Abdominal Compartment Syndrome

DEFINITIONS:
● 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 chronically higher baseline IAP (as
high as 10 to 15 mmHg) without adverse sequelae.
● Intra-abdominal Hypertension
(IAH):- When IAP is consistently > 12 mmHg without
any organ dysfunction.

● Abdominal Compartment
Syndrome (ACS):- When IAP>20 mm Hg or
higher with or without Abdominal Perfusion
pressure <50 mm Hg, it is associated with one or
more organ failure.
 It may be under-recognized because:
- it primarily affects patients who are already quite ill
- organ dysfunction may be incorrectly ascribed to
progression of the primary illness.
● Since treatment can improve organ dysfunction, it is
important that the diagnosis be considered without any
delay.
● Intraabdominal hypertension (IAH) and abdominal
compartment syndrome (ACS) are distinct clinical entities
and should not be used interchangeably.

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

● Abdominal perfusion pressure (APP) was found to be
better than other resuscitation endpoints e.g. hourly
urinary output for predicting the outcomes.
● A target APP of at least 60 mmHg is correlated with
improved survival from IAH and ACS.

● Intraabdominal hypertension (IAH) can be further
graded as follows:
- Grade I = IAP 10 to 15 mmHg
- Grade II = IAP 16 to 25 mmHg
- Grade III = IAP 26 to 35 mmHg
- Grade IV = IAP >36 mmHg

● Hyperacute IAH :
 - Elevation of the IAP lasting only seconds.
 - It is due to laughing, 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 and
can lead to the rapid development of ACS.
● 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.

● Patients with an IAP 10-25
mmHg may or may not have
ACS, depending upon
individual variables such as
blood pressure and abdominal
wall compliance

● Etiology & 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) with or without concomitant trauma are also at risk for ACS.
Importantly, ACS must be distinguished from other intraabdominal
problems that occur in these critically ill patients (eg, necrotizing
enterocolitis, ischemic bowel).
- 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 can increase intraabdominal
pressure.
- Retroperitoneal conditions: Retroperitoneal pathologies, such as
ruptured abdominal aortic aneurysm, pelvic fracture with bleeding,
and pancreatitis, can lead to ACS.
- Medical illness: Conditions that require extensive fluid resuscitation
(e.g. sepsis) and are associated with third spacing of fluids and tissue
edema can increase IAP.
- Post-surgical patients: Patients undergoing operations in which they
are given large volume resuscitation, particularly with crystalloid in
the face of hemorrhagic or septic shock, are at risk for ACS.

● Abdominal wall compliance initially minimizes the
extent to which an increasing abdominal girth can
elevate IAP .
- When a critical abdominal girth is reached,
abdominal wall compliance decreases abruptly.
Further increases in abdominal girth beyond this
critical level result 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
●Secondary
●Recurrent ACS

● Primary ACS:- Intra-abdominal
pathology
➢Trauma
➢Ascites
➢Retro-peritoneal hemorrhage
➢Pancreatitis
➢Pneumoperitoneum
➢Reduction of chronic hernia
➢Complex abdominal procedure and liver
transplantation

●Secondary ACS:- Without intra-
abdominal pathology
➢Shock patients(requires aggressive fluid
resuscitation with crystalloids)
➢Thermally injured
➢Septic shock
Pts with sustained cardiac arrest.

●Recurrent ACS:
➢Is the redevelopment of ACS following previous
surgical or medical treatment of primary or
secondary ACS.

Physiologic consequences
 ● IAH can impair the function of nearly every organ
system, thereby causing ACS .

Pulmonary System:
● Increase IAP, displaces the diaphragm upwards which
leads to decrease in the thoracic volume, compliance and
increase the intra-pleural pressure.
● Results –increase PAP(peak airway pressure), V-P
mismatch, hypoxia,hypercapnia and acidosis.
● IAP -25 leads to increase in end-respiratory pressure to
achieve fixed Tidal Volume.
● Modest IAH can exacerbate ALI, inhalation injury or
respiratory distress syndrome

Cardiovascular System
● IAP >20 mm Hg leads to compression of IVC and PV, decreases
the venous Return.
● So leads to decrease in preload and pooling of blood in
splanchnic and lower vascular beds and increased peripheral
vascular resistance.
● It results in Decreased cardiac output, cardiac index and Rt. Atrial and
pulmonary artery occlusion pressure.
● Increase intra thoracic pressure also leads to decrease left
ventricular compliance which further decreases the cardiac
contractility and compliance.
● IAP 20 to 25- Cardiac output decreases despite normo-volemia and
normal ejection fraction
● IAP >25 –systemic delivery of oxygen decreases and
whole body consumption will reduced
● IAP >30 Ventricular compliance decrease
●

Gastrointestinal System:
● Compression of mesenteric vasculature leads to decrease
in splanchnic perfusion, mesenteric venous hypertension
and decreased hepatic arterial flow.
● Results:-
➢Gastric intra-mucosal acidosis(IAP 15 mm Hg)
➢Intestinal edema
➢Visceral swelling
➢Increased intestinal permeability
➢Bacterial translocation.

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.
● Results – Decreased GFR, renal plasma flow, glucose
absorption and U.O.
● In ICU post operative patients–
If IAP >18 mm Hg renal function impaired by 30%,
independent of pre renal circulation
If IAP >25 mm Hg, renal output decrease in 65% patients
If IAP >35 mm Hg, renal output decrease in 100% patients

Central Nervous System
● Elevated central venous pressure interferes with venous
cerebral outflow leads to cerebral pooling and increase in
intra-cerebral pressure.
● Due to decrease in C.O. and increase in intra-cerebral
pressure
-Decrease in the cerebral perfusion pressure
-Brain anoxia, edema and injury

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.
● Physical signs:
- Nearly all patients with ACS have a tensely distended abdomen. Despite this,
physical examination of the abdomen is a poor predictor of ACS.
- Progressive oliguria and increased ventilatory requirements are also common in
patients with ACS.
- Other findings may include hypotension, tachycardia, an elevated jugular
venous pressure, jugular venous distension, peripheral edema,
abdominal tenderness, or acute pulmonary decompensation.
- 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.
 - CXR 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

2. Clinical manifestations of organ dysfunction
include
respiratory failure
➢Impaired pulmonary compliance
➢Elevated airway pressures
➢Hypoxia
➢Hypercapnia
● Some authors report pulmonary dysfunction as
the earliest manifestation of ACS

● Hemodynamic indicators
➢Increased HR
➢Decreased BP
➢Normal or elevated pulmonary artery
wedge pressure and central venous pressure.
➢Reduced Cardiac Output.
➢Elevated systemic and peripheral vascular
resistance

● Impairment in renal function
➢Oliguria progressing to anuria with
resultant azotemia.
● Renal insufficiency as a result of IAH is
only partly reversible by fluid resuscitation

Diagnostic evaluation
● Definitive diagnosis of ACS requires measurement of the IAP.
● Measurement of intraabdominal pressure:
● Direct Pressure via Intra-peritoneal catheters
● Indirect Pressure
➢Gastric Measure (intragastric)
➢IVC
➢Rectal
➢Urinary bladder pressure – Gold Standard
● Measurement of bladder (ie, intravesical) pressure is the standard
method to screen for IAH and ACS. It is simple, minimally invasive,
and accurate.

Measurement of IAP:
1. Foley’s catheter
2. Three-way Foley’s catheter
3. Foley’s catheter with three-way
stopcock and transducer

Measurement of IAP:
In 1984,Kron et al reported a method to measure
IAP at the bedside with the use of an indwelling Foley
Catheter. Sterile saline (50-100cm3) is injected into the
empty bladder through the indwelling Foley catheter. The
end of the drainage bag tubing is connected to the
Foley catheter. The clamp is released just enough to
allow the tubing proximal to the clamp to flow fluid
from the bladder, then reapplied. A 16-gauge needle is
then used to Y-connect a manometer or pressure
transducer through the aspiration port of the tubing of
the drainage bag. Finally, the top of the symphysis
pubic bone is used as the zero point with the patient
Supine.

Foley’s catheter Bladder pressure monitoring
through the Foley’s catheter is:
● The current standard for monitoring abdominal
pressures
● Comparable to direct intra-peritoneal pressure
measurements.
●More reliable and reproducible than clinical
judgment

Foley’s catheter with three-way
stopcock and transducer

Preventions:
● Primary ACS – leave open peritoneal cavity
● Secondary ACS – if receives 6 litres IVF in 6 hrs then
measure IAP.
● IAP – as routine in critically ill ICU patients because
IAH
is leading cause of chest wall impairment in ARDS
● Monitoring of gastric pH
● Conservative fluid resuscitation, analgesia, sedatives,
paralysis, positioning, drainage of abdominal fluid,
diuretics prevent progression of ACS.

Management approach
● 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:
- Goals:
- Reduction of intraabdominal volume.
- 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.
● Patient should be placed in a supine position.
● Abdominal wall compliance can be improved with
adequate pain control and sedation.

● Ventilatory support:
--Tidal volume reduction, a pressure-limited mode, and/or
permissive hypercapnia 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.
- Some clinicians prefer to use colloids under this circumstance instead
of crystalloids.
● There is no role for diuretic therapy in the resuscitation of patients
with acute ACS.
● The only appropriate management is to open the abdomen.

Surgical decompression
- There is general agreement that surgical
decompression is indicated for ACS.
- Decompressing the abdomen prior to the
development of ACS is becoming increasingly
common and may improve survival.

● 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

● Most surgeons perform decompression and then
maintain an open abdomen using temporary abdominal
wall closure.
● Surgical decompression can be performed in the
operating room if the patient is medically stable for
transfer or at the bedside in the intensive care unit.

● So decompression should be followed by adequate
preload

Open abdomen
● INTRODUCTION:
- 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:
- The most common circumstances that result in open abdomen include the following:
1. Damage control surgery:
- It is an operative strategy that is used to manage immediately life-threatening
conditions by delaying definitive management.
2. Abdominal compartment syndrome (ACS):
-Increased volume in the abdomen is typically the result of an increase in interstitial
fluid as is seen with large volume resuscitation, but space occupying fluid (blood or
ascites) in the peritoneum or retroperitoneum can also contribute.
3. Septic abdomen:
- Bowel perforation with severe contamination of the peritoneal cavity can result in
recurrent intra-abdominal sepsis.
- Under this circumstance, it may be desirable to leave the abdominal wall open
and use negative-pressure wound therapy to remove residual or reaccumulated
fluid or pus.
4. Refractory intracranial hypertension :
- A more controversial indication for open abdomen is refractory intracranial
hypertension associated with traumatic brain injury.

● Complications of open abdomen:
- Fluid loss:
A significant amount of fluid can be lost through an open abdomen.
- Protein loss:
– The fluid that is secreted by the peritoneum is rich in protein with about 2
grams of protein lost from the abdomen for each liter of fluid removed.
-Fistula formation:
– With open abdomen, the bowel is frequently manipulated and is at risk for injury.
- Loss of domain:
- With open abdomen from a midline abdominal incision, the musculature of
the abdominal wall retracts the fascia laterally.
- The use of a negative pressure wound system helps to counteract the lateral
forces on the abdominal wall and may allow primary closure of the fascia and skin .

● 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 — Each time the patient is returned to the operating room,
the abdomen is assessed for potential closure.
● Fascial closure:
1. Primary fascial closure:
- Associated with the lowest rate of complications following management of the
open abdomen.
- Because of the high hernia rate, biologic 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
biologic mesh (in-lay technique).
- Once the biologic mesh is placed, the skin is closed over surgical drains placed
into the subcutaneous space.

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.

Summary and recommendations
● Increased IAP is called intraabdominal hypertension
(IAH). Abdominal compartment syndrome (ACS) refers to
organ dysfunction caused by intraabdominal
hypertension.
● ACS can impair the function of nearly every organ system.
● Diagnosis of ACS requires that IAP be measured.
Symptoms, physical signs, and imaging findings are
insufficient to diagnose ACS.

● Management initially consists of careful observation and supportive
care. In some cases abdominal compartment decompression is
required.
● We suggest that surgical decompression is not delayed until the
development of ACS.
● Following surgical decompression, an open abdomen is maintained
using a variety of temporary abdominal closure techniques.
● Following temporary abdominal closure, the patient is monitored in
ICU.
- Abdominal dressings associated with the closure (adhesive
dressings, gauze, negative pressure systems) are changed, as
needed, and the abdominal contents inspected every two to three
days.

● We suggest the use of a negative pressure system
(towel or sponge based) to control and quantify fluid
loss.
● Once the indication for the open abdomen has
resolved, the abdomen is closed, preferably with a
primary fascial closure. If primary fascial closure
cannot be achieved, functional closure can be
performed.
● If the gap between the fascia is deemed to be too
large for a functional closure, primary skin closure
can be performed, or skin grafts placed once a layer
of granulation tissue has developed.

Abdominal Compartment Syndrome

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