Intraabdominal Pressure in Liver Transplant Recipients: Incidence and Clinical Significance G. Biancofiore, M.L. Bindi, A. Boldrini, G. Consani, M. Bisa`, M. Esposito, L. Urbani, G. Catalano, F. Filipponi, and F. Mosca ABSTRACT Background. The incidence and clinical relevance of increased intraabdominal pressure after orthotopic liver transplantation (OLT) has not yet been evaluated despite the finding that occurrence of this condition in postsurgical critically ill patients may impair various organ functions. The aim of this study was to assess whether the occurrence of abdominal hypertension among a population of OLT recipients was an important cofactor producing early postoperative complications. Method. This prospective clinical study measured abdominal pressure every 6 hours during the intensive care unit (ICU) stay using the urinary bladder method. A value of ⱖ25 mm Hg was considered high. Hemodynamic status was simultaneously evaluated and renal function assessed based on the hourly urinary output, and by calculating serum creatinine on postoperative days 2 and 4. Renal failure was defined as a serum creatinine level of ⬎1.5 mg/dL, or an increase in peak of ⬎1 mg/L within 72 hours of surgery. The filtration gradient and patient outcomes were also considered. Results. Intraabdominal hypertension was observed in 32% of cases. The subjects displaying high IAP showed significantly lower artery pressure values (P ⬍ .01), but did not differ in terms of central venous pressure or cardiac output. High intraabdominal pressure was more frequently associated with renal failure (P ⬍ .01), a lower filtration gradient (P ⬍ .001), delayed postsurgical weaning from the ventilation (P ⬍ .001), and increased ICU mortality (P ⬍ .05). A receiver operator characteristic curve analysis showed that the critical IAP values, namely those with the best sensitivity/specificity, were 23 mm Hg for postoperative ventilatory delayed weaning (P ⬍ .05), 24 mm Hg for renal dysfunction (P ⬍ .05), and 25 mm Hg for death (P ⬍ .01). Conclusions. Abdominal hypertension occurs frequently after OLT and may be associated with a complicated postoperative course.
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ONITORING intraabdominal pressure was first described in the 19th century.1 The effects of intraabdominal hypertension (IAH) have since been evaluated in a variety of clinical situations, including postsurgical patients. Patients undergoing orthotopic liver transplantation (OLT) are at risk of intraabdominal hypertension, not only due to the pathophysiology of their preoperative chronic liver disease but also because of the specific characteristics of the transplant procedure, which include frequent intraperitoneal hemorrhage (due to surgery or to coagulopathy), the use of perihepatic or retroperitoneal packs to control bleeding, bowel congestion due to portal hypertension, © 2004 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710 Transplantation Proceedings, 36, 547⫺549 (2004)
massive fluid administration, and the use of a pneumatic antishock garment. The aim of this prospective study was to evaluate whether abdominal hypertension affects the outcome of OLT recipients.
From the Post-surgical and Transplant ICU, Ospedale di Cisanello, Pisa, Italy (G.B., M.L.B., A.B., G.C., M.B., M.E.); and General and Transplantation Surgery, University School of Medicine, Ospedale di Cisanello, Pisa, Italy (L.U., G.Ca., F.F., F.M.). Address reprint requests to Dr Gianni Biancofiore, UTI Trapianti, Ospedale Cisanello, Via Paradisa 2, 56100 Pisa, Italy. E-mail:
[email protected] 0041-1345/04/$–see front matter doi:10.1016/j.transproceed.2004.02.029 547
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METHODS The study involved 108 consecutive OLT recipients. The only exclusion criterion was preoperative renal dysfunction, which was defined as a serum creatinine level of ⬎1.5 mg/dL. Intraabdominal pressure was measured every 6 hours for at least the first 72 hours after surgery, using the urinary bladder technique.1 Values were considered high at ⱖ25 mm Hg. Hemodynamic measurements, including mean arterial pressure (MAP), central venous pressure, pulmonary artery occluded pressure, and cardiac output, were obtained at the same times. As previously proposed for postsurgical patients, renal function was evaluated on the basis of daily urinary output per hour, and by calculating serum creatinine levels on the second and fourth postoperative days. Acute renal failure was defined as postoperative serum creatinine levels of ⬎1.5 mg/dL or an increase in peak serum creatinine of ⬎1.1 mg/L within 72 hours of surgery. We monitored the filtration gradient (FG), which can be assumed to correspond to the mechanical force across the glomerulus. It was calculated at the patient’s bedside as FG ⫽ MAP (2 ⫻ intraabdominal pressure). The quality of graft function was assessed 7 days after the procedure based upon the aPTT ratio and the incidence of primary graft dysfunction (as judged by the chief surgeon) using standard definitions. After completing the study, patients were divided into two groups: those with at least two consecutive high abdominal pressure measurements (group H), and those with normal or only sporadically high measurements (group N). In fact, it has been reported that the detrimental effects of intraabdominal hypertension occur long before its clinical manifestations. Therefore, the duration of abdominal hypertension, and not just its absolute value, may be a key factor.1
Statistical Analysis The data were analyzed with the Statistical Packages for Social Sciences software (SPSS, Inc., Chicago, Ill) using Student’s t test, the Mann–Whitney U test for nonparametric data (corrected using Bonferroni adjustment), and the Pearson’s chi-square test, as appropriate. Receiver operator characteristic (ROC) curve analysis was used to identify the critical abdominal pressure for respiratory failure, renal failure, and death, and forward stepwise logistic regression analysis was used to evaluate the effects of individual risk factors on renal function. P ⱕ .05 was considered statistically significant.
RESULTS
Thirty-four patients (32%) displayed at least two consecutive high measurements (group H), and 74 (68%) normal or sporadically high abdominal pressure (group N). Although the pressure decreased progressively in both groups, it was always significantly greater in group H (P ⬍ .001 on the operative day and P ⬍ 0.01 on the following 2 days). The monitored hemodynamic parameters generally remained stable. Only the mean artery pressure was consistently higher among group N (P ⬍ .05). Eleven (32%) group H and six (8%) group N patients developed renal failure (P ⬍ .001) with continuous renal replacement therapy required in three of the former (9%) and none of the latter (P ⬍ .01). The subjects without renal impairment had a median intraabdominal pressure (percentiles 25 to 75) of 19 mm Hg (16 to 24), whereas it was 27 mm Hg (20 to 36) among those who developed renal failure (P ⬍ .0001). Intraabdominal
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hypertension was associated with a 9.8 relative risk for acute renal failure, which was higher than the risk associated with sepsis, respiratory failure, congestive cardiac failure, relaparotomy, abdominal pack placement, or high intraoperative blood transfusion. A forward stepwise regression model showed that renal impairment correlated independently with ⬎15 units of intraoperative transfusion, with respiratory failure, and with abdominal hypertension (P ⬍ .01). None of the subjects in group N who showed sporadically elevated intraabdominal pressures experienced acute renal failure. All patients in the group showed significantly higher filtration gradients than those in group H (P ⬍ .001 on the first 2 days, and P ⬍ .01 on the third). Median serum creatinine (percentiles 25 to 75) on postoperative day 2 was 0.9 mg/dL (0.6 to 1.8) in group H and 0.7 mg/dL (0.6 to 0.9) in group N (P ⬍ .01), and 1.1 (0.7 to 2.2) and 0.8 (0.6 to 1) on day 4, respectively (P ⬍ .01). Hourly urine output was similar in the two groups (99 ⫾ 39.5 mL vs 112 ⫾ 51.9 mL; P ⫽ .2), but administration of either low (ⱕ100 mg/d) or high (ⱖ100 mg/d) doses of furosemide was more frequently required by group H patients to maintain adequate urine output (P ⬍ .001 for low doses, and P ⬍ .05 for high doses). There was no difference in the incidence of primary graft dysfunction at 7 days after OLT, but hepatic function, as assessed by the aPTT ratio, was better among group N (P ⬍ .05). The mean duration of postoperative ICU stay was not different between the two groups, but the patients with intraabdominal hypertension showed a lower PaO2/FiO2 ratio (164 vs 271; P ⬍ .05) before weaning from mechanical ventilation, less frequent rapid postoperative extubation (58.8% vs 86.4%; P ⬍ .001), and higher mortality (P ⬍ .05). ROC curve analysis showed that the critical values, namely those with the best sensitivity/specificity, were 23 mm Hg for respiratory failure (P ⬍ .05), 24 mm Hg for renal failure (P ⬍ .05), and 25 mm Hg for death (P ⬍ .01). DISCUSSION
Because the abdominal cavity is a limited space that can be considered a single compartment, any variation in its content increases its pressure, which, in spontaneously breathing normal subjects, is between 0 and 5 mm Hg.1 It has been suggested that loading patients with intravenous fluids may prevent the deleterious effects of intraabdominal hypertension,2 because it counteracts the reduced cardiac output caused by the diminished preload due to hampered venous return to the heart by compression of the inferior and superior venacava compartments.1 Our experience indicates that that this therapeutic approach can successfully keep the hemodynamic parameters of OLT recipients stable, but does not necessarily prevent the onset of renal dysfunction. Local factors1,3 may play a major role in determining renal failure in the presence of intraabdominal hypertension shunting of blood from the cortex to the medulla; direct compression of kidney and renal veins; high renal venous pressure; and high levels of antidiuretic hor-
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mone, renin, and aldosterone. In contrast, urethral compression does not seem to be important.1 In this setting, mean arterial pressure and cardiac performance are better indicators of the need for fluid treatment, because central venous pressure may be misleading, because it has been reported that a high abdominal pressure may affect thoracic pressure through the diaphragm,3 which means that central venous pressure may be spuriously high even in the presence of a reduced total intravascular volume.3 The fact that renal impairment was observed only in recipients with prolonged intraabdominal hypertension, namely at least two consecutive measurements, and not among those with only sporadically high values seems to confirm that the duration of the condition (and not just the absolute IAP value) may play a major role in kidney dysfunction akin to the way that nerve and muscle ischemia begins long before the neuromuscular signs of extremity compartment syndrome. Among the two groups, abdominal hypertension was associated with a need for longer artificial ventilation; there was also a difference in the PaO2/FiO2 ratio before weaning. This may have been due to the deleterious effects of intraabdominal hypertension on the respiratory system, as it has been observed that high pressure may lead to reduced static and dynamic pulmonary compliance, because of the increased intrathoracic pressure caused by the increased abdominal pressure.1,4 High intraabdominal pressure can also reduce total lung capacity, residual functional capacity, and residual volume,4 all of which give rise to ventilation/perfusion anomalies and hypoventilation, with consequent hypoxia and hypercapnia.1 Although there was
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no significant difference in the mean duration of ICU stay between patients with versus without intraabdominal hypertension, graft function assessed by the aPPT at 7 days after the procedure was better among the latter, who also showed a lower mortality rate. In conclusion, our results suggest that intraabdominal hypertension is a frequent finding after OLT. Administration of fluids and optimizing cardiac function are not sufficient to prevent renal failure. Serial monitoring of the filtration gradient may help to ensure timely identification of patients at greater risk of developing postoperative acute renal failure. Routine intraabdominal pressure monitoring should be considered for the management of OLT patients during the postoperative period, because it may help to identify basic physiologic changes. Nevertheless, our study has not provided conclusive evidence as to whether increased intraabdominal pressure is mainly a severity marker that is a consequence of a more complicated postsurgical condition, or a “disease” in itself. REFERENCES 1. Saggi BH, Sugermann HJ, Ivatury RR, et al: Abdominal compartment syndrome. J Trauma 45:597, 1998 2. Meldrum DR, Moore FA, Moore EE, et al: Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 174:667, 1997 3. Ivatury RR, Diebel L, Porter JM, et al: Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin N Am 77:783, 1997 4. Ridings PC, Bloomfield GL, Blocher CR, et al: Cardiopulmonary effects of raised intraabdominal pressure before and after intravascular volume expansion. J Trauma 39:1071, 1995
