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ORIGINAL RESEARCH |
From the Department of Obstetrics and Gynecologic, Lis Maternity Hospital, Tel-Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Address reprint requests to: Sharon Maslovitz, MD, Department of Obstetrics and Gynecology, Lis Maternity Hospital, Tel Aviv Sourasky Medical Center, 6 Weitzman Street, Tel-Aviv 64239, Israel; e-mail: orshma{at}hotmail.co.il.
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ABSTRACT |
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METHODS: We conducted an interventional clinical study of 19 women with severe ovarian hyperstimulation syndrome, manifested by free peritoneal fluid. The subjects were evaluated before and after therapeutic paracentesis by measuring urine output, blood urea nitrogen, intra-abdominal pressure, and renal artery flow measures by Doppler ultrasonography (systolic/diastolic ratio [S/D] and resistance index).
RESULTS: An average of 3,340 mL of ascitic fluid was drained, and the intra-abdominal pressure decreased from 17.5 ± 1.24 cm H2O to 10 ± 1.22 cm H2O. Urine output was increased (by 65%, from 925 ± 248 mL/d before paracentesis to 1,523 ± 526 mL/d on the day after paracentesis, P < .001). The mean renal arterial S/D decreased from 3 ± 0.15 to 2.29 ± 0.13 (P = .001). Most of the decrease in intra-abdominal pressure as well as in renal vasculature resistance was apparent after an initial drainage of 2,000 mL. Additional fluid drainage had only negligible effect on intra-abdominal pressure and renal flow.
CONCLUSION: Paracentesis lowered intra-abdominal pressure and decreased renal arterial resistance (lowered S/D and resistance index), ultimately resulting in increased urine production. It is plausible that the beneficial effects of paracentesis on urine output in ovarian hyperstimulation syndrome are due to improved renal blood flow from a direct decompression effect.
LEVEL OF EVIDENCE: II-3
The management of ovarian hyperstimulation reflects its self-resolving nature and focuses on supportive measures aimed at minimizing the emergence of complications and relieving patients’ discomfort.6 Levin et al7 and others5,6,8,9 studied the beneficial effect of abdominal fluid removal by paracentesis on urinary output and concluded that paracentesis increases urinary output and reduces blood urea nitrogen concentration in women with severe ovarian hyperstimulation syndrome. The mechanism by which paracentesis exerts its effect is still obscure, although 2 possible theories are suggested: One is that of the direct decompression effect, which implies reduced intra-abdominal pressure and thereby enhanced splanchnic perfusion, including renal artery flow, consequently leading to augmented urine production. The other theory relates to the removal of harmful mediators from the peritoneal cavity, thus reversing the pathophysiology of the disease and leading to a cascade that culminates in improved hemodynamic status and urine production. Although both theories are plausible, there is no hard evidence to support or refute either of them.
Assessment of Doppler ultrasound measures such as systolic/diastolic ratio (S/D) and resistance index before and after paracentesis of ascitic fluid may demonstrate alterations in renal arterial flow,10 which are temporarily associated with reduced intra-abdominal pressure. The combination of an untested theory of renal blood flow changes increasing urine production and a readily available tool of assessing these alterations motivated us to conduct a study aimed at evaluating renal arterial Doppler flow indices concurrently with the removal of free peritoneal fluid in patients with severe ovarian hyperstimulation syndrome to evaluate the validity of the direct decompression theory.
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METHODS |
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Excluded from the study were 2 women who could not tolerate the procedure due to pain that necessitated its discontinuation after the removal of only 1,200 mL in one case and 1,900 mL in the other. We also excluded 3 women who had been treated with diuretics and albumin before initial aspiration to avoid any bias originating from variations in treatment regimens. Seventeen women (89%) required repeated aspirations due to reaccumulation of free peritoneal fluid, but only data from the first aspiration in the course of the disease were included in the final analysis of results. Data from reaspirations were excluded because women requiring repeated drainage uniformly needed a modification of their treatment with the addition of albumin, starch, or a diuretic. These treatment modifications may by themselves affect urine production and may interfere with evaluation of the isolated effect of paracentesis on this measure.
After at least 1 day of hospitalization, during which hemodynamic and urinary function data were gathered, all suitable candidates for initial therapeutic paracentesis were referred to the ultrasound unit for further evaluation and aspiration. Before the puncture, a trained ultrasonographist (A.J.) assessed the renal arterial flow by Doppler wave indices taken at both renal hili. Paracentesis was performed and intraperitoneal pressure was measured using a needle connected to a water column system similar to that used for central venous pressure measurements (expressed in cm H2O). Repeated measurements were done after 2,000 mL had been removed, at conclusion of the procedure (ie, when no additional fluid could be drained) and 2 hours later.
Blood sample analyses that included complete blood count, electrolyte levels, and renal function tests (blood urea nitrogen [BUN] and creatinine) were done before the aspiration and were repeated on the day after and on alternating days until discharge, as is routine procedure in our department. Daily urinary output was measured by urinometer, and fluid balance was carefully monitored and recorded.
We compared the values of renal function tests and urine output before and after removal of ascitic fluid. We also evaluated the simultaneous alteration in renal artery flow indices and intra-abdominal pressure to assess whether the increase in urine output that had been previously observed after paracentesis was reflected in a concurrent decreased renal resistance to flow and intra-abdominal pressure.
Due to sample size and lack of demonstrated normality of differences, the nonparametric Wilcoxon matched-pairs signed rank test was used. All statistics were done using SPSS for Windows 11 (SPSS Inc., Chicago, IL). A P value of less than .05 was considered statistically significant.
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RESULTS |
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The mean blood pressure levels measured before and immediately after the procedure were 108 ± 18 mm Hg and 110 ± 15 mm Hg, respectively (P > .05). The mean heart rate remained unaltered as well (approximately 90 beats per minute). On average, the drainage procedure lasted 1.8 hours, during which 3,340 ± 547 mL (range 2,500–4,500 mL) of ascitic fluid were drained. The intra-abdominal pressure measured at puncture was 17.5 cm H2O and it decreased to 10 cm H2O at the conclusion of drainage (P = .001). As shown in Table 1, there was reduced renal artery resistance to flow (expressed by a lower S/D and resistance index) at the conclusion of paracentesis, followed by a marked increase (65%) in urinary output on the subsequent day. No latency period was observed between peritoneal fluid drainage and S/D decrements, and moreover, the S/D remained unaltered at 2 hours and 24 hours after the conclusion of the procedure. There were no significant S/D differences between the left and right kidneys.
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Most of the decline in intra-abdominal pressure, renal artery S/D, and resistance index were observed after draining the first 2,000 mL (the mean intra-abdominal pressure decreased to 11 ± 1.18 cm H2O, P < .01; mean S/D was 2.43 ± 0.12, P < .01). Additional drainage had only negligible effect on both intra-abdominal pressure and S/D (10 cm H2O, P = .09, and 2.29 ± 0.11, P = .1, respectively, at the end of aspiration). As depicted in Figure 1, the curves for intra-abdominal pressure and S/D as a function of the amount of fluid drained nearly overlapped.
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Reaspirations were indicated for reasons other than poor urine production (mainly due to abdominal discomfort accompanying reaccumulation of free peritoneal fluid). Reaspirations were done 3.1 days after the initial drainage and drained less volume as compared with the initial aspiration (2,245 mL compared with 3,520 mL, P < .001). The intra-abdominal pressure measured at the time of repeated aspirations was significantly lower than that measured at the beginning of the initial drainage and averaged 11.8 ± 1.4 cm H2O (P < .001) but was not statistically different from that measured at the conclusion of the initial procedure (P = .09).
Although BUN levels declined after paracentesis, this effect cannot be attributed to increased urine output, because drainage of peritoneal fluid by itself lowers BUN.11 The differences in creatinine and hematocrit levels failed to reach levels of statistical significance.
Five women in our study group were oliguric, defined as daily urine production of less than 500 mL or less than 30 mL/h. Initial intra-abdominal pressure measured before drainage was 17.8 cm H20 (similar to nonoliguric women, P = .21), and decreased to 10.3 cm H20. The mean urine output increased from 21.8 mL/h before aspiration to 48 mL/h (1,152 mL daily) on the day after the procedure. The marked beneficial effect of paracentesis on urine production among that group persisted, with all 5 patients becoming nonoliguric during the day after the procedure and remaining so until discharge. A mean daily urine output of 1,530 mL was measured on discharge day (nearly 3 times the value upon admission).
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DISCUSSION |
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The beneficial effect of paracentesis in ovarian hyperstimulation syndrome was suggested in several reports4,6,17 and confirmed by Levin et al.7 Paracentesis is indicated for tight ascites, deteriorating kidney functions, and symptomatic relief18 and may improve urinary output and creatinine clearance and lead to a decrease in hematocrit, blood osmolarity, and weight.6 Aboulghar et al9 reported decreased hematocrit (by 22%), enhanced creatinine clearance (79.3%), and improved urine output (220.7%) after ascitic fluid aspiration in women with ovarian hyperstimulation syndrome.
Despite the almost undisputed recognition of the advantageous effect of ascitic fluid removal in patients with severe ovarian hyperstimulation syndrome, the mechanism by which paracentesis exerts its action is yet to be elucidated. The most appealing theory centers upon the reduction of intra-abdominal pressure and augmented renal perfusion consequent to a direct decompression effect. Although a few studies indirectly addressed the issue of mechanical decompression, hard evidence for supporting the centrality of this mechanism in alleviating poor urine production among women with ovarian hyperstimulation syndrome is lacking. An alternative theory relates to the removal of harmful mediators, mainly vascular endothelial growth factor, interleukin-2, and interleukin-6, which are abundant in the aspirate. The clearance of such mediators may reverse the pathophysiology of the disease through a cascade culminating in reduced endothelial hyperpermeability and improved hemodynamic status. Although both theories are plausible, there is no hard evidence to support or refute either of them.
Caldwell and Ricotta19 showed that an elevated intra-abdominal pressure compromised the visceral blood flow of several organs including the kidneys, and Cabrera et al20 used a specially designed pneumatic girdle to compress the abdomen to avoid a decrease in intra-abdominal pressure during ascites removal and showed that early hemodynamic changes after paracentesis are prevented if intra-abdominal pressure is maintained at its original level by the inflated girdle. This latter finding is not consistent with the removal of harmful mediators as an explanation for hemodynamic improvement after paracentesis.
Normal values for intra-abdominal pressure vary according to the method of assessment, but it is generally agreed that values from –2 cm H20 to 5 cm H20 are normal.21 We measured a decrement in the intra-abdominal pressure level from 17.5 cm H20 to 10 cm H20, in concordance with earlier publications on ascites decompression in cirrhotic patients.22,23 The impact of this decompression on urine output was already evident by the first day after paracentesis, with the measured urine output having been markedly increased (by 65%), thus supporting the findings of earlier reports.4,6,7,16 We attributed the observed augmentation of urine production to the beneficial effects of paracentesis, because no other treatment modality was implemented.
There are no established, clear-cut, normal values for renal arterial S/D in nonpregnant individuals, although Levine et al24 found that the mean (± standard deviation) values were 2.5 ± 0.20 and 2.6 ± 0.21 for the left and right sides, respectively, in pregnant and nonpregnant subjects. In our current study, the S/D for both kidneys decreased from a value of 3 before intervention to 2.29 immediately after fluid removal. Normal values of the resistance index in nonpregnant are reported to be in the range of 0.58–0.62.25,26 We found higher preprocedure resistance index values (mean 0.67, range 0.64–0.71) in our study group, essentially showing the same trend as the S/D and decreasing from 0.67 to 0.56 instantaneously with decompression.
The curves for intra-abdominal pressure and S/D as a function of the amount of fluid drained almost overlapped. The decrement in both measures was most marked during the drainage of the first 2 L, and then both curves flattened as additional drainage had a minor effect on intra-abdominal pressure. Moreover, there was no latency period between peritoneal decompression and lowered resistance to flow within the renal vasculature, an observation which further supports a direct, causal relationship between decompression and renal flow rather than a cascade of processes reversing the pathophysiology and culminating in increased urine production. Additional volume removal after the first 2,000 mL had negligible effect on renal blood flow, but it may be important in deferring recurrence of symptoms. This issue could not be assessed properly in our population due to the small numbers of patients.
The subgroup composed of oliguric women had a marked increase of urine production on the day after paracentesis (220%) and even nearly tripled their urine output on the day of discharge. The intra-abdominal pressure was not higher among this subgroup, and furthermore, intra-abdominal pressure decrements were not more pronounced nor were volumes of aspirates. This observation is plausible considering the multiple determinants of hemodynamic status in such severely compromised patients, with intra-abdominal pressure being only one component of the whole milieu. Our results reconfirm the marked advantageous effects of paracentesis in oliguric patients and advocate its use in such population.
In conclusion, we demonstrated a temporal and possibly causal relationship between ascites decompression in ovarian hyperstimulation syndrome and instantaneously improved renal blood flow. Despite the lack of decisive and unequivocal evidence regarding the direct decompression effect of paracentesis on renal blood flow, it is improbable that many steps exist between them, because there is no latency period, and the curves for both measures as a function of volume of aspirate overlapped. We suggest that the beneficial effect of paracentesis on urine production in ovarian hyperstimulation syndrome is attributable to improved renal blood flow subsequent to immediate decompression.
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Footnotes |
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10.1097/01.AOG.0000129956.97012.0d
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REFERENCES |
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2. Wang TH, Horng SG, Chang CL, Wu HM, Tsai YJ, Wang HS, et al. Human chorionic gonadotropin-induced ovarian hyperstimulation syndrome is associated with up-regulation of vascular endothelial growth factor. J Clin Endocrinol Metab 2002;87:3300–8.
3. Rizk B, Aboulghar M, Smitz J, Ron-El R. The role of vascular endothelial growth factor and interleukins in the pathogenesis of severe ovarian hyperstimulation syndrome. Hum Reprod Update 1997;3:255–66.
4. Delvigne A, Rozenberg S. Review of clinical course and treatment of ovarian hyperstimulation syndrome (OHSS). Hum Reprod Update 2003;9:77–96.
5. Al-Ramahi M, Leader A, Claman P, Spence J. A novel approach to the treatment of ascites associated with ovarian hyperstimulation syndrome. Hum Reprod 1997;12:2614–6.
6. Borenstein R, Elhalah U, Lunenfeld B, Schwartz ZS. Severe ovarian hyperstimulation syndrome: a reevaluated therapeutic approach. Fertil Steril 1989;51:791–5.[Medline]
7. Levin I, Almog B, Avni A, Baram A, Lessing JB, Gamzu R. Effect of paracentesis of ascitic fluids on urinary output and blood indices in patients with severe ovarian hyperstimulation syndrome. Fertil Steril 2002;77:986–8.[Medline]
8. Thaler I, Yoffe N, Kaftory JK, Brandes JM. Treatment of ovarian hyperstimulation syndrome: the physiologic basis for a modified approach. Fertil Steril 1981;36:110–3.[Medline]
9. Aboulghar MA, Mansour RT, Serour GI, Sattar MA, Amin YM, Elattar I. Management of severe ovarian hyperstimulation syndrome by ascitic fluid aspiration and intensive intravenous fluid therapy. Obstet Gynecol 1993;81:108–11.
10. Yura T, Yuasa S, Fukunaga M, Badr KF, Matsuo H. Role for Doppler ultrasound in the assessment of renal circulation: effects of dopamine and dobutamine on renal hemodynamics in humans. Nephron 1995;71:168–75.[Medline]
11. Chen TW, Huang TP, Liu MC, Wang ML. The removal index for evaluation of dialysis. Perit Dial Int 1996;16:128–34.
12. Guazzi M, Polese A, Magrini F, Fiorentini C, Olivari MT. Negative influences of ascites on the cardiac function of cirrhotic patients. Am J Med 1975;59:165–70.[Medline]
13. Gines P, Arroyo V. Paracentesis in the management of cirrhotic ascites. J Hepatol 1993;17(suppl):14–8.
14. Luca A, Feu F, Garcia-Pagan JC, Jimenez W, Arroyo V, Bosch J, et al. Favorable effects of total paracentesis on splanchnic hemodynamics in cirrhotic patients with tense ascites. Hepatology 1994;20:30–3.[Medline]
15. Wang SS, Lu CW, Chao Y, Lee FY, Chen TW, Lin HC, et al. Total paracentesis in non-alcoholic cirrhotics with massive ascites: mid-term effects on systemic and hepatic haemodynamics and renal function. J Gastroenterol Hepatol 1994;9:592–6.[Medline]
16. Cade R, Wagemaker H, Vogel S, Mars D, Hood-Lewis D, Privette M, et al. Hepatorenal syndrome: studies of the effect of vascular volume and intraperitoneal pressure on renal and hepatic function. Am J Med 1987;82:427–38.[Medline]
17. Chen CD, Yang JH, Chao KH, Chen SU, Ho HN, Yang YS. Effects of repeated abdominal paracentesis on uterine and intraovarian haemodynamics and pregnancy outcome in severe ovarian hyperstimulation syndrome. Hum Reprod 1998;13:2077–81.
18. Navot D, Bergh PA, Laufer N. Ovarian hyperstimulation syndrome in novel reproductive technologies: prevention and treatment. Fertil Steril 1992;58:249–61.[Medline]
19. Caldwell CB, Ricotta JJ. Changes in visceral blood flow with elevated intraabdominal pressure. J Surg Res 1987;43:14–20.[Medline]
20. Cabrera J, Falcon L, Gorriz E, Pardo MD, Granados R, Quinones A, et al. Abdominal decompression plays a major role in early postparacentesis haemodynamic changes in cirrhotic patients with tense ascites. Gut 2001;48:384–9.
21. Aspesi M, Gamberoni C, Severgnini P, Colombo G, Chiumello D, Minoja G, et al. The abdominal compartment syndrome: clinical relevance. Minerva Anesthesiol 2002;68:138–46.
22. Cleva Rd R, Silva FP, Zilberstein B, Machado DJ. Acute renal failure due to abdominal compartment syndrome: report on four cases and literature review. Rev Hosp Clin Fac Med Sao Paulo 2001;56:123–30.[Medline]
23. Milani A, Ciammella AM, Rossi L. The intraabdominal pressure in decompensated cirrhosis: relationship with ascites volume and turn-over. Z Gastroenterol 1994;32:393–5.[Medline]
24. Levine AB, Lockwood CJ, Chitkara U, Berkowitz RL. Maternal renal artery Doppler velocimetry in normotensive pregnancies and pregnancies complicated by hypertensive disorders. Obstet Gynecol 1992;79:264–7.
25. Zimmermann P, Ranta T. Doppler assessment of the maternal interlobar renal and uterine arteries in mid-pregnancy in women at low and high risk for pregnancy-induced hypertension. J Clin Ultrasound 1998;26:239–45.[Medline]
26. Kurjak A, Vidovic MI, Velemir D, Zalud I. Renal arterial Resistance Index in pregnant and nonpregnant women: evaluation with color and pulse Doppler ultrasound. J Perinat Med 1992;20:11–4.[Medline]
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