abdominal compartment syndrome[1]

Abdominal Compartment Syndrome : An Unrecognised Cause of AKI

SAID KHAMIS (MD, KUL Belgium)Professor Of MedicineNephrology ConsultantMenofia University Hospitals

Agenda - IAH and ACS

Definition – what is it? Causes Recent increase in recognition Physiologic Manifestations Prevalence Outcome Treatment Detection:

Bladder pressure monitoring

Abdominal Compartment Syndrome

“…….. multiple organ dysfunction caused by elevated intra-abdominal pressure.”

Tim Wolfe, MD

Definition

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

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)

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

Are we seeing more ACS?

Increased Incidence? Syndromes created by medical

“progress” ICU’s full of sicker patientsFluid resuscitation due to early goal

directed therapy for sepsis?

Increased Recognition?

ACS Literature: Publication explosion

0

20

40

60

80

100

120

140

83-84

87-88

91-92

95-96

99-00

003-04

Research Publications

Physiologic Insult

Ischemia Inflammatory response

Capillary leak

Tissue Edema (Including bowel wall and mesentery)

Intra-abdominal hypertension

Fluid resuscitation

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

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)

Physiologic SequelaeGastrointestinal: 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

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

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 thoraxThe Result: Increased CVP and IJ pressure Increased intracranial pressure Decreased cerebral perfusion pressure Cerebral edema, brain anoxia, brain injury

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)

Physiologic SequelaeMiscellaneous

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

Circling the Drain

Intra-abdominal Pressure

MucosalBreakdown

(Multi-System Organ Failure)

Bacterial translocation

Acidosis

Decreased O2 delivery

Anaerobic metabolism

Capillary leak

Free radical formation

How common is this syndrome?

Malbrain, Intensive Care Medicine (2004):

Abdominal pressure:

Total Prevalence

MICU prevalence

SICU prevalence

IAP > 12 58.8% 54.4% 65%

IAP > 15 28.9% 29.8% 27.5%

IAP > 20 plus organ

failure

8.2% 10.5% 5.0%

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

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.

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

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%

IAH/ACS Management: Decompressive Laparotomy

Rigid Abdomen in ACS Post decompressive laparotomy

Surgical Management of Compartment Syndromes

Compartment

Cranium

Chest

Pericardium

Limb

Pathophysiology

ICP elevation

Tension pneumothorax

Cardiac tamponadeExtremity compartment

syndrome

Surgical Management

Mannitol, Craniectomy, etc..

Chest tube

Pericardiocentesis

Fasciotomy

Decompressive Laparotomy

Delay in abdominal decompression may lead to intestinal ischemia

Decompress Early!

Decompressive Laparotomy

Post-operative dressing Several days post-op

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)

“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 FoleyAssembled sterilely in

proper fashion

University of Utah: IAP monitoring algorithm

Entry criteria defined in table

Nurse is empowered to enter any patient fulfilling these criteria

Final ThoughtDo 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

QUESTIONS?

IAH and ACS Educational Web sites:

www.Abdominalcompartmentsyndrome.org