Abdominal Compartment Syndrome

LITERARY & AHISTORICAL R EVIEW OR IGIN L PA P E R

Abdominal Compartment Syndrome

Abdominal Compartment Syndrome ABSTRACT

Background Abdominal compartment syndrome (ACS) is a systemic syndrome involving derangement in cardiovascular haemodynamics, respiratory and renal functions as a result of sustained increase in intra-abdominal pressure (IAP) ending in multi-organ failure. It is a life threatening emergency and requires prompt action and treatment. For the last 20 years, there has been more awareness among surgeons and intensivists of ACS being a distinct disease entity but still widespread ignorance prevails. Presentation can be acute, chronic and acute on chronic. Initial diagnosis is clinical, confirmed by measurement of IAP. Treatment is abdominal decompression by laparostomy and delayed abdominal closure. Despite prompt treatment mortality remains high. Awareness among surgeons has increased because laparoscopy has resulted in determination of IAP as a readily measurable quantity and also they have been able to appreciate the benefit of abdominal decompression by performing repeated planned laparotomies for trauma. Methods A medline, pubmed and Cochrane database search was performed and the articles found were cross referenced. Results and conclusion Clinical diagnosis is not easy and serial urinary bladder pressure (UBP) monitoring leads to early diagnosis. Treatment is by laprostomy to decompress the abdomen followed by delayed abdominal closure. INTRODUCTION

Abdominal compartment syndrome (ACS) is characterized by tense distended abdomen, raised intra abdominal pressure, increased peak airway pressure, inadequate ventilation with low PO2 and high PCO2, deranged cardiovascular and renal function. There is a significant improvement in patients’ haemodynamic status after abdominal decompression. ACS was first reported in 1876 by Wendt.1 Adverse respiratory effects of raised IAP were first described in late 19th century by Marey and Burt.2 Emerson, in 1911, described the adverse cardiovascular effects and Wendt, in 1913, related the renal dysfunction to raised IAP.3-5 ACS was first described as a separate entity by Baggot in 1951,6 but the term ACS was first coined by Kron in 1984 to describe the syndrome arising from raised IAP following aortic aneurysm surgery.7 Recently Sugrue et al and Ivatury et al have included isolated impairment of gut perfusion to be part of the ACS.8-9

T Bin Saleem1, I Ahmed Airedale General Hospital1, Keighley, West Yorkshire, UK. Queens Medical Centre, Nottingham, UK.

INCIDENCE

Morris et al found the incidence of ACS to be 15% in their trauma admissions,10 while Meldrum et al reported 14% incidence in their patients with blunt abdominal trauma.11 Ivatury et al found an even higher incidence in patients with penetrating abdominal trauma undergoing primary fascial closure (52%) than in patients receiving prophylactic mesh closure (24%).12

PATHOGENESIS

Acute ACS develops within hours after initial insult. Chronic ACS develops in conditions such as morbid obesity, ascites, pregnancy, etc, where there is a gradual increase in the IAP and the abdominal wall adapts by increasing compliance.13 This causes a gradual rise in IAP which is in no respect harmless and does contribute to the morbidity these conditions are associated with.14-17 Normal intra-abdominal pressure is less than 10 mm Hg in supine position.18 In post-operative patients IAP is 3.5 – 10.5 mm Hg in males and 3.3 – 8.8 mm Hg in females.19 Raised IAP causes wide ranging abdominal, cardiovascular, respiratory, renal, and intracranial effects (Table 2).

IRISH JOURNAL OF MEDICAL SCIENCE • VOLUME 175 • NUMBER 1

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R EVIEW OR IGIN A L PA P E R

T Bin Saleem & I�� Ahmed

Table 1 CAUSES OF ABDOMINAL COMPARTMENT SYNDROME

ABDOMINAL

Acute • Abdomino-pelvic trauma • Abdominal packing • Abdominal Aortic Aneurysm rupture and repair • Retro peritoneal bleed & abscess, • Haemorrhagic acute pancreatitis • Paralytic Ileus • Intestinal obstruction • Acute gastric dilatation • Pneumoperitoneum during laparoscopy • Tight abdominal closures, e.g. repair of gastroschisis, omphalocoele and giant hernias • Pneumatic anti-shock garments Chronic • Central obesity, • Ascites • Large abdominal masses, • Pregnancy and delivery • Chronic ambulatory peritoneal dialysis EXTRA-ABDOMINAL • Septic shock • Hypothermic coagulopathy • Burns • Abdominal injury followed by high positive end-expiratory pressure (PEEP) ventilation

There are many factors giving rise to raised IAP. • There is capillary leakage due to ischaemia reperfusion injury, vasoactive substance release and free radical injury compounded by increased extracellular volume due to massive fluid resuscitation. This causes increase in intra abdominal visceral and vascular volume consequently raising IAP.18 • Poor lung function requiring ventilatory support and positive end expiratory pressure (PEEP) causes intra-thoracic pressure to be transmitted into the abdomen further increasing IAP.13, 21

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Table 2 PATHOLOGICAL EFFECTS OF INCREASING INTRA-ABDOMINAL PRESSURE Pressures (mm hg)

INTRA-ABDOMINAL

INTRA-THORACIC

10

•‚ hepatic and portal venous flow •‚ blood flow to rectus sheath

•· Cardiac output •· Venous return (from capacitance vessels)

15

• Intestinal mucosal ischaemia • Bacterial translocation. • �� Oliguria

•‚ venous return

INTRACRANIAL

•· intra cranial pressure

20 •‚ Mesenteric blood flow 25

•· ventilation pressures

30

•‚ cardiac contractility •‚ ventricular compliance

• Intestinal infarction • Anuria +35

•‚ cerebral perfusion

•‚ pO2

• Decreased abdominal wall compliance due to ischaemia and oedema further increase IAP. All these events cause viscous cycle to set in leading to progressive deterioration towards multiple organ failure.20, 22 Evidence supports the association of IAP above 10 mmHg with sepsis, multi-organ failure, re-operations and increased mortality causing anaerobic respiration, acidosis and free radical generation.23-4 This has led to demonstrate that gastric intramucosal pH tonometery may be used to indicate gut ischemia in ACS.23,25




Renal function derangement is due to decreasing glomerular filtration rate which in turn is brought about by reduced cardiac output and increased renal vascular resistance. Factors causing increased renal vascular resistance are compression of renal vein and parenchyma,26,27 secretion of antidiuretic hormone and rennin-angiotensin28 and corticomedullary shunting of renal plasma flow. Decreased abdominal wall compliance is caused by a direct compressive effect on the microvasculature and the inferior epigastric vessel.22,29 Decreased perfusion causes ischemia and oedema leading to decreased compliance further aggravating IAP.20 As collagen deposition and resistance to infection is directly related to tissue perfusion and oxygenation raised IAP can be related to the wound complications like dehiscence, herniation or infection.30 There is compression of inferior vena cava and portal vein in the abdomen causing decreased cardiac output. Increased intra-thoracic pressure causes decreased superior and inferior vena caval flow, decreased ventricular end diastolic volume and increased afterload. These factors decrease stroke volume and cause compensatory tachycardia.31-4

cardiopulmonary functional derangement. These are the direct result of raised central venous and intrathoracic pressures and get reversed after abdominal decompression. Similar changes are seen in morbidly obese in the shape of benign intra-cranial hypertension which improves after weight loss. 43-4

DIAGNOSIS

The usual clinical setting is that of patients in intensive care units on artificial ventilation therefore symptoms are not apparent. Hence it should be suspected in all the unstable critically ill patients with abdominal, cardiovascular and respiratory signs who fail to improve in spite of adequate resuscitation. The diagnosis of ACS is primarily based on serial or renal UBP monitoring in the presence of cardiopulmonary or renal impairment or gastric mucosal acidosis45 (Table 3). Intra-abdominal pressure monitoring is ideally done through an intra-peritoneal catheter. Other methods include gastric, inferior vena cava or urinary bladder pressure monitoring. UBP monitoring remains the most practical and minimally invasive procedure correlating well with IAP over a wide range (15-70 mmHg). 46-7 Table 3 CRITERIA FOR DIAGNOSIS AND LAPAROSTOMY

Increased systemic vascular resistance is due to direct abdominal arteriolar compression and sympathetic reflex to decreased cardiac output.34-5 Inhalational anaesthetics tend to decrease the cardiac output and fluid resuscitation tends to reverse it. Volume expansion before abdominal decompression is recommended for controlling shock seen after such a procedure.36

UBP (MM HG) >18

Chances of deep venous thrombosis increase in obese patients due to chronically raised IAP.37 Respiratory failure with high ventilatory pressures, hypoxia and hypercarbia are the result of raised IAP (acute or chronic).34 Diaphragmatic elevation causes reduction in lung compliance,38-9 total lung capacity and residual volume leading to ventilationperfusion mismatch. 40-1 Pulmonary vascular resistance increases in response to alveolar hypoxia and raised intra-thoracic pressure. 42 Due to these changes the peak inspiratory pressures increase and abdominal decompression reverses these changes immediately.34 Raised IAP causes raised intracranial and cerebral perfusion pressures which are independent of

>20

SYSTEMIC PARAMETERS Gastrointestinal

Gastric pH < 7.15 +/- 0.2

Cardiovascular

Delivery of Oxygen index (DO2I) 45 cm H2O PaCO2 > 50 mm Hg Urine output < 0.5 ml/kg/hour Azotemia

An intravesical Foley’s catheter is used. The bladder is filled with 50-100 mL of sterile saline. Catheter is attached to a water manometer or pressure transducer. Pressure readings are taken using symphysis pubis as the zero reference point. It will not be a reliable reading in the presence of small, neurogenic bladder, bladder with adhesions, abdominal ascites, pregnancy and central obesity. 48 Therefore in patients with chronically raised IAP (e.g. obesity) the periodic rise in the UBP determines progression to ACS.


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R EVIEW OR IGIN A L PA P E R

Using gastric tonometery to assess initial bowel ischaemia with raised IAP is useful as UBP of more than 10 mm Hg has been associated with sepsis, multi-organ failure and mortality.23 Computed tomography findings include round belly sign (increased ratio of anteroposterior to transverse diameter > 0.80), inferior vena caval compression and ascites. 49

TREATMENT

The accepted treatment of the established ACS is decompression of the abdomen which results in an immediate improvement of patient haemodynamic status. Early decompression as guided by UBP gives better survival rate than when it is done in well established ACS.11 Definitive indications for decompression are a UBP of >20 mm Hg with cardiopulmonary or renal impairment or UBP of 15-20 mm Hg with ischemic dusky bowel as examined through silastic closure or indicated by gastric mucosal acidosis not responsive to oxygen therapy (Table 3). Additionally if a patient has head trauma and is on intra-cranial pressure monitoring showing intracranial hypertension not responsive to standard procedures and the UBP exceeds 15-20 mm Hg a decompressive laparotomy is indicated.50 A system of grading UBP is used in trauma patients wherein grade I (0-15 mm Hg) and II (16-25 mm Hg) are treated with volume replacement and expansion respectively. The treatment is aimed to restore splanchnic and renal perfusion by hypervolaemic resuscitation. Grade III (26-35 mm Hg) requires close monitoring and decompression based on the clinical signs. For Grade IV (>35 mm Hg) re-exploration is mandatory. We propose that this method of grading be used for management only in not so well equipped ICUs because now there is a precise definition available for diagnosis of ACS practicable in a modern well equipped ICU. Abdominal decompression leads to abrupt reversal of all physiological abnormalities and should be treated by rewarming, volume loading and reversal of clotting deficiency and acidosis.10 As a preventive measure, temporary abdominal wall closure is preferred for patients with abdominal and thoracic trauma wherein there is cardiovascular

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and pulmonary instability, massive oedema or fluid resuscitation.51-2 Many techniques have been described for temporary abdominal cover. The simplest of these is a towel clip closure.53 Towel clips are applied to the skin 1-2 cm apart and the same distance from the skin edge and covered with moist towel which is sealed with adhesive plastic sheet. Alternatively a silastic bag is fashioned from cutting open sterile 3L Foley irrigation bags to size and sewing to fascia or stapled to skin.54 ‘Bogota’ bag is a commercial product available for covering laparostomies. Plastic sheets, fascial cover, mesh and vacuum pack have been used.54-55 There is considerable fluid loss and the abdomen should be drained by closed drainage systems with or without suction.9 Definitive abdominal closure should be attempted when there is improvement in the general clinical picture evident by reversal of cardiovascular and pulmonary instability, subsidence of visceral and peripheral oedema, high chances of fascial approximation and low probability of bleeding, sepsis and repeat laparotomies.18 Fascial closure primarily or by successive approximation should be the first option. Alternatively if fascial retraction, loss or necrosis precludes primary closure, then granulation over viscera or preferably absorbable mesh with omental cover is encouraged. Later delayed primary skin closure or split thickness skin grafting over granulation tissue is attempted. The resultant ventral hernia can be dealt with by another attempt at fascial closure or plastic mesh implantation after 6-12 months.53

PROGNOSIS

Mortality despite timely and adequate treatment remains high and ranges 63-72%.10-11 This reflects not only the detrimental effects of ACS but also the severity of initial insult. Morbity is also high and relating to wound closure with ventral hernias (63%) and bowel fistulas.55

SPECIAL ISSUES

Conventional laparoscopy uses IAP in the range of 12-15 mm Hg and is associated with gut mucosal and hepatic ischemia with a chance of bacterial translocation.23,56 Also there is a direct relationship between IAP and intracranial pressure.97 Therefore its use in patients with closed head injuries, IRISH JOURNAL OF MEDICAL SCIENCE • VOLUME 175 • NUMBER 1



existing multi-organ failure or sepsis and minimal cardiopulmonary reserve should be with extreme caution. In the realm of paediatric surgery the clinical picture after closure of abdominal wall defect in neonates with gastroschisis and omphalocele resembles the adult ACS.57-61 Chin et al demonstrated that there was a high incidence of ascitic leakage, ventral hernia, lower limb oedema and oliguria in newborns who underwent abdominal wall closure and developed UBP more than 20 mm Hg.59 Lacey et al used UBP as a guide to close abdominal wall defects and found decreased morbidity by this method.58 Rizzo et al in a retrospective study using UBP during abdominal wall defect closure showed reduced hospital stay and cost.58-61

THE FUTURE

Many factors like high injury severity scores (ISS), high transfusion volume, raised arterial lactate and base deficit have been associated with the development of ACS but none are predictive.12 Recently two studies have shown a peak airway pressure of > 44 ± 2 mm Hg on admission to the ICU to be predictive.62-3 Additionally one of these studies has also shown net 24 hours fluid balance to be statistically predictive.63 But neither study establishes intra-operative or early ICU variables like fluid requirements, haemodynamics or blood gas analysis as predictive for ACS. Certain cytokines like IL-1, IL-8 and tumour necrosis factor are raised with an IAP of more than 30 mm Hg. Whether it is a cause or effect of raised IAP and carries any predictive value is yet to be determined.64 Questions regarding predictors of ACS and its early detection and amelioration with regards to outcome need to be explored in terms of reduced mortality and morbidity. The role of minimally invasive techniques for reducing IAP (e.g. splitting the fascia of the rectus muscle to increase the intraabdominal capacity) has to be evaluated.

CONCLUSION

Diagnosis should be suspected in all critically ill patients, particularly those on ventilatory support in intensive care units who are haemodynamically not improving in spite of adequate resuscitation. ACS is a distinct clinical entity developing in the wake of a serious insult to the body affecting multiple organs in a progressive manner. The classical clinical

setting remains of major trauma, massive fluid resuscitation and prolonged operation. The gut mucosa is affected first and gut ischemia develops before renal and cardiopulmonary derangements. Decompressive laparotomy is the mainstay of treatment if the patient is to be saved from multiorgan failure and death despite which mortality is high. ACS should also be considered in patients undergoing laparoscopies and paediatric patients undergoing abdominal wall defect closure.

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Correspondence to: Dr Talha Bin Saleem, Dept. of General Surgery, Airedale General Hospital, Keighley. BD20 6TD, West Yorkshire, UK. Tel: 0044 1535 652 511/0044 1535 654 148 Fax: 0044 1535 292 240 Email: [email protected]


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