Abdominal Compartment Syndrome & Renal Failure
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Transcript Abdominal Compartment Syndrome & Renal Failure
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,
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
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
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
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
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
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
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,
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.