Evaluation of Clinical, Biochemical and Ultrasound Parameters in Diagnosis of Oesophageal Varices

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1 Med. J. Cairo Univ., Vol. 78, No. 2, June: , Evaluation of Clinical, Biochemical and Ultrasound Parameters in Diagnosis of Oesophageal Varices FAWZY A. KHALIL, M.D.*; KHALIL A. KHALIL, M.D.*; TAREK H. KHALIL, M.D.**; ADEL A. HASSAN, M.D.*** and MOHAMAD A. SERWAH, M.Sc.* The Departments of Internal Medicine*, Diagnostic Radiology** and Infectious & Endemic Diseases, Faculty of Medicine, Suez Canal University, Ismailia, Egypt. Abstract Background: Bleeding oesophageal varices (OV) is the most dangerous complication of liver cirrhosis and to reduce the invasive methods and burden that endoscopy units have to bear some studies attempted to identify that non-invasively predict the presence of any OV among patients with liver cirrhosis. Aim of the Work: To assess the presence of OV using noninvasive methods (Clinical, biochemical and ultrasound parameters). Patients and Methods: After approval of our ethics committee, 73 patients (47 males and 26 females, aged years) known to have chronic liver disease (CLD) with liver cirrhosis attending the Gastroenterology Unit, Suez Canal University hospital in Ismailia were evaluated clinically, biochemically and by ultrasonographic studies and upper GI endoscopy. Clinical evaluation included detailed history and complete physical examination. Results: Upper GI endoscopy estimated that 75.3% of the patients had OV. Presence of multiple spider naevi, palmar erythema, lower limb edema and palpable spleen are significantly more common among patients with OV. Low platelet count, low plasma albumin and prolonged PT were significant laboratory findings among patients with OV. Doppler US of hepatic vein showed significant difference between patients with and without OV regarding pattern and direction of blood flow and presence of portosystemic collaterals. Multiple spider naevi, low plasma albumin, low platelet count/spleen diameter ratio, hepatic vein flow pattern and direction of blood flow of portal vein are all independent predictors for presence of OV. Conclusion: Clinical, biochemical and ultrasound parameters can replace the invasive upper GI endoscopy in the detection of the presence of any OV. Key Words: Oesophageal varices Chronic liver disease Upper GI endoscopy Abdominal ultrasound Portal Hepatic vein Doppler. Correspondence to: Dr. Fawzy A. Khalil, The Department of Internal Medicine, Suez Canal University, Ismailia, Egypt. Introduction BLEEDING from ruptured OV is the most severe complications of patients with liver cirrhosis and portal hypertension and is the leading cause of death in approximately one-third of these patients [1]. The prevalence of OV in patients with liver cirrhosis may range from 60% to 80%, with reported mortality from variceal bleeding ranges from 20% to 58% [2]. The Baveno III consensus Conference on Portal hypertension (2000) recommended that all patients with liver cirrhosis should be screened for the presence of OV. Other authors have suggested repeated endoscopies at 2-3 years interval in patients with small varices so as to evaluate the progression of this feature. However endoscopy is not usually accepted by many patients with liver cirrhosis who had never bleed. These recommendations imply a large workload on endoscopy units and a significant cost burden on patients with liver cirrhosis and health care providers [3]. In order to reduce the burden that endoscopy units have to bear, and to reduce the invasive methods some studies have attempted to identify methods that non-invasively predict the presence of OV including biochemical, clinical and ultrasonographic parameters [4-7]. Some studies concluded that high grade varices were predicted by serum albumin less than 2.95gm/dl and portal vein diameter more than 1 1 mm [8]. While other studied showed thrombocytopenia, splenomegaly, or ascitis as unreliable predictors of bleeding OV [9]. Other studies showed that low platelet count, ascities, platelet count/ splenic diameter ratio, and advanced Child Pugh 105

2 106 Evaluation of Clinical, Biochemical & Ultrasound Parameters score are independent predictors of any esophageal varices and large varices [4,5]. In the present study, we aimed to identify the predictive value of clinical, laboratory and ultrasonographic parameters in detection of presence of oesophageal varices among patients with chronic liver diseases and liver cirrhosis. Patients and Methods The study was carried out as a cross sectional study among seventy three patients years old of both sexes known to have chronic liver diseases with liver cirrhosis (compensated and decompensated), with different etiologies who attend the Gastroenterology clinic and the inpatient wards of the GI Department of Suez Canal University hospital. Any patient with any of the following criteria was excluded from the study: 1- Active GI bleeding. 2- Previous endoscopic sclerotherapy or band ligation. 3- Previous transjugular intrahepatic porto-systemic shunt or surgery for portal hypertension. 4- Patients with hepatorenal syndrome or hepatic encephalopathy. All the studied patients were subjected to the following: 1- Complete history taking (personal history and duration, course and treatment of the disease). 2- Full general, chest, heart and abdominal examination. 3- Laboratory investigations: a- Complete blood count and prothrombine time, liver functions tests (alanine aminotransferase (ALT) and aspartate aminotransferase) (AST), total plasma proteins, serum albumin and serum bilirubin), serum creatinine and viral markers (HBsAg, HBcIgG, HCVab). 4- Abdominal Duplex ultrasonography was performed using Colored Duplex Ultrasound model "Esaote MXP10 machine" for assessment of the liver size, presence and grade of periportal thickening [10], hepatic vein flow patterns (triphasic, biphasic, and monophasic [11]. Portal vein (PV) diameter, patency, cross sectional area (A) (cm 2 ), mean PV flow velocity (cm/sec), portal blood flow volume (ml/min), and congestive index (CI) were also assessed. Assessment of splenic vein (SV) diameter, cross sec- tional area, mean SV flow velocity and CI were performed. Ultrasonography also assess the presence and degree of ascitis and presence of portosystemic collaterals. 5- Upper GI endoscopy was performed for all patients in endoscopy unit (Endoscopy Unit, GI Department, Suez Canal University Hospital) using video endoscope (Pentax and Olympus). It was used to assess presence of esophageal varices by expert endoscopist. Based on the results of the upper GI endoscopy, the 73 patients were classified into 2 groups: Group 1: Patients with no esophageal varices. Group 2: Patients with esophageal varices. Statistical analysis: Gathered data were processed using SPSS version 15 (SPSS Inc., Chicago, IL, USA). Quantitative were expressed as means ± SD while qualitative data were expressed as numbers and percentages (%). Student t-test was used to test significance of difference for quantitative variables that follow normal distribution while z-test was used for quantitative data not following normal distribution and Chi Square was used to test significance of difference for qualitative variables. A probability value () <0.05 was considered statistically significant. Results The studied patients were in age group ranging from years old with mean age 50.3 years old. Forty seven were males (64.4%) and twenty six were female (35.6%) were females. Spider naevi, palmar erythema, lower limb edema, palpable spleen and ascites were estimated to be significant findings among patients with oesophageal varices. Other clinical findings including jaundice and palpable liver showed no significant difference between patients with and without varices (Table 1). Assessment of different laboratory parameters showed that platelet count was estimated to be significantly reduced among patients with oesophageal varices (115.2 ±57.9 versus ± 119.1; p- value <0.05). Patients with oesophageal varices showed significantly low plasma albumin and prolonged PT when compared to patients with no OV. Hemoglobin, liver enzymes, ALP and total bilirubin were not significantly different among both groups (Table 2).

3 Fawzy A. Khalil, et al. 107 Among different ultrasonographic (US) findings, huge splenomegaly was more incident significant finding among patients with OV (30.9% versus 5.5%; <0.05). Doppler US of hepatic vein showed significant difference between patients with and without OV regarding pattern and direction of blood flow and presence of portosystemic collaterals (Tables 3,4). Multivariate analysis of different parameters have shown that multiple spider naevi, low plasma albumin, low platelet count/spleen diameter ratio, hepatic vein flow pattern and direction of blood flow of portal vein are all independent predictors for presence of OV (Table 5). Table (1): Clinical of patients with and without esophageal varices. Clinical Jaundice 12 (21.8%) 3 (16.7%) 0.9 Spider naevi 20 (36.4%) 1 (5.6%) 0.03* Palmar erythema 25 (45.5%) 2 (11.1%) 0.01* Lower limb edema 29 (52.7%) 3 (16.7%) 0.02* Palpable liver 8 (14.5%) 3 (16.7%) 0.8 Palpable spleen 39 (70.9%) 3 (16.7%) 0.002* Ascites 41 (74.5%) 6 (33.3%) 0.003* *Statistically significant difference ( <0.05). Table (2): Laboratory of patients with and without esophageal varices. Laboratory Hb (g/dl) 10.3± ± Platelets (x10 3 ) 115.2± ± * AST (U/L) 62.3± ± ALT (U/L) 49.1± ± ALP (U/L) 38.4± ± Total bilirubin (mg/dl) 2.8± ± Albumin (g/dl) 2.7± ± * PT (control = 13 sec) 17.1± ± * HB : Hemoglobin level. ALP: Alkaline phosphatase. * Statistically significant difference ( <0.05). Table (3): Ultrasonographic findings of patients with and without esophageal varices. Ultrasonographic Shrunken liver 25 (45.5%) 7 (38.9%) 0.6 Dilated portal vein 34 (61.8%) 10 (55.6%) 0.6 Huge splenomegaly 17 (30.9%) 3 (5.5%) 0.001* Dilated splenic vein 27 (49.1%) 7 (38.9%) 0.4 Ascites 32 (58.2%) 8 (44.4%) 0.2 * Statistically significant difference ( <0.05). Table (4): Doppler of hepatic and portal vein among patients with and without esophageal varices. Doppler findings Hepatic vein: Biphasin/ monophasic flow pattern Presence of collaterals 37 (67.3%) 0 (0%) 0.001* 24 (43.6%) 4 (22.2%) 0.03* Portal vein: PVD (mm) 14.8± ± PVF (ml/min) 897.6± ± Mean PVV 9.4± ± (cm/sec.) Hepatofugal/ bidirectional 28 (50.9%) 4 (22.2%) 0.003* *Statistically significant difference ( <0.05). PVD : Portal vein diameter. PVF : Portal vein flow. PVV : Portal vein velocity. Table (5): Multivariate analysis of clinical, laboratory and sonographic parameters in detection of presence of OV. Odds ratio Multiple spider naevi * Platelets (x10 3 ) * Albumin (g/dl) * Biphasin/monophasic flow pattern * Hepatofugal/bidirectional direction of portal vein flow * *Statistically significant ( <0.05). Discussion Despite the progress in management achieved over the past decades, bleeding from ruptured esophageal varices is still a leading cause of death in patients with cirrhosis [12]. The possibility of identifying cirrhotic patients with esophageal varices by noninvasive methods is attractive, because it would allow for the restriction of performance of screening endoscopy to patients at high risk of varices [13]. Endoscopic examination is considered an invasive procedure. Moreover, sedation of cirrhotic patient to perform endoscopy may be hazardous. Also, diagnostic upper GI endoscopy may contribute to bacterial infections in patients with liver cirrhosis due to associated disruption of the natural barriers [14]. As a consequence, several noninvasive tools have been evaluated in the search of alternatives to endoscopy. Such tools include clinical and laboratory parameters and abdominal ultrasound with

4 108 Evaluation of Clinical, Biochemical & Ultrasound Parameters or without Doppler quantitative studies [15]. A number of studies have addressed the issue of identifying patients with varices by noninvasive means. A low platelet count has been constantly found to be related to the presence of varices [6,7]. Other prognostic factors identified in different studies include splenomegaly [12], a portal vein diameter on ultrasound scan of 13mm, an advanced Child Pugh class [7], low prothrombin activity [6], and the presence of telangiectasias. This is not the most recent there is Baveno [16] were that there are no satisfactory nonendoscopic indicators of the presence of varices and while further studies are awaited, endoscopic screening is still the best practice to detect varices. The presence of splenomegaly detected clinically and by ultrasonography in the studied patients was significantly higher in patients with varices. Several studies have noted similar findings [17,18]. It is reported that splenomegaly is the most clinical sign of portal hypertension and found almost in all patients [19]. As regarding laboratory parameters, in the present study low platelet count, low plasma albumin and prolonged PT were significant laboratory findings among patients with OV. These data are in agreement with that of Madhotra et al. [5] and Schepis et al. [6]. The association of thrombocytopenia and splenomegaly with the presence of varices is a reflection of the degree of portal hypertension [20]. Doppler examination of the hepatic veins showed that biphasic and monophasic patterns were statistically prevalent in patients with varices which coincided with the results of Ohta et al. [21]. A relationship was noted between the severity of cirrhosis and the disappearance of triphasic Doppler waveform [20]. In the current study, hepatofugal and bidirectional flow in the portal vein were significantly associated with the presence of OV that agreed with the results of Von Herbay et al. [22]. However Taourel and colleagues [23] didn't find any correlation between PV flow and presence of OV. In the present study multivariate analysis showed that multiple spider naevi, low plasma albumin, low platelet count/spleen diameter ratio, hepatic vein flow pattern and direction of blood flow of portal vein are all independent predictors for presence of OV. These findings come in agreement with that of Madhotra et al. [5]. Zaman et al. [7] reported that among all the variants in their study, only Child Pugh score and low platelet count were independent risk factors for the presence of varices. Meanwhile Thomopoulos et al. [17] found that factors independently associated with the presence of large oesophageal varices were platelet count, size of spleen and pressure of ascites by abdominal ultrasonography. In conclusion, the present study stated that clinical, biochemical and ultrasound parameters (mainly presence of multiple spider naevi, low plasma albumin, low platelet count/spleen diameter ratio, hepatic vein flow pattern and direction of blood flow of portal vein) can be used in screening of presence of OV among patients at risk for OV helping to reduce the burden on endoscopy units. References 1- DE FRANCHIS R.: Updating consensus in portal hypertension: Report of the Baveno III consensus workshop on definition, methodology and therapeutic strategies in portal hypertension. J. Hepatol., 33: , KHAN A.N., MAADONALD S., ALI M. and SHERLOCK D.: Portal hypertension D'AMICO G. and MORABITY A.: Noninvasive markers of oeso-phageal varices: not the last. J. Hepatol., 39: 30-34, GIANNINI E., BOTTA F., BORRO P., et al.: Platelets count/spleen diameter ratio: Proposal and validation of a non-invasive parameters to predict the presence of esophageal varices in patients with liver cirrhosis. Gut, MADHOTRA R., MULCAHY H., WILLNER I., et al.: Prediction of oesophageal varices in patients with cirrhosis. J. Clin. Gastroenterol., 34: 4-5, SCHEPIS F., CAMMA C., NICEFORO D., et al.: Which patients with cirrhosis should undergo endoscopic screening for oesophageal varices detection? Hepatol., 136: 157, ZAMAN A., BECKER T., LAPIDUS J., et al.: Risk factors for the presence of varices in cirrhotic patients without history of variceal hemorrhage. Arch. Intern. Med., 161: , SARWAR S., KHAN A.A., ALAM A., et al.: Nonendoscopic prediction of presence of oesophageal varices in cirrhosis. J. Coll. Physicians Surg. Pak., GO S.H., TAN W.P. and LEE S.W.: Clinical predictors of bleeding esophageal varices in the ED. Am. J. Emerg. Med., ABDEL WAHAB M.F., ESMAT G., FARRAG A., et al.: Grading of hepatic shistosomiasis by the use of diagnostic ultrasound. Am. J. Trop. Med. Hyg., 88: , ZWEIBEL W.J.: Introduction to vascular ultrasonography. Saunders Company, Philadelphia, London and Toronto, 4th edition, , CHALASANI N., KAHI C., FRANCOIS F., et al.: Improved patient survival after acute variceal bleeding: A

5 Fawzy A. Khalil, et al. 109 multicenter, cohort study. Am. J. Gastroenterol., 98: , CARBONELL N., PAUWELS A., SERFATY, et al.: Improved survival after variceal bleeding in patients with cirrhosis over the past two decades. Hepatology, 40: , AHUJA A. T.: Diagnostic imaging: Ultrasound. Amirsys company. Canada 1 st edition, 412, BOSCH J. and GARACIA-PAGAN J.C.: Complications of cirrhosis. I Portal hypertension. J. Hepatol., 32 (1): , DE FRANCHIS R.: Evolving consensus in portal hypertension. Report of the Baveno IV Consensus Workshop on methodology of diagnois and therapy in portal hypertension. J. Hepatol., 43: , THOMOPOULOS K., LABROPOU K., MIMIDIS K., et al.: Noninvasive predictors of the presence of large esophageal varices in patients with cirrhosis. Dig. Liv. Dis., 35: , SHARMA P. and AGGARWAL R.: Prediction of large esophageal varices in patients with cirrhosis of the liver using clinical, laboratory and imaging parameters. J. Gastroenterol., SHERLOCK S. and DOOLEY J.: Diseases of the liver and biliary system. Blackwell scientific publications. Oxford (UK): 11 th edition, MARTINS R., SOMBERG K. and MENG Y.: Thrombopoeitin levels in patients with cirrhosis before and after orthotopic liver transplantation. Am. Intern. Med., 127: , OHTA M., HASHIZUME M. and TOMIKAWA M.: Analysis of hepatic vein wave-form by Doppler ultrasonography in 100 patients with portal hypertension. Am. J. Gastroenterol., 89: 170, VON HERBAY A., FRIELING T., HAUS SINGER D., et al.: Doppler sonographic evaluation of spontaneous portosystemic shunts and inversion of portal venous flow in patients with cirrhosis. J. Clin. Ultrasound, 28: , TAUREL P., PERNEY P., DAUZAT M., et al.: Doppler study of fasting and posto/prandial resistant indices in the superior mesentric artery in healthy subjects & patients with cirrhosis. J. Clin. Ultrasound, 26: , 1998.

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