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1996 ACS Article Abstracts

Bloomfield, G. L., P. C. Ridings, et al. (1996). "Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion." J Trauma 40(6): 936-41; discussion 941-3.

OBJECTIVE: To study the effects of elevated intra-abdominal pressure (IAP) upon intracranial (ICP) and cerebral perfusion pressure (CPP) before and after intravascular volume resuscitation. MATERIALS AND METHODS: Intra-abdominal pressure was increased in five anesthetized swine by inflating an intraperitoneal balloon until the IAP was 25 mm Hg above baseline. Intravascular volume was then expanded and finally abdominal decompression was performed. Changes in ICP and systemic and pulmonary hemodynamic parameters secondary to increasing IAP were measured. The effect upon CPP was derived from these measurements. PaO2 and PaCO2 were maintained relatively constant by increasing ventilatory rate. MEASUREMENTS AND MAIN RESULTS: Elevated IAP significantly increased ICP (7.6 +/- 1.2 vs. 21.4 +/- 1.0), pleural pressure and central venous pressure; whereas cardiac index and CPP (82.2 +/- 6.3 vs. 62.0 +/- 10.0) decreased significantly. Intravascular volume expansion further significantly increased ICP (27.8 +/- 1.0), and significantly increased both mean arterial pressure (83.4 +/- 14.0 versus 103.4 +/- 8.9) and CPP (75.6 +/- 9.0). Abdominal decompression returned ICP (11.2 +/- 1.8) toward baseline and further increased CPP (79.8 +/- 9.7). CONCLUSIONS: Elevated IAP increases ICP and decreases CPP and cardiac index. Volume expansion further increases ICP yet improves CPP via its greater positive effect upon mean arterial pressure (*p < 0.05, analysis of variance. All measurements are mean +/- SEM in mm Hg).

Burch, J. M., E. E. Moore, et al. (1996). "The abdominal compartment syndrome." Surg Clin North Am 76(4): 833-42.
1. ACS is caused by an acute increase in intra-abdominal pressure, usually as a result of intra-abdominal hemorrhage. 2. The most common and significant complications are respiratory and renal failure. 3. Abdominal decompression promptly reverses the complications of ACS. 4. Failure to recognize and treat ACS is inevitably fatal.

Hopgood, P., P. Moody, et al. (1996). "The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure." J Am Coll Surg 183(4): 420-2.

MacDonnell, S. P., O. A. Lalude, et al. (1996). "The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure." J Am Coll Surg 183(4): 419-20.

Rizzo, A., P. C. Davis, et al. (1996). "Intraoperative vesical pressure measurements as a guide in the closure of abdominal wall defects." Am Surg 62(3): 192-6.
Increased intra-abdominal pressure represents a difficult problem when closing abdominal wall defects (AWD) and can cause renal insufficiency and vascular injury to the intestine with the development of necrotizing enterocolitis. Urinary bladder pressure measurements have been shown to accurately reflect intra-abdominal pressure in animal models. This study compares outcomes with and without vesical pressure measurements in AWD. Since its description in 1987, these vesical pressure measurements have guided the closure of AWDs. A pressure of <20 cm H2O allows closure by primary fascial, skin, or staged prosthetic closure. All charts of patients who underwent AWD closure from 1981 to 1993 were reviewed and data collected including type of defect and closure, gestational age, weight, age at operation, fluid requirements and urinary outputs, ventilator requirements, days to first and total feeding, total parenteral nutrition (TPN) days, hospital days, hospital charges, morbidity, and mortality. Results were analyzed by paired or unpaired Student's t test or Fisher's exact test. Twenty-seven infants did not receive vesical pressure measurements, whereas 13 did. No significant differences occurred in the parameters recorded in these two diverse groups. When gastroschisis patients only were compared, a significant decrease in intravenous fluid requirements in the vesical measurement group occurred on postoperative Day 2 (155.3+/- 37.5 versus 109.6 +/- 34.3; P = 0.016), and a significant decrease in urinary output occurred on postoperative Day 3 (4.2 +/- 112 versus 3.1+/- 1.1; P=0.044). Ventilator support, TPN days, and oral feeding data were all lower in the vesical measurement group but did not reach statistical significance. Hospital days and hospital changes showed a trend to lower values in the measured group (P values 0.052 and 0.095, respectively). Intraoperative vesical pressure measurements represent a simple, safe, effective method to guide the closing of AWD and result in less capillary leak and more prompt diuresis, and may result in significantly less morbidity, mortality, and cost.


Sugrue, M., F. Jones, et al. (1996). "Intraabdominal pressure and gastric intramucosal pH: is there an association?" World J Surg 20(8): 988-91.
This study evaluated the potential association between increased intraabdominal pressure (IAP) and abnormally low gastric intramucosal pH (pHi) (/= 20 mmHg and a pHi of

Yazigi, A., F. Richa, et al. (1996). "[Comparative measurement of pressure in the abdominal inferior vena cava and in the superior vena cava in adults]." Ann Fr Anesth Reanim 15(5): 681-2.
Abdominal inferior vena cava pressure was compared to intrathoracic central venous pressure in 30 adults admitted in an intensive care unit following coronary artery bypass grafting. Mean pressures were obtained during controlled ventilation with a positive end expiratory pressure (PEEP) of zero and 10 cmH2O respectively, and during spontaneous breathing as well. Ninety measurements were obtained. Limits of agreement between intra-abdominal and intrathoracic cava pressures were below 2.5 mmHg in all cases. In this study, inferior vena cava pressure has predicted central venous pressure in adults during both controlled and spontaneous ventilation.