Compartment syndrome occurs when pressures increase within a fixed cavity of the body, leading to ischemia, muscle damage, and organ dysfunction. These "fixed" spaces are constrained by muscular and facial boundaries which may have limited compliance when they become swollen.
Intra-abdominal hypertension is defined as a sustained abdominal pressure above 12 mmHg.
Abdominal compartment syndrome (ACS) is a very serious illness seen in critically ill patients. ACS results from the progression of steady state pressure within the abdominal cavity to a repeated pathological elevation of pressure above (> 20mmHg) with associated organ dysfunction. Failure to recognize and immediately managed ACS can lend to poor prognosis as ACS is recognized as an independent predictor of mortality. High clinical suspicions with a protocolized monitoring and management should be adapted when treating the critically ill, especially those with large fluid shifts. Clinical diagnosis should be considered in patients with tense or distended abdomen with associated instability, however, it may also be seen without abdominal distention.
The exact clinical conditions that define abdominal compartment syndrome (ACS) are controversial. The dysfunction may be respiratory indicated by high peak airway pressure and inadequate ventilation and oxygenation, decreased urine output caused by falling renal perfusion but is reversible with intervention.
Abdominal Compartment Syndrome has medical and conservative management options, and treatment is aimed at identifying and treating the cause of the compartment syndrome. However, patients with clinical deterioration may require emergent surgical decompression.
Abdominal Compartment Syndrome can be divided and classified into primary and secondary. Primary causes include abdominal blunt or penetrating trauma, hemorrhage, AAA rupture, intestinal obstruction, and retroperitoneal hematoma. Secondary causes include pregnancy, ascites, ileus, burns, intra-abdominal sepsis and large-volume fluid replacement (> 3 Liters). Chronic causes of elevated intra-abdominal pressure include pregnancy, cirrhosis, obesity, intra-abdominal malignancy, and peritoneal dialysis. These are all causes of intra-abdominal hypertension, defined as repeated intra-abdominal pressures > 12 mm Hg. The presence of organ dysfunction in this setting due to compressive symptoms now confirms a diagnosis of Abdominal compartment syndrome.
Studies have shown that mortality after ACS caused by AAA rupture neared 47%. The disease can become devastating once other organ systems become involved due to compression and Primary ACS tends to have a worse outcome.
ACS can develop in all ICU patients. In an identified series of mixed ICU population, 35% of ventilated patients were found to have IAH or ACS. Risks factors include a plethora of medical conditions but may be classified based on abdominal wall mechanics. Risk factors include those that reduce abdominal compliance, increase intra-abdominal contents, increase luminal contents or third space expansion and capillary leak. 
With intraperitoneal bleeding, trauma or abscess, the physiologic response of inflammation and swelling can be held responsible for intra-abdominal hypertension. In the setting of intestinal obstruction, the dilated loops of bowels can cause compressive symptoms within the abdominal cavity. As abdominal pressure increases, the syndrome may begin to involve other organ systems due to further compression.
Intra-abdominal hypertension is graded from I to IV:
Any evidence of repeated intra-abdominal hypertension with organ failure is defined as ACS. However, the incidence of organ failure is far greatest with Grade IV IAH. Organs typically affected include the heart, lungs, kidney.
Physiologic cardiac sequelae include decreased cardiac output and increased CVP due to IVC and portal vein compression, increase SVR leads to hypotension. Pulmonary involvement can include decreased thoracic volumes and elevated peak pressures from compression of the diaphragm, a decrease in P/F ratio and hypercarbia. Renal compression can lead to decreased GFR and low urine output. Visceral blood flow is also decreased. Neurologic symptoms can include increased ICP from the elevated CVP due to IVC compression contributing to a decrease in cerebral perfusion pressure (CPP).
Abdominal compartment syndrome (ACS) is typically only seen in critically ill patients and will likely be a diagnosis made in the ICU setting, rather than in the ER. Clinical suspicion for abdominal compartment syndrome should be high in patients with penetrating abdominal trauma or surgical patients following large abdominal surgery. Patients may present with abdominal pain and distension. However, this is not a sensitive or specific finding. Patients in the ICU setting may present with a wide array of organ failure, not limited to the abdomen which can make the diagnosis difficult.
The physical exam may reveal an increased abdominal girth, tense abdomen, cyanosis, wheezing and difficulty breathing.
In abdominal compartment syndrome, the displacement of the diaphragm cephalad leads to compression of the thorax which causes an increase in work of breathing, ventilation/perfusion inequality, and increases in both peak and plateau pressures.
The extremely tense abdomen also prevents venous return, resulting in elevated intracranial pressure and decreased cerebral perfusion pressure.
While imaging modalities may help in localizing a cause of the elevated abdominal pressure (bleeding, trauma, obstruction, etc.), they are not helpful in making the specific diagnosis of abdominal compartment syndrome. The most accurate manner of confirming this diagnosis is from measured abdominal pressures. The IAP should be measured when any known risk IAH/ACS is present. This can be achieved in many ways including both direct and indirect methods. Direct methods include measurement of abdominal pressure using pressure transducers (e.g. veress needle during laparoscopic surgery) or intraperitoneal catheters (e.g. peritoneal dialysis catheter). Theses methods are highly accurate, however, are limited by their invasiveness. The more commonly used method is an indirect measurement such as intravesicular catheter pressures (e.g. Foley catheter) which has become the gold standard due to its widespread availability and limited invasiveness. Trans-bladder technique involves using aseptic clamping the drainage tubing of the Foley then connecting the Foley to a three-way stop tap adjusted to the level of the mid-axillary line at the iliac crest to zero transducers follow by injecting 25cc of sterile saline into the bladder. Measurements should be taken at end-expiration and complete supine position and expressed in mmHg. Bladder pressures below 5mm Hg are expected in normal patients. Pressures between 10 to 15 mmHg can be expected following abdominal surgery and in obese patients. Bladder pressures over 25 mmHg are highly suspicious of abdominal compartment syndrome and should be correlated clinically. It is recommended that pressure measurements be trended to show and recognize the worsening of intra-abdominal hypertension.
Contraindications to using bladder pressures include bladder trauma, neurogenic bladder, BPH and pelvic hematoma. Bladder pressures may be inaccurate if the patient is not sedated or laying flat.
Ct scan may reveal collapse of the vena cava,, round abdomen, bowel thickening and or bilateral inguinal herniation. The following grading system is used to categorize abdominal compartment syndrome:
Grade I: 10-15 cm H O
Grade II: 15-25 cm H O
Grade III: 25-35 cm H O
Grade IV, greater than 35 cm H O
Non-surgical therapeutic options for treatment of intra-abdominal hypertension involves an overall goal to improve abdominal wall compliance with decreased muscle contraction, evacuate luminal contents by decompression (NG tube), and evacuate abdominal fluid by drainage, and correct positive fluid balance through goal-directed volume resuscitation.
Surgical decompression remains the mainstay treatment of ACS. However, prevention and early treatment of the potential cause may prevent progression of IAH to ACS. The protocol should be used to try to avoid positive cumulative balance in the those at risk. The enhanced ratio of plasma to packed RBC during resuscitation when treating those with massive hemorrhage. Those patients undergoing initial laboratory at risk for ACS be treated with the prophylactic open abdomen. Early recognition involves supportive care to include keeping patients comfortable with pain well controlled. Decompressive procedures such as NG tube placement for gastric decompression, rectal tube placement for colonic decompression and percutaneous drainage of abscesses, ascites or fluid from the abdominal compartment. The neuromuscular blockade has been described to be used as a brief trial in attempt to relax the abdominal musculature, leading to a significant decrease in abdominal compartment pressures in the ventilated ICU patient. If conservative and medical management does not resolve the IAH and further organ damage is noted, surgical decompression using emergent laparotomy may be considered. 
After surgical laparotomy for compartment syndrome, the abdominal fascia may be closed using temporary closure devices such as (vacs, meshes, and zippers). The fascia can be closed properly after 5-7 days and the compartments pressures and swelling have decreased.
With surgical abdominal decompression, organ dysfunction may also improve rapidly as most organ dysfunction is seen as sequelae from compression. With less tension from the inferior portion, the diaphragmatic excursion can increase leading to improved ventilation and reduction of peak airway pressures. Compression of the IVC and circulatory system are relieved, leading to improved cardiac output and ability to wean patients off of vasopressor support. Acute kidney injury can be reversed with less compression of the kidneys and ureters.
If left untreated, abdominal compartment syndrome is fatal. Even delayed treatment is associated with very high mortality rates. Predictors of mortality include a history of diabetes and transfusion of a high volume of blood products. Many series reports that even with treatment, multi-organ failure can delay recovery for weeks or months. Prolonged need for mechanical ventilation, dialysis and longer hospital stay are common in these patients.
After decompression of the abdomen, many patients still require the following treatments:
To prevent abdominal compartment syndrome, many types of mesh are now available for abdominal closure that prevent tension on the abdominal contents. Some studies indicate that abdominal compartment syndrome is less likely to occur in patients resuscitated with FFP and lactate ringers compared to just a pure crystalloid.
Current guidelines with which to be familiar (as presented by the World Society of the Abdominal Compartment Syndrome) include:
1) Intra-abdominal hypertension (IAH) is defined by a sustained or repeated pathological elevation in IAP of =12 mm Hg
2) ACS is defined as a sustained IAP >20 mm Hg associated with organ dysfunction/failure
3) IAH Grade I: IAP 12-15 mm Hg; Grade II: IAP 16-20 mm Hg; Grade III: IAP 21-25 mm Hg; Grade IV: IAP >25 mm Hg
4) A trial of neuromuscular blockade can be used to palliate compressive symptoms in ACS to while awaiting surgical decompression
The diagnosis and management of abdominal compartment syndrome require an interprofessional team approach. The condition can present in subtle ways and the diagnosis can easily be missed. If the abdominal compartment syndrome is not diagnosed or treatment is delayed, the outcome is almost always fatal. Mortality rates of 20-70% have been reported in patients with blunt abdominal trauma, even with treatment. The reason for the high mortality is due to the early involvement of multiple organs. In addition, the higher the abdominal pressure, the higher the mortality. Other factors associated with mortality include surgery lasting more than 2 hours, developing abdominal compartment syndrome within 48 hours of admission and an elevated lactic acid level despite treatment. Even those who survive have significant morbidity from residual deficits like renal failure, muscle wasting, respiratory distress, and liver dysfunction.
The Interprofessional Team
The diagnosis usually requires a systemic approach and discussion with the interprofessional team. Once the diagnosis is made, all patients require ICU care with continuous monitoring. A wound care nurse should assess the wound every day for healing. Since most patients are kept NPO a dietary consult for TPN is necessary. Nurses should ensure that all patients have DVT and pressure sore prophylaxis. In addition, nurses need to weigh the patient daily, measure abdominal girth, assess urine output and organ perfusion. If urine output declines, the nephrologist should be involved early in the care. Any deviation from normal parameters should be immediately conveyed to the interprofessional team. As the patient improves physical therapy should be involved in getting the patient out of bed and encouraging ambulation.
Those who go on to develop chronic abdominal compartment syndrome need lifelong support and monitoring. The current emphasis is on prevention of abdominal compartment syndrome. Various techniques of closure of the abdomen have been described and even the fluid used to resuscitate the patient may make a difference in the outcome. 
The outcomes for most patients with abdominal compartment syndrome are guarded. Those who are diagnosed and treated promptly do have good outcomes but the recovery is often prolonged. Patients with multiorgan dysfunction have a long recovery, marked by wound breakdown, repeated hospitalization and difficulty performing even the most basic daily living activities. (Level V)
|||Ali M, Abdominal compartment syndrome: the importance of urinary catheter placement in measuring intra-abdominal pressure. BMJ case reports. 2018 Oct 21 [PubMed PMID: 30344152]|
|||Ampatzidou F,Madesis A,Kechagioglou G,Drossos G, Abdominal compartment syndrome after surgical repair of Type A aortic dissection. Annals of cardiac anaesthesia. 2018 Oct-Dec [PubMed PMID: 30333346]|
|||Chandra R,Jacobson RA,Poirier J,Millikan K,Robinson E,Siparsky N, Successful non-operative management of intraabdominal hypertension and abdominal compartment syndrome after complex ventral hernia repair: a case series. American journal of surgery. 2018 Oct [PubMed PMID: 30243791]|
|||Vatankhah S,Sheikhi RA,Heidari M,Moradimajd P, The relationship between fluid resuscitation and intra-abdominal hypertension in patients with blunt abdominal trauma. International journal of critical illness and injury science. 2018 Jul-Sep [PubMed PMID: 30181972]|
|||Gray S,Christensen M,Craft J, The gastro-renal effects of intra-abdominal hypertension: Implications for critical care nurses. Intensive [PubMed PMID: 29937073]|
|||Miranda E,Manzur M,Han S,Ham SW,Weaver FA,Rowe VL, Postoperative Development of Abdominal Compartment Syndrome among Patients Undergoing Endovascular Aortic Repair for Ruptured Abdominal Aortic Aneurysms. Annals of vascular surgery. 2018 May [PubMed PMID: 29477687]|
|||Kılıç E,Uğur M,Yetim İ,Temiz M, Effects of temporary abdominal closure methods on mortality and morbidity in patients with open abdomen. Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma [PubMed PMID: 30028489]|
|||Sheldon R,Eckert M, Surgical Critical Care: Gastrointestinal Complications. The Surgical clinics of North America. 2017 Dec [PubMed PMID: 29132517]|
|||Izmaylov SG,Ryabkov MG,Baleyev MS,Mokeyev OA, [Comparative diagnostic value of various methods of intracavitary pressure measurement in abdominal compartment syndrome]. Khirurgiia. 2018 [PubMed PMID: 30113590]|
|||Leclerc B,Salomon Du Mont L,Parmentier AL,Besch G,Rinckenbach S, Abdominal compartment syndrome and ruptured aortic aneurysm: Validation of a predictive test (SCA-AAR). Medicine. 2018 Jun [PubMed PMID: 29923999]|
|||Solórzano Rodríguez E,López Almaraz R,Mendiola Arza J,Astigarraga Aguirre I,Bilbao Salcines N,Álvarez Martínez L, [Paracentesis as abdominal decompression therapy in neuroblastoma MS with massive hepatomegaly]. Cirugia pediatrica : organo oficial de la Sociedad Espanola de Cirugia Pediatrica. 2018 Oct 17 [PubMed PMID: 30371033]|
|||Chabot E,Nirula R, Open abdomen critical care management principles: resuscitation, fluid balance, nutrition, and ventilator management. Trauma surgery [PubMed PMID: 29766080]|
|||Coccolini F,Roberts D,Ansaloni L,Ivatury R,Gamberini E,Kluger Y,Moore EE,Coimbra R,Kirkpatrick AW,Pereira BM,Montori G,Ceresoli M,Abu-Zidan FM,Sartelli M,Velmahos G,Fraga GP,Leppaniemi A,Tolonen M,Galante J,Razek T,Maier R,Bala M,Sakakushev B,Khokha V,Malbrain M,Agnoletti V,Peitzman A,Demetrashvili Z,Sugrue M,Di Saverio S,Martzi I,Soreide K,Biffl W,Ferrada P,Parry N,Montravers P,Melotti RM,Salvetti F,Valetti TM,Scalea T,Chiara O,Cimbanassi S,Kashuk JL,Larrea M,Hernandez JAM,Lin HF,Chirica M,Arvieux C,Bing C,Horer T,De Simone B,Masiakos P,Reva V,DeAngelis N,Kike K,Balogh ZJ,Fugazzola P,Tomasoni M,Latifi R,Naidoo N,Weber D,Handolin L,Inaba K,Hecker A,Kuo-Ching Y,Ordoñez CA,Rizoli S,Gomes CA,De Moya M,Wani I,Mefire AC,Boffard K,Napolitano L,Catena F, The open abdomen in trauma and non-trauma patients: WSES guidelines. World journal of emergency surgery : WJES. 2018 [PubMed PMID: 29434652]|
|||Sakka SG, [The patient with intra-abdominal hypertension]. Anasthesiologie, Intensivmedizin, Notfallmedizin, Schmerztherapie : AINS. 2016 Jan [PubMed PMID: 26863642]|
|||Muresan M,Muresan S,Brinzaniuc K,Voidazan S,Sala D,Jimborean O,Hussam AH,Bara T Jr,Popescu G,Borz C,Neagoe R, How much does decompressive laparotomy reduce the mortality rate in primary abdominal compartment syndrome?: A single-center prospective study on 66 patients. Medicine. 2017 Feb [PubMed PMID: 28151898]|
|||Gupta HP,Khichar PR,Porwal R,Singh A,Sharma AK,Beniwal M,Singh S, The Duration of Intra-abdominal Hypertension and Increased Serum Lactate Level are Important Prognostic Markers in Critically Ill Surgical Patient's Outcome: A Prospective, Observational Study. Nigerian journal of surgery : official publication of the Nigerian Surgical Research Society. 2019 Jan-Jun; [PubMed PMID: 31007504]|