Abdominal Compartment Syndrome

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365b Wittrnann, DH Abdominal Compartment Syndrome, In JP Kirn, RE Condon: Proceedings of the 15th World Congress of the Collegium Internationale Chirurgiae Digestivae Seoul, Korea, September 11-14, 1996. Monduzzi Editore S.p.A., Bologna, Italy, 1996. pp 161-176 Collegium Internationale Chlrurglae Digestivae

Abdominal Compartment Syndrome: what the hell is that? How do you treat it?

XV World Congress Seoul, Korea 11-14 September 1996

D.H. WITTMANN Professor ofSurgery

Medical College ofWisconsin. Milwaukee. Wisconsin (USA)

ABSTRACT Increased intra-abdominal pressure and ils delelerious effects on many organ functions has been weil sludied bolh eHnically and experimentally and is refer enced in literature sinee 1876 (Wendt)! All adverse effects from increased ab· dominal pressure have found a common denominator in lhe Abdominal Com· partment Syndrome (ACS). The ACS. however, has only recently gained eHni· ca! recognilion and is best treated with abdominal decompression utilizing lhe "artificial burr device" (ABO). Intra-abdominal pressure can easily be assessed by indirect measurement of bladder pressure via transurelhral catheter. An intra abdominal pressure of 10 mm HG may impair renal function. Fluid trapped in lhe •••

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Abdominal Compartment

Syndronle:

what the hell is that?

How do you treat it?

Collegium Internationale Chirurglae

Digestivae XV World Congress Seoul, Korea 11-14 September 1996

D.H.WITTMANN Professor ofSurgery

Medical College ofWisconsin, Milwaukee, Wisconsin (USA)

ABSTRACT Increased intra-abdominal pressure and its deleterious effects on many organ funetions has been weil studied both clinically and experimentally and is refer enced in literature since 1876 (Wendt)! All adverse effects from increased ab dominal pressure have found a common denominator in the Abdominal Com partment Syndrome (ACS). The ACS, however, has only recently gained clini cal recognition and is best treated with abdominal decompression utilizing the "artificial burr device" (ABD). Intra-abdominal pressure can easily be assessed by indirect measurement of bladder pressure via transurethral catheter. An intra abdominal pressure of 10 mm HG may impair renal function. Fluid trapped in the peritoneum and peritoneal cavity as weil as in the bowel lumen considerably in creases intra-abdominal pressure. Increased intra-abdominal pressure may cause and exacerbate cardiovascular, respiratory, and renal dysfunction. Addi tionally, its deleterious effects impair hepatic and intestinal or splanchnic perfu sion. The secondary system impairments of ACS in a septic or severely trauma tized patient potentate the development of sequential multiple organ failure in c1uding acute respiratory distress syndrome. Abdominal decompression helps to reverse these effects. Increased intra-abdominal pressure may go along with in creased intra-thoracic pressure produced by respiratory therapy or inhalation anesthesia. In combination with positive end-expiratory pressure (PEEP), it re sults in markedly increased central venous pressure, pulmonary capillary wedge pressure, mean pulmonary artery pressure, and pulmonary vascular resistance. It will decrease venous return to the heart with changes in ventricular compli ance and depression of cardiac funetion. An increase of intra-abdominal pres sure of more than 20 millimeters secondarily increases mean arterial pressure (MAP) and systemic vascular resistance (SVR), and decreases inferior vena

Copyright 1996 by Monduzzi Editore S.p.A.• Bologna (l1aly)

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Collegium Internationale Chirurgiae Digestivae XV World Congress Seoul, Korea 11-14 September 1996

cava flow and cardiac output. The detrimental effects on cardiac, pulmonary, renal, and hepatic function and impairment of intestinal perfusion interferes with post-operative abdominal oxygen supply and energy generation and, in particu lar. impairs anastomotic healing. All these factors adversely affect outcome of both patients with operative and non-operative abdominal trauma, as weil as pa tients with intra"abdominal infections. Effects of increased intra-abdominal pres sure add to the organ injuries from shock-induced oxygen lack. Therapeutically, the abdominal compartment syndrome has been addressed by the method of leaving the abdomen open: The first advocate of the various open abdomen methods, however, did not appreciate pathophysiological consequences of in creased intra-abdominal pressure and the open abdomen methods were dis credited because of serious side effects such as fistula formation and huge inci sional hemias. The operative method of staged abdominal repair (STAR) ad dresses increased abdominal pressure and at the same time, allows for final fascial closure of the abdominal cavity when the artificial burr device (ABO) is used. ABO allows for temporary abdominal closure with the fasciae separated as much as up to 40 cm and permits reapproximation of the fascia as the edema decreases. Fistula and hernia formation are rare. The abdominal compartment syndrome is areal entity. Patients with increased intra-abdominal pressure as a consequence of injury and intra-abdominal infection have a grave prognosis when pressure remains without decompression. The experience of the literature documents a mortality rate of 44%.

INTRODUCTION The abdominal cavity may behave Iike a compartment. Any pressure increase within that compartment then impairs function of organs it contains. Such func tion impairment may negatively influence system function outside of the com partment with a negative feed back to organ function within the compartment. Total 1055 of function may result. These facts are not new. Already in 1876 Wendt reported about renal function ("reduced urine flow") impairment with ris ing intra-abdominal pressure (103) In subsequent years the topic became sub ject of various publications (7,33,64,79,86,100,102), and since 1959 numerous publications deal with increased pressure in the inferior vena cava as weil as about various organ system dysfunction that is aS$ociated with increased intra abdominal pressure. (13.27,32,59,73,84). It became clear, that not only impair ment of renal functions, but also that of liver function, cardiovascular and pul monary function resulted from pressure increase within the abdominal cavity. (24.32,40,50,51,55,72,83,93). Therapeutically the issue was addressed with the introduction of the various open abdomen methods that alleviate intra-abdominal pressure The initially good results with these methods, however. were later offset by too many compi tations such as fistula formation and huge incisional hernias. In spite of the fact, that the open abdomen methods relieves increased abdominal pressure totally, the propagandists of the open abdomen method did not recognize the pitfalls of increased intra-abdominal pressure and never mentioned that increased intra abdominal pressure nor the abdominal compartment syndrome was a reason to leave the abdomen open. (16,17,28,29,35,47,67,74,82) Authors, that favored planned relaparotomy, toD, did not consider danger asso ciated with increased intra-abdominal pressure at all, and c10sed the abdominal cavity under pressure utilizing retention sutures (56,57,98) or a zipper. (65, 88, 95,96,99) Meanwhile the abdominal compartment syndrome became a independent clinical syndrome, that has many causes and that can lead to severe impairment of all organ system necessary for life, and that by itself can result in death. (10,30,89,97,107)

162

In the paper we will present the current knowledge about the physiology and

pathophysiologiy as weil as treatment methods of increased intra-abdominal pressure.

INCREASED INTRA-ABDOMINAL PRESSURE (IAP)

Collegium Internationale Chirurgiae Digestivae XV World Congress

ANATOMICAL & PATHOPHYSIOLOGICAL BASIS

The special anatomy of the peritoneum explains some of the early pathophysi ologicaJ changes seen in intra-abdominal infections. Upon perforation irritaling fluids and bacteria dislocate into the peritoneal cavity, and the host res ponds with inflammation. The inflammatory response evokes a plethora of biochemical inflammatory reaelions resulling, among other things, in peritoneal vasodilatation and shifting of fluid into the peritoneum, peritoneal cavity and intestines. Up to 10 liters of fluid may aceumulate within the peritoneum and its loose subendo thelial conneelive lissue. This massive peritoneal edema raises intra-abdominal pressure, and fluid is removed from central circulation initialing hypovolemic shock. Additionally, ileus develops, and the atonie, dilated bowel, in its lumen, also caplivates intravaseuJar and interstitial f1uid,}urther depleling the macro organism and increasing intra-abdominal pressure. Depending on the magni tude of the insult, inflammatory peritoneal edema may form so quickly as to be manifest c1inically as hypovolemic shock with dehydration, hemoconcentration low blood pressures, poor urinary output, and subtle mental impairment.

Seoul. Korea 11-14 September 1996

Usually, high baeterial numbers or very intense inflammatory challenges are re quired to induce massive peritoneal edema. The peritoneum itself is equipped with effective loeal antibaeterial defenses fostered by its anatomical structure ineluding the omentum, formation of fibrin, and the ubiquitous presence of macrophages and other phagoeytes. Bacteria are quickly c1eared by Iymphatics into the systemie cireulation, endotoxic shock results (44) which in turn may ag gravate function impairment form inereased intra-abdominal pressure. Fluid trapped in the peritoneum and peritoneal cavity as weil as in the bowel lu men considerably inereases intra-abdominal pressure. Inereased intra abdominal pressure not only exaeerbates cardiovascular, respiratory, and renal dysfunction, but also has deleterious effects on hepatic and intestinal or splanchnic perfusion. (4,9,15,21,23,25,40,42,59,83,87,89,91,93,103) All adverse effects from increased abdominal pressure have found a common denominator in the Abdominal Compartment Syndrome: (18,97), These secondary system impairments, in a septie patient, potentiate the development of sequential multi ple organ failure, and death (5,14,19,31,32,37-39,58,60,61,68,70,75,81,101). Abdominal deeompression helps to reverse these effects. Increased intra abdominal pressure may be aeeompanied by increased intra-thoracic pressure produced by respiratory therapy or inhalation anesthesia (9,21,83). In combina tion with positive end-expiratory pressure (PEEP), it results in markedly in creased central venous pressure, pulmonary capillary wedge pressure, mean pulmonary artery pressure, and pulmonary vascular resistance. It will decrease venous return to the heart with changes in ventricular compliance and hormonal depression of cardiae funelion (4,9,42,91). An increase of intra-abdominal pressure of more than 20 millimeters secondarily increases mean arterial pressure (MAP) and systemic vascular resistance (SVR), and deereases inferior vena cava fIow and cardiac output. The in creased pressure also causes renal dysfunction. An abdominal pressure in crease of 51 cm H20 results in a urinary output of less than 10 milliliters per hour.

MEASUREMENT OF INTRA-ABDOMINAL PRESSURE Pressure can be measured by direet and indirect methods Historically, it was measured direetly through a metal cannula or a wide bore needle, inserted into the peritoneal cavity and allaehed to a saline manometer (33,64,79,86,102).

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DIAECT METHODS

Direct measurement using an intraperitoneal catheter connected to apressure transducer has been the preferred method in numerous experimental studies (24,25,48,54,83,84). Occasionally, an inflatable bag was placed into the ab dominal cavity to produce and measure elevated pressure(12) method is famil iar to surgeons who practice laparoscopic procedures during which automatie electronic insufflator provides continuous monitoring of pressure (22,85). INDIAECT METHODS

Inferior vena cava pressure. It has been shown in animal studies that cavaI pressure measured transfemor ally always correlates directly with intra-abdominal pressure in all ranges stud ied (41,84). Although it has been suggested that inferior vena cava pressure measurement could be utilized to determine intra-abdominal pressure in c1inical practice [8], human data are not available.

Intra-gastral Pressure. Intra-abdominal pressure can be measured by water manometry via a nasogas tric or gastrostomy tube (21,36). Gastric pressure is determined by infusing 50 100 ml water through a nasogastric tube into the lumen of the stomach. The proximal end of the open tube is held perpendicular to the floor. The distance fram the water level to the mid-axillary line is taken as the intra-abdominal pres sure in centimeters of water. Pressure thus measured approximately correlates with pressure measured by a Foley catheter in the urinary bladder.

Urinary Bladder Pressure: Method of Choice The bladder behaves as a passive diaphragm when its volume is between 50 and 100 ml. Pressure measurements in animals recorded simultaneously through a urinary bladder catheter and directly via peritoneal catheters were equal for pressures ranging from 5 to 70 mm Hg (48,62). This simple, minimally invasive method can be easily performed at the bedside and appears to be the method of choice(62). Sterile saline is injected into the empty bladder through a Foley catheter, the tubing of the drainage bag is cross-clamped just distal to the culture aspiration port and connected to the catheter; the clamp is released to allow the proximal drainage tubing to fill with saline from the bladder, then reapplied; a 16-gauge needle is inserted through the aspiration port and is connected to a water ma nometer or pressure transducer. Altematively. aT-piece connector or a three way stopcock is added between the catheter and the drainage bag in the patient in the supine position, the zero reference point is the symphysis pubis and the height of the water column above this point represents intra-abdominal pressure in centimeters of water. A neurogenie or small contracted bladder may render the measurements invalid_(52).

THE ABDOMINAL COMPARTMENT SYNDROME ACS Mechanism leading to ACS

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The mechanisms culminating in an ACS are usually multiple. A typical scenario occurs in a patients with diffuse peritonitis or a multiple trauma patient who re ceive a large volume of fluid for resuscitation causing an increase in interstitial fluid volume. The ensuing viscera I and retroperitoneal edema is aggravated by shock-induced visceral ischemia and reperfusion edema, as weil as by tempo rary mesenteric venous obstruction caused by surgical manipulation or the em ployment of packs (3,92). The edematous abdominal wall is c10sed over the bulging abdominal contents under extreme tension (8,77). Following the opera

tion, positive pressure ventilation is often necessary to maintain satisfactory oxygenation, but it further inereases intra-abdominal pressure (9). The potential pressure additive effects of abdominal trauma and its laparoscopic diagnosis (34Lor of abdominal trauma during pregnancy (90) are of concem but as yet un documented.


Normal and Increased Intra-abdominal Pressure Normal mean intra-abdominal pressure is 0 (equals atrnospheric pressure) or less (33,64,79,86,102). Operative laparoscopy is performed with a constant pneumoperitoneum at 10-15 mm Hg pressure (22,85). Elevation of intra abdominal pressure leads to gradual dysfunction of various systems (4,25,26,41,45,46,48,72,83). The magnitude of organs system dysfunction de pends on premorbid physiological reserves and various compounding factors. Conditions associated with elevation of intra-abdominal pressure are listed in Table 1

Seoul. Korea 11-14 September 1996

Elevation of Intra-abdominal Pressure Intra-abdominal pressure may be c1assified as following: 1)

Mild « 20 mm Hg).

2)

Moderate (20-40 mm Hg).

3)

Severe (>40 mm Hg). Mild Eleyation (Mild «20 mm Hgl

Random intra-abdominal pressures measured transvescically during the first 24 hours following elective surgical procedures averaged 3-15 mm Hg (62). At pressures less than 10 mm Hg cardiac output and blood pressure are normal but hepatic arterial blood flow falls significantly (25,26). Intra-abdominal pressure of 15 mm Hg during laparoscopic cholecystectomy produces adverse cardiovascu lar changes (46). Physiological effects are generally weil compensated and thus usually c1inically non-significant. Closure ot"the abdominal wall, however, may become eritical above pressures of 15 mm Hg particularly in the presence of compounding conditions such as sepsis, heart failure, and impairment renal and hepatic function. Perfusion to critical anastomoses may suffer and result in ne eroses to anastomotic tissue with subsequent leak... Moderate Elevation (20-40 mm HG) With sudden moderate elevation of intra-abdominal pressure, a transient in crease in cardiac output is observed as blood is 'squeezed' from the vast splanchnic pool, suddenly increasing the venous retum to the right heart. Sub sequently, cardiac output falls as the abdominal vessels are emptied. This initial momentary 'autotransfusion' effect of inereased intra-abdominal pressure is classically observed during the application of the pneumatic anti-shock garment (69). Intra-abdominal pressure of 20 mm Hg may cause oliguria (41). and re duces hepatic function and splanchnic perfusion significantly, (25,26) which may jeopardize operative results. The abdomen cannot be c10sed with undue tension. Fascial sutures are likely to cause fascial neeroses and neerotizing fas ceitis may result in the presence of intestinal bacteria. Severe Elevation « 40 mm HG) Deleterious consequences appear gradually (4,26,41,45,46,48,83,85). An in erease of Intra-abdominal pressure to 40 mm Hg induces anuria (41), liver and bowel wall neeroses, reduces significanlly cardiac and hepatic dysfunction, in duces pneumonia and healing of intra-abdominal operative and non-{)perative injury is not possible. Patients die from:: LIST see blow

PATHOPHYSIOLOGY OF ACS The main physiological consequences of inereased intra-abdominal pressure are summarized in Tabfe 2.

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Table 1: Conditions associated with elevation of intra-abdominal pressure

ACUTE CONDITIONS I. Spontaneous

Peritonitis, Intra-abdominal infection

Ileus, Intestinal obstruction

Ruptured abdominal aortic aneurysm

Acute pancreatitis

Mesenteric venous thrombosis

Tension pneumoperitoneum

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11. Postoperative Massive operative trauma and fluid overload Ileus, Acute qastric dilatation Intra-peritoneal hemorrhaqe Postoperative peritonitis Intra-abdominal abscess 111. Posttraumatic

Intra/retro-peritoneal bleedinq

Post-resuscitation peritoneal edema

IV. latroqenic

Laparoseopie procedures

Pneumatic anti-shock qarment

Abdominal packing

Reduction of a massive parietal or dia phraqmatic hernia

Abdominal c10sure under excessive tension

CHRONIC CONDITIONS Ascites Large abdominal tumor Chronic amt:lulatory peritoneal dialysis Preqnancv

ABDOMINAL WALL COMPLIANCE.

Intra-abdominal pressure also depends on the stiffness of the abdominal wall. The abdominal cavity dV/dP (pressure-volume, Le,. compliance) curve is not lin ear. As intra-abdominal pressure rises, the sliffness of the abdominal wall in creases; therefore, progressively smaller volume increments are required to fur ther elevate intra-abdominal pressure by given amount (4) Conversely, high intra-abdominal pressure may be dramatically relieved by partial decompression. EFFECTS ON RENAL SYSTEM

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Intra-abdöminal pressure of 15 to 20 mm Hg may produce oliguria; anuria en sues with higher pressures (41,91,100). The decrease in renal blood flow, glomerular filtration rate, urine output and various specific tubular functions (7,73,93) associated with elevated intra-abdominal pressure is of mullifactorial etiology (15,41,52,54,93). Improved cardiac output plays a role in diminished

Table 2: The main physiological consequences of increased intra-abdominal pressure

Increased

Decreased

mean blood pressure

-

heart rate

+

pulmonary capillary wedge pressure

+

peak airway pressure

+

central venous pressure

+ + .'

Parameter

thoracicJpleural pressure In[~rior

\'.ma cava pressure

+

+

systemic vascular resistance

+

cardiac output

-

+

venous return

-

+

renal blood f10w glomerular filtration rate abdominal wall compliance

XV World Congress Seoul, Korea 11·14 September 1996

renal vein pressure

visceral blood flow

Collegium Internationale Chirurgiae Digestivae

+ + + +

renal perfusion but even when cardiac output is maintained at normal or super normal values by blood volume expansion, impairment of renal function persists (41). Renal dysfunction is also caused by compression of the renal vein which causes partial renal blood outflow obstruction (73,93); compression of the ab dominal aorta and renal arteries contributes to increased. renal vascular resis tance (41). Furthermore, direct compression of the kidneys elevates cortical pressures leading to a "renal compartment syndrome" (52,91). Elevation of plasma antidiuretic hormone may represent another etiologic factor (63). Uret eral compression can be excluded as the cause of diminished urine production with elevated intra-abdominal pressure since oliguria was not prevented by placing ureteral stents (16,41). IMPAIRMENT OF INTRA-ABDOMINAL (SPLANCHNIC) BLOOD FLOW

Effects on hepatic function At pressures less than 10 mm Hg hepatie arterial blood f10w falls significantly (26). Increased intra-abdominal pressure is associated with a reduction in he patie blood f10w (12,26,32,49,66); hepatie arterial, portal and microvascular blood f10w are all affected (26). This reduced hepatic function including produc tion of aeute phase proteins, cytokines, immonoglobulins and factors of the other host defense systems. In the presence of such deficiencies and reduced visceral arterial and venous blood flow anastomotie healing may be deeply impaired.

Effects on intestinal blood flow Elevation in intra-abdominal pressure results in decreased mesenteric arterial blood f1ow, intestinal mucosal blood flow (25) and arterial perfusion of the stom-

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ach, duodenum, intestine, panereas and spleen (12). In parallel, assessment of gastrie perfusion by tonometrie intramucosal pH measurements indicate severe ischemia (25). The splanehnie hypoperfusion of the abdominal compartment syndrome favours transloeation of bacteria [DiebeI, presented at WEST 1996] and may contribute to further septie complications fuel ongoing infection. All these changes are greater than can be accounted for by the alterations in cardiae output (12) and also occur when cardiae output and systemie blood pressure are maintained at normal levels (25,55).

Effect on abdominal veins Intra-abdominal pressure is transmitted to all abdominal and retroperitoneal veins. Brief elevations of intra-abdominal pressure in cirrhotie patients cause increases in free and wedged hepatie venous pressures and increased azygos blood flow (an index of gastroesophageal collateral flow). Opposite changes oe cur after ~eduction of intra-abdominal pressure (66).

Effects on Iymph f10w and abdominal Clearance Lymphatie flow in the thoracie duct is significantly decreased when intra abdominal pressure is elevated and promptly increases following abdominal de compression (105). Stretching of the diaphragm decreases the volume of the diaphragmatie Iymphatie lacunae, thus redueing transport of peritoneal fluid into the thoraeie Iymphatics (80). EFFECTS ON RESPIRATORY SYSTEM.

Both hemidiaphragms are pushed upwards due 'to increased intra-abdominal pressure, decreasing thoraeie volume and compliance (21,50). Decreased vol ume within the pleural cavities predisposed to atelectases and decreases alveo lar elearance. Pulmonary infections are the result. Pneumonia is a typical early complication in patients with peritonitis. Further with elevated intra-abdominal pressure peak airway pressure is elevated and higher pressure is needed to deliver a fixed ventilator tidal volume (21,36,55,72,83). The elevated thoraeie and pleural pressure depresses cardiae output as noted above. Pulmonary vascular resistance is elevated (48) and ventilation/perfusion abnormalities occur (21,48). Arterial blood gas measure ments demonstrate hypoxemia, hypercarbia and acidosis, reflecting the physio logical derangements (4,36,48). Meehanical ventilation is required to compen sate but positive end-expiratory pressure (PEEP) ventilation causes further physiologie abnormatities when combined with an increased intra-abdominal pressure (9). EFFECTS ON CARDIOVASCULAR SYSTEM.

Increased intra-abdominal pressure significantly decreases cardiae output (4,9,12,41,45,46,48,50,55,66,72,83,93,104); adverse effects are seen with intra abdominal pressures as low as 10-15 mm Hg (46,48,83,104). Cardiae output (and stroke volume) is eompromised through •

decreased venous return

•

elevated intra-thoraeie pressure.

•

inereased systemie vaseular resistanee,

resulting in increased cardiae afterload and, depressing ventricular funetion.

Decreased venous return (Preload)

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Venous return (preload) is deereased through several mechanisms (11,20,24,50,54,55,66,69,73,83,84,93,104). Elevated pressure is directly transmitted to large retroperitoneal veins resulting in pooling of blood caudally and deereased inferior vena cava flow. In addition, functional narrowing of the inferior vena cava occurs at the diaphragm, just cephaly to the hepatie veins,

because the point of maximal narrowing of a tube always occurs at the transition site from an area of high external pressure (abdomen) into an area of low exter nal pressure (thorax) (27,84). Moreover, anatomical obstruetion of the inferior vena cava can occur by the elevated diaphragmatic crura distorting the dia phragm when intra-abdominal pressure is increased. Decreased venous outflow from the lower extremities during laparoscopic pneu moperitoneum has been observed using duplex ultrasound (6). It is not known whether elevation of intra-abdominal pressure induces deep vein thrombosis.

Collegium Internationale Chirurgiae Digestivae XV War/d Cangress Scoul, Korea 11- 14 September 1996

Decreased Cardiac Output and Increased Intra-thoracic pressure Intra-abdominal pressure increases intrathoracic pressure by elevating the dia phragms. Consequently, ventricular filling pressure increases and cardiac compliance decreases. With increased intra-abdominal pressure, the cardiac output falls and systemic vascular resistance increases. The blood pressure usually remains unaffeeted (50,83,84) although it may fall (55,104) or increase (55~69,1 04). The direetion of response is influenced by the degree of the intra abdominal pressure increase and other compounding faetors discussed below. Tachycardia is the common response to elevated intra-abdominal pressure, compensating for the decrease in stroke volume in order to maintain cardiac output (46,48,55,104).

Increased systemic vascular Resistance The mechanisms of the increase in vascular resistance has not been elucidated but is Iikely to be due to mechanical compression of capillary beds (4,9,12,24,45,46,50,54,66,69,93,104) or reaetive NO deficiency.

Effects on Cardiovascular Monitoring Increased intra-abdominal pressure modifies various cardiovascular parameters commonly monitored. Femoral vein pressure (4,50,55), central venous pressure (9,21,48,55,72,83,87), pulmonary capillary wedge pressure (9,12,21,48,50,62,66), and right atrial pressure (4,41,50,91) increase propor tionally with increasing intra-abdominal pressure. COMPOUNDING FACTORS FOR ACS

In an individual patient, the effects of increased intra-abdominal pressure are not isolated but may be superimposed on multiple co-existent faetors. Only a mild elevation in systemic vascular resistance may severely compromise a marginally functioning myocardium; the elevation in aflerload could lead to both increased myocardial oxygen consumption and myocardial ischemia or congestive heart failure in patients who are susceptible (104). Similarly, a moderate increase in intra-abdominal pressure may suffice to cause anuria in a patient in hemor rhagic shock or when superimposed on chronic renal failure [54}. The intravascular volume status of the patient is crucial; hypovolemia aggra vates the" efteets of increased intra-abdominal pressure while volume expansion with intravenous fluids tends to compensate for the decreased venous return, maintaining cardiac output (21,26,41,50,54,91,104). A similar effeet is achieved by the Trendelenburg position (72,87,104). The additive consequences of PEEP ventilation were mentioned earlier (55,72,104). The cardiovascular disturbances caused an specific injury such as diaphragmatic rupture are more profound when combined with elevated intra-abdominal pressure(2). SIGNS AND SYMPTOMS OF ACS

The clinical syndrome of ACS consists of a need for increased ventilatory pressure, the presence of increased central venous pressure and decreased urinary output, associated with massive abdominal distention (36). Cadio vascular. respiratory. and renal dysfunction became progressively difficult to manage unless the intra-abdominal pressure is reduced (7,21,52,78)..

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Collegium Internationale Chlrurglae Digestivae XV World Congress Seoul, Korea 11·14 September 1996

DECOMPRESSION OF THE PERITONEUM

Abdominal decompression reverses all of the adverse effects of increased intra abdominal pressure (41,46,50,72,83,93). Upon sudden release of intra abdominal pressure, cardiac output and IVC blood f10w increase, but then re turned to base line values within seconds (50). Sudden removal of a large volume of peritoneal fluid is hemodynamically safe in patients who are not volume depleted (53). Removal of ascites in cirrhotic pa tients to decrease intra-abdominal pressure has been associated with a dramatic improvement in renal function(11,87,94), cardiac performance and hepatic per fusion (20,59,66). Clinical experience with decompression of post-traumatic or postoperative ACS in 45 patients in whom abdominal compartment syndrome was recognized and treated (1,15,21,36,43,52,62,71,76,78,91,94) is summarized in Table 5-B After decompression, cardiac, respiratory and renal function are immediately im proved, followed occasionally by transient episodes of hypotension (21,71,91). Immediate post-decompression asystole has been reported in four cases ( 3 fa tal) (71). It has been suggested that following decompression, cardiac output increases while systemic vascular resistance decreases; hypotension occurs because the dilation of peripheral vessels is more profound (91). The hypothe sis that post-decompression cardiovascular collapse results from reperfusion injury, due to release of acid and metabolites from the reperfused ischemic vis cera and lower extremities (21,71) is not weil documented. APPRECIATION OF

ACS

IN PERITONITIS

The increased intra-abdominal pressure as a consequence no only of injury but particularly of infectious abdominal catastrophes identifies a subset of patients with a grave prognosis. The experience from the literature documents a mortal ity rate of 44 percent; 20 out of the 45 patients who underwent decompression died. Only 4 of these fatalities occurred immediately following decompression. Most patients succumbed to a 'Iate' death from their an underlying condition. Abdominal compartment syndrome is areal entity. The detrimental effects of elevated intra-abdominal pressure and the methods and benefits of its decom pression have been weil studied both in the laboratory and clinical practice. Di agnostic suspicion may be confirmed with objective measurements of intra abdominal pressure to select palients who may benefit from decompression us ing the STAR procedure (108). STAR stand for staged abdominal repair. 1I ulil izes the artificial burr devise for temporary abdominal closure (107), that allows for adjustmenl of the abdominal girth to the need dictated by the increased pres sure, and at Ihe same time, Ihal allows for reapproximation of the fascial edges as the pressure decreases with treatment. Finall}(. the abdominal cavity can be c10sed fascia to fascia similar to a one stage laparotomy without an increased risk for hernia formation (106).

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