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 measurementsEvaluate 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.