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Case Presentation Joseph M Brandel, MD Kings County Hospital Center Department of Surgery Friday, November 12, 2004

Case Presentation - SUNY Downstate Medical Center · Case Presentation Joseph M Brandel, MD ... with gas or fluid, as in typhoid fever, ascites, or peritonitis' are caused by 'overloading

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Case Presentation

Joseph M Brandel, MDKings County Hospital CenterDepartment of SurgeryFriday, November 12, 2004

The Abdominal Compartment Syndrome

Definition

A syndrome of intra-abdominal hypertension resulting in organ dysfunction which may be reversed by abdominal decompression

History1863: Etienne-Jules Marey wrote that ‘the effects that respiration produces on the thorax are the inverse of those present in the abdomen’1873: EC Wendt of Germany measured IAP through the rectum, noting that elevated pressures corresponded with diminished excretion of urine1890: Heinricius of Germany found that IAPs between 27 and 46 cmH2O were fatal to animals owing to prevention of respiration

History1911: Haven Emerson publishes his treatise, 'intra-abdominal pressures'contraction of the diaphragm identified as chief factor in the rise of IAP during inspirationexcessive IAP can cause death from cardiac failure even before terminal asphyxia developsObserved that cardiovascular collapse associated with 'distention of the abdomen with gas or fluid, as in typhoid fever, ascites, or peritonitis' are caused by 'overloading the resistance in the splanchnic area' and that 'relief of the laboring heart is constantly seen after removal of ascitic fluid.'

Emerson H. Intra-abdominal pressures. Arch Intern Med 1911;7:754-784

History

1 Ogilvie WH. The late complications of abdominal war wounds. Lancet 1940;2:253-256 2 Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressures a criterion for abdominal re-exploration. Ann Surg 1984;199:28-30

1940: Sir William Heneage Ogilvie1

In a letter to Lancet described ‘a dodge that has twice helped me out’, a technique for avoiding closing a ‘burst abdomen’Sutured vaseline impregnated canvas to wound edges to cover abdominal contents

1984: Kron et al2Published landmark case series on IAH11 patients with elevated IAP after aortic repair (>30 mmHg)7 patients decompressed with immediate diuresisThe other 4 patients died

PathophysiologyCauses of intra-abdominal hypertension

Primary: due to intra-abdominal processTrauma: Intra-abdominal bleeding, MAST, damage control surgeryRetroperitoneal: Pancreatitis, ruptured AAA, abscessIntraperitoneal: Gastric dilatation, bowel obstruction, visceral edema, tension pneumoperitoneumAbdominal wall: Burn eschar, reduction of large hernias

Secondary: due to massive fluid administration for extra-abdominal process

Capillary leakIschemia-reperfusion: release of inflammatory mediators, free radicals

Ivatury RR, Diebel L, Porter JM, Simon RJ. Intraabdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am 1997;77:783–800

Pathophysiology

Increased ICPDecreased CPP

Neurologic

Decreased blood flow to all abdominal organs expect adrenalsDecreased mesenteric and mucosal blood flowDecreased pHi

Intestinal/mucosal

Decreased renal plasma flowDecreased GFRDecreased glucose reabsorptionOliguria or anuria

Renal

Increased peak inspiratory pressuresIncreased airway pressuresDecreased PaO2Increased PaCO2Decreased dynamic compliance

Pulmonary

Decreased cardiac outputDecreased preloadIncreased afterloadIncreased CVP and PCWP

Hemodynamics

Clinical EffectsSystemClinical Effects of Increased Abdominal Pressure

Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intraabdominal pressure in critically ill patients. Crit Care Med 1989; 17:118–121.

Pathophysiology

Decreased cardiac outputDecreased preloadIncreased afterloadIncreased CVP and PCWP

Hemodynamics

Clinical EffectsSystemClinical Effects of Increased Abdominal Pressure

Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. Cardiopulmonary effects of raised intraabdominalpressure before and after intravascular volume expansion. J. Trauma 1995;39:1071–1075.

0

0.2

0.4

0.6

0.8

1

0 10 20 30 40

Intra-abdominal pressure (mmHg)

Car

diac

out

put Elevation of diaphragm

transmits pressure to heart and great vesselsCVP and PCWP are “spuriously” elevated –not a reflection of volume status

Pathophysiology

Increased peak inspiratory pressuresIncreased airway pressuresDecreased PaO2Increased PaCO2Decreased dynamic compliance

Pulmonary

Clinical EffectsSystemClinical Effects of Increased Abdominal Pressure

0

10

20

30

40

50

0 5 10 15 20 25 30 35 40

Intra-abdominal pressure (mmHg)

Peak

airw

ay p

ress

ure

Increases in pleural pressures evident at IAP of 15 mmHg or greaterExacerbated by PEEPNormalizes after surgical decompression

Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. Cardiopulmonary effects of raised intraabdominalpressure before and after intravascular volume expansion. J. Trauma 1995;39:1071–1075.

Pathophysiology

Decreased renal plasma flowDecreased GFRDecreased glucose reabsorptionOliguria or anuria

Renal

Clinical EffectsSystemClinical Effects of Increased Abdominal Pressure

Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intraabdominal pressure in critically ill patients. Crit Care Med 1989; 17:118–121.

IAP of 15-20 mmHg coincides with oliguria; over 30 mmHg causes anuriaCompression of renal vasculature, parenchymaStimulation of juxtaglomerularapparatus

Pathophysiology

Decreased blood flow to all abdominal organs except adrenalsDecreased mesenteric and mucosal blood flowDecreased pHi

Intestinal/mucosal

Clinical EffectsSystemClinical Effects of Increased Abdominal Pressure

Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intraabdominal pressure on mesenteric and intestinal mucosal blood flow. J Trauma 1992;33:45–49.

0

0.2

0.4

0.6

0.8

1

0 20 40

Intra-abdominal pressure (mmHg)

Inte

stin

al m

ucos

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erfu

sion

IAH found to decrease perfusion of every intra-abdominal viscus (except adrenals)Effect persists even when cardiac output is corrected

Pathophysiology

Increased ICPDecreased CPP

Neurologic

Clinical EffectsSystemClinical Effects of Increased Abdominal Pressure

Bloomfield GL, Dalton JM, Sugerman HJ, Ridings PC, DeMaria EJ, Bullock R. Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma 1995;39:1168–1170.

Increase in IAP↓

Increase in ITP↓

Increase in CVP↓

Decrease in CPP

StatisticsReview of 13,817 consecutive trauma admissions revealed incidence of 15% among patients undergoing staged laparotomy with packing1

Of 145 acutely injured patients with ISS ≥ 15, twenty-one (14%) developed ACS2

Review of 70 patients with life-threatening penetrating injuries revealed an incidence of 33%3

In a prospective study of 706 consecutive patients admitted to a trauma ICU incidence of ICH was 2% and ACS 1%4

1 Morris JA Jr, Eddy VA, Blinman TA, Rutherford EJ, Sharp KW. The staged celiotomy for trauma. Issues in unpacking and reconstruction. Ann Surg. 1993 May;217(5):576-84 2 Meldrum DR, Moore FA, Moore EE, Francoise RJ, Sauaia A, Burch JM. Prospective characterization and selective management of the abdominal compartment syndrome. Am JSurg 1997; 174: 667-733 Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM. Intra-abdominal hypertension after life-threateningpenetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominalcompartment syndrome. J Trauma 1998; 44: 1016-214 Hong JJ, Cohn SM, Perez JM, Dolich MO, Brown M, McKenney MG. Prospective study of the incidence and outcome of intra-abdominal hypertension and the abdominal compartment syndrome. Br J Surg. 2002 May;89(5):591-6

DiagnosisHigh index of suspicionClinical signs:

Abdominal distention, tensionDecreased urine output Elevated filling pressuresElevated ICP Worsening acidosis Elevated peak airway pressures

ConfirmationBalogh Z, McKinley BA, Holcomb JB, Miller CC, Cocanour CS, Kozar RA, Valdivia A, Ware DN, Moore FA. Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 2003 May;54(5):848-59

DiagnosisDirect monitoring of IAP

Intraperitoneal catheter connected to water manometer or pressure transducerMost accuratePreferred in experimental studiesClinical use limited by risk of peritoneal contamination, bowel perforation

Diagnosis

Indirect monitoring of IAPMeasuring pressure within abdominal organsLess invasiveLess reliableTransfemoral caval catheterGastric tubeRectal tubeIntravesical pressure monitoring

Diagnosis

Intravesical monitoringMost closely reflects direct monitoring1,2

Foley clamped distal to aspiration port50 to 100 cc saline injected into bladder16-guage needle connected to pressure transducer, inserted into aspiration port

1 Obeid F, Saba A, Fath J, et al. Increases in intraabdominal pressure affect pulmonary compliance. Arch Surg1995; 130:544-5482 Iberti TJ, Kelly KM, Gentili DR, Hirsch S, Benjamin E. A simple technique to accurately determine intraabdominalpressure. Crit Care Med 1987;1140–1142

Treatment: An Ounce of Prevention

Identify patients at riskMajor trauma, damage control surgeryLaparotomy for major bleedingEdematous and/or ischemic bowelAbdominal vascular proceduresMechanically difficult closureHigh-volume resuscitation

Avoid primary fascialclosure

Offner PJ, de Souza AL, Moore EE, Biffl WL, Franciose RJ, Johnson JL, Burch JM. Avoidance of abdominal compartment syndrome in damage-control laparotomy after trauma. Arch Surg 2001;136:676-680

Treatment: An Ounce of Prevention

Treatment: Surgical decompression

Timing of interventionIAH ≠ ACSRecommendations differ

Modest IAH + organ dysfunction1

Marked IAH2

No absolute evidence-based guidelines

1 Meldrum DR, Moore FA, Moore EE, Franciose RJ, Sauaia A, Burch JM. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 1997; 174: 667–6732 Ivatury RR, Sugerman HJ. Abdominal compartment syndrome: a century later, isn’t it time to pay attention? CritCare Med 2000; 28: 2137–2138

Treatment: Surgical Decompression

Abdominal decompression and re-explorationAnuria, decreased cardiac output, raised PAWP

>35IV

Consider abdominal decompressionAnuria, decreased cardiac output, raised PAWP

26–35III

Hypervolemic resuscitation may be employed but could have drawbacks

May have increased PAWP and oliguria16–25II

Maintain normovolemiaNo signs of ACS10–15I

TreatmentAssociated signsIAP (mmHg)Grade

Proposed ACS grading system:

Meldrum DR, Moore FA, Moore EE, Franciose RJ, Sauaia A, Burch JM. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 1997; 174: 667–673

Treatment: Hazards of Laparostomy

“Reperfusion injury”Morris et al1 reported fatal cardiac arrest in 4 of 16 patients undergoing decompressive laparostomyPrevention

Abrupt shift in vent requirementsSudden fluid shiftsLoss of tamponadeComplications of open abdomen

Large surface for fluid lossExposes viscera to trauma, desiccationRoute for infection

Morris JA Jr, Eddy VA, Blinman TA, et al. Staged celiotomy for trauma: issues in unpacking and reconstruction. Ann Surg 1993;217:576-586

Treatment: Nonoperative management

Progression of IAH to ACS may be arrested by nonoperative maneuvers

ParalysisDiuresis or fluid resuscitation

Attempts at management of ACS with percutaneous decompression have been almost universally catastrophic

Patients with ACS secondary to abdominal burns may represent an exceptionAlain and Sherman (2001):

Case series in which ACS in burn patients was managed successfully by percutaneous intraperitoneal drainage catheter

Alain CC, Sherman HF. Percutaneous treatment of secondary abdominal compartment syndrome. J Trauma, 2001;51:1062–1064

Outcome

Intervention successful vis-à-vis early endpointsAirway pressuresCardiac outputUrine output

High mortality rate (10.6-68%)Most commonly succumb to MOF, sepsisPaucity of data on short-term and long-term morbidity

Bailey J, Shapiro MJ. Abdominal compartment syndrome. Crit Care 2000;4(1):23-9

ACS and the General Surgeon

Preponderance of data on ACS based on trauma patientsRetrospective review by McNelis et al of nontraumaSICU admissions developing ACS:

Study population:Eighteen patientsM:F ratio 1:28 AAA repairs6 laparotomies3 cases of pancreatitis1 cerebral aneurysm

Appropriate response to decompression (↑UO, ↓PIP, ↑CO)Mortality 61.1%

Mcnelis J, Soffer S, Marini CP, Jurkiewicz A, Ritter G, Simms HH, Nathan I. Abdominal compartment syndrome in the surgical intensive care unit. Am Surg. 2002 Jan;68(1):18-23

ACS and Acute Pancreatitis

4(80%)3(16.7)7(30.4)Mortality (%)

61751823n

Severe Acute Pancreatitis complicated with ACS3

Infected stage

SIRS stageNo laparostomy performed

Laparostomy performed

Total

Current paradigm for acute pancreatitis:Delayed operation1

Operation for infected necrosis2

Retrospective review of 23 patients with pancreatitis and ACS:

1 Mier J, Leon EL, et al. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg 1997;173:71-5 2 Bradley III EL, Allen KA. Prospective longitudinal study of observation vs surgical intervention in the management of necrotizing pancreatitis. Am J Surg 1991;161:19-243 Tao J, Wang C, Chen L, Yang Z, Xu Y, Xiong J, Zhou F. Diagnosis and management of severe acute pancreatitis complicated with abdominal compartment syndrome. J Huazhong Univ Sci Technolog Med Sci. 2003;23(4):399-402

Conclusions

Abdominal compartment syndrome is a potentially fatal constellation of symptoms with many disparate etiologiesA high index of suspicion and astute decision-making are required for successful managementFurther data would help guide treatment of this syndrome in both the injured and the general surgical population