Abdominal compartment syndrome (ACS) occurs when sustained high intra-abdominal pressure (>20 mmHg) causes organ dysfunction. It is increasingly recognized in critically ill patients and can lead to multi-organ failure if not treated. Intra-abdominal pressure is normally 5-7 mmHg but becomes a concern above 12 mmHg and dangerous above 20 mmHg. Causes include abdominal bleeding, edema from fluid resuscitation, and abdominal wall closure under tension. Early detection by bladder pressure monitoring and treatment by optimizing abdominal perfusion pressure can prevent progression to ACS and improve outcomes. Decompressive laparotomy may be needed for refractory cases.

1. Rana Tanweer Ahmad
Mr.Sheikh Team
Abdominal Compartment Syndrome

2. Outline
 Definitions
 Causes
 Recent increase in recognition
 Detection:
 Physiologic Manifestations
 Prevalence
 Outcome
 Treatment
 discussion

3. Definitions
A. Intra-abdominal Pressure (IAP): Intrinsic pressure within
the abdominal cavity most critically ill patients, an IAP of 5 to
7 mmHg is considered normal, obese and pregnant
individuals may have chronically higher baseline IAP (as
high as 10 to 15 mmHg) without adverse sequelae.
B. Abdominal perfusion pressure (APP): APP =MAP - IAP
Elevated IAP reduces blood flow to the abdominal viscera. A
target APP of at least 60 mmHg is correlated with improved
survival from IAH and ACS. was found to be better than
other resuscitation endpoints e.g. hourly urinary output for
predicting the outcomes.
C. Intra-abdominal Hypertension (IAH): An IAP > 12 mm Hg
(often causing occult ischemia) without obvious organ failure
D. Abdominal Compartment Syndrome (ACS): A sustained
IAP >20 mmHg (with or without APP <60 mmHg) that is
associated with new organ dysfunction.

4. What intra-abdominal pressures are
concerning?
Pressure (mm Hg) Interpretation
0-5 Normal
10-15 Obese and pregnant chronically
high baseline
5-10 Common in most ICU patients
> 12 Intra-abdominal hypertension
15-20 Dangerous IAH - consider non-
invasive interventions
>20-25 Impending abdominal compartment
syndrome - strongly consider
decompressive laparotomy

6. Intraabdominal Hypertension
Hyperacute IAH: lasting only seconds.laughing, coughing,
straining, sneezing, defecation, or physical activity. IAH with
gastric over-distention following endoscopy.
Acute IAH: Develops over hours,trauma or intraabdominal
hemorrhage and can lead to the rapid development of ACS.
Subacute IAH : Develops over days. most common in medical
patients and can also lead to ACS.
Chronic IAH: Develops over months (pregnancy) or years
(morbid obesity). It does not cause ACS, but does place the
individual at higher risk for ACS if they develop superimposed
acute or subacute IAH.
Grade I = IAP 12 to 15 mmHg
Grade II = IAP 16 to 20 mmHg
Grade III = IAP 21 to 25 mmHg

8. Causes of Intra-abdominal Pressure (IAP) Elevation
Retroperitoneal: pancreatitis, retroperitoneal or pelvic
bleeding, contained AAA rupture, aortic surgery,
abscess, visceral edema
Intraperitoneal: intraperitoneal bleeding, AAA rupture,
acute gastric dilatation, bowel obstruction, ileus,
mesenteric venous obstruction, pneumoperitoneum,
abdominal packing, abscess, visceral edema
secondary to resuscitation (SIRS)
Abdominal Wall: burn eschar, repair of gastroschisis or
omphalocele, reduction of large hernias, pneumatic
anti-shock garments, lap closure under tension,
abdominal binders
Chronic: central obesity, ascites, large abdominal

9. Intra-Abdominal Pressure Monitoring
IAP can be measured indirectly using:
1. intragastric
2. intracolonic
3. intravesical (bladder)
4. inferior vena cava catheters
Measurement of bladder (ie, intravesical) pressure is the
standard method to screen for IAH and ACS. It is simple,
minimally invasive, and accurate.

10. Physiologic Insult
Ischemia Inflammatory response
Capillary leak
Tissue Edema
(Including bowel wall and mesentery)
Intra-abdominal hypertension
Fluid resuscitation

11. Physiologic Sequelae:
Elevated intra-abdominal
pressure causes:
•Reduces perfusion of
surgical and traumatic
wounds
•Reduced blood flow to liver,
bone marrow, etc.
•Blood pooling in pelvis and
legs
•“Second hit” in the two
event model of MOF?
The Result:
Poor wound healing and
dehiscence
Coagulopathy
Immunosuppression
DVT and PE risks

12. Circling the Drain
Intra-abdominal Pressure
Mucosal
Breakdown
(Multi-System Organ Failure)
Bacterial translocation
Acidosis
Decreased O2 delivery
Anaerobic metabolism
Capillary leak
Free radical formation

13. Clinical presentation
It is desirable to recognize IAH early, so it can be treated before
progressing to ACS.
Symptoms:
Most patients critically ill and unable to communicate.
symptoms may complain of malaise, weakness,
lightheadedness, dyspnea, abdominal bloating, or abdominal
pain.
Physical signs:
Tensely distended abdomen,the abdomen is a poor predictor
of ACS, Progressive oliguria.
Other findings may include hypotension, tachycardia, an
elevated jugular venous pressure, jugular venous distension,
peripheral edema, abdominal tenderness, or acute
pulmonary decompensation.
There may also be evidence of hypoperfusion, including cool

14. Imaging findings:
- Imaging is not helpful in the diagnosis of ACS.
- CXR may show decreased lung volumes,
atelectasis, or elevated hemidiaphragms.
- Computed tomography (CT) may demonstrate tense
infiltration of the retroperitoneum that is out of
proportion to peritoneal disease, extrinsic compression
of the inferior vena cava, massive abdominal
distention, direct renal compression or displacement,
bowel wall thickening, or bilateral inguinal herniation.

15. How common is this syndrome?
Malbrain, Intensive Care Medicine (2004)
Abdominal
pressure:
Total
Prevalence
MICU
prevalence
SICU
prevalence
IAP > 12 58.8% 54.4% 65%
IAP > 15 28.9% 29.8% 27.5%
IAP > 20
plus organ
failure
8.2% 10.5% 5.0%

16. IAH/ACS Management
 Fluids – two edged sword
 Fluids will absolutely improve cardiac indices if the
patient has inadequate RV filling- so early in the
course they are necessary
 However, over resuscitation will lead to worsened
edema
 Abdominal perfusion pressure - optimize fluids first
then add vasopressors. Shoot for a perfusion
pressure > 60 mm Hg
 Sedation, Paralytics
 Cathaterise / enema to clear bowel?
 Colloids
 Hemofiltration
 Paracentesis
 Need significant free fluid on US
 Decompressive laparotomy

17. IAH/ACS Management : Abdominal Perfusion
Pressure
APP = MAP - IAP
 Abdominal perfusion pressure reflects actual gut
perfusion better than IAP alone.
 Optimizing APP to > 60 mm Hg should probably be
primary endpoint
 Cheatham 2000
 Optimizing APP reduced incidence of
 ACS - 64% versus 48%
 Death - 44% versus 28%

18. Decompressive Laparotomy and Open
Abdomen
Open abdomen is an abdominal wall defect created by
intentionally leaving an abdominal incision open at the
completion of intraabdominal surgery or by opening (or re-
opening) the abdomen because of concern for abdominal
compartment syndrome.
Complications of open abdomen:
1. Fluid loss :Daily fluid balance and the patient’s fluid
intake should be adjusted to prevent hypovolemia.
2. Protein loss : About 2 grams of protein lost from the
abdomen for each liter of fluid removed.
3. Fistula formation : Entero-cutaneous or entero-
atmospheric fistula may be as high as 20 percent and
can occur as early as eight days from the initial
laparotomy.

19. TEMPORARY ABDOMINAL CLOSURE
Once a decision has been made to leave the abdomen open (or
re-open it), the abdominal defect must be covered, which is
termed temporary abdominal closure.
Techniques:
1. Patch techniques
2. Negative pressure wound systems
3. Towel-based
4. Sponge-based
5. Silo techniques
6. Skin-only closures
Mean rates for primary fascial closure are as follows :
 90 percent: Wittmann Patch (4 studies/180 patients)
 85 percent: Dynamic fascial closure (1 study/15 patients)
 60 percent: Sponge-based negative pressure system
(8 studies/251 patients)
 52 percent: Towel-based negative pressure system
(15 studies/1186 patients)

20. ABDOMINAL CLOSURE
1. Fascial closure techniques : Ideal management of the open
abdomen results in closure that brings the edges of the
abdominal fascia together primarily (primary closure). If this is
not feasible, functional closure or simple coverage can be
provided.
2. Primary fascial closure : Primary closure of the fascia refers
to the direct approximation of the fascial edges to each other
and is associated with the lowest rate of complications.
incidence of ventral hernia chances 30%.
3. Functional closure : Functional closure refers to the bridging
of a residual fascial defect with a biologic mesh.
4. Planned ventral hernia: If primary fascial closure or
functional closure cannot be achieved, then planned ventral
hernia is the only option. . Skin coverage over abdominal
viscera can be accomplished in one of two ways:
Skin-only closure

21. Patient outcome?
Ivatury, J Trauma, 1998:
 70 patients with monitored for IAP > 25 mm Hg
 25 had fascial closure at time of surgery:
 52% developed IAP > 25
 39% Died
 45 cases had abdomen left “open”:
 22% developed IAP > 25
 10.6% Died

22. Final Thought
Do NOT wait for signs of ACS to be present before
you decide to check IAP
 By then the patient has one foot in the grave!
 You have lost your opportunity for medical therapy
Monitor ALL high risk patients early and often:
 TREND IAP like a vital sign
 Intervene early, before critical pressure develops

24. Timing Of closure?
Open / closed technique?
Discussion and Thank You