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ABDOMINAL COMPARTMENT SYNDROME. ACS. Reduced cardiac output Oliguria High peak inspiratory pressures Impaired oxygenation Impaired ventilation Reversed by decompression. ABDOMINAL COMPARTMENT SYNDROME Pathophysiology: Viscera. %. IAP (mm Hg). Diebel et al, 1992.
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ABDOMINAL COMPARTMENT SYNDROME
ACS Reduced cardiac output Oliguria High peak inspiratory pressures Impaired oxygenation Impaired ventilation Reversed by decompression
ABDOMINAL COMPARTMENT SYNDROME Pathophysiology: Viscera
% IAP (mm Hg) Diebel et al, 1992
IAP 25 for 60 minutes Bowel TPO2 IAP 15 for 60 minutes Baseline Axillary TPO2 50 100 0 Bongard et al, 1995
IAP and Hepatic flow Decreased HABF 10 mm Hg Decreased HMVBF HABF 45% HMVBF 71% 20 mm Hg PVBF 65% (of control)
IAP and pHi Compared with normal pHi, patients with pHi < 7.32 were 11 times more likely to have a high IAP Sugrue et al, 1996
IAP and pHi Gastric mucosal pH (n=42) With IAH = 11 8 (64%) had acidotic pH 6 of the 8 improved with abdominal decompression 2 with low pHi and IAH died of ACS, MODS Ivatury et al, 1998
IAP and pHi ACS by intraabdominal inflatable balloon in puppies. Baseline: 2 to 5 cm H2O in the stomach and bladder 1 to 3 mm Hg in the intraabdominal catheter = pHi of 7.4. BP and GP of 20 cm, IAP of 10 mm : pHi 7.0 BP 30 cm and GP 20 mm : pHi 6.8 BP 40 cm and GP 30 mm : pHi 6.5 ? Changes in pHi in association with increased IAP may be an early indicator of impending ACS Engum et al, 2002:
IAP and bowel mucosa Quantitatively assessed: mucosal perfusion index, functional capillary density RBC velocity by intravital microscopy At an IAP of 10 and 15 mm Hg: Stewise decrease in all parameters indicating A progressive impairement of Mucosal circulation Samel et al, 2002:
IAP and bowel mucosa Jejunal loop Exposed mucosa Abdominal chamber I V microscope Optical window Samel et al, 2002:
IAP and bowel mucosa Samel et al, 2002:
INTRAABDOMINAL HYPERTENSION IAH 10 (22.2%) 13 (52%) 0.012 Deaths 2 (10.6%)9 (36%) 0.003 MODS 1.3 ± 2.4 3.1 ± 3.9 0.023 Group II: closure Group I: mesh p (n=45) (n=25) Ivatury et al, 1998
INTRAABDOMINAL HYPERTENSION No IAH IAH p (n=47) (n=23) Mortality 4 (8.5%) 10 (43.5%) 0.006 MODS 0.8 ± 1.9 4.3 ± 3.7 0.0001 Ivatury et al, 1998
ACS, MOF and Mortality NO ACS ACS p (n=28) (n=49) Mortality 12% 43% 0.01 0.01 MOF 8% 32% Raeburn et al, 2001
ACS & MOF ACS an independent risk factor for MOF ( OR 9.2, CI 3.8-22.8, p<0001) Mortality (OR 8.4, CI 3.5-20.6, p<0.001) Balogh et al, 2003
? Bacterial translocation E.coli, Enetrobacter in lymph nodes and liver after shock and IAH: Eleftheriadis et al, 1996 Diebel et al, 1997 Gargiulo et al, 1998 No bacterial translocation Jacobi et al, 1997 Doty et al, 2002
ACS & Systemic Cytokines TNF IL-6 PMNs Il-1 ß Rezende-Neto et al, 2002
ACS & Lung pathology Rezende-Neto et al, 2002
Sequential shock & ACS SMAF and CO are reduced to a greater degree by IAH after prior hemorrhage and resuscitation
Sequential shock & ACS Group I animals had Significantly higher BAL PMNs, BAL protein and Lung MPO levels.
ACS as a second-hit in a two-hit model of MODS Hemorrhagic shock-reperfusion in rodents Neutrophil CD-11b expression maximal at 8 hours Lung PMN sequestration (elastase concn) Lung injury (EB dye in BAL) Liver injury (ALT concn) Were maximal with ACS at 8 hours Rezende-Neto et al, 2002
SUMMARY IAH has profound effects on the splanchnic bed. The effects of ischemia-reperfusion and IAH are additive IAH causes systemic inflammatory changes and can serve as the second-hit for the development of MODS IAH and ACS are morbid complications that increase mortality.