Intra-Abdominal Hypertension _IAH_

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Hypertension (IAH)

             Syndrome (ACS)
                   By: Tim Wolfe, MD
• Have you ever seen a critically ill patient
  become progressively more swollen and
  edematous after fluid resuscitation?
• Have any of your ICU patients developed
  renal failure requiring dialysis?
• Have you ever seen a patient develop
  multiple organ failure and die?

   What was their intra-abdominal
           Case: Septic child
5 y.o. female presenting with septic syndrome
• Treatment: Fluids, antibiotics, vasopressors
• 24 hours into therapy develops worsening
  hypotension, oliguria, hypoxemia, hypercarbia.
  PIP rises from 20 to 40 cm
• IAP = 26 mm Hg           decompressive laparotomy
• Immediate resolution of renal, pulmonary and
  hemodynamic compromise
• 7 days later abdomen closed. Alive and well now.
                                  DeCou, J Ped Surg 2000
           Case: Dyspnea in ER
67 y.o. female presenting to ER with pleurisy, dyspnea
• Hypotensive, agitated, H&P suggest liver dz
• IVF resuscitation, intubation, sedation
• Worsened over next 4-6 hours - Difficult to ventilate,
  hypoxic/hypercarbic, hypotension, no UOP.
• IAP = 45 mm Hg, abdominal ultrasound showed tense
  ascites       paracentesis of 4500 cc fluid (IAP = 14)
• Immediate resolution of renal, pulmonary and
  hemodynamic compromise.
• Pathology shows malignant effusion – pancreatic CA.
• Care withdrawn at later time and allowed to expire.
                                      Etzion, Am J EM 2004
        Case: Aspiration patient
77 y.o. male aspirated on ward. Transferred to ICU
  where he required intubation, developed hypotension
• 10 liters IVF overnight, Norepi 1.0 mcg/kg/min.
• Anuric (35 ml urine in 8 hours). Lactate = 4.6
• IAP = 31 mm Hg. KUB – massively distend small and
  large bowel. US shows no free ascitic fluid.
• Surgeon consulted for possible decompressive surgery
• Rx: NGT, Rectal Tube, oral cathartics, neuromuscular
• 1 hour later: IAP 12 mm Hg, UOP 210 ml,
  norepinephrine discontinued.
                                    Cheatham, WSACS 2006
                  Case Points
• Trauma is not required for ACS to develop:
   – Intra-abdominal hypertension and ACS occur in many
     settings (PICU, MICU, SICU, CVICU, NCC, OR, ER).
• IAP measurements are clinically useful: Help to
  determine if IAH is contributing to organ
  dysfunction (i.e. useful if normal or abnormal)
• “Spot” IAP check results in delayed diagnosis:
   – Waiting for clinically obvious ACS to develop before
     checking IAP changes urgent problem to emergent one.
• IAP monitoring will allow early detection and early
  intervention for IAH before ACS develops.
            Outline / Objectives
•   Definition – what is it?
•   Causes
•   Physiologic Manifestations
•   Prevalence
•   Outcome
•   Treatment
•   Detection:
    – Bladder pressure monitoring
• University of Utah/WSACS treatment algorithm
            WCACS, Antwerp Belgium 2007

• Intra-abdominal Pressure (IAP): Intrinsic
  pressure within the abdominal cavity
• Intra-abdominal Hypertension (IAH): An
  IAP > 12 mm Hg (often causing occult
  ischemia) without obvious organ failure
• Abdominal Compartment Syndrome (ACS):
  IAH with at least one overt organ failing
         Types of IAH /ACS
            WCACS, Antwerp Belgium 2007

• Primary – Injury/disease of abdomino-
  pelvic region, “surgical”

• Secondary – Sepsis, capillary leak, burns,

• Recurrent – ACS develops despite surgical
  What intra-abdominal pressures
         are concerning?
Pressure (mm Hg)     Interpretation
 0-5                  Normal
 5-10                 Common in most ICU patients
 > 12 (Grade I)       Intra-abdominal hypertension
16-20 (Grade II)      Dangerous IAH - begin non-
                       invasive interventions
>21-25 (Grade III)    Impending abdominal compartment
                        syndrome - strongly consider
                        decompressive laparotomy
Physiologic Insult/Critical Illness
  Ischemia           Inflammatory response

                           Fluid resuscitation
              Capillary leak

               Tissue Edema
      (Including bowel wall and mesentery)

     Intra-abdominal hypertension
        Causes of Intra-abdominal
        Pressure (IAP) Elevation
• Major abdominal /
  retroperitoneal problem

• Ischemic insult / SIRS
  requiring fluid resuscitation
  with a positive fluid balance
  of 5 or more liters within 24
  hours – (10 lb weight gain)

Where does all that
    fluid go?
Right Here!!
Intra-abdominal Hypertension
  Abdominal Compartment
      Physiologic Sequelae
Physiologic Sequelae
• 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, decreased ScvO2
   –   Misleading elevations of CVP and PAWP
   –   Cardiac insufficiency       Cardiac arrest
Catheter PA          Pressure  Volume
                            Pleural Pressure
                                                       Airway resistance
   Lung compliance                                     pressure

                         PEEP              PIP
                                                            Thoracic cage

                                                 Changing Ventricular
                                                 compliance, Valvular
              Intra-                             disease
                                     Intra-abdominal pressure
 CVP, PAOP & CI in the presence
 of Intra-abdominal Hypertension
                   r = -0.33                         r = -0.33

Poor, inverse correlation between CVP, PAOP and Cardiac Index
                                              Cheatham, Malbrain 2005
Ridings, et al 1995
Cheatham, Malbrain 2005
Physiologic Sequelae
• Increased intra-abdominal pressures causes:
   – Elevation of the diaphragms with reduction in lung
     volumes, stiffening of thoracic cage, reduced alveolar
     inflation, increased intersitial fluid
   – 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 - VILI, atelectasis, hypoxia, hypercarbia
   – ARDS (indirect - extrapulmonary)
Physiologic Sequelae
• Increased intra-abdominal pressures causes:
   – Compression / Congestion of mesenteric veins and
   – 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
              IAP vs Organ perfusion
Δ – hepatic a. flow; O – cardiac output; ◊ - SMA flow; □ - intest. flow

                          Diebel, J Trauma 1992
  Physiologic Sequelae
• Elevated intra-abdominal pressure causes:
   – Compression of renal veins, parenchyma
   – Reduced cardiac output to kidneys
   The Result:
   – Reduced blood flow to kidney
   – Renal congestion and edema
   – Decreased glomerular filtration rate (GFR)
      • FG = GFP-PTP so FG = (MAP-IAP)-IAP so FG = MAP-(2 x IAP)
   – Renal failure, oliguria/anuria
      • Top 4 causes of renal impairment in SICU: hypotension, sepsis, age
        > 60 and elevated IAP
      • Mortality of renal failure in ICU is over 50% - DO NOT WAIT for
        this to occur!
        Normal Abdominal CT
                         Normal kidney

Note that
abdomen is
oval, not

                        Inferior Vena Cava
                Abdominal CT in ACS – Renal
                          compression Kidneys are
Pickhardt, AJR 1999
Note that                                     patient is
abdomen is                                    anuric
round, not

  Retroperitoneal hemorrhage    Flattened Inferior Vena Cava
 Physiologic Sequelae
• Elevated intra-abdominal pressure causes:
   – Increases in intrathoracic pressure
   – Increases in superior vena cava (SVC) pressure with
     reduction in drainage of SVC into the thorax
   The Result:
   –   Increased central venous pressure and IJ pressure
   –   Increased intracranial pressure
   –   Decreased cerebral perfusion pressure
   –   Cerebral edema, brain anoxia, brain injury
        • Maryland Shock Trauma unit now decompresses abdomens in
          patients with intractable intra-cranial hypertension
                          Direct impact of IAP on
                           common pressure
                          • IAP elevation causes
                            immediate increases in
                            ICP, IJP and CVP (also in

15 liter bag placed on abdomen
(Citerio 2001)
                     Circling the Drain

                         Intra-abdominal Pressure

    Capillary leak              Breakdown               Decreased O2 delivery

Free radical formation   (Multi-System Organ Failure)   Anaerobic metabolism
                          Bacterial translocation

  How common is this syndrome?
Malbrain, Intensive Care Medicine (2004):
  Prevalence of intra-abdominal hypertension in
  critically ill patients: a multicentre epidemiological
   – Prospective, multi-center trial
      • 13 ICU’s, 6 countries
  – Every patient in ICU with expected stay > 24
    hours had IAP measured q6 hours.
      • 97 patients entered
  How common is this syndrome?
    Malbrain, Intensive Care Medicine (2004):
 Abdominal              Total       MICU         SICU
  pressure:          Prevalence   prevalence   prevalence
  IAP > 12             58.8%        54.4%         65%
  IAP > 15             28.9%        29.8%        27.5%
  IAP > 20             8.2%         10.5%        5.0%
plus organ failure
   How common – Septic* Patients
     Efstathiou et al, Intensive Care Med 2005;31 supp1 1: S183 Abs 703

 Abdominal              Total            Medical            Surgical
  pressure:          Prevalence         prevalence         prevalence
  IAP > 12              58%               52.1%               67%
  IAP > 15              29%                27.6%              25.2%
  IAP > 20               6%                9.3%                4.1%
plus organ failure

*Hernandez showed 51% incidence of IAP > 20 mm Hg in septic shock
  patients at the same conference.
SEPSIS/SEPTIC SHOCK                                     Early Goal
      Titrate to                                        Algorithm

No                 Yes                                      IAH/ACS!!

              Hypotension              Ischemia

         No                    Yes

           Drotrecogin alpha
   How good is clinical judgment for
       detecting elevated IAP?
                               Prospective, blinded trial - Staff
                                 physician judgment

                               Results: < 50% of the time was
                                 the clinician able to determine
                                 when IAP was elevated.

                               “…findings suggest that more
                                 routine measurements of
                                 bladder pressure…”
Kirkpatrick, Can J Surg 2000
Does IAH / ACS affect patient outcome?

                     •IAH predicted mortality

                        IAH > 12 mortality 38.8%
                        No IAH - mortality: 22.2%

                         Malbrain, Crit Care Med, 2005
     Does IAH / ACS affect patient
Pupelis, 2002: Clinical significance of increased intra-
  abdominal pressure in severe acute pancreatitis.
37 cases of severe pancreatitis
• 26 cases with IAP < 18 mm Hg (25 cm H2O) :
  19% SIRS & MODS 0 % mortality
  Mean ICU LOS 9 days
• 11 cases with IAP > 18 mm Hg (25 cm H2O) :
  64% SIRS & MODS 36 % mortality
  Mean ICU LOS 21 days
     Does IAH / ACS affect patient
Ivatury, J Trauma, 1998: Intra-abdominal hypertension
  after damage control surgery.
• 70 patients monitored for IAP > 18 mm Hg (25 cm H2O)
   – 25 had facial closure at time of surgery:
      • 52% developed IAP > 18 mm Hg
      • 39% Died
   – 45 cases had abdomen left “open”:
      • 22% developed IAP > 18 mm Hg
      • 10.6% Died
       Does IAH / ACS affect patient
Cheatman, Is the evolving management of IAH/ ACS improving
  survival? Acta Clinica Belgica 2007;62 supp1 1:268 Abs O61
• Prospectively collected data base in hospital with >10 yrs of ACS experience
• Year 2002: 53 cases of abdominal decompression for IAH/ACS
       34% successful same admission closure    49% mortality
       Median hospital LOS 28 days
• Year 2005: Implementation of IAH treatment protocol
• Year 2006: 75 cases of abdominal decompression for IAH
  before or early after the onset of ACS
       61% successful same admission closure    29% mortality
       Median hospital LOS 18 days
Author points: Despite same age and severity of illness they
  achieved a much better outcome with similar or less resource
  utilization by implementing aggressive treatment protocol.
     Does IAH / ACS affect patient
• IAH and ACS are common entities in the critical care
  environment (including your own).
• IAH and ACS increase morbidity, mortality and ICU
  length of stay…………
• Clinical signs of IAH are unreliable and only show up
  late in the clinical course …..SO
• Early monitoring (TRENDING) & detection of IAH
  with early intervention is needed to reduce these
Management of IAH
    and ACS
           IAH/ACS Management
• Position
• 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 (> 60 mm Hg)
    optimize fluids, then add vasopressors
•   Sedation, Paralytics
•   NGT / Cathartics / enema to clear bowel?
•   Colloids / diuretics?
•   Hemofiltration
•   Paracentesis
•   Surgical decompression
IAH/ACS Management :

      Malbrain, CCM 2003
   IAH/ACS Management: Optimize
       fluids, consider colloids
Issues: Judicious fluid management may prevent IAH
• Too much fluid leads to increased capillary leak but elevated IAP
  elevates CVP potentially causing inadequate fluid resuscitation.
• Suggestions for resuscitation:
   – Serial IAP measurements – once IAP rises over 10, do not rely
     on CVP, PAWP measurements
       • Assess volumes status using volume index catheter, echo, pulse contour
         analysis to assist in determining ventricular filling
   – Resuscitate with crystalloids - consider HS, colloids
   – Assess afterload, RVEF (or GEF) to determine next step in
     patients who have not met perfusion parameters
       • Low afterload – vasopressor, Normal EF – fluids, Low EF - inotropes
    IAH/ACS Management :
  Abdominal Perfusion Pressure
             APP = MAP - IAP
• Abdominal perfusion pressure reflects
  actual gut perfusion better than IAP alone
  (esp. pediatrics).
• 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: Paralysis




                  De Waele, Crit Care Med 2003
  IAH/ACS Management: Colloids
O’Mara, 2005: Prospective randomized evaluation of IAP
  with crystalloid and colloid resuscitation in burns
• 31 cases with >25% burn plus inhalation or >40% burn
  without inhalation
   – Randomized to saline vs plasma
• Results post resuscitation:
   – Crystalloid IAP mean 26.5 mm Hg
   – Plasma IAP mean 10.6 mm Hg
          IAH/ACS Management:
Oda, 2005: Management of IAH in patients with severe
  acute pancreatitis using continuous hemofiltration.
• 17 cases of severe pancreatitis and IAH
   – Treated with hemofiltration PRIOR to developing renal
     insufficiency (maintained adequate serum oncotic pressure
     with albumin)
• Results:
   – Interleukin (IL-6) cytokine levels cut in half
      • Reduced vascular permeability and interstitial edema
   – Mean IAP value dropped from 15 mm to less than 10 mm
   – 16 of 17 patients discharged alive without complications
          IAH/ACS Management:
Multiple case series reporting successful treatment
 of IAH and ACS:
  –   Latenser 2002: Burn patient management
  –   Reckard 2005: Peripancreatic fluid filled mass
  –   Sharp 2002: Pediatric blunt trauma
  –   Etzion 2004: Malignant ascites therapy
          IAH/ACS Management:
Sun, 2006: Indwelling peritoneal catheter vs
  conservative measures in fulminant acute pancreatitis.
• 110 cases of severe fulminant pancreatitis - RCT
   – Control group: Routine ICU supportive care
   – Study group: Routine ICU supportive care PLUS
      • IAP monitoring (mean pressure 21 mm Hg on day 1)
      • Indwelling peritoneal drain catheter (drain 1800 cc on day 1)
   – Outcome:
      • Control -           20.7% mortality
      • Study group -       10.0% mortality (p<0.01)
        IAH/ACS Management
Decompressive Laparotomy:
• Err on the side of early vs late intervention
   – Less bowel edema or cell damage, better chance of early
     closure and early recovery.
• Be aware that delaying care until this complication
  occurs is VERY expensive – more expensive the
  longer you wait:
   – Vanderbilt costs for open abdomen:
      • Same admission closure - $150,000
      • Failure to close on initial admission $250,000 (estimate at least as
        much over next year by time ventral hernia finally repaired).
      IAH/ACS Management:
     Decompressive Laparotomy

Rigid Abdomen in ACS
                       Post decompressive laparotomy
Decompressive Laparotomy

              • Delay in
                may lead to
                intestinal ischemia
              • Decompress Early!
      Decompressive Laparotomy

Post-operative dressing   Several days post-op
        Surgical Management of
        Compartment Syndromes
Compartment      Pathophysiology      Surgical Management

Cranium           ICP elevation       Craniotomy, etc..

Chest         Tension pneumothorax    Chest tube

Pericardium    Cardiac tamponade      Pericardiocentesis

Limb          Extremity compartment   Fasciotomy
  Management of Compartment

• Abdominal compartment syndrome =
    Emergent Surgical Disease.

• Intra-abdominal hypertension =
      Urgent Medical Disease.
Intra-Abdominal Pressure
       Intra-Abdominal Pressure
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 (Fusco 2001, Davis
    2005, Risin 2006, Schachtrupp 2006)

  – 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
  – 1 needle / angiocath
  – Clamp for Foley
  Assembled sterilely in
    proper fashion
           “Home Made” Pressure
            Transducer Technique
• Home-made:
   – No standardization
   – Sterility issues
• Time consuming – therefor it is used infrequently due to
  the hassle factor (i.e. not monitoring - waiting for ACS)
• Data reproducibility errors - what are the costs /
  morbidity of inaccurate or delayed information?
• Other: Needle stick, Recurrent penetration of sterile
  system, Leaks, re-zeroing problems, failure to trend
      Bladder Pressure Monitoring:
              How to do it
Commercially available devices :
  –   Foley Manometer – (Bladder manometer)
  –   CiMon (Gastric)
  –   Spiegelberg (Gastric)
  –   AbViser – (Bladder transduction)

  Advantages – Simple, Standardized, Reproducible,
      Time efficient, Sterile
Intra-Abdominal Pressure Monitoring Kit
 Closed system in-line
   with the Foley catheter.
 • Once attached it is left in
   place during entire time
   IAP is measured.

 • 30 seconds to measure IAP

 • Standardized measurement

 • No reproducibility errors
                  AbViser: Reproducibility Study
                 Inter-observer Scatterplot (r = 0.922, p < 0.001)
First Observer


                               0    5      10         15          20     25        30
                                                Second Observer

                                                           Kimball, Int Care Med 2007
     Intra-Abdominal Pressure
• How much fluid should be infused into the
  – The minimal amount of fluid required to obtain a
    reliable IAP measurement.
  – Too much fluid leads to bladder over distention and
    bladder wall compliance issues
  – Currently it appears that one never needs more than 25
    ml in an adult, less (10-20 ml) is probably adequate
  – Pediatric data shows 1 ml/kg best (Davis, 2005)
                                   How much fluid should be
                                     infused into bladder?       Bladder compliance curve


                                   bladder: Measured
                                   pressure increases as
                              30   volumes exceed 50 ml of                                                    bladder:
       IAP measured (mm Hg)

                                   infusion                                                                   Measured pressure
                              25                                                                              changes very little
                                                                                                               IAP - complaint bladder
IAP                                                                                                           with higher
                                                                                                               IAP - noncomplaint bladder
Measured                                                                                                      volumes of fluid
(mm Hg)                       15


                                   10   15     20   50      75           100       125      150   175   200
                                                         Volume of infusion (ml)

                                             Volume of infusion (ml)
      IAP transduction to monitor
Proper transduction
• Respiratory
  variation noted
• Oscillation test
• Reproducible
  over several
 Cheatham, ICM 2006
    University of Utah IAP
monitoring & treatment algorithm

 • Entry criteria defined in prior table
 • Nurse is empowered            to enter any patient
   fulfilling those criteria
  IAH/ACS Medical Management
  – Perform measurement Q2-
    4h until < 12 mmHg
  – Medical therapy for IAH

  – Primary…decompression
  – Secondary…medical tx
    with surgical backup
                         IAP Monitoring Protocol
                                   IAP monitoring Q 2 hours for first
                                             24-48 hours

             IAP               IAP 12 to 15         IAP 15-20 mm Hg       IAP >20-25 mm Hg
          consistently           mm Hg               with no evidence        or evidence of
          <12 mm Hg                               of organ dysfunction/   organ dysfunction/
                        Optimize Abdominal           ischemia (ACS)         ischemia (ACS)
                         perfusion pressure
                     •Careful fluid management

          Reduce IAP                           Medical Management
         measurements                         • Sedation/pain control
         to Q4-6 hours                        • Empty GI tract
          for 24 hours                              -Gastric suction, cathartics
                                                    -Rectal tube/enemas
                                              • Neuromuscular blockade
                                                                               Consider Surgical
 “Second Hit” pt.        IAP remains          • Colloids/diuretics               Decompression
  develops new           <12 mm Hg            • Paracentesis
indication for IAP        discontinue         • CVVH plus Colloids
    monitoring            monitoring
               Final Thought
Do 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
   IAH and ACS
 Educational Web sites:

       My email:
• Ridings PC, et al. Cardiopulmonary effects of raised intra-abdominal pressure
  before and after intravascular volume expansion. J Trauma 1995;39:1071-5.
• Citerio G, et al. Induced abdominal compartment syndrome increases
  intracranial pressure in neurotrauma patients: a prospective study. Crit Care
  Med 2001;29:1466-71.
• Malbrain ML, et al. Prevalence of intra-abdominal hypertension in critically ill
  patients: a multicentre study. Intensive Care Med 2004;30:822-9.
• Kirkpatrick AW, et al. Is clinical examination an accurate indicator of raised
  intra-abdominal pressure in critical patients? Can J Surg 2000;43:207-11.
• Ivatury RR, et al. Intra-abdominal hypertension after life-threatening
  penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to
  gastric mucosal pH and abdominal compartment syndrome. J Trauma
• De Waele JJ, et al. A role for muscle relaxation in patients with abdominal
  compartment syndrome? Intensive Care Med 2003;29:332.
• Malbrain ML, et al. Incidence and prognosis of intraabdominal hypertension
  in a mixed population of critically ill patients: a multiple-center
  epidemiological study. Crit Care Med 2005;33:315-22.
• O'Mara MS, et al. A prospective, randomized evaluation of intra-abdominal
  pressures with crystalloid and colloid resuscitation in burn patients. J Trauma
• Oda S, et al. Management of Intra-abdominal Hypertension in Patients With
  Severe Acute Pancreatitis With Continuous Hemodiafiltration Using a
  Polymethyl Methacrylate Membrane Hemofilter. Ther Apher Dial
• Syndrome WSoAC. Consensus Definitions and Recommendations [WSACS
  web site]. Available at: 2005.
• Reckard JM, et al. Management of intraabdominal hypertension by
  percutaneous catheter drainage. J Vasc Interv Radiol 2005;16:1019-21.
      Are your patients at risk for

• 30-50+% of all ICU patients have some IAH
  and are at risk for ACS

• 1 In 11 suffer full blown abdominal
  compartment syndrome
   Should you monitor bladder
           pressures ?

• IAP is directly related to organ failure
  and mortality
• Directly impacts other important
  monitoring capabilities
• Clinical exam is very inaccurate
   Can you make a difference?

• Early intervention and management can
  impact patient survival
     Does IAH / ACS affect patient
Joseph 2004: Decompressive laparotomy to treat
  intractable intracranial hypertension
• 17 patients with intractable ICP despite maximal therapy
  (including decompressive craniectomy in 14)
   – Mean ICP 30 mm Hg, Mean IAP 27 mm Hg
   – All 17 underwent decompressive laparotomy
      • 100% had drop in the ICP immediately or in few hours
          – To mean of 17 mm Hg
      • 11 had persistent reduction in ICP
          – These 11 all survived and with “good neurologic outcome”
“Decompression should almost certainly be performed before
  obvious symptoms of abdominal compartment syndrome are

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