IntraAbdominal Hypertension IAH

1
Intra-Abdominal Hypertension (IAH)
Abdominal CompartmentSyndrome (ACS)
By Tim Wolfe, MD Associate Professor, University
of Utah Medical Director, Wolfe Tory Medical
2
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
3
Case Complicated pulmonary embolism

• 46 yo male with PE on SQ enoxaparin
• Acutely decompensated, requiring IVF,
  vasopressors and blood for retroperitoneal
  hematoma
• Became anuric, BP dropped again, difficult to
  ventilate
• IAP measured at 68 cm H2O (50 mm Hg)
• Decompression resulted in immediate resolution of
  anuria, hypotension and ventilator pressure
  issues
• Eventually discharged alive and well

Dabney, Intensive Care Med 2001
4
Case Dyspnea in ER

• 67 y.o. female presenting to ER with pleurisy,
  dyspnea
• Initially vitals stable, HP suggest liver dz
• Over 2 hours developed agitation, hypotension,
  hypoxemia, oliguria hypercarbia.
• IAP 45 mm Hg, abdominal ultrasound showed tense
  ascites paracentesis of 4500 cc fluid.
• Immediate resolution of renal, pulmonary and
  hemodynamic compromise.
• Pathology showed malignant effusion pancreatic
  CA.
• Care withdrawn at later time and allowed to
  expire.

Etzion, Am J EM 2004
5
Case Chest and Pelvic trauma

• 54 y.o. male fell 15 feet broke ribs, pelvis,
  L-spine
• External fixation of pelvis, posterior spine
  stabilized
• 2 days later developed increasing pulmonary
  difficulty and was intubated
• Persistent pulmonary deterioration with
  hypotension requiring fluids, then dobutamine
  epinephrine
• Pulmonary catheter showed good preload, but
  oliguria developed
• Bladder pressure 46 cm when measured
  Decompressed
• Initially had immediate improvement of
  cardiopulmonary status, but progressively
  worsened and died 9 days later of MSOF.

Kopelman, J Trauma 2000
6
Case Points

• Intra-abdominal hypertension and ACS occur in
  many ICU settings (PICU, MICU, SICU).
• Trauma is not required for ACS to develop.
• Bladder pressure measurements are valuable in
  assessing whether IAH is contributing to organ
  dysfunction.
• Spot IAP checks when clinical syndrome has
  developed result in delayed diagnosis
• IAP monitoring allows early detection and early
  intervention for IAH before ACS develops.

7
Questions about past experiences

• Have you ever had an ICU patient become
  progressively more swollen edematous after
  fluid resuscitation?
• Have you ever had an ICU patient develop
  progressive renal failure and need dialysis?
• Have you ever had an ICU patient die of multiple
  organ failure?
• What was their intra-abdominal pressure?

8
Outline - IAH and ACS

• Definition what is it?
• Causes
• Recent increase in recognition
• Physiologic Manifestations
• Prevalence
• Outcome
• Treatment
• Detection
• Bladder pressure monitoring
• University of Utah treatment algorithm

9
Abdominal CompartmentSyndrome (ACS) Definition
.. multiple organ dysfunction caused by
elevated intra-abdominal pressure. Tim Wolfe, MD
10
What intra-abdominal pressures are concerning?
Pressure (mm Hg) Interpretation 0-5
Normal 5-10 Common in most
ICU patients gt 12
Intra-abdominal hypertension 15-20
Dangerous IAH - consider non- invasive
interventions gt20-25 Impending
abdominal compartment syndrome -
strongly consider decompressive
laparotomy
11
Intra-abdominal pressure vs organ dysfunction
12
Analogy Monroe-Kellie Doctrine

• At a critical volume pressure rises dramatically
  with any additional edema.
• This pressure rise leads to reduced perfusion
  pressure and reduced blood flow

13
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)
• 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

14
Recent increases in ACS Recognition
15
Are we seeing more ACS?

• Increased Incidence?
• Syndromes created by medical progress
• ICUs full of sicker patients
• Fluid resuscitation due to early goal directed
  therapy for sepsis?
• Increased Recognition?

16
ACS Literature Publication explosion
17
Intra-abdominal Hypertension Abdominal
Compartment Syndrome

• Physiologic Sequelae

18
Physiologic Insult

• Ischemia

Inflammatory response
Capillary leak
Fluid resuscitation
Tissue Edema (Including bowel wall and
mesentery)
Intra-abdominal hypertension
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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

20
Physiologic Sequelae

• Detailed Cardiac effects - Cardiac contractility
  
• Reduction in thoracic cavity volume plus increase
  in ITP results in increased pulmonary artery
  pressures and reduced return of blood to left
  heart.
• Pulmonary hypertension leads to RV dilation,
  ventricular septal deviation into LV and higher
  RV wall tension. This leads to increased RV work
  and oxygen consumption.
• Reduced blood return to left heart plus
  obstructive impact of ventricular septum leads to
  reduced cardiac output.
• END RESULT Right coronary artery blood flow
  drop with resultant RV subendocardial ischemia
  and worsening cardiac dysfunction.

21
Physiologic Sequelae

• Detailed Cardiac effects - Preload impact
• IAH pushes diaphragms up, resulting in
  compression of intra-thoracic organs and reduced
  intra-thoracic volume.
• This plus positive pressure ventilation lead to
  elevated intra-thoracic pressure (ITP).
• Elevated ITP impedes blood flow into the thorax.
• Elevated diaphragms compress vena cava as it
  enters chest.
• Elevated IAP compresses vena cava leading to
  pooling of blood in the pelvis and legs
• END RESULT Dramatic reduction in venous return
  to the heart (preload).

22
Physiologic Sequelae

• Detailed Cardiac effects - Afterload impact
• IAH causes some direct arterial compression
  resulting in increased afterload.
• More importantly, reduced cardiac output leads to
  an elevation of SVR in attempt to maintain blood
  pressure.
• END RESULT Elevated SVR leads to reduced blood
  flow to organs already suffering from ischemia
  and venous engorgement. They are now more
  ischemic and the capillary leak worsens, further
  exacerbating the syndrome.

23
Catheter PA
Pleural Pressure
Airway resistance pressure
Lung compliance pressure
PIP
PEEP
Thoracic cage Compliance pressure
Intra-cardiac pressure
Intra-abdominal pressure
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Physiologic Sequelae

• Hemodynamic monitoring
• Elevated intra-thoracic/transpleural pressure
  directly impacts traditional pressure-based
  cardiac filling measurements such as CVP and PAOP
  (wedge).
• These pressure measurements are elevated and do
  not reflect actual fluid resuscitation
  end-points.
• END RESULT Reliance on unadjusted
  pressure-based cardiac indices may lead to
  inadequate fluid resuscitation, persistent global
  organ ischemia and higher instances of MOF and
  death .
• Correction factor CVP(corrected) CVP meas -
  IAP/2

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Physiologic Sequelae

• Detailed Cardiac effects - Hemodynamic
  monitoring
• Volumetric indices such as RVEDVI and GEDVI
  accurately reflect fluid volume status in the
  face of elevated IAP and ITP.
• END RESULT Focusing volume resuscitation end
  points on a volume-based index will result in
  improved cardiac function and reduced organ
  failure.

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(No Transcript)
27
Ridings, et al 1995
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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)

29
Physiologic Sequelae

• Gastrointestinal
• 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

30
Physiologic Sequelae

• Schwarte, Anesthesiology 2004
• Prospective study investigating gastric mucosa
  oxygen saturation during elective laparoscopic
  surgery

31
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

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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 thorax
• The Result
• Increased central venous pressure and IJ pressure
• Increased intracranial pressure
• Decreased cerebral perfusion pressure
• Cerebral edema, brain anoxia, brain injury

33
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)
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Physiologic Sequelae

• Miscellaneous
• 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

35
Circling the Drain
Intra-abdominal Pressure Mucosal Breakdown (
Multi-System Organ Failure) Bacterial
translocation Acidosis
Decreased O2 delivery Anaerobic metabolism
Capillary leak Free radical formation
MSOF
36
Physiologic Sequelae at increasing pressures

• 0-9 mm Hg
• Cytokine release capillary leak
• 3rd spacing of resuscitative fluid
• Decreasing venous return and preload
• Ridings Surg Forum. 1994
• Early effects on ICP and CPP
• Bloomfield Crit Care Med 1997

37
Physiologic Sequelae at increasing pressures

• 10-15 mm Hg
• Abdominal wall perfusion decreases 42
• Diebel Am Surg 1992
• Marked reduction in intestinal and
  intra-abdominal organ blood flow leading to
  regional acidosis and free radical formation.
• Schwatre Anesthesiology 2004
• Deibel Trauma 1992
• Bacterial Translocation across bowel wall
• Eleftheriadis World J Surg 1996
• Deibel J Trauma 1997

38
Physiologic Sequelae at increasing pressures

• 16-25 mm Hg
• Worsening hemodynamics
• Markedly decreased venous return, CO and
  splanchnic perfusion
• Increased SVR, CVP, PAWP
• Pulmonary compromise
• Decreased TLC, FRC, RV.
• Increased vent pressures, hypercapnia, hypoxia-
• Ridings et al

39
Physiologic Sequelae at increasing pressures

• 16-25 mm Hg
• Bowel ischemia
• Reduction to 61 of baseline mucosal blood
  flow-Deibel et al
• Increasing gut acidosis-Timmer , Ivatury et al
• Renal Dysfunction
• Oliguria, anuria, etc
• Cerebral perfusion problems
• Worsening CPP with increasing ICP

40
Physiologic Sequelae at increasing pressures

• 26-40 mm Hg
• Hemodynamic collapse, worsening acidosis,
  hypoxia, hypercapnia, anuria.
• Flow in Celiac A. 58, SMA 39, Renal A. 30
• Barnes, AM J Physiol 1985
• 80 reduction in flow to abdominal wall
• Deibel et al
• Inability to oxygenate, ventilate or resuscitate

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How common is this syndrome?

• Malbrain, Intensive Care Medicine (2004)
  Prevalence of intra-abdominal hypertension in
  critically ill patients a multicentre
  epidemiological study.
• Prospective, multi-center trial
• 13 ICUs, 6 countries
• Every patient in ICU with expected stay gt 24
  hours had IAP measured q6 hours.
• 97 patients entered

42
How common is this syndrome?

• Malbrain, Intensive Care Medicine (2004)

43
How good is clinical judgment for detecting
elevated IAP?

• Kirkpatrick, Can J Surg (2000). Is clinical
  examination an accurate indicator of raised
  intra-abdominal pressure in critically injured
  patients?
• Prospective, blinded trial - Staff physician
  judgment
• Results Less than 50 of the time was the
  clinician able to determine when IAP was
  elevated.
• These findings suggest that more routine
  measurements of bladder pressure in patients at
  risk for intra-abdominal hypertension should be
  performed.

44
Does IAH / ACS affect patient outcome?

• Tao, 2003 Diagnosis and management of severe
  acute pancreatitis complicated with abdominal
  compartment syndrome.
• 23 cases of severe pancreatitis with ACS
• 18 cases were emergency decompressed 16.7
  mortality
• 5 cases were not decompressed
  80 mortality
• All cases with decompression within 5 hours or
  less of diagnosis survived.
• Early diagnosis, emergency decompressive
  celiotomy and temporary abdominal closure .. are
  the keys to the management of the condition.

45
Does IAH / ACS affect patient outcome?

• Pupelis, 2002 Clinical significance of increased
  intra-abdominal pressure in severe acute
  pancreatitis.
• 37 cases of severe pancreatitis
• 26 cases with IAP lt 25 mm Hg
• 19 SIRS MODS 0 mortality
• Mean ICU LOS 9 days
• 11 cases with IAP gt 25 mm Hg
• 64 SIRS MODS 36 mortality
• Mean ICU LOS 21 days

46
Does IAH / ACS affect patient outcome?

• Biancofiore 2004 Intra-abdominal pressure in
  liver transplant recipients incidence and
  clinical significance.
• Prospective observational study in 108 liver
  transplants
• 32 developed IAP gt 25 mm Hg
• Renal failure in 32 permanent dialysis 9,
  higher mortality
• 68 with IAP lt 25 mm Hg
• Renal failure 8 permanent dialysis 0
• The critical IAP values with the best
  sensitivity specificity, were 23 mm Hg for
  postoperative ventilatory delayed weaning (P
  lt.05), 24 mm Hg for renal dysfunction (P lt.05),
  and 25 mm Hg for death (P lt.01).

47
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 gt 25 mm Hg
• 25 had facial closure at time of surgery
• 52 developed IAP gt 25
• 39 Died
• 45 cases had abdomen left open
• 22 developed IAP gt 25
• 10.6 Died

48
Does IAH / ACS affect patient outcome?

• Raeburn 2001 The abdominal compartment syndrome
  is a morbid complication of post-injury damage
  control surgery.
• 77 patients monitored for IAH /ACS
• 36 developed IAP gt 20 mm Hg
• Longer ICU LOS
• Longer ventilator times
• Higher MSOF
• Higher mortality

49
Does IAH / ACS affect patient outcome?

• Malbrain, Crit Care Med, 2005 Incidence and
  prognosis of intra-abdominal hypertension in a
  mixed population of critically ill patients A
  multicenter epidemiological study.
• Prospective, multi-center trial
• 14 ICUs, 6 countries
• Every patient in ICU with expected stay gt 24
  hours had IAP measured q12 hours.
• 265 patients entered

50
Does IAH / ACS affect patient outcome?
Malbrain, Crit Care Med, 2005

• Development of sub-ACS levels of IAH (IAP gt 12 mm
  Hg) predicted mortality
• IAH gt 12 - mortality 38.8
• No IAH - mortality 22.2

51
Does IAH / ACS affect patient outcome?

• Sugrue, Arch Surg, 1999 Intra-abdominal
  hypertension is an independent cause of
  postoperative renal impairment.
• Prospective study investigating IAP monitoring
• 263 patients monitored for IAH gt 18 mm Hg
• 156 cases with IAP lt 18 14.1 renal impairment
• 107 cases (41) with IAP gt 18 32.7 renal
  impairment
• This study shows that IAP is an independent
  cause of renal impairment, and it ranks in
  importance after hypotension, sepsis, and age
  older than 60 years.

52
Does IAH / ACS affect patient outcome?

• Michael Sugrue, MD World expert in IAH and ACS
  (over 1800 measurements done, 10 publications)
  Personal communication June 2, 2004.
• Evidence is clear regarding renal impairment.
• Not every patient will respond to decompression
• About 25-30 benefit if some delay in
  decompression occurs
• Probably 60-70 benefit if you decompress early
• Still has substantial morbidity and mortality.

53
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.

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IAH/ACS Management

• Close Monitoring
• Serial evaluation of
• vent settings
• hemodynamics
• urine output
• bladder pressures
• Understanding monitoring pitfalls
• CVP, SVR, CO, PAOP, peak pressures, UOP, IAP, etc
  are all affected and inter-related. These values
  may be misleading if entire clinical picture is
  not available.

55
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 gt 60 mm Hg
• Sedation, Paralytics
• Cathartics / enema to clear bowel?
• Colloids
• Hemofiltration
• Paracentesis
• Need significant free fluid on US
• Decompressive laparotomy

56
IAH/ACS Management Abdominal Perfusion Pressure

• APP MAP - IAP
• Abdominal perfusion pressure reflects actual gut
  perfusion better than IAP alone.
• Optimizing APP to gt 60 mm Hg should probably be
  primary endpoint
• Cheatham 2000
• Optimizing APP reduced incidence of
• ACS - 64 versus 48
• Death - 44 versus 28

57
IAH/ACS Management Paralysis
IAP
UOP
De Waele, Crit Care Med 2003
58
IAH/ACS Management Colloids

• OMara, 2005 Prospective randomized evaluation
  of IAP with crystalloid and colloid resuscitation
  in burns
• 31 cases with gt25 burn plus inhalation or gt40
  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

59
IAH/ACS Management Hemofiltration

• 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
• 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

60
IAH/ACS Management Paracentesis

• Latenser, 2002 Percutaneous decompression for
  abdominal compartment syndrome in burn patients.
• 9 cases with IAP gt 25-30 mm Hg
• Treated with percutaneous catheter (paracentesis)
  to drain ascitic fluid
• Results
• 5 responded with drop in IAP - 60 survival
• 4 failed to respond and IAP increased - 0
  survival

61
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.
• Can be performed bedside for unstable patients

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IAH/ACS Management Decompressive Laparotomy
Rigid Abdomen in ACS
Post decompressive laparotomy
63
Surgical Management of Compartment Syndromes

• Compartment
• Cranium
• Chest
• Pericardium
• Limb

Pathophysiology ICP elevation Tension
pneumothorax Cardiac tamponade Extremity
compartment syndrome
Surgical Management Mannitol, Craniectomy,
etc.. Chest tube Pericardiocentesis Fasciotom
y
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Decompressive Laparotomy

• Delay in abdominal decompression may lead to
  intestinal ischemia
• Decompress Early!

65
Decompressive Laparotomy
Post-operative dressing
Several days post-op
66
Intra-Abdominal Pressure Monitoring
67
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)

68
Intra-Abdominal Pressure Monitoring

• How much fluid should be infused into the
  bladder?
• The minimal amount of fluid required to obtain a
  reliable IAP measurement.
• Too much fluid leads to bladder over distention
  and compliance issues (see next slide)
• Currently it appears that one never needs more
  than 50 ml in an adult, less (10 ml) is probably
  adequate
• Pediatric data shows 1 ml/kg best (Davis, 2005)

69
How much fluid should be infused into bladder?
Non-compliant bladder Measured pressure
increases as volumes exceed 50 ml of infusion
Compliant bladder Measured pressure changes very
little with higher volumes of fluid infusion
IAP Measured (mm Hg)
Volume of infusion (ml)
70
Fluid-Column Manometry

• Simple method of measuring bladder pressure via
  fluid column in a Foley catheter.
• Requires disconnection of the Foley to instill
  saline and careful bending of the Foley to ensure
  accurate measurement.

Sedrak M, Major K, Wilson M. Simple Fluid-column
manometry to monitor for the development of
abdominal compartment syndrome. Contemporary
Surgery 2002,58227-229
71
Fluid-Column Manometry

• Problems
• Failure to pay extreme attention to detail may
  lead to errors
• Siphon effect leads to false elevations
• Pinching of Foley can lead to inability to
  equilibrate
• Failure to hold tube vertical can lead to
  inaccuracies
• Inadequate volume of infusion will lead to
  falsely low measurements
• Need to infuse urine back into patient

72
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 Foley
• Assembled sterilely in proper fashion

73
Home Made Pressure Transducer Technique

• PROBLEMS
• Home-made
• No standardization
• Sterility issues
• Time consuming Done infrequently
• Data reproducibility errors - what are the
  costs / morbidity of inaccurate information?
• Other Needle stick, Recurrent penetration of
  sterile system, Leaks, re-zeroing problems/errors

74
AbViser Intra-Abdominal Pressure Monitoring Kit

• AbViser Tray
• Contains all materials needed for IAP monitoring
  except transducer and saline bag.
• Integrates into any ICU using their established
  transducer, cabling and monitors.

75
AbViser 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

76
AbViser Intra-Abdominal Pressure Monitoring Kit
77
AbViser Intra-Abdominal Pressure Monitoring Kit

• Advantages
• Kit contains everything you need
• Standardized measurement
• No reproducibility errors
• Ease simplicity of use
• Time savings
• 30 seconds to get data.
• Closed system
• No needles
• No contamination risks

78
AbViser Reproducibility Study
Inter-observer Scatterplot (r 0.922, p lt 0.001)
79
AbViser Purchase Justification

• If you SPOT CHECK to confirm clinical suspicion
  of advanced disease (i.e. to confirm ACS)
• The AbViser is not for you.
• If your goal is to
• Detect IAH early
• Establish a trend in IAP to assist in clinical
  management
• Utilize IAP to accurately interpret hemodynamics
  and other organ function
• Prevent abdominal compartment syndrome
• Decrease patient morbidity, mortality and LOS
• Then the AbViser is your tool

80
University of Utah IAP monitoring algorithm

• Entry criteria defined in table
• Nurse is empowered to enter any patient
  fulfilling these criteria

81
University of Utah IAP Monitoring Protocol
IAP monitoring Q1-2 hours for first 12 hours
IAP consistently lt12 mm Hg
IAP 12 to 15 mm Hg
IAP 15-20 mm Hg with no evidence of organ
dysfunction/ ischemia (ACS)
IAP gt20 mm Hg OR APPlt 50-60 mm Hg? Plus evidence
of organ dysfunction/ ischemia (ACS)

• Optimize Abdominal perfusion pressure
• Careful fluid management
• Pressors

Reduce IAP measurements to Q4-6 hours for 24
hours

• Consider Medical Management
• Sedation/Neuromuscular blockade
• Paracentesis of free fluid
• Other options
• Gastric suction, cathartics
• Rectal tube/enemas
• Continuous filtration
• Colloids

Surgical Decompression
Second Hit pt. develops new indication for
IAP monitoring
IAP remains lt12 mm Hg discontinue monitoring
82
SummaryAre your patients at risk for ACS?

• 30-50 of all ICU patients have some IAH and are
  at risk for ACS
• 1 In 11 suffer full blown abdominal compartment
  syndrome

83
SummaryShould you monitor bladder pressures ?

• IAP is directly related to organ failure and
  mortality
• Directly impacts other important monitoring
  capabilities
• Clinical exam is very inaccurate

84
SummaryCan you make a difference?

• Early intervention and management can impact
  patient survival

85
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

86
QUESTIONS?
IAH and ACS Educational Web sites www.Abdominalc
ompartmentsyndrome.org www.wsacs.org My email
twolfe_at_wolfetory.com