*From the Pritzker School of Medicine (Mr. Tsuang), University of Chicago, Chicago, IL; Section of Pulmonary and Critical Care Medicine (Drs. Pohlman and Hall), University of Chicago Medical Center, Chicago, IL.
Correspondence to: Jesse Hall, MD, Section Chief, Pulmonary and Critical Care Medicine, MC 6076, University of Chicago Medical Center, 5841 South Maryland Ave, Chicago, IL 60637; e-mail: email@example.com
A 25-year-old woman with type II diabetes and hypertension presented to the emergency department complaining of abdominal pain and nonbloody, nonbilious emesis for 1 day. She denied fevers, chills, or dysuria. Due to mental status changes, she required intubation and transfer to the medical ICU.
The patient’s vital signs were as follows: temperature, 35.8°C; BP, 98/73 mm Hg; pulse 118 beats/min; and respiration, 18 breaths/min. Her body mass index was 33 kg/m2, she was intubated and sedated, and a central venous catheter was in place. The patient’s lungs were clear to auscultation bilaterally. She was tachycardic, with a regular rhythm. The abdomen was distended, there were decreased sounds, and it was diffusely tender. The patient’s extremities were cool to the touch, she had poor nail bed return, and her radial and pedal pulses were not palpable. Central venous pressure was 7 mm Hg.
Hemoconcentration was suggested by a hemoglobin concentration of 19 g/dL and a hematocrit of 54%. The levels of lipase (7,430 U/L) and ionized calcium (2.7 mg/dL) were consistent with acute pancreatitis, and a triglyceride level of 6,280 mg/dL indicated hypertriglyceridemia as a cause. Arterial blood gas measurements made at hospital admission while the patient was breathing 10 L of O2 via facemask revealed the following: pH, 7.24; Paco2, 30 mm Hg; Pao2, 173 mm Hg; and calculated HCO3 concentration, 13 mm/L. The anion gap was 20, and glucose concentration was 566 mg/dL. Urine was negative for ketones.
The patient received 17 L of IV fluid resuscitation in the first 20 h after hospital admission. At this time, the patient’s condition deteriorated relatively rapidly with a BP decline from 100/60 to 71/31 mm Hg despite titrating norepinephrine from 6 to 20 μg, as well as adding vasopressin and dobutamine to therapy. Concurrently, the ventilator fraction of inspired oxygen was increased from 60 to 100%, although oxygen saturation decreased from 100 to 70%. Peak airway pressure increased from 45 to 74 cm H2O, and bladder pressure transduced from the urinary catheter increased from 29 mm Hg at hospital admission to 54 mm Hg. A chest radiograph (Fig 1
) and an abdominal CT scan (Fig 2
) are shown.
Abdominal compartment syndrome (ACS) is best described as intraabdominal hypertension (IAH) impeding tissue perfusion and causing end-organ damage. A recent consensus conference defined IAH as an abdominal pressure (AP) of ≥ 12 mm Hg, and ACS as an AP of ≥ 20 mm Hg with evidence of organ failure. A study of a mixed population of critically ill patients found that the conditions of 32% of patients who had been admitted to the hospital for > 24 h over 4 weeks fit the definition of IAH (> 12 mm Hg) on hospital admission. ACS eventually developed in 13% of patients with IAH.
Among patients with acute pancreatitis, the incidence of IAH is as high as 78%. Our patient’s pancreatitis caused the massive release of proinflammatory cytokines into the retroperitoneum. The resulting systemic inflammatory response syndrome increases capillary fluid leak and edema formation in the mesentery and bowel wall, which leads to the increased AP. The rising AP expands the abdominal cavity, and the abdominal wall is compliant but only to a degree. Rising AP can have deleterious effects on multiple organ systems, which worsen when abdominal wall compliance reaches its maximum.
While fluid resuscitation is a standard treatment for acute pancreatitis, the fluid can exacerbate edema formation, raise AP, and contribute to IAH and ACS. Thus, acute pancreatitis presents a challenge in which hypovolemia management must be balanced against worsening the edema and contributing to IAH and ACS.
Pancreatitis or other inflammatory processes can cause IAH and ACS, but the majority of cases are from massive fluid resuscitation, trauma, abdominal surgery, and liver transplantation. In situations involving trauma or surgery, there is mesentery and bowel hypoperfusion, which leads to cell death, necrosis, and then inflammation. The inflammation contributes to edema and rising AP, and is exacerbated by fluid resuscitation. The organ system effects of ACS are discussed below.
Rising AP mechanically elevates the diaphragm and increases intrathoracic pressure. The compressed thoracic space increases peak airway pressure, which was evident in our patient. In addition, there is an increase in plateau pressure, and decreases in total lung capacity, residual volume, and functional residual capacity. The consequences of these mechanical events include atelectasis, edema, hypoxemia, and increased alveolar dead space. Chest radiographs demonstrate elevated hemidiaphragms, and blood gas levels often show hypoxemia and hypercapnia.
Diaphragmatic elevation and increased intrathoracic pressure can compress the heart, decreasing muscle compliance and contractility. Vena cava and portal vein flow can be impeded, reducing venous return and cardiac preload and output, and manifesting clinically as hypovolemic shock. Central venous pressure may overestimate intravascular volume due to the elevated measurements of intrathoracic pressures.
High AP can cause tissue hypoperfusion and ischemia throughout the bowel via direct compression of the mesenteric arteries, veins, and capillaries. The ischemia contributes to acidosis and breakdown of the intestinal epithelial barrier, leading to bacterial translocation.
ACS may cause acute renal failure via renal vein obstruction, which can manifest with decreased urine output and rising creatinine levels. The obstruction leads to decreased renal blood flow and glomerular filtration rate.
High intrathoracic pressures may compress the jugular veins, obstruct cerebral venous outflow, and increase intracranial pressure.
The “gold standard” for AP monitoring is direct transduction of a catheter into the peritoneal space. However, the risk of infection is high, and this method can be impractical in the critically ill. The most commonly used method is bladder pressure measurement, which correlates closely with AP when compared to other monitoring methods. Consensus meetings have established that AP should be measured via the bladder, with the patient supine and the transducer at the level of the mid-axillary line. In our patient, while the differential diagnosis for cardiopulmonary failure is broad, the increasing bladder pressure confirmed the development of ACS and that surgical intervention was required. A normal AP is near zero. A physical examination is inadequate for assessing or following AP.
ACS treatment involves emergent surgical decompression, and if performed in a timely matter, there is a reversal of end-organ damage. Even with laparotomy, outcomes are mixed, and the mortality rate approaches 50%. Intervening prior to the development of ACS has been suggested yet is controversial. However, most investigators agree that surgical decompression should occur with evidence of organ failure. In the setting of acute pancreatitis, because the massive release of proinflammatory cytokines triggers the cascade toward IAH and ACS, there have been reports successfully using hemofiltration to remove inflammatory cytokines, and also of using hemofiltration in combination with an indwelling catheter and other nonsurgical measures before there is progression to ACS.
In our patient, ACS was suspected given the increase in bladder and airway pressures, and the accompanying cardiopulmonary deterioration. The patient was sent for emergent laparotomy. On entering the abdomen, the pancreas, stomach, and small bowel were dusky in color and grossly ischemic; but, after decompression, normal coloration returned. Postoperatively, the abdomen remained open with resolution of hypotension (BP of 121/101 mm Hg without use of vasopressors), and decreased airway pressure (36 cm H2O) and bladder pressure (13 mm Hg). Figure 3
shows the dramatic improvement of the patient after surgery.
While IAH and ACS are frequently seen in cases of massive fluid resuscitation and trauma, there is a high incidence in acute pancreatitis. In patients with pancreatitis, the massive release of inflammatory cytokines causes systemic inflammatory response syndrome and edema formation that increases AP.
AP should be measured noninvasively via bladder pressure, and frequent monitoring is needed to detect IAH and ACS. A physical examination alone is insufficient.
The current treatment for ACS is urgent decompression, often with laparotomy. To avoid ACS in patients with pancreatitis, therapies involving hemofiltration are being explored.
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
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