Abdominal compartment syndrome: what is it, symptoms, treatment, prognosis

What is Abdominal Compartment Syndrome?

Abdominal compartment syndrome (AKC) is a serious illness seen in critically ill patients. ACS occurs as a result of a sustained increase in pressure in the abdominal cavity above 20 mm Hg. Art. with concomitant organ dysfunction. Failure to recognize and immediately treat ACS can lead to a poor prognosis, as ACS is recognized as an independent predictor of mortality. Increased pressure reduces blood flow to the abdominal organs and impairs lung function. cardiovascular system, kidney and gastrointestinal tract, causing multiple organ syndrome failure and death.

The specific cause of abdominal compartment syndrome is unknown, although some causes may be sepsis and severe abdominal trauma.

Signs and symptoms

Abdominal compartment syndrome is usually seen only in critically ill patients and is more likely to be diagnosed in the ICU rather than in the emergency department. The clinical suspicion of the syndrome should be high in patients with penetrating abdominal trauma or surgical patients after major abdominal surgery. Patients may experience abdominal pain and bloating. However, this is not a delicate or specific indication. Patients in the intensive care unit can have a wide range of organ failure beyond the abdominal cavity, which can make diagnosis difficult.

Physical examination may reveal an increased girth of the abdomen, a tense abdomen, cyanosiswheezing and shortness of breath (dyspnea).

In abdominal compartment syndrome, the displacement of the diaphragm towards the head leads to compression of the chest, which causes increased respiratory work, ventilation / perfusion inequality and an increase in both peak and plateau pressure.

A tense abdomen also prevents venous return, which results in increased intracranial pressure and decreased cerebral perfusion pressure.

Causes and risk factors

Abdominal compartment syndrome can be divided into two groups: primary and secondary ACS. Primary causes of AKC include blunt or penetrating abdominal trauma, bleeding, rupture abdominal aortic aneurysm (ABA), intestinal obstruction and retroperitoneal hematoma. Secondary causes include pregnancy, abdominal ascites, intestinal obstruction, burns, intra-abdominal sepsis and replenishment of a large volume of fluid (> 3 liters).

Chronic causes of increased intra-abdominal pressure include pregnancy, cirrhosis of the liver, obesity, intra-abdominal malignant neoplasms and peritoneal dialysis. These are all causes of intra-abdominal hypertension, defined as pressure above 12 mm Hg. Art. in adults. Initially, this increase in pressure does not cause organ failure, but interferes with the normal functioning of the organs. ACS is determined by stable IAP (intra-abdominal pressure) above 20 mm Hg. Art. with new-onset or progressive organ failure.

Studies have shown that the mortality rate from AAA caused by ruptured AAA is approaching 47%. The disease can become devastating if other organ systems are involved due to compression and the primary ACS tends to have an increasingly poorer prognosis.

Epidemiology

ACS can develop in all patients in the intensive care unit (ICU). In the identified series of a mixed ICU population, 35% of patients on mechanical ventilation had intra-abdominal hypertension or abdominal compartment syndrome. Risk factors include many diseases, but they can be classified based on the mechanics of the abdominal wall. Risk factors include those that decrease abdominal compliance, increase intra-abdominal contents, increase the contents of the lumen or expansion of the third space and cause leakage capillaries.

Pathophysiology

With intraperitoneal bleeding, injury, or abdominal abscess the physiological response of inflammation and edema may be responsible for intra-abdominal hypertension. In the setting of intestinal obstruction, dilated bowel loops can cause symptoms of contraction in the abdomen. As abdominal pressure increases, the syndrome may begin to affect other organ systems due to further compression.

Intra-abdominal hypertension is classified from I to IV:

• I degree: IAP 12-15 mm Hg.
• II degree: IAP 16-20 mm Hg.
• III degree: IAP 21-25 mm Hg.
• IV degree: IAP> 25 mm Hg.

Any evidence of ongoing intra-abdominal hypertension with organ failure is defined as ACS. However, the frequency of organ failure is highest in patients with grade IV IBH. Organs such as the heart, lungs, and kidneys are usually affected.

Physiologic cardiac effects include decreased cardiac output and increased central venous pressure (CVP) due to compression of the inferior vena cava (IVC) and portal vein, an increase in systemic vascular resistance leads to hypotension. Pulmonary involvement can be manifested by a decrease in chest volumes and an increased peak pressure due to diaphragm compression, a decrease in the PaO2 / FiO2 ratio, and hypercarbia. Compression of the kidneys can lead to decreased GFR and low urine output. Visceral blood flow also decreases. Neurological symptoms may include increased intracranial pressure (ICP) due to increased CVP due to IVC compression, which contributes to a decrease in cerebral perfusion pressure (CPP).

Diagnostics

Although imaging techniques can help localize the cause of the increased abdominal pressure (bleeding, trauma, obstruction), they do not help to make a specific diagnosis of the syndrome. The most accurate way to confirm the diagnosis is to measure the pressure in the abdominal cavity. IAP should be measured in the presence of any known risk of intra-abdominal hypertension (IAP). This measurement can be achieved in a variety of ways, including both direct and indirect methods. Direct methods include measuring abdominal pressure using pressure transducers (for example, a Veress needle in time of laparoscopic surgery) or intraperitoneal catheters (for example, a catheter for peritoneal dialysis). These methods are very accurate; however, they are limited by their invasiveness. The most commonly used method is an indirect measurement such as intravesical pressure through a catheter (e.g. Foley catheter), which has become the gold standard due to its widespread availability and limited invasiveness.

Computed tomography can also reveal several things, such as collapse of the vena cava, round abdomen, thickening of the intestines, and / or bilateral inguinal hernia. The following scoring system is used to classify the abdominal compartment syndrome:

• 1st degree: 10-15 cm H2O. Art.
• 2nd degree: 15-25 cm of water. Art.
• Grade 3: 25-35 cm H2O. Art.
• 4 degree, more than 35 cm of water. Art.

Treatment

Non-surgical therapeutic options for the treatment of intra-abdominal hypertension include the overall goal of improving the following: abdominal wall compliance with reduced muscle contraction, evacuation lumen content by decompression (nasogastric tube), evacuation of abdominal fluid by drainage and correction of positive fluid balance due to targeted volumetric resuscitation.

The primary treatment for abdominal compartment syndrome is surgical decompression. However, early use of nonsurgical interventions can prevent the progression of intra-abdominal hypertension to ACS. Early recognition includes supportive care, including keeping patients comfortable with well-controlled pain. Decompression procedures such as nasogastric tube placement to decompress the stomach, rectal tube placement to decompress the colon, and percutaneous drainage abscesses, ascites, or abdominal fluid. It has been described that neuromuscular blockade was used as a short test in an attempt to relax abdominal muscles, which led to a significant decrease in pressure in the abdominal cavity in a patient Mechanical ventilation. If conservative and medical treatment does not correct the IHD and further damage is noted organ, the possibility of surgical decompression using emergent laparotomy.

After surgical laparotomy for compartment syndrome, the abdominal fascia can be closed with temporary closure devices. The fascia can be properly closed 5-7 days after the pressure and edema are relieved.

With surgical abdominal decompression, organ dysfunction can also improve rapidly, as most organ dysfunctions are seen as a consequence of compression. Lower abdominal stress may increase the excursion of the diaphragm, resulting in improved ventilation and a decrease in peak airway pressure. Compression of the inferior vena cava and the circulatory system is relieved, resulting in improved cardiac output and the ability to wean patients from vasopressor support. Acute kidney injury is repaired by less compression of the renal arteries and ureters.

Forecast

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 large quantities of blood products. Many studies report that even with treatment, multiple organ failure can delay recovery by weeks or months. Patients often have a prolonged need for mechanical ventilation, dialysis, and longer hospital stays.

Complications

Complications include:

• renal failure;
• intestinal ischemia;
• respiratory distress syndrome;
• increased cranial pressure;
• low cardiac output and shock.