Abdominal compartment syndrome (ACS) occurs when the abdomen becomes subject to increased pressure reaching past the purpose of intra-abdominal hypertension (IAH). ACS is present when intra-abdominal pressure rises and is sustained at 20 mmHg and there's new organ dysfunction or failure. ACS is assessed into three groups: Primary, secondary and recurrent ACS. it's not a disease and intrinsically it occurs in conjunction with many disease processes, either thanks to the first illness or in association with treatment interventions. Specific explanation for abdominal compartment syndrome isn't known, although some causes are often sepsis and severe abdominal trauma. Increasing pressure reduces blood flow to abdominal organs and impairs pulmonary, cardiovascular, renal, and gastro-intestinal (GI) function, causing multiple organ dysfunction syndrome and death.
Abdominal compartment syndrome occurs when tissue fluid within the peritoneal and retroperitoneal space (either edema, retroperitoneal blood or free fluid within the abdomen) accumulates in such large volumes that the wall compliance threshold is crossed and therefore the abdomen can not stretch.
Once the wall can not expand, any longer fluid leaking into the tissue leads to fairly rapid rises within the pressure within the closed space. Initially this increase in pressure doesn't cause organ failure but does prevent organs from working properly – this is often called intra-abdominal hypertension and is defined as a pressure over 12 torr in adults. ACS is defined by a sustained IAP(intra-abdominal pressure) above 20 torr with new-onset or progressive organ failure. Severe organ dysfunctionent syndrome. These pressure measurements are relative. young children get into trouble and develop compartment syndromes at much lower pressures while young previously healthy athletic individuals may tolerate an abdominal pressure of 20 torr alright . The underlying explanation for the disease process is capillary permeability caused by the systemic inflammatory response syndrome (SIRS) that happens in every critically ill patient. SIRS results in leakage of fluid out of the capillary beds into the interstitial space within the entire body with a profound amount of this fluid leaking into the gut wall, mesentery and retroperitoneal tissue.
· Peritoneal tissue edema secondary to diffuse peritonitis, abdominal trauma
· Fluid therapy thanks to massive volume resuscitation
· Retroperitoneal hematoma secondary to trauma and aortic rupture
· Peritoneal trauma secondary to emergency abdominal operations
· Reperfusion injury following bowel ischemia thanks to any cause
· Retroperitoneal and mesenteric inflammatory edema secondary to acute pancreatitis
· Ileus and bowel obstruction
· Intra-abdominal masses of any cause
· Abdominal packing for control of bleeding
· Closure of the abdomen under undue tension
· Ascites (intra-abdominal fluid accumulation)
· Acute pancreatitis with abscesses formation
Abdominal compartment syndrome is de?ned as an intra-abdominal pressure above 20 mmHg with evidence of organ failure. Abdominal compartment syndrome develops when the intra-abdominal pressure rapidly reaches certain pathological values, within several hours (intra-abdominal hypertension is observed), and lasts for six or more hours. The key to recognizing abdominal compartment syndrome is that the demonstration of elevated intra-abdominal pressure which is performed most frequently via the bladder , and it's considered to be the "gold standard". Multiorgan failure includes damage to the cardiac, pulmonary, renal, neurological, gastrointestinal, wall , and ophthalmic systems. The gut is that the most sensitive to intra-abdominal hypertension, and it develops evidence of end-organ damage before alterations are observed in other systems. during a recent systematic review, Holodinsky et al. described 25 risk factors related to IAH (intra-abdominal hypertension) and 16 with ACS (abdominal compartment syndrome). These are often roughly categorized in three categories, which can be more helpful at the bedside to spot patients in danger. Especially noteworthy is that the potential role of fluid resuscitation within the development of IAH and ACS. Recognizing the pivotal role of fluid resuscitation within the pathogenesis of IAH and ACS supplies the clinician with a target for preventive measures. Large volume resuscitation with crystalloids should be avoided in patients with or in danger of ACS.
The deathrate related to abdominal compartment syndrome is critical, ranging between 60% and 70%. The poor outcome relates not only to abdominal compartment syndrome itself but also to concomitant injury and hemorrhagic shock. The surgical decompression of the abdomen remains the treatment of choice of abdominal compartment syndrome; this usually improves the organ changes and is followed by one among the temporary abdominal closure techniques so as to stop secondary intra-abdominal hypertension. Surgical decompression is often achieved by opening the wall and abdominal fascia anterior so as to physically create more room for the abdominal viscera. Once opened, the fascia is often bridged for support and to stop loss of domain by a spread of medical devices (Bogota bag, artificial bur, and vacuum devices using negative pressure wound therapy.
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