سندرم کمپارتمان شکمی
Be Alert for the Development of Abdominal Compartment Syndrome
Awori J. Hayanga MD
The terms intra-abdominal hypertension and abdominal compartment syndrome have sometimes been used interchangeably. However, it is important to recognize there is a distinction between these entities. Intra-abdominal hypertension exists when intra-abdominal pressure exceeds a measured numeric parameter. This parameter has generally been set at between 20 and 25 mm Hg. Abdominal compartment syndrome exists when intra-abdominal hypertension is accompanied by manifestations of organ dysfunction, with reversal of these pathophysiologic changes upon abdominal decompression. These include the pulmonary, cardiovascular, renal, splanchnic, musculoskeletal/ integumentary (abdominal wall), and central nervous system.
The exact incidence of abdominal compartment syndrome is yet to be established, but it is clearly increased in certain population groups. These include patients with the following:
- severe blunt and penetrating abdominal trauma
- ruptured abdominal aortic aneurysms
- retroperitoneal hemorrhage
- massive ascites
- liver transplantation
- massive fluid resuscitation
- accumulation of blood and clot
- bowel edema
- forced closure of a noncompliant abdominal wall
- circumferential abdominal burn eschars
In one prospective series of 145 patients who were identified as being at risk for development of the abdominal compartment syndrome, the reported incidence was 14%. The incidence following primary closure after repair of ruptured abdominal aortic aneurysm was reported in one series as 4%.
In the trauma population, the group that is especially at risk includes those patients undergoing abbreviated or â€œdamage controlâ€
laparotomy, especially with intra-abdominal packing. It must be noted that having an open abdomen does not necessarily preclude the diagnosis of intra-abdominal hypertension or abdominal compartment syndrome, particularly where intra-abdominal packing has been used.
Signs And Symptoms
Clinical manifestations of organ dysfunction in abdominal compartment syndrome include respiratory failure that is characterized by impaired pulmonary compliance that results in elevated airway pressures with progressive hypoxia and hypercapnia. In this situation, extremely high driving pressures may be required to maintain minimally sufficient tidal volumes, often with loss of delivered tidal volume by distension of ventilatory tubing. The high airway pressures are needed to overcome high extrathoracic pressure exerted through the diaphragmand not to overcome an intrinsic lung problem. Some authors report pulmonary dysfunction and elevated peak airway pressures as the earliest manifestation of abdominal compartment syndrome. Chest radiography may show elevated hemidiaphragms with loss of lung volume.
Hemodynamic indicators consistent with abdominal compartment syndrome include elevated heart rate, hypotension, elevated pulmonary artery wedge pressure and central venous pressure, reduced cardiac output, and elevated systemic and pulmonary vascular resistance. In this situation measurement of right ventricular end-diastolic volume may be a more accurate predictor of a patient's position on the Starling curve. The pathophysiology is related to decreased venous return.
In abdominal compartment syndrome impairment in renal function is manifested by oliguria progressing to anuria with resultant azotemia. Renal insufficiency as a result of intra-abdominal hypertension is only partly reversible by fluid resuscitation. Renal failure in the absence of pulmonary dysfunction is not likely to be the result of intra-abdominal hypertension. Elevated intracranial pressure is an additional clinical manifestation of abdominal compartment syndrome.
Clinical confirmation of intra-abdominal hypertension requires bedside measurements indicative of intra-abdominal pressure. Experimental and clinical data indicate that intra-abdominal hypertension is present when intra-abdominal pressure exceeds 20 mm Hg. Contemporary measurement of intra-abdominal pressure outside of the laboratory is accomplished by a variety of means. These include direct measurement of intra-abdominal pressure by means of an intraperitoneal catheter, as is done during laparoscopy. Bedside measurement
of intra-abdominal pressure has been accomplished by transduction of pressures from indwelling femoral vein, rectal, gastric, and urinary bladder catheters. Of these methods, measurement of urinary bladder and gastric pressures are the most common clinical applications. In 1984, Kron et al. reported a method to measure intra-abdominal pressure at the bedside with the use of an indwelling Foley catheter as follows:
- Sterile saline (50 to 100 cc) is injected into the empty bladder through the indwelling Foley catheter.
- The sterile tubing of the urinary drainage bag is clamped just distal to the culture aspiration port.
- The end of the drainage bag tubing is connected to the Foley catheter.
- The clamp is released just enough to allow the tubing proximal to the clamp to drain fluid from the bladder, then reapplied.
- A 16-gauge needle is then used to Y-connect a manometer or pressure transducer through the culture aspiration port of the tubing of the drainage bag.
- Finally, the top of the symphysis pubic bone is used as the zero point with the patient supine.
An alternative bedside technique has been described in which intragastric pressure measurements are taken from an indwelling nasogastric tube. This method has been validated and found to vary within 2.5 cm H2O of urinary bladder pressures. Of these techniques, measurement of urinary bladder pressure appears to have gained widest clinical acceptance and application.
One final note is that the clinician must know if the pressure readings have been reported in cm H2O or mmHg. To convert cm H2O to mm Hg, multiply the reported value by 0.736.
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