Pulmonary impact of intra-abdominal hypertension and abdominal compartment syndrome
IAH and pulmonary mechanics:
The early effects of IAH on pulmonary function are largely mechanical. As intra-abdominal pressure increases, it pushes the diaphragms cephalad. This results in reduced intra-thoracic volume (reduced functional residual capacity, total lung capacity and residual volume), reduced chest wall compliance and increased intra-pleural pressure. Simultaneously there is alveolar collapse due to the smaller intra-thoracic space and the higher intra-thoracic pressure.[1, 2] This leads to atelectasis, ventilation-perfusion mismatching, hypoxia, hypercarbia and respiratory acidosis. To maintain ventilation, airway pressures must be increased and high peak airway and plateau pressures are often generated as is the work of breathing (see figures). The combination of elevated intrathoracic pressure and hypoxic pulmonary vasoconstriction can also lead to pulmonary hypertension.[3]
Figures describing the effect of IAH on pulmonary mechanics and function as well as recommendations for optimizing ventilation and PEEP.
IAH,
ACS and ARDS:
Elevated intra-abdominal pressure initially causes direct mechanical pulmonary problems as described above. However, as the pressure remains elevated and ischemic injury progresses, inflammatory mediators are released from the damaged alvolar membrane as well as from the gut. These inflammatory mediators cause pulmonary capillary damage leading to interstitial edema and an ARDS like syndrome.[1, 4]
Figure: Histologic sample of the lung in two pigs with ACS. The first was observed, the second nearly normal tissue was from an animal that had aggressive management of their ACS with open abdomen and drainage of cytokines, reduction in IAP
The ARDS that evolves as the result of ACS is a combination of alveolar collapse, high intra-thoracic pressure and interstitial edema. Ventilatory strategies such as PEEP, inspiratory recruitment and prone positioning more effectively improve respiratory mechanics, alveolar recruitment and gas exchange in these patients than in those with direct pulmonary injury.[1, 2]
IAH effect on the lung results in much longer ICU stays and
higher morbidity:
This IAH induced pulmonary dysfunction has a profound effect on patient morbidity – study after study demonstrates that IAH leads to longer times on the ventilator with resulting increases in costs and complications. Cheatham, Kimball and Batacchi have all demonstrated that active treatment aimed at reduction of IAP leads to more rapid weaning from the ventilator and shorter times in the ICU.[5-7] Kimball additionally noted less ventilatory associated pneumonia (VAP) in the treatment arm likely due to earlier removal of the endotracheal tube.
| Author | Vent days control | Vent days intervention | VAP control | VAP intervention |
| Kimball 2009 | 12 days | 8 days | 29% | 12% |
| Cheatham 2010 | 16 days | 12 days | ||
| Batacchi 2009 | 8 days | 5 days |
PEEP and IAH
Questions frequently arise regarding the interrelationship of PEEP and IAP. Interestingly there is relatively little literature on the topic. However, in 2010 Verzilli and colleagues investigated this relationship in 30 adults suffering from acute lung injury.[17] The authors noted relatively little impact of PEEP levels up to 12 cm water if the patients had normal IAP (less than 12 mm Hg). However, in patients with baseline intraabdominal hypertension (IAP of 12 mm Hg or higher) increasing levels of PEEP led to rises in IAP and decreases in abdominal perfusion pressure. They conclude that patients with acute lung injury in whom PEEP is applied likely need to have IAP measured and methods to moderate IAP using body position, sedation and other medical treatment modalities should be implemented to moderate any IAP increases seen with PEEP.
Figure 1 from Verzilli [17]: Impact of PEEP on IAP - note how the IAP is more significantly impacted by PEEP in patients with IAH than those without
Clinical implications:
Dr. Pelosi, a pulmonologist with research insight into IAH and ACS, reviewed the effects of IAP on respiratory mechanics in 2007 and made these observations and recommendations (Click here for the article)[2]:
“The interactions between the abdominal and the thoracic compartment pose a specific challenge to the ICU physician. Both compartments are linked via the diaphragm and on average a 50% transmission (range 25-80%) of IAP to the intra-thoracic pressure has been noted in previous animal and human studies.[8] Patients with primary ACS will often develop a secondary ARDS and will require a different ventilation strategy and more specific treatment than a patient with primary ARDS.[9, 10] The major problem lays in the reduction of the functional residual capacity (FRC). However some key issues to remember are:”
· IAH decreases total respiratory system compliance, while lung compliance remains unchanged.[11]
· The best PEEP should be set to counteract IAP while also avoiding overinflation of already well-aerated lung. [12]
· ARDS consensus definitions should take into account PEEP and IAP values.
· During lung protective ventilation, the plateau pressures should be limited to transmural plateau pressures below 35 cm H2O.[12-14]
o Pplat™ = Pplat – IAP/2
· The pulmonary artery occlusion pressure (PAOP) criterion in ARDS consensus definitions is futile in the case of IAH and should not be adopted (most patients with IAH and secondary ARDS will have a PAOP above 18 mm Hg).
· IAH increases lung edema. Within this concept monitoring of extravascular lung water index seems warranted.[15]
· The combination of capillary permeability, positive fluid balance and elevated IAP puts patients in extreme danger for lung edema.
· Body position affects IAP
o Obese patients in upright position can develop IAH
o The abdomen needs to hang freely during prone positioning
· Reluctance to use muscle relaxation must be balanced against the beneficial effects on IAP, APP and lung mechanics. It can be useful during patient-ventilatory dyssynchrony to reduce ETCO2 production and IAP.[16]
· The presence of IAH will lead to pulmonary hypertension via increased ITP with direct compression of lung parenchyma and vessels and via diminished left and right ventricular compliance.
Summary:
In summary, elevated intra-abdominal pressure causes direct mechanical effects on the lung and chest wall, which result in reduced intra-thoracic volume and elevated intra-thoracic pressure. These mechanical effects cause increasing posterior atelectasis, higher intrathoracic pressure, worsening gas exchange with resulting hypoxia and hypercarbia, rising peak inspiratory pressures and barotrauma. Eventually, the ischemia that develops due to hypoxia and reduced cardiac output to the gut results in inflammatory mediator release, which can cause an ARDS syndrome to occur. Interventions designed to reduce IAP result in improved ability to wean patients off the ventilator, earlier extubation and reduced risk of ventilator-induced complications including ventilator associated pneumonia.
References:
1. Pelosi, P., et al., Pulmonary and extrapulmonary acute respiratory distress syndrome are different. Eur Respir J Suppl, 2003. 42: p. 48s-56s.
2. Pelosi, P., M. Quintel, and M.L. Malbrain, Effect of intra-abdominal pressure on respiratory mechanics. Acta Clin Belg Suppl, 2007(1): p. 78-88.
3. Hunter, J.D. and Z. Damani, Intra-abdominal hypertension and the abdominal compartment syndrome. Anaesthesia, 2004. 59(9): p. 899-907.
4. Kubiak, B.D., et al., Peritoneal Negative Pressure Therapy Prevents Multiple Organ Injury in a Chronic Porcine Sepsis and Ischemia/Reperfusion Model. Shock, 2010.
5. Cheatham, M.L. and K. Safcsak, Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med, 2010. 38(2): p. 402-7.
6. Kimball, E.J., et al., A Prospective Evaluation of the Protocolized Management of Intra-abdominal Hypertension and the Abdominal Compartment Syndrome Acta Clinica Belgica, 2009. 64(3): p. 272 (Abstract 110).
7. Batacchi, S., et al., Vacuum-assisted closure device enhances recovery of critically ill patients following emergency surgical procedures. Crit Care, 2009. 13(6): p. R194.
8. Malbrain, M.L.N.G., D. Deeren, and T.J. De Potter, Intra-abdominal hypertension in the critically ill: it is time to pay attention. Curr Opin Crit Care, 2005. 11(2): p. 156-171.
9. Gattinoni, L., et al., Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med, 1998. 158(1): p. 3-11.
10. Ranieri, V.M., et al., Impairment of lung and chest wall mechanics in patients with acute respiratory distress syndrome: role of abdominal distension. Am J Respir Crit Care Med, 1997. 156(4 Pt 1): p. 1082-91.
11. Mutoh, T., et al., Volume infusion produces abdominal distension, lung compression, and chest wall stiffening in pigs. J Appl Physiol, 1992. 72(2): p. 575-82.
12. Malbrain, M.L.N.G., Is it wise not to think about intraabdominal hypertension in the ICU? Curr Opin Crit Care, 2004. 10(2): p. 132-45.
13. Talmor, D., et al., Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med, 2008. 359(20): p. 2095-104.
14. Kubiak, B.D., et al., Plateau and Transpulmonary Pressure With Elevated Intra-Abdominal Pressure or Atelectasis. J Surg Res, 2009.
15. Quintel, M., et al., An increase of abdominal pressure increases pulmonary edema in oleic acid-induced lung injury. Am J Respir Crit Care Med, 2004. 169(4): p. 534-41.
16. De Waele, J.J., et al., A role for muscle relaxation in patients with abdominal compartment syndrome? Intensive Care Med, 2003. 29(2): p. 332.
17. Verzilli, D., et al., Positive end-expiratory pressure affects the value of intra-abdominal pressure in acute lung injury/acute respiratory distress syndrome patients: a pilot study. Crit Care, 2010. 14(4): p. R137. (Open access article - click here for full reference)