Abdominal Compartment
Syndrome & Renal Failure
PEGGY BEELEY, MD
O C T O B E R 1 2 TH, 2 0 1 1
Case
 49 yo female admitted with cirrhosis and worsening ascites,
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Cr 2.8 on admission
Had diagnostic paracentesis on admission negative for
infection
Nephrology consulted. Urine sediment c/w ATN with prerenal
component suspected
Large volume paracentesis of 3.5 L, next diagnostic tap 4 days
later was bloody
Cr began to climb, bladder pressure was 32-34 mmHg
Large volume paracentesis removed 5 L of bloody fluid,
bladder pressure 24 mmHg
Cr continued to climb, comfort care measures instituted
Patient died
Objectives
 Understand pathophysiology of increased
intraabdominal pressure (IAP) and organ
failure
 Learn current methods used in determining
IAP
 Learn limitations of such measurements
 Evaluate literature for use in cirrhotic
patients with ascites
ACS: Importance in Hospitalist Medicine
 Occurs in
 Patients with rapid volume resuscitation (especially in
early goal directed therapy for sepsis)
 Acute formation of ascites
 In visceral edema
 May see this more commonly as we see more
acutely ill patients
 High mortality rate associated with ACS
 Early recognition leads to improved outcomes
History of Abdominal Compartment Syndrome
(ACS)
 Wendt in 1876 the association of intra-abdominal
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hypertension (IAH) and renal dysfunction
Recognized as a complication in trauma surgery in
1970s
Most early descriptions in trauma literature
Now recognized as occurring in critically ill patients
and in medical conditions
Not universally appreciated across different
specialties
Not much in nephrology literature by my search
Abdominal Compartment Syndrome (ACS)
 Rotondo, et al 1983 recognized that IAH as cause
of multi-organ failure
 ↓preload, ↑afterload and extrinsic compression
leads to decreased oxygen delivery in abdominal
organs
 Resultant pressure-volume dysregulation
syndrome is known as ACS
World Society of the ACS
The mission of the
WSACS is to promote
research, foster
education, and improve
the survival of patients
with intra-abdominal
hypertension (IAH)
and/or abdominal
compartment
syndrome (ACS) All
who have an interest in
the diagnosis,
management, and/or
treatment of IAH / ACS
are invited to join the
Society.
Definitions
 Normal intraabdominal pressure (IAP) is <5-7 mmHg
 Upper limit of normal IAP is 12 mmHg
 > 12 mmHg is Intraabdominal Hypertension (IAH), must
be sustained to meet criteria
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Grade I is 12-15 mm Hg
Grade II is 16-20 mm Hg
Grade III 21-24 mm Hg
Grade IV > 25 mm Hg
 ACS : sustained IAP >20 mmHg that is associated with
new organ dysfunction
 Morbidly obese and pregnant women may have pressure
as high as 10-15 mmHg without adverse sequela
Primary vs. Secondary ACS
 Primary ACS injury or dz within abd or pelvis
 Surgical interventions often needed
 Secondary ACS
 Often from conditions outside the abd or pelvis., e.g.
burns, sepsis
 Recurrent ACS
 Condition in which ACS redevelops following previous
surgical or medical treatment of primary or secondary
ACS
Mechanism of Organ injury in ACS
 Ischemia, either venous or arterial
 Release of vasodilatory substances
 As ischemia progresses capillary integrity
fails and leads to extravasation of fluid,
lytes, proteins
 Increased distance between tissue and
capillaries
 Viscous cycle compromises organ viability
Renal Injury due to ACS
 First oliguria
 Then rise in serum creatinine
 Rise of < 0.3 mg in creatinine = AKI
 Rise of more that 0.3 mg = ARF
 As oliguria worsens no amount of fluid resuscitation
will help
 ATN occurs upon reperfusion, usually by abdominal
decompression
Cirrhosis and Ascites in ACS
 Mentioned in several articles as potential cause of
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ACS
Removal of ascites in IAPs > 18.4 mmHg does
improve renal function
Intravasc volume may improve renal function in
chronic ascites where ACS it does not
Most cirrhotics tolerate > 15 liters of ascites w/o
renal failure or organ ischemia
Abdominal wall compliance remains if fluid
accumulation is slow
Renal Failure in Cirrhotics with Ascites
IAH/ACP
Hepato-renal
 Oliguria
 Oliguria
 Often looks like ATN
 Bland urine sediment
 Acute ischemia to
kidney
 Vasodilators: Lactate
and adenosine
 Elevated ADH, usually
increased more than
twice baseline
 Slowly progressive
ischemia
 Vasodilator: Nitric
Oxide, ?prostaglandins
 Salt conserving state,
elevated ADH
Incidence of IAH and ACS in Critically ill
 Multicenter prospective study of 265 patients
admitted to ICU
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32% IAH
4% ACS
53% normal IAP
 IAH was strongly associated with multi-organ
dysfunction and nearly all had ARF
 Another prospective study of 706 pts at U of Miami
showed an incidence of 2% IAH and 1% ACS in
trauma population
Malbrain et al, Crit Care Med 2005 ; 33
Hong et al Br J Surg 2002: 89
Associated signs and organ failure in ACS
 Hypovolemic shock
 ↓ SBP,↓ pulse pressure, lactic acidosis, tachy
 Increased core to peripheral temp grad, weak pulses, abnormal
mentation
 Acute kidney injury/acute renal failure
 Acute respiratory failure
 Hypoxia & hypercarbia
 Increased peak airway pressures
 ↓tidal volume
 Acute hepatic failure
 ↑LFTs, coagulopathy
Estimating & Measuring IAP
 Bladder pressure
 NGT pressure
 Condom Cath measurement
 Gastric tonometry
 Direct measurements by laparoscopy
 Direct measurement in femoral vein or
inferior vena cava
Validity of Bladder Pressure as an estimation of IAP
 37 patients undergoing laparoscopy
 Measured direct IAP with laparoscopic insufflation
 Simultaneously measured bladder pressure
 At O ml bladder volume
 50 ml, 100 ml, 150 ml, & 200 ml
 1110 data points of bladder pressure at various IAPs
were collected
 Findings showed high correlation of bladder
pressure to IAP (R2 = 0.68)
 Least bias with the 50 ml instillation
Fusco et al, J of Trauma,: 2001: 50
Measuring Bladder Pressure
Cheatham et al J Am Coll Surg 1998
Other Causes of Elevated IAP Estimates in Bladder Pressure
 Central Obesity
 Pregnancy
 Not reliable in the following
 Low
intrinsic bladder compliance
 bladder trauma
 Pelvic hemorrhage
 Overestimated in these conditions
Therapeutic Interventions
 Laparotomy with temporary closure to enlarge
peritoneal space
 Non-surgical
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Catheter drainage
Therapeutic paracentesis
Dialysis
Neuromuscular blockage
Prokinetic agents if intestinal distension is present.
Control underlying etiology (hemorrhage, ascites)
 No prospective RCT have been done to compare
efficacy of Non-surgical decompression vs. surgical
Nonoperative Management of IAH & ACS
 Evacuate intraluminal contents
 Evacuate intraabdominal space-occupying
lesions
 Improve abdominal wall compliance
 Optimize fluid administration
 Optimize systemic and regional tissue
perfusion
Cheatham, World J Surg 2009 33
Case
 49 yo female admitted with cirrhosis and worsening
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ascites, Cr 2.8 on admission
Although patient did have a slowly worsening ascites, she
develop hemorrhage after paracentesis
High risk patient
Acute on chronic elevation in IAP could have led to ACP
Therapeutic tap seemed reasonable, did we not take off
enough?
May have been Hepatorenal but bladder pressure of 32
made ACP a compelling diagnosis
Recommendations
 Consider ACS in your differential diagnosis,
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especially after rapid fluid resuscitation
Acute ACS is generally a surgical disease with
abdominal decompression
If recommended by consultant, ask to review rational
Remember to do albumin replacement in large
volume paracentesis
Group did not come to clear consensus about how to
use bladder pressures in cirrhotic patients with
ascites.