Overall breakdown of the relation between intra-abdominal pressure (IAP) and renal function. The asterisk indicates that the relative risk of renal impairment is 2.32 (95% confidence interval, 1.45-3.72).
First day on which intra-abdominal hypertension (IAHT) occurred after abdominal surgery.
Sugrue M, Jones F, Deane SA, Bishop G, Bauman A, Hillman K. Intra-abdominal Hypertension Is an Independent Cause of Postoperative Renal Impairment. Arch Surg. 1999;134(10):1082–1085. doi:10.1001/archsurg.134.10.1082
Intra-abdominal hypertension exerts an effect on renal function independent of other confounding variables.
A prospective study of all patients admitted to an intensive care unit following abdominal surgery was undertaken between September 1, 1994, and July 31, 1997, in a single university hospital.
Main Outcome Measures
Intra-abdominal pressure (IAP) was measured every 8 hours (normal IAP, 0-17 mm Hg); 18 mm Hg or higher was considered increased. Forward stepwise logistic regression determined whether intra-abdominal hypertension is an independent cause of renal impairment.
A total of 263 patients (174 after emergency surgery), whose mean±SD age was 61.0±18.7 years and Acute Physiology and Chronic Health Evaluation II score was 14.6±7.7, were studied. Intra-abdominal pressure was increased in 107 (40.7%) of the 263 patients. Renal impairment occurred in 35 (32.7%) of the 107 patients with intra-abdominal hypertension and in 22 (14.1%) of the 156 with a normal IAP (odds ratio, 1.62-5.42). Using the Wald maximizing model, renal impairment was independently associated with 4 antecedent factors: hypotension (P=.09), sepsis (P=.006), age older than 60 years (P=.03), and increased IAP (P=.004).
To our knowledge, for the first time in a large clinical study, IAP has been shown to be an independent cause of renal impairment, and it ranks in importance after hypotension, sepsis, and age older than 60 years. Surgeons need to be aware of the importance of intra-abdominal hypertension in patients postoperatively.
INTRA-ABDOMINAL pressure (IAP) has become an important issue in the postoperative management of patients undergoing abdominal surgery.1,2 The importance of intra-abdominal hypertension (IAHT) has been heightened by its recognized association with the abdominal compartment syndrome.3,4 For more than a century, it has been recognized that increases in IAP are associated with renal impairment.5- 7 To our knowledge, an independent association between renal impairment and IAHT has not been shown previously. While we have previously reported that IAP was associated with a statistically increased odds ratio of developing renal impairment, we did not allow for potentially confounding coexisting predisposing factors for renal failure. Conclusions about the causal role of IAP in renal impairment could not be made from this and other studies.7,8
This article establishes whether IAHT is an independent causal factor for renal impairment in patients admitted to the intensive care unit (ICU) following abdominal surgery.
A prospective study of patients undergoing intraperitoneal abdominal surgery and admitted to the ICU of Liverpool Hospital, University Teaching Hospital, Sydney, Australia, was undertaken from September 1, 1994, to July 31, 1997. Patients transferred to the ICU from the ward or other hospitals, who had undergone abdominal surgery within the preceding 2 weeks, were also included. The study was approved by the South Western Sydney Area Health Service Ethics Committee. Patients who had abnormal renal function (serum creatinine level >130 µmol/L [>1.47 mg/dL]) on admission to the ICU were not included.
In addition to baseline information, the predominant cause of IAHT and the presence of preexisting conditions or factors known to promote renal impairment were noted daily.9 In determining the cause of IAHT, intra-abdominal sepsis was defined as the presence of organisms or greater than 3 polymorphonuclear leukocytes on Gram stain. The volume of blood and fluid in the peritoneal cavity was measured, and retroperitoneal hematomas were documented. Sterile fluid was classified as ascites. All patients were followed up daily until discharge from the hospital or death. Acute Physiology and Chronic Health Evaluation II scores were calculated on admission to the ICU.10 Renal impairment was defined as a postoperative serum creatinine level greater than 130 µmol/L (>1.47 mg/dL) or an increase in serum creatinine level greater than 100 µmol/L (>1.13 mg/dL) within 12 days of surgery.7 Intra-abdominal hypertension was chosen as an IAP of 18 mm Hg or higher, based on values used in 2 major previous studies.7,8 Oliguria was defined as less than 600 mL of urine excreted in a 24-hour period.11 Standard definitions for sepsis and hypovolemia were used.12 Hypotension was defined as a systolic blood pressure lower than 100 mm Hg or a reduction of greater than 40 mm Hg from the patient's baseline, if normally hypertensive. Intra-abdominal pressure was measured every 8 hours using a modification of the Kron technique.13
In evaluating whether IAHT may be an independent causal factor for renal impairment, the following factors were deemed important in testing the hypothesis. Is there evidence from human experiments? Does it make scientific sense? Is there a strong association consistent from study to study? Is the temporal relation right? Is there a dose-response relation and is it reversible? Is the association independent of other confounding factors?14 The management of IAHT was not part of this study.15 Standard mortality rates (SMRs) were reported using the observed to expected death rates based on Acute Physiology and Chronic Health Evaluation II norms.
Correlation coefficients were used to determine correlations between continuous variables. Logistic regression analysis was performed using a forced-entry model to determine the likelihood ratios. Forward stepwise logistic regression was used to evaluate the effect of each risk factor on the risk of renal impairment after adjustment for the other factor. Statistical significance was set at P=.01 for bivariate and χ2 analyses and at P=.05 for multivariate analysis. Values are reported as means and SDs.
Two hundred seventy-six patients admitted to the ICU following abdominal surgery were studied; 13 were excluded, 9 having developed renal impairment before documentation of increased IAP and 4 having had no IAP reading performed. The remaining 263 patients (156 men) were aged 61.0 ±18.7 years, and their Acute Physiology and Chronic Health Evaluation II score was 14.6±7.7 (range, 1-37). The predominant type of surgery undertaken in the study population of 263 was upper gastrointestinal tract (n=131), lower gastrointestinal tract (n=70), aortic vascular (n=57), and other (n=5). In 156 of the 263 patients, the surgery was emergency rather than elective. Of the 263 patients, 232 (88.2%) were enrolled into the study within 24 hours of surgery, 22 (8.4%) within 48 hours, and 9 (3.4%) after 48 hours. Figure 1 provides an overall breakdown of the distribution of IAP in the study group. Of the 263 patients, 107 (40.7%) had IAHT and 156 (59.3%) had a normal IAP. Of the 107 patients with IAHT, 35 (32.7%) developed renal impairment compared with 22 (14.1%) of the 156 with a normal IAP. The suspected predominant cause of IAHT was intra-abdominal sepsis (n=16), ileus or bowel obstruction (n=10), tissue edema (n=26), hemorrhage or hematoma (n=6), fluid collection or ascites (n=1), or a combination of factors (n=48). Most patients had a combination of reasons for elevated IAP, although tissue edema and sepsis were the most common single factors. The day on which IAHT occurred is shown in Figure 2.
The relation of IAP to the nature of primary surgery is shown in Table 1. An overview of the prevalence of risk factors for renal impairment in patients is shown in Table 2. According to bivariate analysis, IAP, sepsis, hypotension, preexisting hypertension, age older than 60 years, and aortic clamping are significantly associated with renal impairment. Multivariate analysis using a forced-entry logistic model is shown in Table 3. When using a forward stepwise model, renal impairment was significantly and independently associated with 4 factors: hypotension, sepsis, age older than 60 years, and increased IAP (≥18 mm Hg). The forward stepwise Wald maximizing model rated hypotension as most critical in the model followed by age older than 60 years, sepsis, and increased IAP, as judged by the level of significance.
Using Acute Physiology and Chronic Health Evaluation II norms, the observed-expected ratio for death in those with a normal IAP was 1:17 (SMR, 0.06) and 6:6 (SMR, 1.0) for the normal and abnormal renal function groups, respectively. Similarily, in those with IAHT, the SMR ratios were 2:16 (SMR, 0.13) and 19:15 (SMR, 1.3) for the normal and impaired renal function groups, respectively. Of the 35 patients with IAHT who experienced renal failure, the mean time to onset of IAHT and to renal impairment was 1.7±1.4 and 4.3±6.5 days, respectively. The mean lag time between onset of increased IAP and renal impairment was 2.7±6.5 days. The relation between renal impairment and the level of IAP is shown in Table 4. The prevalence of renal impairment increases significantly as the level of IAP increases.
This large prospective study has identified that IAP is an important independent cause of renal impairment in patients postoperatively. This is the first such study, to our knowledge, to report this independent relation; IAHT rated as the fourth most important causal factor of renal impairment in the patients postoperatively, after hypotension, sepsis, and age older than 60 years. While our previous study15 of 88 patients has shown a significant association between IAHT and renal impairment, the present study adjusted for other risk factors. The present study validated the prevalence of IAHT in patients who were admitted to the ICU after laparotomy, with IAHT occurring in 40.7% (107/263) of the patients. Ivatury and colleagues4 reported the incidence in excess of 50% in patients undergoing fascial closure.
The evidence that IAP is an independent causal factor in renal impairment is supported by the strong clinical association between IAHT and renal impairment. This association would appear to be consistent from study to study.3,6,16,17
The concept of increasing IAP exerting adverse renal effects is physiologically and scientifically acceptable. The actual mechanism remains uncertain.
Intra-abdominal hypertension is caused by multiple factors working in concert in the individual patient. We found a dominant cause in 57 of 107 patients but recognize that in the remainder the exact cause is not possible to define.
Initial reports3,7 of IAHT were often following aortic surgery with postoperative hemorrhage from the graft suture line. These patients may constitute a different subgroup from those with secondary and tertiary peritonitis, in whom tissue edema and intra-abdominal sepsis are the dominant cause of IAHT, rather than free intraperitoneal or retroperitoneal blood.
Our study supports the concept that renal impairment is dose related, with the incidence of renal impairment doubling once the pressure goes above 25 mm Hg. We chose 18 mm Hg as a cutoff based on previous studies7,8 but could have used 15 or 20 mm Hg. Others18 have suggested that 10 to 15 mm Hg is a critical value for IAP.
The most likely direct effect of IAHT is an increase in the renal vascular resistance coupled with a moderate reduction in cardiac output. Ulyatt19 suggested that the filtration gradient (FG) is a key to renal impairment in patients with IAHT. The FG is the mechanical force across the glomerulus and is equal to the difference between the glomerular filtration pressure and the proximal tubular pressure, thus FG=glomerular filtration pressure−proximal tubular pressure. Where IAP is elevated, proximal tubular pressure can be equated with IAP, and glomerular filtration pressure is estimated by the difference between mean arterial pressure and IAP. The FG can, therefore, be calculated by the following formula: FG=mean arterial pressure−(2×IAP). Therefore, changes in IAP will have a much greater effect on urine formation than the effect of a corresponding alteration in mean arterial pressure.19 Pressure on the ureter is not a key factor in renal impairment.20 Other potential factors include humeral factors, such as increased antidiuretic hormone levels, increased plasma renin and aldosterone activity,21,22 and increased catecholamine concentrations.23
It would make sense in high-risk patients to combine IAP monitoring with visceral perfusion monitoring and have a low threshold for considering abdominal decompression and temporary abdominal closure. The value of such approaches, while conceptually acceptable, is not supported by class 1 scientific evidence.24
Demonstration of a temporal relation between IAHT and renal impairment is a clinical challenge; also, increase in serum creatinine level occurs some time after the onset of renal dysfunction. Of the 35 patients who developed renal impairment in this study, there was a mean lag period between IAHT and renal impairment of 2.7 days (range, 0-35 days). The effect of IAHT on renal function would appear to be gradual rather than immediate.
This study did not attempt to answer the question of whether renal impairment caused by increasing IAP could be reversed by abdominal decompression and temporary abdominal closure. It has been claimed that abdominal decompression reverses the sequelae of IAHT. Recent work15 from our unit suggests that while patients undergoing abdominal decompression and temporary abdominal closure have a lower SMR than expected, it does not universally reverse renal failure.
In conclusion, this study demonstrated that IAHT exerts an effect on renal function independent of other confounding variables. The associated dysfunction usually occurs 1 to 2 days after the onset of IAHT. The importance of IAHT cannot be overemphasized, with up to 40% of patients experiencing pressures greater than 18 mm Hg.
Consideration to adopting a more routine approach to IAP measurement, every 8 hours in patients in the ICU, particularly those undergoing emergency surgery, should be undertaken. Perhaps IAP measurement should be undertaken in the operating room, at the end of abdominal closure, or in the recovery room.
The concept of nonclosure of the abdomen or early decompression should be considered a potential option. While this study has identified that IAHT independently affects renal function, many other systems are often affected and the increase in mortality is not just related to renal dysfunction.
Reprints: Michael Sugrue, FRCSI, FRACS, Department of Trauma, Liverpool Hospital, Elizabeth Street, Liverpool, Sydney 2170, Australia (firstname.lastname@example.org).