Intra-abdominal
Hypertension
Leanna R. Miller
RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP
Definitions
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 abdominopelvic region, “surgical”
• Secondary – Sepsis, capillary leak,
burns, “medical”
• Recurrent – ACS develops despite
surgical intervention
Physiologic Insult/Critical Illness
Ischemia
Inflammatory response
Fluid resuscitation
Capillary leak
Tissue Edema
(Including bowel wall and mesentery)
Intra-abdominal hypertension
Intra-abdominal Hypertension
Compartment syndrome occurs
when the pressure within a closed
anatomic space increases to the
point where vascular tissue is
compromised with subsequent loss
of tissue viability and function. This
can occur within any closed body
cavity.
Intra-abdominal Hypertension
Increased IAP leads to decreased
mesenteric blood flow (MBF) and to
bacterial translocation (BT), which may
contribute to later septic complications
and organ failure.
Intra-abdominal Hypertension
• IAH provokes the release of proinflammatory cytokines which may
serve as a second insult for the
induction of MOF.
• production of interleukin-1 (IL-1
beta), interleukin-6 (IL-6), tumor
necrosis factor (TNF-)
Intra-abdominal Hypertension
• Symptomatic organ dysfunction that results
from increased intra-abdominal pressure (IAP)
• Increased IAP is an under-recognized source
of morbidity and mortality.
• 1-day point-prevalence observational trial
conducted in 13 medical ICUs of six countries
with 97 patients, 8% had IAP > 20mmHg.1
• The incidence of ACS in trauma patients is
estimated to be between 2 and 9 percent.2
1Crit
Care Med 2005; 33:315.
2Am
J Surg 2002; 184:538.
Intra-abdominal Hypertension
Etiology
• massive volume resuscitation is the leading
cause of ACS.
• inflammatory states with capillary leak, fluid
sequestration, inadequate tissue perfusion,
and lactic acidosis can develop ACS.
• gastric overdistention following endoscopy
has resulted in ACS.
Intra-abdominal Hypertension
• trauma (blunt or open), as a result of the
accumulation of blood, fluid or edema.
• gastrointestinal hemorrhage can also
lead to increased pressure in the
abdominal compartment as ischemic
cells swell or fluids collect.
• pancreatitis
• pneumoperitoneum
Intra-abdominal Hypertension
• syndrome may follow a ruptured
abdominal aortic aneurysm
• intra-abdominal infection
• coagulopathies with abdominal
bleeding
• cirrhosis
• profound hypothermia
Intra-abdominal Hypertension
• massive intra-abdominal
retroperitoneal hemorrhage
• severe gut edema
• intestinal obstruction
• ascites under pressure
• neoplasm
Intra-abdominal Hypertension
• Patients who have undergone long surgical
procedures with intraoperative hypotension
and large fluid requirements are at significant
risk, particularly if the abdomen has been
closed under pressure in the OR.
• External pressure from circumferential burns
about the abdomen, application of military
anti-shock trousers (MAST), or even tight
abdominal restraint devices can cause
tension within the abdomen due to external
forces and result in ACS
Intra-abdominal Hypertension
Recently, awareness of the ACS has increased
for 2 primary reasons.
• First, the increased use of laparoscopy among
general surgeons has brought with it an appreciation
of IAP as a readily quantifiable entity.
• Second, the more frequent use of planned repeat
laparotomy for trauma has allowed both surgeon and
intensivist to appreciate the beneficial effects of
abdominal decompression upon removal of packing
or evacuation of hematoma.
Intra-abdominal Hypertension
• Interpreting IAP
 0 – 5 mm Hg
 6 – 11 mm Hg




12 – 15 mm Hg
16 – 20 mm Hg
21 – 15 mm Hg
> 25 mm Hg
normal
minimal elevation
common finding in ICU
Grade I
Grade II
Grade III – high risk for ACS
Abdominal Compartment
Syndrome
Intra-abdominal Hypertension
Abdominal Compartment Syndrome
“. . . . . . .the end result of a progressive,
unchecked increase in intra-abdominal
pressure from a myriad of disorders that
eventually leads to multiple organ dysfunction”
Intra-abdominal Hypertension
Grading System for ACS
Grade
Bladder pressure
(cm water)
Indication of
surgical
decompression
I
10-15
No evidence of
ACS
II
15-25
Based on patient
condition
III
25-35
Decompression
indicated
IV
>35
Immediate
decompression
Elevated IAP
Intra-abdominal Hypertension
•
•
•
IAH may develop rapidly
Monitor the trend: rising IAP or
sustained IAH
poor prognosis
Recommendation: Measure IAP at
each Urine Output determination
Physiologic Sequelae
The Pathophysiology of IAH
IAP
VASCULAR
COMPRESSION
RVP
IVC
Flow
DIAPHRAGMATIC
ELEVATION
Cardiac
compression
DIRECT ORGAN
COMPRESSION
Intrathoracic
pressure
Cardiac preloadCardiac contractility Systemic afterload
PV pressure
CARDIAC OUTPUT
Renal Vascular
Resistance
RENAL FAILURE
Splanchnic
Vascular Resistance
ABDOMINAL WALL
ISCHAEMIA/OEDEMA
RESPIRATORY
FAILURE
ICP SPLANCHNIC
ISCHAEMIA
Effects on CVS
• As intra-abdominal pressure increases above
10 mmHg, cardiac output declines, despite
normal arterial pressures.
• Additionally, whole body oxygen consumption,
pH, and PO2 decrease.
• Intra-abdominal hypertension affects cardiac
function by pushing the hemi-diaphragms
upward, thus transmitting the abdominal
pressure to the heart and its vessels.
• This decreases preload and increases
afterload on the left ventricle and at the same
time creates a hemodynamic picture of low
cardiac output and high filling pressures
35
3.5
3
2.5
25
2
1.5
15
1
0.5
Wedge pressure (mmHg)
Cardiac index (L/min/m 2)
4
Cardiac index
Wedge pressure
0
0
5
10
15
20
25
IAP (mmHg) above baseline)
Effect of increased intra-abdominal pressure on cardiac
index and pulmonary artery occlusion pressure (J Trauma
1995; 39:1071-1075)
Physiologic Sequelae
Cardiac:
• Increased intra-abdominal pressures cause:
– Compression of vena cava with reduced venous
return
– Elevated intra-thoracic pressure with multiple
negative cardiac effects
• Result:
–
–
–
–
–
Decreased cardiac output, increased SVR
Increased cardiac workload
Decreased tissue perfusion
Misleading elevations of CVP and PAOP
Cardiac insufficiency; cardiac arrest
Effects on Pulmonary System
• most commonly noted effects of IAH on the
pulmonary system are:
– elevated peak inspiratory pressures
– decreases in PaO2
– increases in PaCo2
• requires the use of complete ventilatory support
to maintain adequate oxygenation and
ventilation.
• positive end-expiratory pressure has been
shown to exacerbate the cardiac and
respiratory consequences of IAH .
Physiologic Sequelae
Pulmonary:
• Increased intra-abdominal pressures causes:
– Elevated diaphragm, reduced lung volumes &
alveolar inflation, stiff thoracic cage, increased
interstitial fluid
• 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)
Pulmonary Effects of IAH
• mechanical ventilation
often necessary
• high peak airway
pressures 
barotrauma
• high PEEP often
required  further
compromising CO
Pulmonary Effects of IAH
Pressure on the IVC
predisposes to
venous stasis and
increased risk of
thromboembolism
IAH and Splanchnic Flow
• increases in IAP have
adverse effect on
splanchnic flow
• >15mmHg  SM blood
flow
• marked reduction in hepatic
artery and portal venous
blood flow
• leads to mucosal acidosis
and edema
IAH and Splanchnic Flow
Splanchnic
hypoperfusion
Hepatic
ischemia
Gut mucosal acidosis
IAH
Bowel edema
Coagulopathy
hypothermia
Unrelieved
acidosis
Intraabdominal
bleeding
Free oxygen radicals
Distant organ damage
ACS
Intra-abdominal Hypertension
• measured mucosal and intestinal blood flow and
intramucosal pH (pHi) and found that mesenteric
and mucosal blood flow decreased when IAP
reached 20 mmHg, with intestinal mucosal flow
declining to 61% of baseline
• At an IAP of 40 mmHg, intestinal flow decreased to
28% of baseline
• Intestinal mucosa showed signs of a severe degree
of acidosis, measured by tonometer. These
changes in splanchnic blood flow occurred despite
maintenance of baseline cardiac output with
volume loading
Intra-abdominal Hypertension
• blood flow to virtually every abdominal
organ decreased significantly. The only
exception was the adrenal gland; the
reason this organ is not affected is
unknown ?
Physiologic Sequelae
Gastrointestinal:
• Increased intra-abdominal pressures causes:
– Compression/Congestion of mesenteric veins and
capillaries
– Reduced cardiac output to the gut
• Result:
– Decreased gut perfusion, increased gut edema and
leak
– Ischemia, necrosis
– Bacterial translocation
– Development and perpetuation of SIRS
– Further increases in intra-abdominal pressure
Effects on Renal System
• decreased renal plasma flow, glomerular
filtration rate, and glucose reabsorption.
• oliguria also occurs, with anuria noted in
animal models when IAP reaches 30
mmHg
• effects occur without significant decreases
in blood pressure (mechanical, ↑ PVR,
compression of renal vein→ outflow
obstruction→ ↑ intraparenchymal pressure
→ shunting of blood from renal cortex)
Effects on Renal System
• improvement of cardiac output does
not improve renal function, nor do renal
blood flow and glomerular filtration rate
improve.
• the placement of ureteral stents failed
to improve renal function.
• improvement in renal function occurred
only after abdominal decompression
Intra-abdominal Hypertension
• These findings suggest that the effects of IAH on
renal function are related to compression of the
renal parenchyma itself and to compression of
renal vasculature and are not related to
decreased cardiac output.
• other mechanisms proposed include shunting of
blood away from the renal cortex into the
medulla, decreased renal arterial flow with a
concomitant increase in renal vascular
resistance, and the presence of high levels of
renin, aldosterone, and antidiuretic hormones.
Physiologic Sequelae
Renal:
• Elevated intra-abdominal pressure causes:
– Compression of renal veins, parenchyma
– Reduced cardiac output to kidneys
• Result:
–
–
–
–
Reduced blood flow to kidney
Renal congestion and edema
Decreased glomerular filtration rate (GFR)
Renal failure, oliguria/anuria
• Mortality of renal failure in ICU is over 50% DO NOT WAIT for this to occur!
Effects on CNS
• The rise in intra-abdominal pressure,
intrathoracic pressure leads to a rise in
central venous pressure which prevents
adequate venous drainage from the brain,
leading to a rise in intracranial pressure and
worsening of intracerebral edema.
Intracranial Derangements
• IAH associated with
– ICP
– CPP
cerebral ischemia
• ?Why?
• may be due to
impairment of
cerebral venous
outflow
Central Nervous System Implications
ICP
CPP
retinal capillaries rupture
Valsalva retinopathy
Sudden decrease of central vision
Intra-abdominal Hypertension
• increased intrathoracic pressure causing
increased resistance to cerebral venous
return associated with IAH( ?pseudotumor
cerebri).
• Volume expansion further increased ICP.
Cerebral perfusion pressure declined as
ICP increased and cardiac output declined.
• Only abdominal decompression reversed
effects of IAH.
• The exact level of IAH that results in
elevated ICP and decreased CPP in the
brain injured patient is unknown
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
• Result:
– Increased central venous pressure and IJ
pressure
– Increased intracranial pressure
– Decreased cerebral perfusion pressure
– Cerebral edema, brain anoxia, brain injury
Multisystem Organ Failure
Intra-abdominal Pressure
Capillary leak
Mucosal
Breakdown
Decreased O2 delivery
Free radical formation
(Multi-System Organ Failure)
Anaerobic metabolism
Bacterial translocation
Acidosis
IAH / ACS Affects Outcome
Points:
• 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…………
However:
• 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
complications.
Measurement of IAP
Diagnosis of ACS
• Intra – abdominal pressure  25 mmHg or 30 cmH20/ urine
• One or more of the following signs of clinical deterioration
– ↑ pulmonary pressures
– ↓ cardiac output
– ↓ urinary output
– acidosis
– hypoxia
– hypotension
• abdominal decompression results in clinical improvement
Indications for IAP Monitoring
•
•
•
postoperative (abdominal surgery)
ventilated pts with other organ failure
patients with signs of ACS:
– oliguria, hypoxia, hypotension, acidosis, mesenteric
ischemia, ileus, elevated ICP.
•
•
high cumulative fluid balance
abdominal packing
Intra-abdominal Hypertension
Abdominal compartment pressure monitoring is
done to help recognize life threatening elevations
in pressure before ischemia or infarction of the
abdominal organs occurs. When a patient exhibits
a distended and taut abdomen, the measurement
of abdominal compartment pressure can provide
direction regarding the need for decompressive
surgery
Measurement of IAP
Direct Monitoring
• The most direct, accurate way to measure
intraabdominal pressure is through an
intraperitoneal catheter attached to a water
manometer or pressure transducer, the
preferred method in most experimental studies
of IAH.
• Its use in the clinical situation is limited by the
potential complications, specifically the risk of
peritoneal contamination or bowel perforation.
• Abdominal pressure measured during
laparoscopy is another example of direct
measurement
Indirect Monitoring
• Intraabdominal pressure may be indirectly
measured by measuring pressure within certain
abdominal organs.
• The first indirect method described involves
placement of transfemoral catheters into the
inferior vena cava .The associated risks of this
procedure include infection and thrombus
formation.
• measurement of gastric pressure through
gastrostomy or nasogastric tubes
• esophageal stethoscope catheter
• urinary bladder pressure measurement
Bladder Pressure Monitoring
• at intravesical volumes less than 100 mL,
the bladder acts as a passive reservoir,
accurately reflecting intra-abdominal
pressure within a range of 5 to 70 mmHg
• when bladder volumes exceed 100 mL, the
intrinsic contraction of the bladder wall
causes bladder pressure to increase.
Intra-abdominal Hypertension
• the basic technique of bladder pressure
measurement is not complicated. Fifty to 100
mL of sterile saline is injected into the
bladder through a Foley catheter while the
tubing to the drainage bag is clamped distal
to the aspiration port
• the clamp is then opened to allow fluid to fill
the tubing proximal to the clamp and the
tubing is then reclamped
“Home Made” Pressure Monitoring
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
Intra-abdominal Hypertension
Intra-abdominal Hypertension
“One Step” Infusion of saline into
bladder:
1. Aspirate 20 ml saline into the
syringe.
2. Compress the syringe to infuse
the saline.
3. Read the IAP
4. Repeat as needed
Measure
Drain
That’s all – no valves or clamps or easily made errors
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 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
Intra-abdominal Hypertension
• patient positioning affects the accuracy of
bladder pressure measurements.
• monitoring should occur with the patient
supine so that the weight of the abdominal
contents pressing on the bladder does not
falsely elevate the reading.
• if patient is unable to remain supine, the
position at which the first measurement is
taken should be noted and subsequent
measurements taken with the patient in that
position
• although the individual reading may be
inaccurate, trends in abdominal pressure can
still be assessed
Intra-abdominal Hypertension
• Unfortunately, this procedure requires that
the closed urinary drainage system be
opened each time pressure is measured,
placing the patient at increased risk of
infection.
• Strict aseptic technique is essential. A
sterile towel should be placed under the
Foley catheter to maintain sterility .
Intra-abdominal Hypertension
In patients with a neurogenic bladder or in
those having a small contracted bladder
(e.g., after radiotherapy), measurements
may be inaccurate.
Management of IAH
and ACS
Abdominal Perfusion Pressure (APP)
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
IAP Monitoring Protocol
IAP monitoring Q1-2 hours for first
12 hours
IAP
IAP 12 to 15
IAP 15-20 mm Hg
IAP >20 mm Hg
consistently
mm Hg
with no evidence
OR
<12 mm Hg
of organ dysfunction/ APP< 50-60 mm Hg?
ischemia (ACS)
Plus evidence of
Optimize Abdominal
organ dysfunction/
perfusion pressure
ischemia (ACS)
•Careful fluid management
•Vasopressors
Reduce IAP
measurements
Consider Medical Management
to Q4-6 hours
• Sedation/Neuromuscular blockade
for 24 hours
• Paracentesis of free fluid
“Second Hit” pt.
develops new
indication for IAP
monitoring
IAP remains
<12 mm Hg
discontinue
monitoring
•Other options
Surgical
-Gastric suction, cathartics Decompression
-Rectal tube/enemas
-Continuous filtration
-Colloids
Intra-abdominal Hypertension
Pressure
Grade
Management
10-15 mm Hg
I
maintain
normovolemia
16-25 mmHg
II
26-35 mmHg
III
hypervolemic
resuscitation
decompression
> 35 mm Hg
IV
decompression
and re-exploration
Prevention of ACS
Most commonly used open Current opinion does
abdomen techniques
not support liberal
include
use of an open
abdomen technique
• bogota bag (25%)
to prevent ACS
• absorbable mesh (17%)
• prolene mesh (14%)
• silastic mesh (7%)
• miscellaneous (28%)
The Journal of Trauma, Infection and
Critical Care 1999;47 :509-511
Intra-abdominal Hypertension
• an alternative technique is the 'vacuum-pack'
technique. Here the 3 liter bag is opened and
placed into the abdomen to protect the gut
contents, under the sheath.
• two large caliber suction drains are placed over
this, and a large adherent steridrape placed over
the whole abdomen.
• suction catheters are connected to highdisplacement suction to provide control of fluid
losses and create the 'vacuum-pack' effect
Operative Decompression
Vacuum-assisted
temporary
abdominal closure
device:
A thin plastic sheet,
a sterile towel,
closed suction
drains, and a large
adherent operative
drape. This
dressing system
permits increases
in intra-abdominal
volume, without a
dramatic elevation
in IAP.
Decompressive Laparotomy
• Delay in abdominal decompression
may lead to intestinal ischemia
• Decompress early!
Case Presentations
Case: Septic Patient
45 y.o. female presenting with septic syndrome
• Treatment: Culture, Antibiotics, Fluids, Vasopressors
• 24 hours into therapy develops worsening hypotension,
oliguria, hypoxemia, hypercarbia. PIP rises from 20 to
40 cm H2O
• IAP = 26 mm Hg
decompressive laparotomy
• Immediate resolution of renal, pulmonary and
hemodynamic compromise
• 7 days later abdomen closed.
• Alive and well now.
Case: Dyspnea in ER
67 y.o. female presenting to ER with pleurisy, dyspnea
• Hypotensive, agitated, H&P suggest liver disease
• 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 general medicine floor.
Transferred to MICU & intubated; hypotensive.
• 10 liters IVF overnight, Levophed 40 mcg/min.
• Anuric (35 ml urine in 8 hours).
• IAP = 31 mm Hg. KUB – massively distended
small and large bowel. U/S shows no free ascitic
fluid.
• Surgeon consulted for possible decompressive
surgery
• Rx: NGT, Rectal Tube, oral cathartics
• 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)
Case Points
• “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.
WSACS Guidelines
Cheatham, ICM 2006
Intra-abdominal Hypertension
WSACS recommendations
•
•
Non-surgical treatment options:
– paracenthesis
– Gastric suctioning, enemas
– Gastro/colon prokinetics
– Furosemide, with or without albumin
– CVVH with aggressive ultrafiltration
– Sedation
Surgical: Decompression
Intra-abdominal Hypertension
Summary
• ACS is a clinical entity caused by an acute,
progressive increase in IAP.
• Multiple organ systems are affected, usually in a
graded fashion.
• The gut is the organ most sensitive to IAH.
• Treatment involves expedient decompression of the
abdomen.
• Since this syndrome affects patients who are already
physiologically compromised, a high degree of
suspicion and a low threshold for checking bladder
pressures are required to prevent the mortality
associated with this complex problem.
Final Thoughts
Do NOT wait for signs of ACS 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
• 30-50+% of all ICU patients have some IAH and
are at risk for ACS
• 1 in 11 suffer full blown abdominal compartment
syndrome