
  • definition 8 – intra-abdominal hypertension is divided into four degrees:

I    – IAP 12-15 mm Hg (1.6-2.0 kPa)

II   – IAP 16-20 mm Hg (2.1-2.6 kPa)

III  – IAP 21-25 mm Hg (2.8-3.3 kPa)

IV  > IAP > 25 mm Hg (>3.3 kPa)

  • definition 9 – abdominal compartment syndrome (ACS) – a continuous IAP >20 mm Hg (>2.6 kPa) with or without reduced APP < 60 mm Hg (<8.0 kPa) with coexisting organ dysfunction or failure,
  • definition 10 – primary ACS – the condition related to trauma or disease in the abdominal cavity or pelvis, which often requires prompt surgical intervention,
  • definition 11 – secondary ACS – the condition, whose primary cause is not associated with the abdomen or pelvis,
  • definition 12 – recurrent ACS – when ACS returns despite conservative or surgical treatment of primary or secondary ACS [2].

Intra-abdominal hypertension affects abdominal organs due to the transfer of pressures, yet it also has an impact on more remote organs. The animal and human studies have demonstrated that 20-80% of IAP is transferred to the thoracic cavity. Increased thoracic pressure decreases the blood inflow to the heart and the end-diastolic volume of ventricles, which results in lower contractility of the myocardium. All this leads to a decrease in cardiac output [3]. Increased IAP transferred to the thoracic cavity affects the measurements of CVP and PCWP. Many authors suggest that in patients with IAH, the extent of vascular bed filling should be assessed using parameters measured by thermodilution methods [4, 5, 6]. If this is not possible, measurements of CVP and PCWP should be corrected by subtracting half of intra-abdominal pressure [3, 7].

Moreover, transfer of intra-abdominal pressure to the thorax has adverse effects on the respiratory system. An elevation of the diaphragm reduces the functional residual volume and compliance of the thoracic walls; thus, the risk of atelectasis in the basal segments of lungs and development of pneumonia increases [8]. Due to these phenomena in patients with IAH requiring substitutive ventilation, PEEP equalling IAP should be used; in cases of sparing ventilation of the lungs, the peak or plateau airway pressure should be reduced by half of IAP (as in the case of the circulatory system) [3, 8]. 

Furthermore, a direct relation between intra-abdominal pressure and intra-cranial pressure was demonstrated [9, 10]. An increase in intra-cranial pressure results from increased thoracic pressure due to transmission of the pressure from the abdominal cavity [11]. Hindered venous outflow from the cranial cavity caused by increased thoracic pressure is likely to lead to cerebral oedema or enhance the existing one. This phenomenon, combined with decreased mean arterial pressure induced by reduced venous return to the heart, results in a decrease in cerebral perfusion pressure with all its negative consequences. The available studies have demonstrated a high usefulness of decompressive laparotomy for reduction of intra-cranial pressure and improvement of cerebral perfusion pressure in patients with recurrent, drug-resistant intra-cranial hypertension [12]. Relaxation of striated muscles may also be beneficial. Due to the reasons mentioned, the measurement of IAP is recommended in all patients with the pathology likely to increase intra-cranial pressure, particularly in patients with IAH risk factors [3]. Any action that may increase IAP should be avoided (positive fluid balance, excessive volume of enteral nutrition in cases of abnormal intestinal peristalsis). Increased intra-cranial pressure has also been observed during diagnostic laparoscopies, therefore this procedure is not recommended in patients with cerebro-cranial trauma [13].

Increased intra-abdominal pressure markedly impairs the renal function. The compression of renal veins, direct pressure on the renal cortical layer and reduced arterial inflow to the kidneys cause a substantial decrease in filtration gradient and diuresis leading to anuria. Reduced renal flow also leads to activation of the rennin-angiotensin-aldosterone system [14]. Additionally, in IAH, increased ADH secretion was observed [15].

In cases of intra-abdominal hypertension a decrease in the flow both in hepatic arteries and in branches of the portal vein is found [16], which may be accompanied by impaired function of hepatic cells; however, this phenomenon has been demonstrated only in rabbits at IAP >30 mm Hg (>4.0 kPa) [17].

Impaired flow in mesentery vessels caused by IAH induces intestinal ischaemia, abnormal functioning of the intestinal barrier and subsequently increased transfer of toxins and bacteria from the intestinal lumen to blood [18].

Many risk factors of IAH and ACS have been identified. Those related to reduced compliance of abdominal integuments include: mechanical lung ventilation, particularly combined with the lack of patient-ventilator synchronization, high PEEP, the presence of auto-PEEP, basal pneumonia, increased body mass index (BMI), post-abdominal surgery conditions, prone positioning of the patient, haematomas in abdominal integuments, conditions after repair of large hernias, burns with extensive scars. The factors associated with increased abdominal content are obstruction with abdominal distension, tumours, haematomas, intra-abdominal abscesses, hepatic dysfunction with ascites, acute pancreatitis, peritonitis, abdominal oedema, and enteral feeding in malabsorption cases. The other IAH risk factors include diseases related to increased permeability of the vascular endothelium and fluid resuscitation, i.e. acidosis (pH <7.2), hypothermia, coagulopaties, massive fluid resuscitation, severe sepsis, septic shock, and massive b
urns [3].

In obese patients, IAP may reach 13.2 or even 13.7 mm Hg (1.7-1.8 kPa) [19]. Clinical implications of IAP abnormalities in morbidly obese patients have not been studied yet.

In critically ill patients, the value of IAP changes depending on the type and severity of disease. An increase in IAP >15 mm Hg (>2.0 kPa) may cause marked dysfunctions of internal organs and lead to death. Once ACS develops, the mortality reaches 42%. The conclusive diagnosis is possible only on the basis of IAP measurements [3]. Physical examinations are insufficient as their sensitivity is 40% and specificity 77% [19]. WSACS advises screenings and evaluation of all patients admitted to ITU for risk factors of IAH. If two or more factors are detected, IAP measurements are recommended. Such measurements are particularly justifiable in patients after extensive abdominal surgeries or abdominal trauma, with ACS symptoms (oliguria, hypoxia, metabolic acidosis), and after intensive fluid therapy (>5000 mL 24 h-1) [3].

Intra-abdominal pressure may be measured directly using a large-lumen catheter inserted into the abdominal cavity and connected to a manometric set or electronic transducer through the fluid column. Another direct method of IAP measurement is the determination of pressure of the gas insufflated to the peritoneal cavity during laparoscopic procedures. At present, such direct measurements are of a historic or research value. They were replaced by equally reliable yet less invasive and more convenient indirect measurements. Indirect measurements are based on the assumption that abdominal hydrostatic pressure is equally distributed over all fluid spaces in the abdominal cavity. Various methods were designed to measure IAP in almost all cavities or spaces within the abdominal cavity: the urinary bladder, stomach, uterine cavity, rectum and through the catheter placed in the inferior vena cava [21]. In European ITUs and postoperative wards, bladder measurements are most popular (92.3%). Direct and indirect measurements in the stomach are used less frequently (4.2 and 2.8%, respectively) [1]. At present, IAP measurements based on determinations of elasticity and compliance of abdominal integuments are being introduced.

The pressure in fluid spaces is assessed using manometric sets which measure hydrostatic pressure in a given space, e.g. in the urinary bladder, or transducer sets which change hydrostatic pressure into electrical signals. Moreover, sets with micro-processors are increasingly popular, which are placed at the end of catheters introduced to particular spaces. Such devices are much better for continuous measurements.

According to the WSACS guidelines, IAP should be measured in the urinary bladder filled with 25 mL of sterile solution of 0.9% NaCl. If the volume of filling is higher, the pressure values may be overestimated [22]. To prevent VAP, ITU patients are placed in the semi-recumbent position, which additionally substantially overestimates the IAP value. The formula correcting the pressure value in this position compared to the horizontal positioning is still lacking yet some studies are being carried out [23, 24]. The bed head positioning-dependent difference in IAP has been demonstrated, 1.2 mm Hg (0.1 kPa) for 10˚, 2.9 mm Hg (0.4 kPa) for 20˚, 5.0 mm Hg (0.6 kPa) for 30˚ and 7.4 mm Hg (1.0 kPa) for 45˚. Since the difference of 7 mm Hg (0.9 kPa) may result in the change of IAH classification even by 2 degrees, standard determination of IAP in the horizontal position causes underestimated incidence of clinically significant IAH. This problem requires further studies and multi-centre strategies [19].

A compromise between the necessity to prevent VAP and avoidance of elevated IAP is the anti-Trendelenburg position. However, even in this position IAP will be higher although not so high as in the 45º position [9]. In should be remembered that the prone position used to improve ventilation in patients with severe lung pathologies may also increase the IAP values [28].

The extensive management in IAH involves: normalization of circulatory parameters, suitably chosen pulmonary ventilation, intensive nutritional therapy, control of blood glucose levels, meticulous control of fluid balance with renal replacement therapy administered if need be. If the pressure is lower than 20 mm Hg (2.6 kPa), conservative treatment first involves evacuation of digestive contents through the gastric or rectal tube and enema. In some cases, endoscopic decompression of the alimentary tract is needed. The therapy with prokinetic drugs, such as metoclopramide, erythromycin or neostigmine is justifiable. Moreover, normalization of electrolyte disturbances is essential as hypokalaemia, hypomagnesaemia, hypophosphataemia or hypercalcaemia may impair the alimentary motor activity [7]. In cases of mild or moderate IAH ( I and II degree), enteral nutrition is not contraindicated and may even be beneficial as it has prokinetic effects, prevents the spread of bacteria outside the alimentary canal and imp
roves the immune system function [25]. In patients with severe IAH (III and IV degree), enteral feeding should be abandoned [7, 26].

In cases of enhanced tone of abdominal integuments, IAH may be decreased by increased doses of hypnotic drugs as they reduce the striated muscle tone and increase the compliance of abdominal integuments. Moreover, such drugs provide better patient-ventilator synchronization [7]. In severe hypertension (III and IV degree) and lack of explicit indications for laparotomy, relaxants of striated muscles are effective [26]. Their use should be as short as possible due to the risk of adverse effects.

In patients with IAH, the institution of excessive fluid resuscitation doubles the incidence of multiorgan failure compared to patients with more limited fluid supply [7]. Ambulation and elimination of tissue swellings are also relevant. Diuretics with colloids are used to transfer water to the intravascular space [29]. Moreover, normalization of blood albumin levels is essential. When diuretics are ineffective or renal failure develops, dehydration using the continuous renal replacement techniques is required [7].

If the conservative treatment is found ineffective and IAP <20 mm Hg (<2.6 kPa) cannot be achieved or ACS develops, invasive methods of therapy should be considered. The first-line strategy is percutaneous (USG- or CT-guided) evacuation of the abdominal fluids, blood and pus. If intra-abdominal pressure is markedly high, evacuation of only several hundred millilitres of contents may result in a substantial decrease in IAP, improved organ perfusion and better prognosis [30].

The next stage of invasive therapy is decompressive laparotomy. The method poses the risk of numerous complications therefore is should be performed only in patients with ACS resistant to other forms of treatment. In any case, the decision should be prompt as delayed laparotomy is associated with significantly higher mortality [7, 31, 32]. In patients undergoing surgeries due to other reasons and at risk of ACS, the abdomen should be left open. In both cases, the “open” abdomen should be secured with special plastic dressings (in some cases with the suction option). The use of suction dressings reduces the number of infections within the abdominal cavity; compared to suction drainages, it may decrease the incidence of fistulae formed [3, 7].

During each stage of IAH therapy, adequate abdominal perfusion pressure should be maintained >60 mm Hg (>8.0 kPa).

Lower values affect the mortality rates. APP, having the component determining the mean arterial pressure (MAP) and the component describing the limited venous outflow (IAP) is of a higher prognostic value compared to single parameters [33].

Nowadays, the management of patients in ITUs is extremely complex and is based on many data from monitoring of numerous vital parameters. Extensive monitoring of the circulatory, respiratory and clotting systems is widely used. Monitoring of the function of abdominal organs, particularly of intestines, is definitely less developed. Intra-abdominal pressure measurements appear to be a valuable supplement to those methods.

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address:

*Dariusz Onichimowski

Oddział Anestezjologii i Intensywnej Terapii
Wojewódzki Szpital Specjalistyczny w Olsztynie
ul. Żołnierska 18, 10-501 Olsztyn
tel.: 0-89 538 64 42
e-mail: onichimowski@wp.pl

received: 30.12.2009
accepted: 18.03.2010