peggy beeley, md october 12 th, 2011 abdominal compartment syndrome & renal failure
TRANSCRIPT
PEGGY BEELEY, MDOCTOBER 12 T H , 2011
Abdominal Compartment Syndrome & Renal Failure
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 mmHgLarge volume paracentesis removed 5 L of bloody fluid,
bladder pressure 24 mmHgCr continued to climb, comfort care measures institutedPatient 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 ACSEarly 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 literatureNow recognized as occurring in critically ill
patients and in medical conditionsNot universally appreciated across different
specialtiesNot 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 mmHgUpper 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 arterialRelease of vasodilatory substancesAs 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 oliguriaThen rise in serum creatinine Rise of < 0.3 mg in creatinine = AKIRise of more that 0.3 mg = ARFAs oliguria worsens no amount of fluid
resuscitation will helpATN 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
IAH/ACP Hepato-renal
OliguriaOften looks like ATNAcute ischemia to
kidneyVasodilators: Lactate
and adenosineElevated ADH, usually
increased more than twice baseline
OliguriaBland urine
sedimentSlowly progressive
ischemiaVasodilator: Nitric
Oxide, ?prostaglandins
Salt conserving state, elevated ADH
Renal Failure in Cirrhotics with Ascites
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 ; 33Hong 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 mentationAcute kidney injury/acute renal failureAcute respiratory failure
Hypoxia & hypercarbia Increased peak airway pressures ↓tidal volume
Acute hepatic failure ↑LFTs, coagulopathy
Estimating & Measuring IAP
Bladder pressureNGT pressureCondom Cath measurementGastric tonometryDirect measurements by laparoscopyDirect measurement in femoral vein
or inferior vena cava
Validity of Bladder Pressure as an estimation of IAP
37 patients undergoing laparoscopyMeasured direct IAP with laparoscopic
insufflationSimultaneously 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 instillationFusco 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 ObesityPregnancyNot 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 contentsEvacuate intraabdominal space-
occupying lesionsImprove abdominal wall complianceOptimize fluid administrationOptimize 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 patientAcute on chronic elevation in IAP could have led to
ACPTherapeutic 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.