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Abdominal compartment syndrome
1. ABDOMINAL
COMPARTMENT
SYNDROME (ACS)
Leor Arbel, MS-3
Source: DeCou, JM et al. Abdominal compartment syndrome in children: Experience
with three cases. Journal of Pediatric Surgery, Volume 35, Issue 6, 840-842.
2. What is Abdominal Compartment Syndrome (ACS)?
Refers to organ dysfunction caused by intraabdominal hypertension
Tx can improve organ dysfunction, so it’s important to consider this diagnosis
Primarily affects pts who are already very ill – thus, S/Sx of ACS can be mistakenly
attributed to progression of the primary illness → heightened awareness of ACS is
needed!
Intra-Abdominal Hypertension (IAH) is not the same thing as ACS; IAH = sustained
Intra-abdominal Pressure (IAP) ≥ 12 mmHg
Note: IAP in critically ill pts between 5 – 7 mmHg is considered normal
For research purposes, ACS = sustained IAP > 20 mmHg
Clinically, however, there is no IAP value that reliably diagnoses ACS in all pts.
Therefore, it is more helpful to think of ACS as IAH-induced new organ dysfunction
That said, pts w/IAP < 10 mmHg generally do not have ACS and pts w/IAP > 25 mmHg usu
do have ACS
3. Primary vs Secondary ACS
Primary ACS Secondary ACS
▪ Due to abdominopelvic injury or
disease
▪ Examples: Trauma,
Hemoperitoneum, Pancreatitis
▪ Due to conditions that do NOT
originate in abdominopelvic region
but which require extensive fluid
resuscitation (→ splanchnic
reperfusion)
▪ Examples: Fluid resuscitation,
Burns, Sepsis
4. Who gets ACS?
ACS is MC seen in pts who are critically ill, but there is a wide variety in their
underlying medical/surgical conditions. Examples include:
TRAUMA – Injured pts in shock who need aggressive fluid resuscitation
BURNS – Pts with burns involving >30% of body surface area
ACS vs NEC vs Ischemic bowel
SEPSIS – Along with other medical conditions that require extensive fluid
resuscitation and are a/w 3rd spacing of fluids & tissue edema
LIVER TRANSPLANTATION
RETROPERITONEAL PATHOLOGIES – Eg ruptured AAA (8% of these pts develop ACS),
pelvic fractures, pancreatitis
POST-SURGICAL – Pts undergoing operations in which they are given large volume
resuscitation, esp with crystalloid in the face of hemorrhagic or septic shock
5. Physiologic Manifestations of ACS
Intra-abdominal Hypertension (IAH)
can cause dysfunction in nearly
every organ system, thereby
causing ACS
Table shows a summary of the key
physiologic effects a/w elevated
intra-abdominal pressure
Physiologic deterioration frequently
manifests as end-organ sequelae
eg:
↓ urine output
↑ pulmonary inspiratory pressure
↓ cardiac preload
↑ cardiac afterload
Source: UpToDate
6. Physiologic Manifestations of ACS (cont’d)
This is a better visual
representation of the
effects discussed on
the previous slide
Source: Brunicardi FC,
Andersen DK, Billiar TR, Dunn
DL, Hunter JG, Matthews JB,
Pollock RE. Trauma.
Schwartz's Principles of
Surgery, 10e (2014)
7. Signs & Symptoms
Pt is usually critically ill, unable to communicate.
Rarely, the pt is verbal & conveys symptoms of malaise, weakness, abdominal pain and bloating.
Tensely distended abdomen
Progressive oliguria
Increased ventilatory requirements, acute pulmonary decompensation
Hypotension
Tachycardia
Elevated JVP, JVD
Hypoperfusion → cool skin, obtundation, lactic acidosis
8. Diagnosis
Dx requires that IAP be measured. IAP cannot be reliably determined via
physical exam, and S/Sx and imaging findings are also insufficient for Dx.
IAP can be approximated by measuring the patient’s bladder pressure
50 mL saline instilled into bladder via aspiration port of Foley catheter with the drainage
tube clamped
3-way stopcock and water manometer are placed at level of pubic symphysis
Bladder pressure can then be viewed (in cm of water) on the manometer
9. Management
No specific bladder pressure prompts therapeutic intervention (unless the pressure is >
35 mmHg)
Emergent decompression is warranted when IAH reaches a level at which end-organ
dysfunction is observed
Decompression is usu performed operatively (decompressive laparotomy)
In operative decompression with egress of the abdominal contents → temporary
coverage using a subfascial sterile drape and Ioban application is placed over the
abdominal viscera
If significant intra-abdominal fluid is a primary component of the pt’s ACS (as opposed
to bowel or retroperitoneal edema), decompression can be achieved non-operatively via
Percutaneous Drain
Most applicable to pts with major liver injuries
Mortality is directly affected by the timing of decompression:
60% mortality if presumptive decompression
70% mortality if delayed decompression
Nearly 100% mortality if no decompression
11. Complications & Other Surgical Considerations
Recognition of ACS and performance of damage control surgery have ↑ pt survival,
but at the cost of an open abdomen
Pts with an open abdomen lose btwn 500-2500 mL per day of abdominal effluent (albumin rich
fluid). Appropriate volume compensation for this loss remains controversial, both wrt amount and
type of replacement (crystalloid vs colloid).
Interestingly, despite having a widely open abdomen, pts can develop recurrent ACS (this ↑
morbidity & mortality)
Therefore, recommended to monitor bladder pressure q4hr. Significant increases in pressure may
warrant repeat operative decompression
Following resuscitation & management of specific injuries where applicable, goal of
operative team is to close the abdomen as quickly as possible! Doing so promotes
fascial closure and minimizes morbidity as well as cost of care.
Delayed abdominal wall reconstruction = greater pt morbidity & resource invasive
Advent of wound VAC technology has revolutionized fascial closure
Authors used a sequential closure technique with the wound VAC device on constant fascial tension
with return to the OR every 48 hrs until closure is complete with a success rate of 95%
Mgmt requires frequent operative/percutaneous drainage of abscesses, fistula
control and prolonged TPN
12. Sequential Closure Technique for Open Abdomen with Wound VAC
Source: Brunicardi FC,
Andersen DK, Billiar TR,
Dunn DL, Hunter JG,
Matthews JB, Pollock RE.
Trauma. Schwartz's
Principles of Surgery,
10e (2014)
Authors’ sequential
closure technique for
the open abdomen
13. References
DeCou, JM et al. Abdominal compartment syndrome in children: Experience with three cases. Journal of
Pediatric Surgery, Volume 35, Issue 6, 840-842.
Burlew Cn, Moore EE. Trauma. In: Brunicardi F, Andersen DK, Billiar TR, Dunn DL, Hunter JG, Matthews JB,
Pollock RE. eds. Schwartz's Principles of Surgery, 10e New York, NY: McGraw-Hill;
2015. http://accessmedicine.mhmedical.com/content.aspx?bookid=980§ionid=59610848. Accesse
d March 04, 2017.
Gestring, M. Abdominal Compartment Syndrome in Adults. In: UpToDate, Post TW (Ed), UpToDate,
Waltham, MA. (Accessed on March 4, 2017).
Editor's Notes
Image from: DeCou, JM et al. Abdominal compartment syndrome in children: Experience with three cases. Journal of Pediatric Surgery, Volume 35, Issue 6, 840-842.
Note: For pts with severe burns, ACS must be distinguished from other abdominal pathologies seen commonly in this population such as Necrotizing Enterocolitis and ischemic bowel.
As you can see, a recurring theme here is that ACS is often related to the need for and extent of rapid volume resuscitation. This can likely be attributed to splanchnic reperfusion following massive resuscitation.
This is a somewhat more visual representation of the effects outlined in the previous slide.
The performance of damage control surgery and recognition of abdominal compartment syndrome have dramatically improved patient survival, but at the cost of an open abdomen. Several management points deserve attention. Despite having a widely open abdomen, patients can develop recurrent abdominal compartment syndrome, which increases their morbidity and mortality; therefore, bladder pressure should be monitored every 4 hours, with significant increases in pressures alerting the clinician to the possible need for repeat operative decompression. Patients with an open abdomen lose between 500 and 2500 mL per day of abdominal effluent. Appropriate volume compensation for this albumin-rich fluid remains controversial, with regard to both the amount administered (replacement based on clinical indices vs. routine ½ mL replacement for every milliliter lost) as well as the type of replacement (crystalloid vs. colloid).
The authors’ sequential closure technique for the open abdomen. A. Multiple white sponges (solid arrow), stapled together, are placed on top of the bowel underneath the fascia. Interrupted No. 1 polydioxanone sutures are placed approximately 5 cm apart (dashed arrow), which puts the fascia under moderate tension over the white sponge. B. After the sticky clear plastic vacuum-assisted closure (VAC) dressing is placed over the white sponges and adjacent 5 cm of skin, the central portion is removed by cutting along the wound edges. C and D. Black VAC sponges are placed on top of the white sponges and plastic-protected skin with standard occlusive dressing and suction. E. On return to the operating room (OR) 48 hours later, fascial sutures are placed from both the superior and inferior directions until tension precludes further closure; skin is closed over the fascial closure with skin staples. F. White sponges (fewer in number) are again applied and fascial retention sutures are placed with planned return to the OR in 48 hours.