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Abdominal Compartment Syndrome Riwanto Bagian I. Bedah FK.

UNDIP/ Rs Dr Kariadi KASUS > Laki-laki 24 tahun, pasca laparatomi trauma abdomen, ditemukan ruptur hepar yang sulit diatasi perdarahannya dilakukan packing dan dilakukan penjahitan primer dinding abdomen > Di ICU 5 jam pasca bedah: RR 36/ menit, T 100/ 80 mm Hg, Nadi 112/ menit, abdomen distensi, CVP 18 Cm H2O, PH: 7,31, Urine 0 cc sejak dari operasi. The Goals Understand & able : > Definition, > Factors contributing, > Adverse Physiologic effect, > Clinical finding and diagnosis, > Measurement of Intra-abdominal pressure, > Treatment and prevention,of Abdominal Compartment Syndrome. Compartment Syndrome (CS) : A condition in which increased pressure in a confined anatomical space adversely affects the circulation and threatens the function and viability of tissues therein. Example:  Fascial space of extremities (CS)  Orbital globe (Glaucoma)  Abdominal Cavity (Abdominal Compartment Syndrome): little attention
(Schein et al. JACS june 1995)

Abdominal Compartment Syndrome (ACS) > Alterations in cardiovascular hemodynamics, respiratory mechanics and renal function that occur as a result of a sustained increase in intra-abdominal pressure. > Awareness of the ACS has increased: 1. Laparoscopy 2. Planned repeat laparotomy for trauma
(Nathens et al. CJS Vol 40, 1997)

Factors contributing to increased intra-abdominal pressure (Schein et al, JACS Vol 180, 1995) Adverse physiologic effects of IAH (Schein et al, JACS Vol 180, 1995) (Nathens et al. CJS Vol 40, 1997) Mattox KL et al. Trauma:Trauma Damage Control Int Ed 2000 (Hiatt JR. Trauma Secrets 2nd, 2003) Adverse physiologic effects of IAH A. Respiratory  Elevated diaphragm: decrease thoracic volume  increased thoracic pressure and decreased dynamic compliance  Increased Peak Respiratory Pressure: ventilation-perfusion abnormality  Increased Pulmonary Vascular resistance - Intrapulmonary shunt

. 1995) The Viscious Circle created by IAH Splachnic hypoperfusion Hepatic ischemia Gut mucosal acidosis . Splanchnic Blood  Decreased Hepatic Blood Flow   decreased hepatocyte mitochondrial function  Decreased Mesenterial Blood Flow  Promote gut mucosal ischaemia  acidosis. Abdominal Wall  Decreased Abdominal Wall Blood Flow (IAP 10 mm Hg: blood flow reduce 60%)  Pressure-volume curve is not linear (the IAP rises. hypercarbia. acidosis Adverse physiologic effects of IAH B. Intra-Cranial Pressure  Decrease cerebral venous outflow  Increased Intra-Cranial Pressure (ICP)  Decreased cerebral perfusion pressure. Blood pressure usually unaffected  Pooling blood in the extremities: bilateral deep vein thrombosis Adverse physiologic effects of IAH C. SVR  Decrease in Venous Return due to .  Increased wound infection & fascial dehiscence Adverse physiologic effects of IAH E. Oliguria is often in earliest sign of ACS (IAH 15-20 mmHg) Adverse physiologic effects of IAH D. PCWP. Cardiovascular  “False” increases in CVP. stiffness of abdominal wall increases) so progressively smaller volume increments are required to further elevate IAP. JACS Vol 180.  Decrease in Cardiac output Tachycardia. may potentially aggravate neuronal disease. Physiological consequences of elevated intra-abdominal pressure (summary) ((Schein et al.retroperitoneal vein compression pooling blood caudally. Hypoxemia.narrowing IVC at the diaphragm due to elevated diaphragm. bowel edema and production of oxygen free radicals  possible bacterial translocation Adverse physiologic effects of IAH F. Renal  Increased renal vascular resistance  Direct compression (“renal compartment syndrome”)  Increased plasma renin and aldosteron  Decrease RBF  Reduce urine output  Oliguria  Anuria.

Clin. UO= Urine output Meldrum DR et al Am J Surg 1997.DO2I=Oxygen Delivery Index. Hiat JR. Surg.Trauma Secret 2 nd ed. Al Surg.76:838. Percentage of patients with respective organ dysfunction per grade of ACS Grade UO<0.  High index of suspicion must be maintained to make diagnosis and intervene early in the course of ACS Grading system for ACS Grade Bladder pressure (Cm H2O) mmHg I II III IV 10-15 15-25 25-35 >35 7.North Am 1997.Bowel edema Coagulopathy Hypotermia Acidosis Intra-abdominal Bleeding IAH unrelieved ACS Free Oxygen Radicals Distant organ damage Ivatury RR et. 2003. Acidosis 2) Elevated central venous pressure 3) Decreased urine output 4) Massive abdominal distention 5) Reversal of this derangements with abdominal decompression. Trauma Secrets 2nd. BJA Vol 77.11 11-18 18-26 >26 Burch JM et al. Hypercarbia. Clin North Am 1996.5 PAP>45 SVR>1000 DO2I <600 ml/kg/hr (Cm H2O) (dyne/sec/cm2) (mlO2/min/m2) I II III IV 0% 0% 65% 100% 0% 40% 78% 100% 0% 20% 65% 100% 0% 20% 57% 100% PAP=Peak Airway Pressure).174:667 . 1996) Clinical Finding of Abdominal Compartment Syndrome: five key features (Hiatt JR. SVR= Systemic Vascular Resistance. 2003) 1) Elevated ventilatory pressures ( Peak inspiratory pressures> 85 cm H2O)  Hypoxia.77:796 MODEL OF POSTINJURY MOF (Biffl et al.

JACS june 1995)  Gastric Pressure: • Infusing 50-100 ml water into NGT • Connecting to water manometer • 0 level: mid axillary line     Bladder pressure Infusing 50-100 ml water to empty bladder Connecting to water manometer 0 level: symphysis pubis Pressure 5-70 mm Hg: equal to direct method. attaching to a saline manometer or pressure transducer  During laparoscopy: automatic electronic insufflator provides continuous monitoring of pressure. Abdominal Perfusion Pressure (APP)  A superior parameter in the assessment of IAH  Appears to be clinically useful resuscitation end point and predictor of patient survival during treatment for IAH & ACS  APP > 50 mmHg should be considered a potential resuscitation end point in the patient with elevated IAP Cheatham ML et al J.  Indirect method  Measurement of:  Bladder pressure (most popular)  Gastric pressure (NGT/ Gastrostomy tube)  Inferior Vena Cava Pressure Gastric & Bladder Pressure (Schein et al.49(10):621-627 Abdominal Perfusion Pressure  APP = Abdominal Perfusion Pressure  MAP = Mean Arterial Pressure  IAP = Intra Abdominal Pressure  SP = Systolic Pressure  DP = Diastolic Pressure Diagnosis of ACS  High index of suspicion  • • Clinical syndrome Abdominal distention Peak inspiratory pressure . Trauma 2000.Measuring Intra Abdominal Pressure (IAP)  Direct method  Directly placing a catheter into the peritoneal cavity.

The Am.Trauma Secret 2nd ed.76:838. Hiat JR. Clin North Am 1996. . 1997) -Retrospective analysis of case series -University-based level I trauma center -Case: patients underwent celiotomy for abdominal trauma Group I: Primary mesh closure Group II: Delayed mesh mesh closure Group III: Control Grading of ACS related to its proposed management Grade Bladder pressure Recommendation Cm H2O (mm Hg) I 10 -15 7-11 Maintain normovolemia (Normal post-op. treated it promptly  Patients treated by Damage Control Surgery (DCS) are particularly prone to IAH. III 25 -35 18-26 Most require decompression IV > 35 >26 All require decompression and re-exploration Burch JM et al. Meldrum DR et al Am J Surg 1997. press) II 16 -25 11-18 Closed monitoring Hypervolemic resusc. Surgeon Vol 64. Vol 132. Surg. if persistently high. consideration should be given to prevent IAH Prophylaxis and Treatment of IAH  Temporary closure of fascia to patients at high risk for IAH  ICU/SICU management  Monitoring gastric mucosal pH and use this variable as end-point of resuscitation  IAP is measured every 4-6 hours / more frequently  Persistent evaluation>20-25 mm Hg is an indication for re-exploration Temporary closure of abdominal wall (Sherck et al.174:667.• CVP (if patients euvolumic) • Oliguria • Hypercarbia Diagnosis of ACS  Measuring IAP  IAP> 25 mmHg correlates with renal dysfunction  IAP> 25 mmHg in postoperative patients with adequate blood volume and oliguria indication for decompression laparotomy Management of IAH and ACS  IAH is detrimental to organ function.  IAP should be monitored frequently. it should be anticipated and prevented. 2003. 1998) Prevention of Abdominal Compartment Syndrome by Absorbable Mesh Prosthesis Closure (Mayberry et al Arch Surg.

Rapid decompression  Pulmonary embolism (MacDonnell et al JACS 1996) Effort to reduce the side effect of abdominal decompression  Decompress in hemodinamically stable.45% Normal saline + 50 g manitol + 50 mEq NaHCO3 pre & post operatively  Slowly opening the abdomen for decompression (in severe case. hypothermia and coagulation defects corrected. CJS Vol 40. decompress in ICU is possible)  Prophylactic insertion of a vena cava filter before decompression?  Temporary abdominal closure. . severe abdominal injury. 1997) Abdominal Decompression Complication:  Rapid decompression abrupt drop in central filling pressure and systemic vascular resistance  hypotension. Surgical intervention should be indicated by IAH and delayed until ACS is clinically apparent. with anuria. oxygen delivery maximized. 1997)  ACS Venous Thrombosis. after repair of abdominal aortic ruptured. (Nathena et al.Response to abdominal decompression(Nathens et al. When clinical deterioration is marked.  2 l infusion of 0. CJS Vol 40.  Viable bowel. diminishing abdominal girth. Abdominal re-closure (Schein et al.  Early recognition and urgent abdominal decompression: improve the prognosis. CJS Vol 40. ventilatory dysfunction and hemodynamic instabillity. 1995) SUMMARY  IAH causes multiple and profound physiologic abnormalities both within and outside of abdomen  IAP monitoring is easily performed through bladder  Careful monitoring & prompt recognition & treatment of IAH are critical in patients after DCS because IAH is extremely common in this patients SUMMARY  Use of temporary fascial prosthesis or the alternatives at the initial laparotomy as prophylaxis measures  IAH should be considered an earlier manifestation of ACS. Majority: critically ill patients (severe abdominal sepsis. coagulopathy corrected)  3-4 days after: brisk diuresis. JACS june 1995)  Well resuscitated patients (tissue oxygenation restored. hypothermia. decreasing peripheral edema. adequacy debridement of necrotic tissue: try to close fascia and cek intra abdominal pressure: Excessive tension temporary closure Prognosis  Dead rate: 42-71%  Considered in the context of the patients underlying disease. abdominal decompression my be needed before the therapeutic goals have been reached.  Rapid washout and systemic circulation of acid and metabolites from the reperfused viscera and lower extremities (Ischemia-Reperfusion Injury /IRI)  episodes of asystole and supraventricular arrhytmia (Nathens et al.  Slowly opening of the abdomen for decompression is important key to reduce the effect of reperfusion syndrome. hypovolemia.