This document discusses abdominal compartment syndrome (ACS), an underrecognized cause of acute kidney injury. It defines ACS as multiple organ dysfunction caused by elevated intra-abdominal pressure. The document outlines various causes of increased intra-abdominal pressure and the physiologic manifestations of ACS, which can impact the cardiac, pulmonary, gastrointestinal, renal and neurological systems. Left untreated, ACS can lead to multi-system organ failure and death. Early detection of increased intra-abdominal pressure and treatment, including decompressive laparotomy if needed, are important to prevent complications of ACS.

1. Abdominal Compartment Syndrome :
An Unrecognised Cause of AKI
SAID KHAMIS (MD, KUL Belgium)
Professor Of Medicine
Nephrology Consultant
Menofia University Hospitals

2. Agenda - IAH and ACS
 Definition – what is it?
 Causes
 Recent increase in recognition
 Physiologic Manifestations
 Prevalence
 Outcome
 Treatment
 Detection:
 Bladder pressure monitoring

3. Abdominal Compartment Syndrome
Definition
“…….. multiple organ dysfunction caused by
elevated intra-abdominal pressure.”
Tim Wolfe, MD

4. What intra-abdominal pressures
are concerning?
Pressure (mm Hg) Interpretation
0-5 Normal
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

5. 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)

6. Causes of Intra-abdominal Pressure
(IAP) Elevation
 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
tumors, PD, pregnancy

7. Are we seeing more ACS?
 Increased Incidence?
 Syndromes created by medical
“progress”
 ICU’s full of sicker patients
 Fluid resuscitation due to early goal
directed therapy for sepsis?
 Increased Recognition?

8. ACS Literature: Publication
explosion
140
120
100
80
60
Research Publications
40
20
0
83- 87- 91- 95- 99- 00
84 88 92 96 00 3-
04

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

10. Physiologic Sequelae
Cardiac:
 Increased intra-abdominal pressures
causes:
 Compression of the vena cava with reduction in
venous return to the heart
 Elevated ITP with multiple negative cardiac
effects
 The result:
 Decreased cardiac output increased
SVR
 Increased cardiac workload
 Decreased tissue perfusion, SVO2
 Misleading elevations of PAWP and CVP
 Cardiac insufficiency Cardiac arrest

11. Physiologic Sequelae
Pulmonary:
 Increased intra-abdominal pressures
causes:
 Elevation of the diaphragms with reduction in
lung volumes
 Cytokines release, immune hyper-responsiveness
The result:
 Elevated intrathoracic pressure (which further
reduces venous return to heart, exacerbating
cardiac problems)
 Increased peak pressures, Reduced tidal volumes
 Barotrauma, atelectasis, hypoxia, hypercarbia
 ARDS (indirect - extrapulmonary)

12. Physiologic Sequelae
Gastrointestinal:
 Increased intra-abdominal pressures
causes:
 Compression / Congestion of mesenteric
veins and capillaries
 Reduced cardiac output to the gut
The result:
 Decreased gut perfusion, increased gut
edema and leak
 Ischemia, necrosis, cytokine release,
neutrophil priming
 Bacterial translocation
 Development and perpetuation of SIRS
 Further increases in intra-abdominal
pressure

13. Physiologic Sequelae
Renal:
 Elevated intra-abdominal pressure
causes:
 Compression of renal veins and arteries
 Reduced cardiac output to kidneys
The Result:
 Decreased renal artery and vein flow
 Renal congestion and edema
 Decreased glomerular filtration rate (GFR)
 Acute tubular necrosis (ATN)
 Renal failure, oliguria/anuria

14. Physiologic Sequelae
Neuro:
 Elevated intra-abdominal pressure causes:
 Increases in intrathoracic pressure
 Increases in superior vena cava (SVC) pressure with
reduction in drainage of SVC into the thorax
The Result:
 Increased CVP and IJ pressure
 Increased intracranial pressure
 Decreased cerebral perfusion pressure
 Cerebral edema, brain anoxia, brain injury

15. Physiologic
Sequelae
Direct impact of IAP
on common
pressure
measurements:
 IAP elevation causes
immediate increases
in ICP, IJP and CVP
(also in PAOP)
15 liter bag placed on abdomen
(Citerio 2001)

16. Physiologic Sequelae
Miscellaneous
 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

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

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

19. Does IAH / ACS affect patient
outcome?
Ivatury, J Trauma, 1998: Intra-abdominal
hypertension after life-threatening penetrating
abdominal trauma: prophylaxis, incidence, and
clinical relevance to gastric mucosal pH and
abdominal compartment syndrome.
 70 patients with monitored for IAP > 25 mm
Hg
 25 had facial closure at time of surgery:
 52% developed IAP > 25
 39% Died
 45 cases had abdomen left “open”:
 22% developed IAP > 25
 10.6% Died

20. Does IAH / ACS affect patient
outcome?
Points:
 Clinical signs of IAH are unreliable and only
show up late in clinical course (once ACS
occurs).
 IAH and ACS increase morbidity, mortality
and ICU length of stay.
 Preventive therapy plus early detection and
intervention can reduce these complications in
many patients.
 Monitoring early (not waiting for clinical signs)
in all high risk patients allows early detection
and early intervention.

21. 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
 Cathartics / enema to clear bowel?
 Colloids
 Hemofiltration
 Paracentesis
 Need significant free fluid on US
 Decompressive laparotomy

22. 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%

23. IAH/ACS Management:
Decompressive Laparotomy
Rigid Abdomen in ACS
Post decompressive laparotomy

24. Surgical Management of
Compartment Syndromes
Pathophysiology
Compartment Surgical Management
ICP elevation
Cranium Mannitol,
Craniectomy, etc..
Tension
Chest pneumothorax Chest tube
Pericardium Cardiac tamponade Pericardiocentesis
Extremity
Limb compartment Fasciotomy
syndrome

25. Decompressive Laparotomy
 Delay in
abdominal
decompression
may lead to
intestinal
ischemia
 Decompress
Early!

26. Decompressive Laparotomy
Post-operative dressing Several days post-op

27. Intra-Abdominal Pressure
Monitoring
Bladder pressure monitoring through
the Foley catheter is:
 The current standard for monitoring
abdominal pressures (Consensus, World
Congress ACS Dec 2004)
 Comparable to direct intraperitoneal
pressure measurements, but is non-
invasive (Bailey, Crit Care 2000)
 More reliable and reproducible than
clinical judgment (Kirkpatrick, CJS 2000;
Sugrue World J Surg 2002)

28. “Home Made” Pressure
Transducer Technique
Home-made assembly:
 Transducer
 2 stopcocks
 1 60 ml syringe,
 1 tubing with saline
bag spike / luer
connector
 1 tubing with luer
both ends
 1 needle / angiocath
 Clamp for Foley
Assembled sterilely in
proper fashion

29. University of
Utah: IAP
monitoring
algorithm
 Entry criteria
defined in table
 Nurse is empowered
to enter any patient
fulfilling these
criteria

30. 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

31. QUESTIONS?
IAH and ACS Educational Web
sites:
www.Abdominalcompartmentsyndrome.
org