Intra-Abdominal

Hypertension
Trina Banerjee
Outline

Definitions/Categories/Stages
Incidence
Causes
Diagnosis
Pathophysiology
Treatment
Definitions I

Intra-abdominal pressure (IAP):

Pressure within the abdominal cavity
<5-7 mm Hg, with upper limit 12 mm Hg

Abdominal Perfusion Pressure (APP):

MAP (mean arterial pressure) IAP
Normal is 60 mm Hg and above
Definitions II

Intra-abdominal Hypertension (IAH):

IAP >10-12 on three different
measurements or
APP<60mmHg on two separate
occassions

Abdominal CompArtment Syndrome

(ACS):
Subcategory of IAH
Sustained IAP>20 with organ dysfunction
Categories

Primary :
Either Hyperacute (second to minutes) or
Acute (Hours)
Results from abdominal trauma
Secondary:
Either Subacute (days) or Chronic
(Months )
Results from extrabdominal causes
Stages

Stage I : 12-15

Stage II : 16-20

Stage III : 21-24

Stage IV : >25
Incidence

In mixed ICU population the incidence

of IAH can be 30-50%

In mixed ICU populations the

incidence of ACS can be 4-8%
Causes

Conditions that Decrease abdominal

wall compliance
Conditions that increase intraluminal
contents
Conditions related to abdominal
collections of fluid, air, or blood
Conditions related to capillary leak and
fluid resucitation
Decreased abdominal
wall compliance
Mechanical ventilation
PEEP
Basal pneumonia
High BMI
Pneumoperitoneum
Abdominal surgery with tight closure
Anti-shock garments
Prone positioning
Abdominal wall bleeding or rectus sheath
hematomas
Correction of large hernias, gastroschisis, or
omphocele
Burns with abdominal eschars
Increased Intraluminal
Contents
Gastroparesis
Gastric distension
Ileus
Volvulus
Colonic pseudo-obstruction
Abdominal tumor
Retroperitoneal/Abdominal wall hematoma
Enteral feeding
Abdominal wall tumor
Damage control laparotomy
Collections of fluid, air, or
blood
Ascites
Abdominal infection
Hemoperitoneum
Pneumoperitoneum
Laparoscopy with excesive inflation
pressures
Major trauma
PD
Capillary leak and fluid
resucitation
pH<7.2
Hypothermia
Coagulopathy
Polytransfusion
Sepsis
Transfusions with capillary leak
Major burns
Diagnosis
Physical Exam:
Highly inaccurate
Direct:
Intraperitoneal catheter attached to a pressure
transducer
Indirect:
Transduction of a bladder, colonic, gastric, or
uterine pressure from a balloon
Measure at end expiration in the supine position
with absent abdominal wall contractions, at the
level of the midaxillary line at the iliac crest after
the instillation of a volume of 20-25 cc
Pathophysiology
General
Pathophysiology I
The Pressure in ACS decreases venous
return:
Increased IAP compromises venous return, by
compressing the portal vein and IVC.
There is also increased afterload because of the
increased abdominal pressure and thoracic
pressure.
Cardiac output then goes down (this occurs at a
IAP of 10), and therefore oxygen delivery
This leads to decreased arterial pressure, resulting in
deceased MAP
General
Pathophysiology II
Decreased MAP causes Ischemic
Organs:
Organs become ischemic and then swell. Local
release of lactate and adenosine.
Abdominal viscera swelling limits diaphragmatic
movement, which limits alveolar recruitment.
There is hypoxia and hypercapnia. Increased
intrathoracic pressure which further limits
venous return. It also increases central venous
pressure. It also compresses the heart
The venous return sits in the liver and kidneys
Intest. Pathophysiology

The rise in pressure causes decreased

blood flow to the gut, resulting in
bacterial translocation

Can result in abdominal wall ischemia

Liver Pathophysiology

There is decreased blood flow to the

liver causing impaired hepatocellular
function
Liver dysfunction starts at a IAP of 10
Decreased hepatic artery flow, decreased
venous portal flow, increase in the
portacollateral circulation
Reduced lactate clearance, altered
glucose metabolism, altered
mitochondrial function
Brain Pathophysiology

Cerebral perfusion pressure decreases

because of the increase in
intrathoracic pressure, resulting in an
obstruction of cerebral venous outflow
Renal Pathophysiology I

IAP Thresholds:
Reduction in renal plasma flow and GFR
starting at IAP 15-20 mm Hg
Oliguria starts at 15mmHg
Anuric above 30 mm Hg
Numbers refer to a normovolemic patient.
In a septic patient the numbers may be
lower
Renal Pathophysiology II
Pre-renal, Renal, and Postrenal
Pre-renal:
Cardiovascular dysfuntion, both from decreased
venous return and from compression of the heart, and
from increased afterload
Increase in ADH response, and can be an Increase in
renin/aldosterone/and plasma catecholamines
Renal:
Increased pressure on the kidneys and release of
inflammatory markers
Post-renal:
Direct compression of the ureters
A study in the Annals of Surgery in 1982 did not
improve with the insertion of ureteral stents
Calculations

IAP may affect the kidneys more than

changes in MAP
RPP=MAP-IAP
FG=GFR-IAP=(MAP-IAP)-IAP=MAP-
2(IAP)
Time Frame

Mean time from IAH to ARF is 2.7 days

May take between 0-35 days

Archives of Surgery 1999
Study
Tried to determine if IAH was an
independent risk factor for AKI
263 after abdominal surgery
Elevated IAP was =/>18mmHg
32.7% of patients with IAH developed
AKI
Mean time between onset of IAH and
AKI 2.7 +/- 6.5 days
Intensive Care Medicine
2008 Study
Determine at what IAP AKI develops
123 patients admitted > 24 hours in a
MICU
Bladder Pressure Q24 hours
Renal failure associated with IAH if
time interval <48 hours
37 patients (30%) developed IAH
16 in the IAH group developed AKI
Threshold of IAH 12mmHg
Treatment
General Principles

Serial monitoring of IAP

Optimization of systemic perfusion
Medical procedures to reduce IAP
Prompt surgical decompression for
refractory ACS
Serial Monitoring of IAP

High risk patients every 4-6 hours

IAH >12, increase monitoring to
hourly or continuous while treatment
is being implemented
Discontinue when the risk factors of
IAH go away or there are no signs of
acute organ dysfunctino and IAH
measurements have been less than
10-12 for 24-48 hours
Optimization of systemic
perfusion
Fluids increase circulating blood
volume

Too much fluid may result in IAH

To get around this, some practioners

have been using hypertonic solutions
Journal of Trauma 2006
Study
Determine if Hypertonic fluids
decrease risk of IAH
48 patients admitted to the burn unit
between 2002 and 2004 with
burns>40% of their body
Patients were given either hypertonic
LR (14) or LR (22).
IAH was a IAP greater than 30mmHg.
 Journal of Trauma 2006
Study
LR was given at 4mls/kg per percentage
of TBSA per 24 hours with a goal of 0.5-
1ml/kg per hour
IAH was a IAP greater than 30mmHg
Hypertonic LR had 40% less volume
infused than the group with the LR
Journal of Trauma 2006
Study
14% of patients in the hypertonic LR
group developed IAH vs. 50% of the
patients in the LR group

Serum sodium between 136 and

138meq/L 24 hours after injury in the
LR group and 150.7+/-10meq/L in the
HLS group, which then decreased to
an acceptable level within 2 hours
Medical procedures to
reduce IAP
Bowel Decompression

Decrease Intra-abdominal Fluid

Increase Abdominal Compliance

Correction of Capillary Leak

Bowel Decompression

Bowel obstruction through either ileus

or other causes leads to bowel dialtion
and mucosal edema, which will
increase the intra-abdominal pressure
Correct Electrolytes, stop medications
that impair bowel motility, can use
gastro-kinetcs (reglan and
erythromycin) or colo-kinetics
(neostigmine)
Decrease Intra-
abdominal Fluid

May be done with lasix/albumin

May be done with CRRT

Increase abdominal
Compliance
Muscle relaxants

Fentanyl may increase IAH

Correction of Capillary
Leak
Low dose dobutamine corrects
intestinal mucosal perfusion
Prompt surgical
decomporession for
refractory ACS
50% mortality rate, but 100% without
decompression

If the abdominal pressure is dropped

too quickly there can be reperfusion
injury