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Abdominal compartment syndrome Marilyn J. Borst, M.D.*, Andrew B. Peitzman, M.D.* * The Department of Surgery, University of Pittsburgh School of Medicine.

Address correspondence to: Andrew B. Peitzman, M.D. Room A1010, Presbyterian University Hospital, Pittsburgh, PA 15213.

SUMMARY An IAP greater than 25 mmHg in a patient with adequate blood volume and oliguria is an indication for decompressive laparotomy. Renal and splanchnic dysfunction occur with IAP of 10-15 mmHg. Forced fascial or skin closure over swollen bowel or intra-abdominal packs must be avoided. This will often prevent the development of ACS in the patient at high risk after laparotomy. Surgeons caring for patients at risk for development of ACS must be cognizant of the multiple organ systems affected by an increasing IAP. Surgeons caring for multiply injured trauma patients, especially those with combined abdominal and head trauma, must be particularly aware of the effects of increased IAP upon the CNS. Key word: Abdominal compartment syndrome. Abdominal hypertension. The abdominal compartment syndrome (ACS), also known as intra-abdominal hypertension, is the development of physiologic dysfunction in intra-abdominal and extra-abdominal organs as 1-5 the result of increased intra-abdominal pressure (IAP) . The elevated IAP is a function of the rate of fluid accumulation within the abdominal cavity and the compliance of the abdomen. The 6 pressure-volume curve for the abdominal cavity is nonlinear . Due to the decreasing compliance of the abdomen, as fluid within the peritoneal cavity progressively accumulates, a greater increase in IAP results. The ACS may occur in patients with a variety of conditions in which increased IAP occurs. Clinical settings which have been associated with the syndrome include ruptured abdominal aortic aneurysm, ascites, intraperitoneal hemorrhage, abdominal trauma, 1,4,5,7-14 ovarian tumors, liver transplantation, and hemorrhagic pancreatitis . Trauma patients with hepatic or intra-abdominal vascular injuries are particularly susceptible to

the impact of intravascular volume status on depression of CO in ACS was assessed. The use of increasing PEEP can exacerbate cardiovascular and hemodynamic abnormalities in the patient with elevated IAP. central venous pressure (CVP). In 15 . Cardiovascular system.The measured PAWP and CVP are each the sum of pleural pressure and the intravascular filling pressures and 17 thus spuriously elevated . Continued impairments in 15 ventilation and oxygenation result in hypercarbia. The magnitude of the depression of CO is dependent on the intravascular volume status. ongoing surgical bleeding (missed injuries). Increasing positive end-expiratory pressure (PEEP) is required to oxygenate the patient. As the IAP increases. abdominal closure under excessive tension. acidosis. abdominal compartment syndrome may occur in the patient who has been massively fluid resuscitated without an associated intra-abdominal injury. The CVP and PAWP are elevated due to an increased pleural pressure secondary to the increased IAP. The hemidiaphragms are elevated due to the increased IAP. or bleeding controlled with intraabdominal packs (damage control laparotomy).the development of ACS. Cardiac output (CO) decreases progressively as the IAP increases . A decrease in thoracic volume and compliance results. and progressive hypoxemia . On rare occasion. pulmonary artery 15 wedge pressure (PAWP). Other factors which may contribute to the development of increased IAP in the trauma patient include retroperitoneal bleeding. cardiovascular. Elevation in intracranial pressure (ICP) and depression of cerebral perfusion pressure (CPP) may also result from increased IAP. Ventilationperfusion abnormalities occur. Increasing bowel wall edema and third-space fluid losses due to large volumes of blood products and nonsanguinous solutions used in resuscitation also contribute to the increased IAP. and systemic vascular resistance increase . pneumatic antishock garments. In an interesting laboratory study. The increased IAP in these patients develops from increasing hemoperitoneum compounded by hypothermia and coagulopathy. Peak inspiratory pressure and pulmonary vascular resistance increase. Higher pressures are required to deliver a set tidal volume. Respiratory system. and renal systems. SYSTEMIC MANIFESTATIONS OF INCREASED INTRA-ABDOMINAL PRESSURE Increased IAP results in dysfunction of the respiratory.

In addition. Intravenous volume expansion will increase the cardiac output and central filling pressures in ACS. Using a dog model. decreased hepatic blood flow resulting from increased IAP was found to impair hepatic energy production and 23 reduce the hepatic energy level . are exacerbated by hypovolemia. renal vascular resistance increases several-fold in ACS. but will not correct the other manifestations of ACS. including depressed renal function and splanchnic bloodflow. Caldwell and Ricotta demonstrated a decreased organ blood flow index (organ blood flow/cardiac output) with increased IAP in all major abdominal organs. In a swine model. including depression of cardiac output. The renal vein and inferior vena cava are compressed. Ileal and gastric mucosal blood flow are decreased with increased IAP 24-26 21 . and hepatic microcirculatory 22 blood flow decreased significantly with increasing IAP . renal bloodflow and glomerular filtration rate were 25% of normal at an IAP of 20 mmHg and only 7% of normal at 19 an IAP of 40 mmHg . Renal system. and in 18 hypervolemic animals. hepatic arterial. In a pig model. as well 18 as impairment of venous return . Clinically. Oliguria is often the earliest sign of ACS and anuria 15 follows if the IAP is not reduced .hypovolemic animals. An actual depression of myocardial function occurs with ACS due to marked increase in afterload. except the adrenal glands. Abdominal decompression in combination with intravascular volume expansion reversed the effects upon renal function and the renin20 angiotensin-aldosterone system . CO increased 50% in the setting of ACS . Small bowel tissue . Oliguria occurs with IAP >15 mmHg. All effects of ACS. in euvolemic animals. Oliguria develops despite measured normal or mildly elevated CVP and PAWP. elevated IAP was found to decrease urine output and up-regulate the hormonal output of the renin-angiotensin-aldosterone system. the abdominal girth increases and the abdomen becomes more tense as the IAP increases. Direct compression of the renal parenchyma also contributes to the renal dysfunction. Blood flow and glomerular filtration in the kidney are diminished. portal venous. In a rabbit model. CO declined 53%. In an animal study. and anuria results with IAP >30 mmHg. CO declined 17%. Splanchnic blood flow decreases as ACS develops. Abdominal and visceral effects.

28 models . Clinically. The proposed mechanism is functional obstruction of jugular venous drainage due to the elevated pleural pressures and CVP. Increased IAP has been associated with the rupture of retinal capillaries. Due to the Monroe-Kellie doctrine. In a porcine model. If a patient with ACS develops visual changes. this increase in intracranial blood volume results in elevation of the ICP. Bloomfield et al have demonstrated significant effects of elevated IAP upon the central nervous system (CNS). this observation (confimed clinically) is important. and hypercarbia . These studies have identified physiologic derangements that occur with increased IAP which may play a role in the development of sepsis and systemic inflammatory response syndrome (SIRS) in patients with ACS. a diagnosis of ACS should be made on the basis of clinical suspicion and decompressive 35 laparotomy performed without attempts at measuring IAP . Abdominal decompression resulted in a return toward 30 baseline for ICP and an improvement in the CPP . measurement of the gastric pressure. Methods of measuring IAP include measurement of bladder pressure.35 euvolemic). measurement of IAP is useful. Often. Decompressive 32 laparotomy in this patient resulted in a dramatic reduction in ICP . valsalva retinopathy should be considered and an appropriate ophthalmic examination performed. Eyes. when oliguria may be the only sign. or measurement of the 27 . the syndrome consists of the association of abdominal distention with increasing peak inspiratory pressures. increased central venous pressure (if the patient is 15. Central nervous system.oxygenation is decreased in ACS . Bacterial translocation has been demonstrated in rat 24. With the common association of abdominal injury and closed head injury. oliguria. In the early phases of ACS. a high index of suspicion must be 34 maintained . elevated IAP resulted in 29-31 increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP) . DIAGNOSIS To diagnose and intervene early in the course of ACS. It has been described in a number of settings in which a sudden increase in IAP or intra-thoracic pressure has occurred. resulting in the sudden onset of decreased central vision (valsalva retinopathy). The retinal hemorrhage usually resolves within days to months and no specific treatment is 33 necessary .

To measure the bladder pressure. connect the end of the drainage bag tubing to the indwelling Foley catheter. instead of a transducer . During decompression of the abdomen. TREATMENT If ACS is present based on the measured IAP or clinical suspicion. prompt diuresis occurs and polyuria often develops. Therefore. maximization of oxygen delivery.IAP using a long femoral venous catheter placed in the inferior vena cava36. an IAP greater than 25 mmHg in a post-operative patient with an 1 adequate blood volume and oliguria is an indication for decompressive laparotomy . via the culture aspiration port of the tubing. Measurement of IAP. determine the IAP from the transducer using the top of the symphysis pubis bone as the zero point with the patient supine. As mentioned earlier. the operating room must be prepared to accept the patient if surgically correctable bleeding is identified at the time of decompressive 35 laparotomy . Peak airway pressure . the following actions should be taken to prevent hemodynamic decompensation: restoration of the intravascular volume. A hand-held manometer connected to the Foley catheter via the column of fluid in the tubing may 1. After decompression. the operating room is preferable. a decompressive laparotomy should be performed. Y-connect a pressure transducer to the drainage bag. however. The bladder pressure is essentially equivalent to the IAP. The most accurate and simple way to determine the IAP is indirectly by measurement of the bladder pressure using a Foley catheter. using a 16-gauge needle. release the clamp just enough to allow the tubing proximal to the clamp to fill with fluid from the bladder then reapply the clamp.37 be used to determine the pressure. an IAP greater than 15-25 mmHg has been found to induce renal dysfunction. correction of hypothermia. inject 50-100 ml of sterile saline into the Foley catheter via the aspiration port. The abdomen may be opened in the surgical intensive care unit (SICU). If the abdomen is opened in the SICU. and correction of coagulation 15 defects .10. cross-clamp the sterile tubing of the urinary drainage bag just distal to the culture aspiration port.

a variety of materials (absorbable/nonabsorbable. the skin may be closed or left open.15 bloodpressure results . or polytetrafluoroethylene (PTFE) . sterile dressings and an adhesive drape (Vi-drape™ or Steri Drape™). Temporary abdominal closure. If the fascia is closed with synthetic material. An 15. The first decision to be made is whether to close the fascia with synthetic material or leave the fascia open. If closure of the skin alone causes an increase in the IAP.45% normal saline with 50 g of mannitol and 50 mEq of sodium bicarbonate . sterile x-ray cassette bags . A 2 l solution is prepared consisting 33 of 0. absorbable material is preferred. Closure with an artificial burr (Velcro-like) device 38. After decompressive laparotomy.43 44 may be closed using sutures. The skin 42. or mesh. dramatic decrease in systemic vascular resistance and increase in cardiac output. a temporary abdominal closure is performed.38 5. The bowel is covered with a nonadhesive.39 . necessitating simultaneous adjustments of the ventilator . it is covered with moist. If the fascia is left open and the abdomen packed. polypropylene (Marlex™) . including polyglycolic 35.decreases as the abdomen is opened. The second mechanism proposes a reperfusion syndrome from the 15. and Silastic sheets have been used. towel clips . The fascia should not be closed primarily. rather than to the fascia. If mesh is sutured to the skin. preserves the fascia for later definitive closure. Suturing the synthetic material to the skin. the skin is left open. 15 porous/nonporous) may be used . Two possible etiologies have been proposed for this phenomenon.35 release of acid and metabolites from reperfused tissues . This reperfusion syndrome may be ameliorated by using a solution containing mannitol and sodium bicarbonate for the initial volume resuscitation following decompressive laparotomy.38 38 acid (Vicryl™) . Esmarch latex bandage . nonporous material (such as a bowel bag or adhesive drape folded 35 . Decompression of the abdomen results in acute. an acute drop in 14. followed by permanent abdominal closure at a later date.40 38 41 intravenous fluid bag (“Bogotá bag”) . this is associated with a high reoccurrence of ACS. Immediate aystole may occur upon opening the abdomen. Several methods of temporary abdominal closure may be utilized. Various types of mesh may be used.

Next. a “separation of parts” technique may be required to reapproximate the 38. In an interesting animal model in which sternotomy and .46 fascia .48 nonabsorbable mesh . abdominal wall 15. If mesh was placed as the temporary abdominal closure (preferably an absorbable material). hypothermia. Permanent abdominal closure. Several methods of abdominal closure have been described.35 after abdominal decompression . However. sterile towels are placed. followed by an adhesive drape (Vidrape™ or Steri Drape™) which sticks to the abdominal wall and further prevents evisceration. coagulapathy.upon itself so that the adhesive side sticks to itself). Various methods of reconstruction have been described.45. The edges of the nonadhesive.38. it may be possible to close the fascia without significant tension. Direct application of the adhesive drape to the bowel increases the risk of enterocutaneous fistula and is not advised. PREVENTION Prevention of the ACS must be the goal of surgeons caring for patients at risk for the development of this syndrome.46 abdominus muscle and its fascia with or without skin-relaxation incisions . including bilateral medial advancement of the rectus 32. If the fascia was not closed and the patient is left with an abdominal wall defect. the mesh may be left in situ for two weeks then covered with partial thickness skin grafts to the underlying granulation tissue. which is usually three to four days 15. Permanent abdominal closure is performed after hypovolemia. Primary closure of the fascia may be performed or a skin graft may be placed followed by delayed abdominal wall reconstruction. Subcutaneous 47 tissue expanders followed by bilateral myocutaneous advancement flaps have also been used .45. The mesh will usually be incorporated into the granulation tissue at this point in time.36 reconstruction may be performed six to twelve months later . and acidosis have been corrected. Mid-line abdominal defects may require flap reconstruction or reconstruction with 38. After significant mobilization of fluids. and fluid losses from the open abdomen. desiccation of the bowel. nonporous material are tucked under the edges of the anterior abdominal wall in order to prevent evisceration of the bowel.

Blood warmers should be used for administration of blood products and intravenous fluids. Most patients suffer late deaths resulting from the underlying insult and multiple organ dysfunction syndrome.5% of patients with ACS 15. A forced fascial closure of the abdomen should be avoided. such as in patients with massive retroperitoneal hematoma. as previously discussed. 40 to 62. Ongoing nonsurgical bleeding can lead to an increased IAP even in patients in whom the fascia was left open but the skin closed. visceral edema. Thus. High mortality rates are found in patients who develop ACS.35 will die . Coagulopathy should be corrected by restoration of normal temperature and replacement of 36 coagulation factors . 31 Only depression of the cardiac output persisted . Loose closure of the abdomen is the most direct means to accomplish this. The skin should usually be left open as well. MORBIDITY AND MORTALITY Morbidity in patients with ACS is often due to sepsis and multiple organ failure. RESUMEN Una presión intrabdominal mayor de 25 mmHg en un paciente con oliguria y volumen saguíneo adecuado es una indicación para una laparotomía decompresiva. Se debe evitar el cierre forzado de fascia . La disfunción renal y esplénica ocurre con una presión intrabdominal de 10-15 mmHg. The abdominal fascia should not be closed in patients who are hypothermic. the majority of the systemic effects of abdominal compartment syndrome were preventable in the setting of increased intra-abdominal pressure . a means for decompression of the abdominal compartment in our patients can prevent the systemic consequences in our patients. Hypothermia should be prevented. Patients should be externally warmed using warming lights and special warming blankets. or intra-abdominal packs.The following actions should be taken to prevent the development of increased IAP and ACS. coagulopathic. The resuscitation area and operating room should be warm.pleuropericardiotomy were performed . or on whom a damage control laparotomy was required. The development of these clinical conditions may be associated with the splanchnic hypoperfusion resulting from increased IAP.

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