The Abdominal Compartment Syndrome

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Syndrome

Moshe Schein

In surgery, physiology is the king, anatomy the queen; you can be the prince, but only provided you have the judgment . . .

At Thanksgiving, a national holiday here in the United States, many millions of turkeys – also called “thanksgiving birds” – are tightly stuffed with various sorts of ingredients (mine would include chickpeas, garlic, wine-soaked bread, and thyme) and served to the assembled members of American families. Bear in mind, however, that these large birds are stuffed post-mortem but imagine what would happen to the poor bird if it were tightly stuffed alive? First, the bird would stop flying and then gradually it would hypoventilate, collapse and die. Surely, you could attribute the death of the stuffed avis to bad lungs, old heart, toxins produced by the ingredients used in the stuffing and as a last resort – you could blame the anesthetist.

But frankly there is a huge body of first grade scientific evidence to prove beyond any doubt that the tragic outcome for your bird was the result of elevation of her intra-abdominal pressure (IAP), causing intra-abdominal hypertension (IAHT), which in turn led to the abdominal compartment syndrome (ACS).

Does Abdominal Compartment Syndrome Exist?

Much good evidence now supports the concept that elevated IAP or IAHT may impair physiology and organ function by producing the abdominal compartment syndrome (ACS). Complex, adverse physiological consequences of increased IAP develop as the pressure is transmitted to adjacent spaces and cavities, decreasing cardiac output, restricting pulmonary ventilation, diminishing renal function and visceral perfusion, and increasing cerebrospinal pressure (^>Table 36.1, Fig. 36.1).

How Do You Measure IAP?

At the bedside, IAP is best measured through the urinary bladder catheter connected to a manometer or a pressure transducer. In fact, all you need to measure IAP is a Foley catheter: disconnect it from the urine bag; instill 100 ml saline into

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Table 36.1. Physiological consequences of intra-abdominal hypertension

Increased Decreased No change

Mean blood pressure – – x

Heart rate x – –

Peak airway pressure x – –

Thoracic/pleural pressure x – –

Central venous pressure x – –

Pulmonary capillary wedge pressure x – –

Inferior vena cava pressure x – –

Renal vein pressure x – –

Systemic vascular resistance x – –

Cardiac output – x –

Venous return – x –

Visceral blood flow – x –

Gastric mucosal pH x

Renal blood flow – x –

Glomerular filtration rate – x –

Cerebro-spinal fluid pressure x

Abdominal wall compliance – x –

Fig. 36.1. The abdominal compartment syndrome

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the bladder and elevate the disconnected catheter perpendicular to the supine patient and his bed. The height of the water-urine column in the catheter is the IAP in cmH2O (1 cm H2O=0.735 mmHg). The level will fluctuate with the patient’s respiratory cycle – up during inspiration, down during expiration – following the movements of the diaphragm. A neurogenic or small contracted bladder may render the measurements invalid. Errors can also occur if the catheter is blocked or in the presence of a pelvic hematoma which may selectively compress the bladder.

Because the Trendelenburg position (or its reverse) may affect intra-bladder pressure, accurate measurements are best achieved in the supine position.

Deleterious Consequences of Raised IAP Appear Gradually

At pressures less than 10 mmHg cardiac output and blood pressure are normal but hepatic arterial blood flow falls significantly; IAP of 15 mmHg produces adverse, but easily compensable, cardiovascular changes; IAP of 20 mmHg may cause renal dysfunction and oliguria, and an increase to 40 mmHg induces anuria. In an indi- vidual patient,the effects of increased IAP are not isolated but usually superimposed on multiple underlying and co-existent factors, the most notable being hypo- volemia, which aggravates the effects of increased IAP.

Why Didn’t You Notice IAHT and ACS Before?

Because you – or your mentors – did not know that this entity exists!

(^>Fig. 36.2) Any increase in the volume of any of the contents of the abdomen or

the retroperitoneum elevates IAP. Clinically significant elevation of IAP has been observed in a variety of contexts (^>Table 36.2), such as: postoperative intra- abdominal hemorrhage,after complicated abdominal vascular procedures or major operations like hepatic transplantation, in association with severe abdominal trauma accompanied by visceral swelling, hematoma or the use of abdominal packs, severe peritonitis,necrotizing pancreatitis,use of the pneumatic anti-shock garment, and tense ascites in cirrhotic patients. Peritoneal insufflation during laparoscopic procedures is currently the most common (iatrogenic) cause of IAHT. Note that severe intestinal edema causing IAHT has been described following massive fluid resuscitation for extra-abdominal trauma. The combination of severe abdominal wall burns – producing a tight-constricting eschar, and fluid resuscitation causing visceral edema – could lead to ACS in the burned patient.

Be aware that morbid obesity and pregnancy (^>Chap. 31) are “chronic” forms of IAHT; various manifestations associated with such conditions (e.g.hypertension, pre-eclampsia) are attributed to IAHT. Note that anything can cause IAHT and

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Fig. 36.2. “What? Abdominal compartment syndrome? Never heard of it!”

Table 36.2. Etiology of increased intra-abdominal pressure. The list cannot be considered

“complete” as any increase, of any etiology, in the volume of the intra- or retro-peritoneal space will increase intra-abdominal pressure

Condition Etiology

ACUTE

I. Spontaneous Peritonitis, intra-abdominal abscess, ileus, intestinal obstruction, ruptured abdominal aortic aneurysm, tension pneumoperitoneum, acute pancreatitis, mesenteric venous thrombosis

II. Postoperative Postoperative peritonitis, paralytic ileus, acute gastric dilatation, intra-peritoneal hemorrhage

III. Posttraumatic Intra/retro-peritoneal bleeding, post-resuscitation visceral edema

IV. Iatrogenic Laparoscopic procedures, pneumatic anti-shock garment, abdominal packing, reduction of a massive parietal or diaphragmatic hernia, abdominal closure under excessive tension

CHRONIC Ascites, large abdominal tumor, chronic ambulatory peritoneal dialysis, pregnancy, morbid obesity

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ACS – irrespective of the ingredients used in the “stuffing” or its flavor. The “stuffing” can even be composed of feces:

An elderly lady presented with poor peripheral perfusion,blood pressure of 70/40,and respiratory rate of 36/min. Her abdomen was very distended, diffusely tender with guard- ing. Rectal examination revealed a large amount of soft impacted feces. Blood urea nitrogen (BUN) and creatinine levels were 30 mg% and 2 mg%, respectively. Arterial blood gases showed a metabolic acidosis with pH of 7.1. Her IAP was 25 cm H₂O. She survived following a decompressive laparotomy and resection of the partially ischemic rectosigmoid.

Only a few years ago we would have described this patient as suffering from

“septic shock” due to “colonic ischemia”. We would have attributed the cardiovascular collapse and acidosis to the consequences of endotoxemic sepsis. But today it is clear to us that the mass effect created by the extreme dilatation of the rectum produced severe IAHT, causing cardiovascular and respiratory collapse and renal dysfunction – representing a typical ACS. This further decreased splanchnic perfusion, thus aggravating colorectal ischemia. Rectal disimpaction and abdominal decompression rapidly reversed the adverse physiological manifestations of the abdominal hypertension.Being more aware that IAHT is a “real problem”and liberally measuring IAP, we recognize it with an increasing frequency in our daily clinical practice.

The Mechanisms Culminating in an ACS Are Usually Multiple

The typical scenario occurs in a multiple trauma or post-emergency laparotomy patient who receives a large volume of fluid for resuscitation, causing an increase in interstitial fluid volume.The ensuing visceral and retroperitoneal edema is aggravated by shock-induced visceral ischemia and reperfusion edema, as well as by temporary mesenteric venous obstruction caused by surgical manipulation or the employment of hemostatic packs. The edematous abdominal wall is closed over the bulging abdominal contents under extreme tension.

The Clinical Syndrome

The clinical syndrome of ACS consists of:

 Need for increased ventilatory pressure

 Presence of decreased cardiac output

 Decreased urinary output

 Abdominal distension

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These abnormalities are often present despite apparently normal cardiac filling pressures because transmission of increased IAP to the thorax elevates central venous pressure (CVP), right atrial pressure and pulmonary capillary wedge pressure. Cardiovascular, respiratory and renal dysfunction become progressively dif- ficult to manage unless IAP is reduced. Rarer consequences of ACS have been described,such as intestinal ischemia following laparoscopic cholecystectomy or spinal cord infarction in the setting of IAHT following a perforation of a gastric ulcer.

When Should You Consider Abdominal Decompression?

The decision to decompress the abdomen should not be taken based on isolated measurements of IAP without taking into account the whole clinical picture.

Early or mild physiological abnormalities caused by IAHT can be managed by fluid administration or afterload reduction.(Note,however,that increasing cardiac filling offers only a temporary solution and that fluid administration may in fact increase tissue edema and thus aggravate IAHT). In patients receiving mechanical ventila- tion muscle paralysis may decrease IAP by relaxing the abdominal wall.

Established ACS,however,mandates an emergency decompressive laparotomy, which, when performed in the well-resuscitated patient, promptly restores normal physiology.To prevent hemodynamic decompensation intravascular volume should be restored, oxygen delivery maximized, and hypothermia and coagulation defects corrected. Following decompression, the abdominal skin and fascial edges are left open using one of the temporary abdominal closure devices (TACD) described

in ^>Chap. 46.

Prevention

In order to avoid IAHT and ACS, forceful closure of the abdomen in patients having massive retroperitoneal hematoma, visceral edema, severe intra-abdominal infection, or a need for hemostatic packing, should be avoided (^>Chap. 38). Leaving the fascia open, closing only the skin with sutures or towel clips to protect the bulging viscera, has been recommended. Occasionally, however, the skin closure alone may produce IAP of 50 mmHg or more. Certainly, leaving both fascia and skin unsutured offers maximal reduction in IAP but may result in fistula and evisceration. Bridging the fascial gap with a TACD circumvents these problems

(^>Chaps. 38, 46, and 47).

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Would Decompression Benefit Patients with Only a Moderate IAHT?

That the “extreme” case of ACS as described above necessitates an urgent abdominal decompression is obvious. But what about a less extreme case? Would decompression benefit a postoperative patient in whom the moderately increased IAP of 20 mmHg is compensated by appropriate fluid and ventilatory therapy?

We believe that the available evidence suggests that the detrimental effects of IAHT take place long before the manifestations of ACS become clinically evident – just as nerve and muscle ischemia begins long before neuromuscular signs of the extremity compartment syndrome are evident. IAHT may cause gut mucosal acidosis at relatively low pressures, long before the onset of clinical ACS. Uncorrected, it may lead to splanchnic hypoperfusion,distant organ failure and death.Prophylactic non- closure of the abdomen may facilitate the prevention, early recognition and treat- ment of IAHT and reduce these complications. It appears that “borderline” IAHT contributes to the overall morbidity but the risk/benefit ratio of abdominal decompression in such patients is not yet clear.

In Conclusion

IAHT is yet another factor to consider in the overall management of the emergency abdominal patient. It may be obvious –”crying” for abdominal decompression. More commonly, however, it is relatively silent but contributing to your patient’s SIRS (systemic inflammatory response syndrome), organ dysfunction and death. So now you know better, you know that your patient is not a dead turkey to be stuffed. Bon appetit!

Be as aware of intra-abdominal hypertension as you are of arterial hypertension. It is much more common and clinically relevant than you have suspected hitherto.