Case Presentation

Joseph M Brandel, MD
Kings County Hospital Center
Department of Surgery
Friday, 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

History

1863: 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 urine
1890: Heinricius of Germany
found that IAPs between 27 and
46 cmH2O were fatal to animals
owing to prevention of respiration

History

1911: Haven Emerson publishes his treatise,

'intra-abdominal pressures'
contraction of the diaphragm identified as chief
factor in the rise of IAP during inspiration
excessive IAP can cause death from cardiac
failure even before terminal asphyxia develops
Observed 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

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 al2

Published landmark case series on IAH
11 patients with elevated IAP after aortic
repair (>30 mmHg)
7 patients decompressed with immediate
diuresis
The other 4 patients died

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

Pathophysiology

Causes of intra-abdominal hypertension

Primary: due to intra-abdominal process

Trauma: Intra-abdominal bleeding, MAST,

damage control surgery
Retroperitoneal: Pancreatitis, ruptured AAA,
abscess
Intraperitoneal: Gastric dilatation, bowel
obstruction, visceral edema, tension
pneumoperitoneum
Abdominal wall: Burn eschar, reduction of large
hernias

Secondary: due to massive fluid administration

for extra-abdominal process

Capillary leak
Ischemia-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;77:783800

Pathophysiology
Clinical Effects of Increased Abdominal Pressure
System

Clinical Effects

Hemodynamics

Decreased cardiac output

Decreased preload
Increased afterload
Increased CVP and PCWP

Pulmonary

Increased peak inspiratory pressures

Increased airway pressures
Decreased PaO2
Increased PaCO2
Decreased dynamic compliance

Renal

Decreased renal plasma flow

Decreased GFR
Decreased glucose reabsorption
Oliguria or anuria

Intestinal/mucosal

Decreased blood flow to all abdominal organs expect adrenals

Decreased mesenteric and mucosal blood flow
Decreased pHi

Neurologic

Increased ICP
Decreased CPP

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; 17:118121.

Pathophysiology
Clinical Effects of Increased Abdominal Pressure
System

Clinical Effects

Hemodynamics

Decreased cardiac output

Decreased preload
Increased afterload
Increased CVP and PCWP

Cardiac output

0.8
0.6

0.4
0.2
0
0

10

20

30

Elevation of diaphragm
transmits pressure to
heart and great vessels
CVP and PCWP are
spuriously elevated
not a reflection of volume
status

40

Intra-abdominal pressure (mmHg)

Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. Cardiopulmonary effects of raised intraabdominal
pressure before and after intravascular volume expansion. J. Trauma 1995;39:10711075.

Pathophysiology
Clinical Effects of Increased Abdominal Pressure
Clinical Effects

Pulmonary

Increased peak inspiratory pressures

Increased airway pressures
Decreased PaO2
Increased PaCO2
Decreased dynamic compliance

Peak airway pressure

System

50

40
30
20

10

0
0

10

15

20

25

30

35

Increases in pleural
pressures evident at IAP
of 15 mmHg or greater
Exacerbated by PEEP
Normalizes after surgical
decompression

40

Intra-abdominal pressure (mmHg)

Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. Cardiopulmonary effects of raised intraabdominal
pressure before and after intravascular volume expansion. J. Trauma 1995;39:10711075.

Pathophysiology
Clinical Effects of Increased Abdominal Pressure
System

Clinical Effects

Renal

Decreased renal plasma flow

Decreased GFR
Decreased glucose reabsorption
Oliguria or anuria

IAP of 15-20 mmHg

coincides with oliguria;
over 30 mmHg causes
anuria
Compression of renal
vasculature, parenchyma
Stimulation of
juxtaglomerular
apparatus

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; 17:118121.

Pathophysiology
Clinical Effects of Increased Abdominal Pressure
Clinical Effects

Intestinal/mucosal

Decreased blood flow to all abdominal organs except adrenals

Decreased mesenteric and mucosal blood flow
Decreased pHi

Intestinal mucosal perfusion

System

0.8
0.6
0.4

0.2
0
0

20

IAH found to decrease

perfusion of every intraabdominal viscus (except
adrenals)
Effect persists even
when cardiac output is
corrected

40

Intra-abdominal pressure (mmHg)

Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intraabdominal pressure on mesenteric and intestinal
mucosal blood flow. J Trauma 1992;33:4549.

Pathophysiology
Clinical Effects of Increased Abdominal Pressure
System

Clinical Effects

Neurologic

Increased ICP
Decreased CPP

Increase in IAP

Increase in ITP

Increase in CVP

Decrease in CPP
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;39:11681170.

Statistics

Review 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: 667-73
3 Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM. Intra-abdominal hypertension after life-threatening
penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal
compartment syndrome. J Trauma 1998; 44: 1016-21
4 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

Diagnosis

High index of
suspicion
Clinical signs:

Abdominal distention,
tension
Decreased urine
output
Elevated filling
pressures
Elevated ICP
Worsening acidosis
Elevated peak airway
pressures

Confirmation

Balogh 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

Diagnosis

Direct monitoring of
IAP
Intraperitoneal catheter
connected to water
manometer or pressure
transducer
Most accurate
Preferred in
experimental studies
Clinical use limited by
risk of peritoneal
contamination, bowel
perforation

Diagnosis

Indirect monitoring of IAP

Measuring

pressure within
abdominal organs
Less invasive
Less reliable
Transfemoral caval catheter
Gastric tube
Rectal tube
Intravesical pressure
monitoring

Diagnosis

Intravesical monitoring
Most

closely reflects
direct monitoring1,2
Foley clamped distal to
aspiration port
50 to 100 cc saline
injected into bladder
16-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 Surg
1995; 130:544-548
2
Iberti TJ, Kelly KM, Gentili DR, Hirsch S, Benjamin E. A simple technique to accurately determine intraabdominal
pressure. Crit Care Med 1987;11401142

Treatment: An Ounce of
Prevention

Identify patients at risk

Major trauma, damage

control surgery
Laparotomy for major
bleeding
Edematous and/or
ischemic bowel
Abdominal vascular
procedures
Mechanically difficult
closure
High-volume resuscitation

Avoid primary fascial

closure
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 intervention
IAH

ACS
Recommendations differ
Modest IAH + organ dysfunction1
Marked IAH2

No

absolute evidence-based
guidelines

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: 667673
2
Ivatury RR, Sugerman HJ. Abdominal compartment syndrome: a century later, isnt it time to pay attention? Crit
Care Med 2000; 28: 21372138

Treatment: Surgical
Decompression

Proposed ACS grading system:

Grade

IAP (mmHg)

Associated signs

Treatment

1015

No signs of ACS

Maintain normovolemia

II

1625

May have increased PAWP and oliguria

Hypervolemic resuscitation may be employed but

could have drawbacks

III

2635

Anuria, decreased cardiac output, raised

PAWP

Consider abdominal decompression

IV

>35

Anuria, decreased cardiac output, raised

PAWP

Abdominal decompression and re-exploration

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: 667673

Treatment: Hazards of
Laparostomy

Reperfusion injury
Morris et al1 reported fatal cardiac
arrest in 4 of 16 patients undergoing
decompressive laparostomy
Prevention

Abrupt shift in vent requirements

Sudden fluid shifts
Loss of tamponade
Complications of open abdomen

Large surface for fluid loss

Exposes viscera to trauma, desiccation
Route 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

Paralysis
Diuresis 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 exception
Alain 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;51:10621064

Outcome

Intervention successful vis--vis early endpoints

Airway

pressures
Cardiac output
Urine output

High mortality rate (10.6-68%)

Most

commonly succumb to MOF, sepsis

Paucity 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

patients
Retrospective review by McNelis et al of nontrauma
SICU admissions developing ACS:

Study population:

Eighteen patients
M:F ratio 1:2
8 AAA repairs
6 laparotomies
3 cases of pancreatitis
1 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

Current paradigm for acute pancreatitis:

Delayed operation1
Operation for infected necrosis2

Retrospective review of 23 patients with pancreatitis and

ACS:
Severe Acute Pancreatitis complicated with ACS3

1
2

Total

Laparostomy
performed

No laparostomy
performed

SIRS stage

Infected
stage

23

18

17

Mortality
(%)

7(30.4)

3(16.7)

4(80%)

Mier J, Leon EL, et al. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg 1997;173:71-5

Bradley III EL, Allen KA. Prospective longitudinal study of observation vs surgical intervention in the management of
necrotizing pancreatitis. Am J Surg 1991;161:19-24
3
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 etiologies
A high index of suspicion and astute decisionmaking are required for successful management
Further data would help guide treatment of this
syndrome in both the injured and the general
surgical population