ABDOMINAL COMPARTMENT
SYNDROME
GUIDE: DR. ABHIJEET
DR. SANKET, DR. POOJA THORAT SIR
Intraabdominal pressure (IAP):
It is the steady state pressure concealed
within
the abdominal cavity. For most critically
ill patients, an IAP of 5 to 7 mmHg is
considered normal.
Patients with increased abdominal girth
that
developed slowly e.g. the morbidly
obese and
pregnant individuals may have
Intra-abdominal Hypertension (IAH):-
When IAP is consistently more than 12
mmHg without any organ dysfunction.
Abdominal Compartment Syndrome(ACS):-
When IAP is 20 mm Hg or higher with or
without Abdominal Perfusion pressure <
50 mm Hg, it is associated with one or
more organ failure.
Since treatment can improve organ
dysfunction, it is important that the
diagnosis be considered without any
delay.
Abdominal perfusion pressure (APP):
It is calculated as the mean arterial pressure
(MAP) minus the IAP
APP = MAP - IAP.
• Elevated IAP reduces blood flow to the
abdominal
viscera
A target APP of at least 60 mmHg is
correlated with improved survival from IAH
and ACS.
Grading of Intraabdominal hypertension
(IAH)
Grade I : IAP 12 to 15 mmHg
Grade II : IAP 16 to 25 mmHg
Grade III : IAP 26 to 35 mmHg
Grade IV : IAP > 35 mmHg
• Hyperacute IAH:
Elevation of the IAP lasting only seconds.
It is due to coughing, straining, sneezing,
defecation or physical activity. IAH with ACS
due to gastric over-distention following
endoscopy has been described.
• Acute IAH:
Elevation of the IAP that develops over hours.
It is usually the result of trauma or
intraabdominal
hemorrhage
• Subacute IAH:
Elevation of the IAP that develops over days.
It is most common in medical patients and can also
lead to ACS.
• Chronic IAH:
Elevation of IAP that develops over months
(pregnancy) or years (morbid obesity).
It does not cause ACS, but does place the individual at
higher risk for ACS if they develop superimposed acute
or subacute IAH.
Etiology and risk factors:
ACS generally occurs in patients who are
critically ill due to any of a wide variety of
medical and surgical conditions. Some of these
include:
Trauma : Injured patients in shock who require
aggressive fluid resuscitation are at risk for ACS.
Burns: Patients with severe burns (>30 percent
total body surface area)
Liver transplantation: IAH (IAP >25 mmHg) was
found following liver transplantation in 32%
patients.
Abdominal conditions: Massive ascites, bowel
distension, abdominal surgery or intraperitoneal
bleeding
Retroperitoneal conditions: ruptured abdominal
aortic aneurysm, pelvic fracture with bleeding,
and pancreatitis
Medical illness: Conditions that require
extensive fluid resuscitation (e.g. sepsis)
tissue edema can increase IAP.
Post-surgical patients: large volume
resuscitation, in the case of hemorrhagic
or septic shock are at risk for ACS.
Abdominal wall compliance
When a critical abdominal girth is reached,
abdominal wall compliance decreases
abruptly. Further increase in abdominal girth
beyond this critical level results in a rapid
rise of IAP and ACS if untreated.
Increased abdominal wall compliance due
to chronic increased abdominal girth(e.g.
pregnancy, cirrhosis with ascites, morbid
obesity) may protect against ACS.
Types of ACS
Primary ACS : It is associated with injury
or disease in the abdominopelvic region
Trauma
Retro-peritoneal hemorrhage
Ascites
Pancreatitis
Pneumoperitoneum
Reduction of chronic hernia
Complex abdominal procedure and liver
transplantation
Secondary ACS
It develops without intra- abdominal
pathology
Shock patients (requires aggressive fluid
resuscitation with crystalloids)
Massive burns
Sustained cardiac arrest.
Recurrent ACS:
It is the redevelopment of ACS following
previous surgical or medical treatment of
primary or secondary ACS.
Pathophysiology
Cardiovascular System
IAP >20 mm Hg leads to compression of IVC and
PV that decreases the venous return to the heart
Decrease in preload and cardiac output
Less blood and oxygen delivery to peripheral
tissues
Increased intra thoracic pressure places direct
pressure on the heart , ultimately decreasing
ventricular compliance
Pulmonary system
Increase IAP displaces the diaphragm
upwards which leads to decrease in the
thoracic volume, compliance and
increase the intra-pleural pressure.
Airway pressure increases and alveoli
exhibit atelectasis increasing the dead
space
Gas exchange is affected leading to
hypoxia and hypercarbia
Renal system
Direct compression of kidneys and obstruction of
venous outflow leads to increase in pre-renal vascular
resistance and shunting of blood from cortex to
medulla.
This causes decreased GFR and urine output leading
to acute kidney injury.
The renin-angiotensin-aldosterone system is activated:
• increased systemic vascular resistance through
angiotensin
• Increased resorption of Na & water by aldosterone
IAP > 15mmhg – Oliguria
IAP > 30mmhg - Anuria
Gastrointestinal System:
Compression of mesenteric vasculature leads
to decrease in splanchnic blood flow causing
tissue hypoxia, increased capillary
permeability and edema.
It further leads to intestine malperfusion that
increases the risk of bacterial translocation
and infection.
The hepatic system is also affected as
decreased hepatic flow leads to impaired
Nervous system
Elevated IAP decreases venous drainage
from the brain, which increases
intracranial pressure and decreases
cerebral blood flow.
Increased PaCO2 also causes increased
arterial blood flow to the brain, further
increasing intracranial pressure.
Clinical presentation
Symptoms:
Most patients who develop ACS are
critically ill and unable to communicate.
The rare patient who is able to convey
symptoms may complain of malaise,
weakness, lightheadedness, dyspnea,
abdominal bloating or abdominal pain.
Signs
Nearly all patients with ACS have a tensely distended
abdomen.
Progressive oliguria and increased ventilatory
requirement.
Other findings may include
.Hypotension
. Tachycardia
. an elevated jugular venous pressure
. peripheral edema
. abdominal tenderness
There may also be evidence of hypoperfusion, including
cool skin, obtundation, restlessness or lactic acidosis
DIAGNOSIS:
1. Imaging findings:
Imaging is not helpful in the diagnosis of ACS.
-Chest xray may show decreased lung volumes,
atelectasis, or elevated hemidiaphragms.
- Computed tomography (CT): may demonstrate tense
infiltration of the retroperitoneum that is out of
proportion to peritoneal disease, extrinsic compression
of the inferior vena cava, massive abdominal
distention, direct renal compression or displacement,
bowel wall thickening, or bilateral inguinal herniation
Definitive diagnosis of ACS requires
measurement of the IAP.
Measurement of intraabdominal
pressure:
• Direct method include using Intra-
peritoneal
Catheters [eg. Peritoneal dialysis catheter]
or pressure transducers[eg. Veresse
needle during laparoscopic surgery]
These methods are highly accurate but
invasive.
Indirect method
The most accepted method of measuring
IAP is through intravesicular cathetar
pressures
In 1984,Kron et al reported a method to
measure IAP at the bedside with the use
of an indwelling Foley Catheter.
Management
Management of IAH and ACS consists of
supportive care and when needed
abdominal decompression.
Some exceptions include escharotomy
release to relieve mechanical limitations
due to burn eschars and percutaneous
catheter decompression to relieve tense
ascites.
Supportive care:
Measures to improve abdominal wall compliance.
• Nasogastric and rectal drainage are a simple means
for reducing IAP in patients with bowel distension.
• Hemoperitoneum, ascites, intraabdominal abscess
and retroperitoneal hematoma occupy space and
can elevate IAP. In some cases, these collections
can be evacuated using percutaneous techniques.
• Abdominal wall compliance can be improved with
adequate pain control and sedation.
• Ventilatory support:
Tidal volume reduction, a pressure-limited
mode may be necessary.
Positive end-expiratory pressure (PEEP)
may reduce ventilation-perfusion
mismatch and improve hypoxemia.
• Hemodynamic support:
For patients with IAH, limiting the amount
of fluid administration may decrease the
risk of developing ACS.
Surgical decompression
Decompression - not based on IAH alone but
also on presence of organ dysfunction.
Grade III IAH + tense abdomen + signs of
ventilatory dysfunction + oliguria
Grade IV IAH+ signs of ventilatory
dysfunction + renal failure
Severe head injury + IAP >20 mm Hg
Intractable intra cranial hypertension without
obvious head injury
Open abdomen
Refers to a defect in the abdominal wall that
exposes the abdominal viscera.
Damage control surgery associated with
trauma and ACS is the most frequent reason
for open abdomen.
Etiology of open abdomen
1.Damage control surgery
2. Abdominal compartment syndrome
(ACS)
3. Septic abdomen
4. Refractory intracranial hypertension:
Complications of open
abdomen:
Fluid loss
Protein loss
Fistula formation
Loss of domain
Temporary closure techniques:
In some patients, delayed primary
closure of the abdominal fascia is
possible once edema subsides. However,
if closure is premature, ACS can recur.
ABDOMINAL CLOSURE -
1. Primary fascial closure:
- Associated with the lowest rate of
complications
- Because of the high hernia rate, biological
mesh
reinforcement during primary fascial closure is
frequently used.
2. Functional closure:
- Functional closure refers to the bridging
of a residual fascial defect with a
biological mesh (in-lay technique).
3. Planned ventral hernia:- If primary fascial closure
or functional closure cannot be achieved.
Skin-only closure: A skin-only closure approximates the
skin over the fascial defect leaving a ventral hernia.
Split-thickness skin graft:
If the skin cannot be approximated, the viscera within
the wound are allowed to adhere to each other and to
the abdominal wall. Once the abdominal contents have
solidified and there is a healthy bed of granulation
tissue overlying the bowel, a split-thickness skin graft
can be placed.
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