Abdominal Compartment Syndrome

Bendahan, Jose; Coetzee, C.J.; Papagianopoulos, Costas; Müller, Richard

doi:10.1097/00005373-199501000-00034

Cited by 50 publications

(15 citation statements)

References 16 publications

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“…Abdominal compartment syndrome became recognized as a cause of significant morbidity and mortality in the late 1980s, particularly in cases of trauma and vascular surgery [11,12]. Small increases in intraabdominal pressure can result in renal and respiratory failure, as well as impaired venous return.…”

Section: Discussionmentioning

confidence: 99%

Staged reduction of gastroschisis using preformed silos: practicalities and problems

Lansdale

Hill

Gull-Zamir³

et al. 2009

Journal of Pediatric Surgery

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Section: Discussionmentioning

confidence: 99%

Staged reduction of gastroschisis using preformed silos: practicalities and problems

Lansdale

Hill

Gull-Zamir³

et al. 2009

Journal of Pediatric Surgery

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“…Noradrenaline, endothelin-1, and angiotensin II are all vasoconstrictive agents. We do not know for sure, however, if the renal vasoconstriction that occurs under increased IAP is due to one or more of these hormones, or to other agents.Several studies [1,12,20] have shown that increased IAP results in reduced urinary output or anuria and that this condition can be reversed by abdominal decompression. The diuresis is regulated by several factors, such as renal blood flow, glomerular filtration rate, and reabsorption of sodium and water [11].…”

mentioning

confidence: 99%

“…Several studies [1,12,20] have shown that increased IAP results in reduced urinary output or anuria and that this condition can be reversed by abdominal decompression. The diuresis is regulated by several factors, such as renal blood flow, glomerular filtration rate, and reabsorption of sodium and water [11].…”

mentioning

confidence: 99%

Role of angiotensin II under prolonged increased intraabdominal pressure (IAP) in pigs

et al. 2003

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“…[1][2][3] The exact pressure thresholds that signify both intra-abdominal hypertension (IAH) and correlate with ACS are controversial. Its precise incidence in critically ill patients is also unclear, but most likely approximates 1% to 14% depending on the population.…”

Section: Discussionmentioning

confidence: 99%

Tertiary Abdominal Compartment Syndrome in the Burn Injured Patient

Ball

Kirkpatrick

Karmali

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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A bdominal compartment syndrome (ACS) has not been commonly reported in burn patients, although it is becoming more frequently recognized. We present a case of secondary ACS that was further complicated by an episode of tertiary ACS in a severely burned patient. CASE REPORTA previously healthy 42-year-old, 80-kg man presented to our regional trauma referral center with direct partial and full thickness flame burns covering 52% of his total body surface area (TBSA). The burns were located on his anterior thorax, abdomen, upper extremities, and buttocks.At presentation the patient was alert and normotensive, but tachycardic at 124 beats per minute. He displayed evidence of significant inhalational injury and was intubated. During the following 24 hours, the patient required vigorous fluid resuscitation with intravenous crystalloid (18.4 L) (4.42 mL/kg/% TBSA), packed red blood cells (8 units) and fresh frozen plasma (4 units) to maintain urine output, normalize his vital signs, and correct his anemia and coagulopathy.Within 12 hours of admission, the patient became profoundly hypoxemic and difficult to ventilate. His peak inspiratory pressures (PIP) rose to greater than 50 cm H 2 O. Initially this was thought to be a result of his constrictive thoracic burns. Escharotomies of his chest and abdomen, however, resulted in only transient improvements in oxygenation and airway pressures. His urine output subsequently decreased to less than 25 mL/hr (0.3 mL/kg/hr) and his intravesicular and pulmonary artery wedge (PAWP) pressures increased to 38 and 40 mm Hg, respectively. Secondary ACS was diagnosed and an urgent midline decompressive celiotomy, extending from the sternum to approximately 10 cm above the pubis, was performed. The viscera were edematous, but well perfused with no other pathology noted. Intraoperative monitoring included standard vital signs, central venous pressure, pH, lactate, base deficit, and urine output. The abdomen was left open, but temporarily sealed using a sterile clear X-ray cassette bag, which was cut to size and inserted (not sutured) deep into the surrounding fascia (Fig. 1). Two overlying Jackson-Pratt drains connected to low continuous suction were then placed along the fascial-plastic interface. This was followed by a large antimicrobial, adherent clear drape applied over the entire closure. Decompression resulted in remarkable improvements in oxygenation, urine output (125 mL/ hr), PIP (32 cm H 2 O), bladder pressure (12 mm Hg), and PAWP (16 mm Hg).During the following days the patient underwent excision of deep burns with split thickness skin grafting. On his third hospital day, he sustained a significant episode of hypovolemic shock after a difficult burn excision that required aggressive fluid resuscitation. A total of 22.9 L (5.50 mL/ kg/% TBSA) of crystalloid fluid had been infused since his decompressive celiotomy. Recurrent ACS was suggested by the onset of oliguria at 30 mL/hr (0.4 mL/kg/hr) and increased PIP (52 cm H 2 O), PAWP (26 mm Hg), and bladder pressure (29 mm Hg). Thes...

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Abdominal Compartment Syndrome

Cited by 50 publications

References 16 publications

Staged reduction of gastroschisis using preformed silos: practicalities and problems

Staged reduction of gastroschisis using preformed silos: practicalities and problems

Role of angiotensin II under prolonged increased intraabdominal pressure (IAP) in pigs

Tertiary Abdominal Compartment Syndrome in the Burn Injured Patient

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