Download Intra-Abdominal Hypertension

Intra-Abdominal
Hypertension
Trina Banerjee
Outline
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Definitions/Categories/Stages
Incidence
Causes
Diagnosis
Pathophysiology
Treatment
Definitions I
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Intra-abdominal pressure (IAP):
– Pressure within the abdominal cavity
– <5-7 mm Hg, with upper limit 12 mm Hg
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Abdominal Perfusion Pressure (APP):
– MAP (mean arterial pressure) – IAP
– Normal is 60 mm Hg and above
Definitions II
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Intra-abdominal Hypertension (IAH):
– IAP >10-12 on three different
measurements or
– APP<60mmHg on two separate
occassions
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Abdominal CompArtment Syndrome
(ACS):
– Subcategory of IAH
– Sustained IAP>20 with organ dysfunction
Categories
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Primary :
– Either Hyperacute (second to minutes) or
Acute (Hours)
– Results from abdominal trauma
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Secondary:
– Either Subacute (days) or Chronic
(Months )
– Results from extrabdominal causes
Stages
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Stage I :
12-15
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Stage II :
16-20
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Stage III :
21-24
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Stage IV :
>25
Incidence
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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
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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
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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
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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
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Ascites
Abdominal infection
Hemoperitoneum
Pneumoperitoneum
Laparoscopy with excesive inflation
pressures
Major trauma
PD
Capillary leak and fluid
resucitation
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pH<7.2
Hypothermia
Coagulopathy
Polytransfusion
Sepsis
Transfusions with capillary leak
Major burns
Diagnosis
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Physical Exam:
– Highly inaccurate
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Direct:
– Intraperitoneal catheter attached to a pressure
transducer
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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
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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
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This leads to decreased arterial pressure, resulting in
deceased MAP
General
Pathophysiology II
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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
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The rise in pressure causes decreased
blood flow to the gut, resulting in
bacterial translocation
Can result in abdominal wall ischemia
Liver Pathophysiology
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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
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Cerebral perfusion pressure decreases
because of the increase in
intrathoracic pressure, resulting in an
obstruction of cerebral venous outflow
Renal Pathophysiology I
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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
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Pre-renal, Renal, and Postrenal
– Pre-renal:
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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:
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Increased pressure on the kidneys and release of
inflammatory markers
– Post-renal:
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Direct compression of the ureters
A study in the Annals of Surgery in 1982 did not
improve with the insertion of ureteral stents
Calculations
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IAP may affect the kidneys more than
changes in MAP
– RPP=MAP-IAP
– FG=GFR-IAP=(MAP-IAP)-IAP=MAP2(IAP)
Time Frame
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Mean time from IAH to ARF is 2.7 days
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May take between 0-35 days
Archives of Surgery 1999
Study
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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
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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
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Serial monitoring of IAP
Optimization of systemic perfusion
Medical procedures to reduce IAP
Prompt surgical decompression for
refractory ACS
Serial Monitoring of IAP
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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
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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
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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
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LR was given at 4mls/kg per percentage
of TBSA per 24 hours with a goal of 0.51ml/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
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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
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Bowel Decompression
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Decrease Intra-abdominal Fluid
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Increase Abdominal Compliance
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Correction of Capillary Leak
Bowel Decompression
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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 Intraabdominal Fluid
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May be done with lasix/albumin
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May be done with CRRT
Increase abdominal
Compliance
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Muscle relaxants
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Fentanyl may increase IAH
Correction of Capillary
Leak
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Low dose dobutamine corrects
intestinal mucosal perfusion
Prompt surgical
decomporession for
refractory ACS
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50% mortality rate, but 100% without
decompression
If the abdominal pressure is dropped
too quickly there can be reperfusion
injury