J VASC ENDOVASC SLRG 2006;13:73-6
Abdominal compartment syndrome after ruptured abdominal aortic aneurysm D. MAYER
1, T. PFAMMATTER 2, J. M. GAUER 1, M. WILHELM L . LABLER 3, D. WEBER 1, M . GENONI 1, M . LACHAT
The mortality rate after ruptured abdominal aortic aneurysm 'Clinic for Cardiovascular Surgery (rAAA) has remained nearly constant during the last 50 years, University Hospital Zurich, Zurich, CH with multiple organ failure (MOF) representingthe leading cause 2Znstitute of Diagnostic Radiology University Hospital Zurich, Zurich, CH of death in those patients surviving operative repair. MOF is 3Traurna Centre, University Hospital Zurich, Zurich, CH generally a consequence of intra-abdominalhypertension 0, which occurs when hematoma from aortic rupture and edema from fluid resuscitationreduce abdominal free space. Abdominal compartment syndrome (ACS) is the condition where IAH edema from fluid resuscitation reduce abdominal free induces organ dysfunction. ACS without expedient decompression laparotomy has up to 100% mortality. Although the role of space. Abdominal compartment syndrome (ACS) is ACS in aortic surgery has been pointed out during the last decade, the condition where IAH induces organ dysfunction. the literature dealing with it is still rather scarce and sometimes ACS without expedient decompression laparotomy confounding. Moreover, most contemporary reports about rAAA has up to 100%mortality. still do not describe IAH andlor ACS, which has to be interpretCompartment syndrome has been identified within ed as an underscoring of that entity. This review describes effec- the thorax (pericardialtamponade, pneumothorax andlor tive management strategies for reducing the significant morhemothorax with mediastinal shift syndrome), the cerebidity and mortality of IAWACS. bro-spinal space and the extremities. In all of these locaKEY WORDS: Aortic aneurysm, abdominal - Aortic rupture tions, early recognition and treatment do significantly Compartment syndromes.
increase organ function as well as patient outcome and nowadays failed recognition and/or treatment is considhe mortality rate after ruptured abdominal aortic ered to be a malpractice. ACS in aortic surgery has been aneurysm (rAAA) has remained nearly constant pointed out more than 20 years ago by Kron et a1.,2 but during the last 50 years,] with multiple organ failure most contemporary reports about rAAA still do not (MOF) representing the leading cause of death in those describe intra-abdominal pressure (TAF') andlor IAWACS, patients surviving operative repair. MOF can be due to which has to be interpreted as an underscoring of that low cardiac output syndrome or acute embolization entity.3.4 Recently, the World Society of Abdominal of atherosclerotic material, but generally it is a con- Compartment Syndrome (WSACS) was founded "to sequence of intra-abdominal hypertension (IAH), promote research, foster education, and improve the surwhich occurs when hematoma from aortic rupture and vival of patients with IAWACS by bringing together physicians, nurses, and others from a variety of clinical disciplines to share information on effective manageAddress reprint requests to: M. Lachat, Clinic for Cardiovascular ment strategies for reducing the significant morbidity Surgery, University Hospital Zurich, 8091 Zurich, CH. E-mail: and mortality of IAHIACS" (http://www.wsacs.org).
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*.J
Vol. 13- No. 2
THE ITALIAN JOURNAL OF VASCULAR AND ENDOVASCULAR SURGERY
ABDOMINAL COMPARTMENT SYNDROME AFTER RUPTURED ABDOMWAL AORTIC ANEURYSM
Physiopathology of abdominal compartment syndrome A rapid reduction of the abdominal free space can lead to IAH and, as a consequence, to ACS. In patients with rAAA abdominal free space can acutely be reduced by retro- and/or inhaperitoneal bleeding or hematoma. Massive fluid resuscitation and ischemiareperfusion injury secondary to a shock state produce abdominal organ swelling, additionally reducing intraabdominal free space and decreasing abdominal wall compliance. PostoperativeACS occurs typically 7-25 h after abdominal closure.2.5 IAP is usually measured with a Foley winary catheter. The urinary bladder is filled with 50-100 rnL of saline solution, the Foley urinary catheter clamped and a pressure line connected to a pressure transducer.2 The bladder pressure correlates well with direct IAP measurement within the range of 5-50 mmHg. At physiological conditions, IAP ranges from -2 mmHg to 8 mmHg. Continuous IAP measurement shows a very good correlation with intermittent IAE' measurement and is far less time consuming.6 IAH has generally been described as IAP between >10 mmHg and 20 mmHg.7 WSACS defines IAH more precisely at an IAP level 212 mmHg. ACS is defined as a sustained IAP >20 mmHg that is associated with new organ dysfunction/failure.W A C S affect intra- andlor extra-abdominal organs (central nervous, respiratory, cardiovascular, renal and gastrointestinal systems).7-10The pressure threshold above which each organ hnction is altered is variable. The gastrojntestinal system is affected at levels as low as 10 mmHg, while the central nervous system is unaffected until pressure exceeds 20 rnmHg. IAP above 20 mmHg increases resistance to blood flow in the portal circulation and vena cava. Therefore, venous return to the heart is reduced and low cardiac output results. Moreover, IAH leads to increased intra-thoracicpressure further reducing cardiac preload and the resulting diastolic heart dysfunction (tamponade like state) further reduces cardiac output. Respiratory dysfunction appears at IAP of 15 rnmHg and is due to a reduction of lung and thoracic compliance. Reduced lung capacity and compliance do alter gas exchange and increase vascular pulmonary resistance. As a consequence, right heart failure with a further increase of central venous pressure and hypoxemia ensue. Severe renal dysfunction occurs at an IAP of 20-30 mmHg. Low cardiac output syndrome does induce a prerenal insufficiency, whereas the increased IAP induces a com-
TABLE1.-Predisposing
factors for ACS.
Severe shock BP sys
