Abdominal Compartment Syndrome (ACS) & : Abdominal Compartment Syndrome (ACS) & By: Tim Wolfe, MD
Associate Professor, Univ. of Utah
Medical Director Wolfe Tory Medical Intra-Abdominal Hypertension (IAH)
Case: Septic child: Case: Septic child 5 y.o. female presenting with septic syndrome
Treatment: Fluids, vasopressors, antibiotics
24 hours into therapy develops worsening hypotension, oliguria, hypoxemia, hypercarbia. PIP rises from 20 to 40 cm
IAP = 26 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: Complicated pulmonary embolism: 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 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
Case: Chest and Pelvic trauma: 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
Case Points: 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 measurement is valuable in assessing whether IAH is contributing to organ dysfunction.
IAP monitoring allows early detection of IAH, probably allowing clinicians to intervene earlier and avoid morbidity, mortality and prolonged ICU stay associated with delayed diagnosis of ACS.
Outline: Outline Definition – what is Intra-abdominal Hypertension and the Abdominal Compartment Syndrome?
Causes
Recent increase in recognition
Physiologic Manifestations
Prevalence
Outcome
Treatment
Detection:
Bladder pressure monitoring
Abdominal Compartment Syndrome (ACS): Definition: Abdominal Compartment Syndrome (ACS): Definition
“……..the end result of a progressive, unchecked increase in intra-abdominal pressure from a myriad of disorders that eventually leads to multiple organ dysfunction.”
John Hunt, MD
What intra-abdominal pressures are concerning?: What intra-abdominal pressures are concerning? Pressure (mm Hg) Interpretation
0 Normal
1-10 Common in most ICU patients
> 10-12 Intra-abdominal hypertension
15-20 Dangerous IAH - consider non-
invasive interventions
>20-25 Impending abdominal compartment
syndrome - strongly consider
decompressive laparotomy
Slide9: 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
Recent increases in ACS Recognition: Recent increases in ACS Recognition
Are we seeing more ACS?: Are we seeing more ACS? Increased Incidence? - Maybe (Definitely once early goal directed therapy for sepsis becomes standard)
Increased Recognition? - Definitely
Syndromes created by medical “progress”? - Definitely
ACS Literature: Publication explosion: ACS Literature: Publication explosion
Intra-abdominal Hypertension & Abdominal Compartment Syndrome: Intra-abdominal Hypertension & Abdominal Compartment Syndrome
Physiologic Sequelae
Physiologic Sequelae: 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
Compression of the aorta and systemic arterial tree
The result:
Decreased cardiac output
Increased cardiac workload
Decreased SVO2, elevations of PAWP and CVP
Cardiac insufficiency and eventually Cardiac arrest
Physiologic Sequelae: 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).
Physiologic Sequelae: 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.
Physiologic Sequelae: 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.
Physiologic Sequelae: Physiologic Sequelae Detailed Cardiac effects - Hemodynamic monitoring:
Elevated intra-thoracic pressure directly impacts traditional pressure-based cardiac filling measurements such as CVP and PAOP (wedge).
These pressure measurements are erroneously elevated and do not reflect actual fluid resuscitation end-points.
END RESULT: Failure to understand this, and reliance on pressure-based cardiac indices will lead to inadequate fluid resuscitation, persistent global organ ischemia and higher instances of MOF and death .
Physiologic Sequelae: 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.
Slide20: PEEP PIP Intra-abdominal pressure Thoracic cage
Compliance
pressure Pleural Pressure Lung compliance
pressure Airway resistance
pressure Intra-cardiac
pressure Catheter PA
Monitoring Pitfalls: Monitoring Pitfalls Abdominal exam can be misleading
“Poor sensitivity and accuracy. Low PPV ”
Kirkpatrick et al J Crit Care., 43:3 2000
Beware the PA Catheter
Physiologic Sequelae: Physiologic Sequelae Pulmonary:
Increased intra-abdominal pressures causes:
Elevation of the diaphragms with reduction in lung volumes
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
Physiologic Sequelae: Physiologic Sequelae Gastrointestinal:
Increased intra-abdominal pressures causes:
Compression of mesenteric arteries
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
Bacterial translocation
Development and perpetuation of SIRS
Further increases in intra-abdominal pressure
Physiologic Sequelae: 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: 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
Physiologic Sequelae: 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 Sequelae: Physiologic Sequelae Miscellaneous
Elevated intra-abdominal pressure causes:
Reduces perfusion of surgical and
traumatic wounds
Reduced blood flow to critical organs and tissues
The Result:
Poor wound healing and dehiscence
Coagulopathy
Immunosuppression
Physiologic Sequelae at increasing pressures: Physiologic Sequelae at increasing pressures 0-9mm 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
Physiologic Sequelae at increasing pressures: Physiologic Sequelae at increasing pressures 10-15mm 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
Physiologic Sequelae at increasing pressures: Physiologic Sequelae at increasing pressures 16-25mm Hg:
Worsening hemodynamics:
Markedly decreased venous return, CO and splanchnic perfusion
Increased SVR, CVP, PAWP
Pulmonary Spiral:
Decreased TLC, FRC, RV.
Increased vent pressures, hypercapnia, hypoxia-
Ridings et al
Physiologic Sequelae at increasing pressures: Physiologic Sequelae at increasing pressures 16-25mm 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
Physiologic Sequelae at increasing pressures: Physiologic Sequelae at increasing pressures 26-40mm 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
Slide33: 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
How good is clinical judgment for detecting elevated IAP?: 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.”
How common is this syndrome?: 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 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?: How common is this syndrome? Malbrain, Intensive Care Medicine (2004):
How common is this syndrome?: How common is this syndrome? Malbrain, Intensive Care Medicine (2004):
“Our study suggests that there is no specific type of patient or disease or treatment that reliably indicates when IAP needs to be measured, or when measurement is not necessary in a mixed ICU population. Indeed, it seems that .. IAP should be routinely measured.”
Does IAH / ACS affect patient outcome?: 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.”
Does IAH / ACS affect patient outcome?: 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 25 mm Hg:
64% SIRS & MODS 36 % mortality Mean ICU LOS 21 days
“Routine measurement of the intra-abdominal pressure is rational in the clinical setting of the ICU and gives additional criteria for the evaluation of the clinical course and the effectiveness of the treatment .”
Does IAH / ACS affect patient outcome?: 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 > 20 mm Hg:
Longer ICU LOS
Longer ventilator times
Higher MSOF
Higher mortality
Does IAH / ACS affect patient outcome?: 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 IAH > 25 mm Hg
25 had facial closure at time of surgery:
52% developed IAH > 25
39% Died
45 cases had abdomen left “open”:
22% developed IAH > 25
10.6% Died
Does IAH / ACS affect patient outcome?: 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 > 25 mm Hg:
Renal failure in 32%; permanent dialysis 9%, higher mortality
68 with IAP < 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 <.05), 24 mm Hg for renal dysfunction (P <.05), and 25 mm Hg for death (P <.01).”
Does IAH / ACS affect patient outcome?: Does IAH / ACS affect patient outcome? Sugrue, Arch Surg, 1999: Intra-abdominal hypertension is an independent cause of postoperative renal impairment.
Large Prospective study investigating IAP monitoring
263 patients monitored for IAH > 18 mm Hg
156 cases with IAP 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.”
Does IAH / ACS affect patient outcome?: 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.
Evolving area of research / understanding
IAH and patient outcome: Abdominal Perfusion Pressure: IAH and patient outcome: Abdominal Perfusion Pressure APP = MAP - IAP
Abdominal perfusion pressure reflects actual gut perfusion better than IAP alone.
Optimizing APP to > 50-60 mm Hg should probably be primary endpoint
Cheatham 2000
Optimizing APP reduced incidence of
ACS - 64% versus 48%
Death - 44% versus 28%
Does IAH / ACS affect patient outcome?: Does IAH / ACS affect patient outcome? Points:
IAH and ACS increase morbidity, mortality and ICU length of stay
Early detection and intervention reduces these complications in some patients
Clinical signs of ACS are unreliable and only show up late in clinical course
Monitoring early (not waiting for high clinical suspicion) all high risk patients allows early detection and early intervention.
IAH/ACS Management: IAH/ACS Management Close Monitoring
Serial evaluation of:
bladder pressures
vent settings
hemodynamics
urine output
Understanding monitoring pitfalls:
CVP, SVR, CO, PAOP, peak pressures, UOP, etc are all affected and may be misleading
IAH/ACS Management: IAH/ACS Management Fluids – two edged sword
Fluids will absolutely improve cardiac indices if the patient has inadequate RVEDVI - 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 on perfusion pressure > 60 mm Hg
Paralytics
Cathartics / enema to clear bowel?
Paracentesis
Need significant free fluid on US
Can place temporary catheter
Latenser et al J Burn Care Rehabil 23:190 2002
Decompressive laparotomy
IAH/ACS Management: IAH/ACS Management Decompression 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
IAH/ACS Management: IAH/ACS Management Decompression Laparotomy:
Rigid Abdomen in ACS Post decompressive laparotomy
Decompressive Laparotomy: Decompressive Laparotomy Delay in abdominal decompression may lead to intestinal ischemia
Decompress Early!
IAH/ACS Management: IAH/ACS Management Post-operative dressing Several days post-op Decompression Laparotomy:
IAH/ACS Management: IAH/ACS Management Decompression Laparotomy:
Anticipate significant physiologic changes at decompression if you have waited too long
Cardiovascular: asystole, dysrhythmias, hypertension-turn down pressors
Pulmonary: Barotrauma, hyperoxia-dial down pressures and FI02, pulmonary embolism
Acidosis from reperfusion: consider Morris cocktail (Volume with Bicarb, glucose, insulin…)
Renal/Fluids: Ongoing 3rd spacing and need for resuscitaion
IAH/ACS Management: IAH/ACS Management Post-laparotomy ACS:
Same problem-same treatment
Be aware that ACS can recur following a decompression laparotomy
Score or replace dressing to treat recurrence
Gracias et al Arch Surg 2002;137:1298-1300
Intra-Abdominal Pressure Monitoring: Intra-Abdominal Pressure Monitoring
Intra-Abdominal Pressure Monitoring: Intra-Abdominal Pressure Monitoring Bladder pressure monitoring through the Foley catheter is:
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)
Becoming a standard method for monitoring abdominal pressures (Fritsch, Crit Care Nurse 2000)
Allows early detection of intra-abdominal hypertension, allowing intervention before ACS develops (Sugrue, Intensive Care Med 2002)
Intra-Abdominal Pressure Monitoring: 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 is probably adequate
Pediatric data is unavailable, I would suggest 20 ml or 1 ml/kg
Bladder compliance curve: Bladder compliance curve Non-compliant bladder: Measured pressure increases as volumes exceed 75 ml of infusion Compliant bladder: Measured pressure changes very little with higher volumes of fluid infusion Volume of infusion (ml) IAP
Fluid-Column Manometry: 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 2002,58:227-229
Manometry Accuracy Study: Manometry Accuracy Study Inadequate volume results in falsely low pressure when pressure is elevated Siphon effect results in falsely elevated pressure when pressure is low
Manometry: Difference between measured and gold standard pressure at 30 cm water pressure: Manometry: Difference between measured and gold standard pressure at 30 cm water pressure Siphon effect Inadequate volume effect Bland Altman analysis
Fluid-Column Manometry: Fluid-Column Manometry Problems:
Failure to pay extreme attention to detail may lead to errors
Siphon effect leads to false elevations
Pinching of tube 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
“Home Made” Pressure Transducer Technique: “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
“Home Made” Pressure Transducer Technique: “Home Made” Pressure Transducer Technique PROBLEMS:
Home-made:
No standardization
Sterility issues
Data reproducibility / variability issues and costs / morbidity of inaccurate information
Requires recurrent penetration of closed urinary drain system with needle or some form of connection. Leaks, re-zeroing problems
Time consuming data acquisition limits utility
“Home Made” Pressure Transducer Technique: “Home Made” Pressure Transducer Technique QUESTIONS TO CONSIDER:
Who is “building” your home-made devices
Are all nurses adept? Is it done is sterile fashion
How reproducible is the data you obtain
Are there variations? Does this lead to confusion regarding care and therapy?
How often are you measuring IAP?
Most only measure 2-4 time a day due to hassle, but IAH occurs rather quickly in many cases
What are the hidden costs in delayed or missed diagnosis, time requirements of homemade device, etc
What is the big deal about data reproducibility?: What is the big deal about data reproducibility? Reliable, reproducible data is imperative to properly manage critically ill patients whose physiology is in a state of rapid fluctuation.
Inaccurate or flawed data may lead:
to errors of omission (failure to recognize a disease process, leading to failure to intervene)
errors of commission (inaccurate identification of a disease process that does not exist, leading to unnecessary interventions).
What is the big deal about data reproducibility?: What is the big deal about data reproducibility? Failure to identify IAH / ACS may lead to:
Organ failure &/or Death
Prolonged ICU length of stay
Misidentification of IAH / ACS may lead to:
Use of inaccurate CVP, cardiac data with resultant errors in fluid/pressor management
Unnecessary decompressive laparotomy.
In either case, substantial increases in morbidity and cost of care may occur.
AbViser Intra-Abdominal Pressure Monitoring Kit: 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.
A simple valve twist allows fluid infusion and pressure measurement.
Twist back to drain.
30 seconds to measure IAP
AbViser Intra-Abdominal Pressure Monitoring Kit: AbViser Intra-Abdominal Pressure Monitoring Kit Advantages:
Standardized measurement
No reproducibility errors
Ease & simplicity of use
Time savings
30 seconds to get data.
Closed system
No needles
No contamination risks
Slide70: Study Aims: Evaluate intra and inter-observer variability when intra-abdominal pressures are measured using the AbViser - a newly developed intra-abdominal pressure monitoring kit.
Two phases:
Bench top model - eliminates all uncontrolled variables to ensure device is accurate
Clinical setting - validates device data reproducibility in real environment.
AbViser: Reproducibility Study
AbViser Reproducibility Study: Methods: AbViser Reproducibility Study: Methods Bench-Top:
Gold standard pressure -
Water column depth created to mimic pressures of 5, 10, 15, 20, 25, 30 and 40 mm Hg
1.36 cm water equals 1 mm Hg
Study variable measured - Transduced pressure recorded on hemodynamic monitor using AbViser intra-abdominal pressure monitoring kit.
11 participant, 5 measurements each
Clinical Inter-observer variability:
“Gold standard pressure”-
Primary nurse measured IAP on patient using AbViser, then drained bladder
Study variable measured -
Second nurse measured IAP on same patient within 20 minutes of first measurement and the measurements were compared.
AbViser Reproducibility Study: Results: AbViser Reproducibility Study: Results Bench-top data:
No differences greater than 2 mm Hg occurred at any pressure.
Mean Differences
Actual vs. Measured Pressure
0.206 (95%CI 0.165, 0.248)
(Volume = 50 ml)
Clinical Data:
Measurement differences greater than 3 mm Hg were uncommon.
Mean differences
First nurse vs. second nurse
0.265 (CI -0.217 to 0.748)
Limits of agreement (Reference Range for difference): -3.096 to 3.626
AbViser: Reproducibility Study : AbViser: Reproducibility Study Bench - 15 mm Hg Clinical - Interobserver
Conclusions: Conclusions The AbViser, a newly developed intra-abdominal pressure monitoring kit:
Provides very accurate pressure measurements when compared to a known gold standard.
Provides reproducible pressure measurements without little or no intra or interobserver variability both in an intra-abdominal pressure model as well as in a clinical setting.
As would be predicted, slight increases in variability occur in the clinical setting, but these are rarely of clinical significance.
University of Utah: IAP monitoring algorithm: University of Utah: IAP monitoring algorithm Entry criteria defined in table
Nurse is empowered to enter any patient fulfilling these criteria
University of Utah: IAP Monitoring Protocol: University of Utah: IAP Monitoring Protocol IAP monitoring Q1-2 hours for first
12 hours IAP
consistently
20 mm Hg
OR
APP< 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 “Second Hit” pt.
develops new
indication for IAP
monitoring IAP remains
<12 mm Hg
discontinue
monitoring Consider Medical Management
Neuromuscular blockade
Paracentesis of free fluid
Other options
Gastric suction, cathartics
Rectal tube/enemas
Continuous filtration
Surgical
Decompression
Summary Are your patients at risk for ACS?: Summary Are 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
Summary Should you monitor bladder pressures ?: Summary 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
Summary Can you make a difference?: Summary Can you make a difference? Early intervention and management can impact patient survival
QUESTIONS?: QUESTIONS?