Concurrent devascularization and splenectomy …of a pathological increase in portal vein pressure...

Research Article

Gastroenterology, Hepatology and Endoscopy

Gastroenterol Hepatol Endosc, 2018 doi: 10.15761/GHE.1000160 Volume 3(3): 1-10

ISSN: 2398-3116

Concurrent devascularization and splenectomy versus splenectomy alone in patients with hypersplenism but silent esophageal varicesAhmed Hammad1, Ahmed M Abdel Modaber1* and Vusal Aliyev2

1Department of General Surgery, Faculty of Medicine, Mansoura University Hospitals, Egypt2Department of General Surgery, Emsey Hospital, İstanbul, Turkey

AbstractBackground: Bleeding esophageal varices is a catastrophic event with high mortality; every effort should be exerted to prevent such a consequence. Primary prophylaxis against the first variceal bleeding has been adopted worldwide with different modalities and techniques for prophylaxis.

Hypothesis: We hypothesize that concurrent devascularization could reduce at least half the number of bleeding episodes.

Objectives: The aim of this study was to assess the effect of splenectomy alone or with vasoligation (devascularization of the upper 2/3 of the greater curvature of the stomach and left gastric vein ligation) on the evaluation of the esophageal varices in those patients with hypersplenism secondary to portal hypertension.

Patients and methods: This is prospective simple randomized trial including 34 patients who presented with hypersplenism and asymptomatic esophageal varices during the period from March 2014 to March 2015. These patients were randomizing into two groups; in group I, patients were managed by splenectomy alone and patients in group II were managed by splenectomy and vasoligation. These patients had different presenting complaints such as pain in the left hypochondrium, bleeding tendency or easy fatigability. Any patient with history of hematemesis and melena were excluded from our study. Before treatment, all patients were evaluated clinically, laboratory, radiological evaluation and esophago-gastro-duodenoscopy. Also, portal vein diameter was measured to all patients in this study. All patients were evaluated at one month and three months postoperatively.

Results: There was no much difference between the two groups in the postoperative course as regard to hospital stay or complication. Both groups of patients showed decrease of the portal vein diameter; this may be indicative for decreased portal pressure after both types of surgery which needs farther evaluation and measurement of the portal vein pressure. There was no change in the grade of varices in group I after surgery. But there was statistically significant improvement of the grade of varices in group II postoperatively, although no patient showed eradication of varices in this group.

Conclusion: We found that vasoligation when combined to splenectomy can give beneficial effect to the patient by decreasing the grade of varices, but the patients are still in need to be scheduled on a program to assess the efficacy of vasoligation on long term follow up.

*Correspondence to: Ahmed Abdel Modaber, Department of General Surgery, Faculty of Medicine, Mansoura University Hospitals, Egypt, Tel: +20 50 2202876; E-mail: [email protected]

Key words: devascularization, splenectomy, portal hypertension, esophageal varices, hypersplenism

Received: May 11, 2018; Accepted: May 28, 2018; Published: May 31, 2018

IntroductionPortal hypertension is a clinical syndrome which is a consequence

of a pathological increase in portal vein pressure due to various causes, liver cirrhosis being the most common. The basic pathophysiological characteristic of portal hypertension is resistance to portal vein flow or an increase in portal vein flow, which results in elevation of pressure in the portal vein and its tributaries and the formation of collateral circulation. Portal hypertension can be manifested by splenomegaly, hypersplenism, esophagogastric variceal bleeding, hepatoencephalopathy and ascites [1].

Bleeding from esophageal varices is still a lethal complication in cirrhotic patients with portal hypertension. Approximately 5-10% of patients with cirrhosis will develop esophageal varices per year, and about 25-30% of cirrhotic patients with esophageal varices and without previous variceal hemorrhage will bleed from ruptured varices [2].

Most patients with esophagogastric varices have cirrhosis and portal hypertension; for patients in advanced stages of liver failure, liver transplantation is the optimal treatment, although shunting or non-shunting operations can be considered for treatment of bleeding complications [3].

Compared with the risk of postoperative hepatic encephalopathy in surgical shunts and trans jugular intrahepatic portosystemic shunt (TIPS), non-shunting procedures maintain postoperative portal perfusion and long-term hepatic and systemic hemodynamics in patients with cirrhosis, which results in a low incidence of postoperative encephalopathy [3].

Bleeding of gastroesophageal varices is the most hazardous complication of portal hypertension. Similarly, hypersplenism prevents safe application of the treatments for hepatitis C. Thus, Hassab’s operation, which involves devascularization of peri-gastroesophageal vessels and splenectomy, has a new role as a procedure for cirrhotic patients [4].

Hammad A (2018) Concurrent devascularization and splenectomy versus splenectomy alone in patients with hypersplenism but silent esophageal varices

Volume 3(3): 2-10Gastroenterol Hepatol Endosc, 2018 doi: 10.15761/GHE.1000160

3. Laboratory investigations in the form of complete blood count, kidney and liver function tests, viral markers, anti-bilharzial antibody titre, bone marrow aspirate and bleeding profile to aid in the assessment of patient fitness.

4. Radiological investigations in the form of pelvic-abdominal US with Doppler study on the portal vein to report the presence of cirrhosis, size of the spleen and perihilar varices and the portal vein calibre and patency.

5. Upper GI endoscopy.

Manoeuvre descriptionPreoperative preparation

Pneumococcal vaccine, the Hemophilus influenzae type B vaccine, and the meningococcal vaccine were administrated 2 weeks preoperatively.

Preoperative blood grouping and cross matching was done.

Preparation of platelets for intraoperative transfusion.

Shaving of the hair in the anterior abdominal wall for males before surgery.

Stop all forms of solid food and any fluid with residue to be taken orally 6 hours preoperatively and only plain fluids can be taken and stopped just 4 hours preoperatively.

Operative procedures

A. Splenectomy alone procedure:

•• The procedure is done under general anesthesia.

•• 1 gm of 3rd generation cephalosporin is given IV at the induction of anesthesia.

•• The patient was placed in a supine position over the operating table.

•• The abdomen is prepared and draped in a standard fashion.

•• Counting the laparotomy pads.

•• A midline or left paramedian incision was performed (Figure 1).

•• Exploration of the abdomen.

•• Ligation of the splenic artery in the lesser sac

Opening of the lesser sac through the gastrocolic ligament was done to expose the upper border of the pancreas; the splenic artery can be palpated as it courses along the upper pancreatic border. Once the splenic artery was identified, the peritoneum over the artery is opened and right-angle clamp passed around the splenic artery and encircled with 2-0 silk ligature (Figures 2-4).

•• Mobilizing the spleen. The spleen retracted with the left hand in a medial direction and the assistant retracts the abdominal wall with a retractor laterally to expose the splenophrenic and lienorenal ligaments (Figure 5). The ligaments were divided with electrocautery and ligation of the prominent vessels in these ligaments. Several moist gauze pads were applied to the splenic bed.

The splenocolic ligament was divided releasing the colon from the lower pole of the spleen. Division of the peritoneum over the splenic hilum was done from the lower pole to the upper pole (Figure 6). The short gastric (Figure 7) vessels were divided carefully by suture ligation with care not to take a part of the gastric wall in the ligature. At this

Splenectomy in compensated cirrhosis with hypersplenism is safe, corrects cytopenia, made HCV cirrhotic are eligible for specific antiviral treatment and improvement of Child's score at long term follow up [5].

The rate of bacteremia in splenectomised cirrhotic patients after esophageal injection sclerotherapy is higher than non-splenectomised cirrhotic patients. Band ligation should replace injection sclerotherapy in this category of patients. Those patients may need strong parental antimicrobial combination coverage before the endoscopy apart from they received vaccinations or not [6].

In this study, we define, which operation is better to the patient; splenectomy or splenectomy with vasoligation for management of hypersplenism with asymptomatic esophageal varices.

Patients and methodsPatients with hypersplenism with asymptomatic esophageal varices

were included in this prospective simple randomized. The study was approved by the ethics and institutional review board and was registered in the clinical trial registry of the provincial medical board.

Inclusion criteria

1. Aged 18-70 years.

2. Both sexes.

3. Patients with hypersplenism and any grade of oesophageal varices and have no history of bleeding oesophageal varices.

4. Compensated liver disease with child Pugh of A score.

Exclusion criteria

1. Age <18 - >70.

2. Patients with hypersplenism and has no oesophageal varices.

3. Patients with history of bleeding oesophageal varices.

4. Patients with decompensated liver disease; Child's B and C score.

5. Current pregnancy.

Method of randomization

The patients signed informed consent regarding the procedure and its sequelae.

Each patient who fulfilled the inclusion criteria was numbered sequentially. Subsequently, these patients were divided into two groups according simple randomization with patients of odd numbers underwent splenectomy alone and those with even numbers underwent splenectomy with vasoligation.

Group I

17 patients were subjected to mere splenectomy.

Group II

17 patients were managed using splenectomy with vasoligation.

Methods1. Proper history taking.

2. Examination searching for pallor, jaundice, petechial haemorrhage, abdominal examination for detection of splenomegaly, ascites caput medusa.



Figure 1. Photograph showing the anterior abdominal wall, the costal margin is marked above, the midline incision is marked. The shaded area represents the enlarged spleen. Figure 4. Photograph shows ligated splenic artery in the leaser sac.

Figure 2. Photograph of identification of the splenic artery at the superior border of the pancreas after the entrance to the leaser sac.a

Figure 5. Photograph shows opening of the linorenal ligament to help the mobilization of the spleen.

Figure 3. Photograph shows opening of the peritoneum over the splenic artery in the leaser sac. Figure 6. Photograph shows division of the peritoneum over the hilum.



stage the spleen was fairly mobile and attached only by the vessels at the splenic hilum.

•• Ligation the Splenic Vessels at the hilum. The mobilized spleen could be elevated out of the abdominal cavity. Clamming, division and ligation of the splenic vessels at the hilum was done with care to avoid injury of the tail of the pancreas (Figures 8 and 9).

•• Any remaining peritoneal attachments were divided, and the spleen was removed.

•• Hemostasis was then checked (Figure 10): the inferior surface of the diaphragm, the region of the short gastric vessels at the greater curvature of the stomach and the splenic hilum. This was done by a rolled laparotomy pad into the left upper quadrant and rolling it, exerting downward, with medial traction on the stomach and hilar region to permit visualization of the undersurface of the diaphragm. The pad was then rolled toward the midline to permit visualization of the site of the divided short gastric vessels at greater curvature of the stomach. The final step was uncovering the hilar dissection; and hemostasis was secured.

•• A tube drain was inserted at the splenic bed

•• Counting the laparotomy pads

•• Close the abdominal wounds in a standard way.

B. Splenectomy and vasoligation procedure

•• The same as splenectomy alone with devascularization of the upper 2/3 of the greater curve of the stomach and left gastric vein ligation.

•• Left gastric vein ligation was dissected until the left gastric artery and vein were exposed while the greater curvature was lifted up with a retractor (Figure 11).

Postoperative care

•• IV Analgesics was given when indicated (e.g. paracetamol infusion and Pethidine if needed).

•• IV Fluids were given until oral feeding can be started.

•• IV Antibiotics were given in the form of 3rd generation Cephalosporins (cefotaxim 1 gm/8 h) for 5 days.

•• Oral feeding was started in the form of plain fluids just the patient had audible intestinal sounds.

•• The tube drains were removed when no more than 50 ml of drained fluid per day after the patients starts full form of oral intake.

•• Postoperative follow up

•• Clinical evaluation of all patients and any complications, minor and major, were registered.

•• Wound complications in the form of wound dehiscence and burst abdomen.

•• Postoperative laboratory investigations (CBC, liver function tests, kidney function tests and coagulation profile were done postoperatively, after a month and after 3 months.

•• Postoperative ultrasound portal vein Doppler.

•• Length of hospital stay will be recorded.

•• Post splenectomy follow up upper GI endoscopy postoperatively during the hospital admissions well as 1and 3 months postoperatively.

•• Length of postoperative hospital stay: the operation day was considered day 0 (Figure 12 and 13).

Statistical analysis

Data were statistically described in terms of mean and standard deviation (SD), median and range, or frequencies (number of cases) and percentages when appropriate.

Figure 7. Photograph shows dissection of the short gastric vessels to help complete mobilization of the spleen.

Figure 8. Photograph shows dissection of the splenic vessels at the splenic hilum.

Figure 9. Photograph shows dissection and ligation of the splenic vessels at the splenic hilum.



Figure 10. Photograph shows checking of the haemostasis after removal of the spleen.

Figure 11. Photograph shows dissected left gastric vein after upwards retraction of the stomach. The left gastric vein is marked by the white arrow.

Figure 12. Photographs show the esophageal varices in a patient preoperatively (A) and 3 months after splenectomy and vasoligation in the same patient (B). Notice the change in the grade of varices from grade II to grade I.

Figure 13. Photographs show the esophageal varices in patient preoperative (the right photo) and 3 months after splenectomy in the same patient (the left photo). Notice there is no significant change in the grade of varices.

Comparison of numerical variables between the study groups was done using Man Whitney U test for independent samples and paired t test for dependent samples.

The Pearson correlation coefficient is used to measure the strength of a linear association between two variables.

For comparing categorical data, Chi square (X2) test was performed. Exact test was used instead when the expected frequency is less than 5. (P) Values less than 0.05 was considered statistically significant.

All statistical calculations were done using computer programs SPSS (Statistical Package for the Social Science; SPSS Inc., Chicago, IL, USA) version 15 for Microsoft Windows.

ResultsGender distribution into males and females in each group shows

that most of our patients were females as shown in Figure 14.

Patients’ age ranged from 26 to 60 years with the mean age 44 years in group I and 48.1 years old in group II. The most common cause of portal hypertension is liver cirrhosis due to viral hepatitis. Most patients were presented by left hypochondrial pain (47.05% in each group of patients), then left hypochondrial swelling (29.4% in group I and 35.29% in group II) (Table 1).

Thrombocytopenia was found in all cases of our study either alone or in combination of leucopoenia, anemia or both. The was no preoperative statistically significant difference between group I and group II as regard to blood cells affection (Table 2).

In both groups of patients, there were significant changes in all items except between preoperative HB and early postoperative HB also between preoperative HB and one-month postoperative HB, also HB and three months postoperative HB (Tables 3 and 4). All patients of our study showed dilated portal vein which ranged from 12 to 19 mm with mean diameter 13.94 mm in group I and 14.64 in group II. There was no statistically significant difference between both groups preoperatively (Table 5).

Although all patients had dilated portal vein there was no significant correlation between portal vein diameter and the grade of the varices (Table 6).

There was significant reduction in the portal vein diameter after surgery in both groups of patients (Table 7).

All grades of varices were found in our study with grade II and III esophageal varices were more prevailing. There was no statistically



Figure 14. Distribution of patients according to gender.

Group I Group II

SexMales 7 (41.2%) 8 (47.1%)Females 10 (58.8%) 9 (52.9%)minimum 26 37

Age

maximum 60 56Mean ± SD 44.41 ± 9.695 48.17 -2: 5.615t-test 1.313P value 0.103HCV 10 (58.8%) 8 (47.1%)HBV 1 (5.9%) 1 (5.9%)

Aetiology of Portal hypertension

Bilhasiasis 4 (23.5%) 2 (11.8%)HCV + HBV 1 (5.9%) 2 (11.8%)HCV + Bilhasiasis 1 (5.9%) 4 (23.5%)Chi-Square (X2) 3.0222P value 0.554

Presentation

Swelling 5 (29.4%) 6 (35.29%)Pain 8 (47.05%) S (47.05%)Bleeding tendency 3 (17.6%) 3 (17.6%)Refrained before antiviral therapy 1 (5.9%) -Chi-Square (X2) 1.09P value 0. 779

Table 1. Demographic data, aetiology of portal hypertension and presentation.

No cytopenia ThrombocytopeniaTwo cell affection

Pancytopenia Total X2 p↓Plat + ↓WBCs ↓Plat + ↓RBCs

Group I 0 (0%) 7 (-41.17%) 4 (-215%) 3(17.6 90) 3 (-17.6%) 171.8 0.179Group II 0 (0 96) 6 (-35.29%) 3 (-17.6%) 4 (-215%) 4 (23.5 96) 17

Total' 0 (0%) 10 (-29.4%) 7 (-20.6%) 10 (-29.4%) 7(20.6 96%) 34

Table 2. Preoperative distribution of blood cell affection in both groups.

N Min Max Mean ± SD t p

Group I

platelets

Pre-op 17 28 70 46.17± 11.89Early post-op 17 160 243 189.70 ± 24.9 -20.68 0

One-month post-op 17 156 262 204.35 ± 28.6 -18.81 03-months post-op 17 180 243 201.41 ± 19.06 -25.19 0

RBC

Pre-op 17 3.1 5.8 4.43 ± 0.76 -5.022 0Early post-op 17 4.7 5.9 5.41 ± 0.40

One-month post-op 17 4.7 5.9 5.32 ± 0.35 -4.753 03-months post-op 17 4.7 5.9 5.41 ± 0.36 -6.019 0

HB

Pre-op 17 9.8 13.1 11.69 ± 1.17Early post-op 17 10.8 13.4 12.09 ± 0.65 -1969 0.066

One-month post-op 17 11.2 13.1 12.11 ± 0.54 -1.553 0.1393-months post-op 17 11.3 12.8 12.20 ± 0.46 -1.851 0.082

WBC

Pie-op 17 1.9 8.2 4.85 ± 2.147Early post-op 17 4.8 12.5 9.33 ± 2.207 -5.767 0


Table 3. Blood picture comparison at different times of follow up to the preoperative one in group I.



Preoperative Portal vein diameter

Group N Min Max Mean ± SD t P valueGroup I 17 12 19 13.94 ± 2.304

-1.33 0.096Group II 17 12 19 14.64 ± 2.059

Table 5. The mean portal vein diameter the patients preoperatively.

N Pearson correlation between PVD and the grade of EV P value SignificanceGroup I 17 0.364 0.151 No statistically significant relation

between PVD and the grade of EVGroup II 17 -0.02 0.939

Table 6. The correlation between portal vein diameter and the grade of varices.

N Min Max Mean ± SD Paired t P Value

Group I

Preoperative PVD 17 12 19 13.94 ± 2.3042.704 0.015

PVD weak postoperative 17 12 17 13.41 ± 1.662Preoperative PVD 17 12 19 13.94 ± 2.304

3.771 0.002PVD month postoperative 17 12 16 13.00 ± 1.369


PVD 3 months postoperative 17 12 16 12.94 ± 1.390Preoperative PVD 17 12 19 14.64 ± 2.059

2.704 0.016

Group II

PVD weak postoperative 17 12 17 14.17 ± 1.424Preoperative PVD 17 12 19 14.64 ± 2.059

3.801 0.002PVD month postoperative PVD 17 12 17 14.00 ± 1.457


PVD 3 months postoperative 17 12 16 13.70 ± 1.424

Table 7. The change in the portal vein diameter after surgery.

significant difference between both groups of patients preoperatively as regard to the grade of esophageal varices (Table 8).

Postoperatively there was no improvement in the grade of varices in group I but there was some improvement of the grade of varices among patients in group II (Table 9).

All of our patients had preoperative compensated liver function (child A score). We considered the patient had impaired liver functions if he had either ALT >40 u/L, bilirubin >1.2 mg/dl or albumin <3.5 g/dl. From this point, impaired liver function doesn't reflect the child score of the patient. Liver functions was significantly impaired at early postoperative period in both group of patients which improved gradually, there was no significant changes between the preoperative liver functions and 3 months postoperative follow-up liver functions (Table 10).

The most common postoperative complication we had found in this study is postoperative fever most commonly due to chest infection (Table 11).

There was no significant difference between the two groups of patients as a regard to the postoperative hospital stay with the average postoperative hospital stay about 5 days (Table 12).

DiscussionMassive hemorrhage of the upper gastro-intestinal tract resulting

from esophageal varices, which are mainly supplied by an enlarged left gastric vein originating from the portal vein, is a major complication of liver cirrhosis. At least two-thirds of patients with cirrhosis develop the varices, and approximately 10-60% of patients experience variceal bleeding [7].

Liver transplantation is the only effective treatment for treating severe liver cirrhosis, but patients without an appropriate potential donor cannot undergo liver transplantation. For such patients, splenectomy may offer another treatment option. Splenectomy can decrease the inflow into the portal system, resulting in a decreased

Table 4. Blood picture comparison at different times of follow up to the preoperative one in group II.

N Min Max Mean ± SD t P

GroupII

Platelets

(Pre-op 17 28 64 43.294 ± 10.82Early post-op 17 153 217 178.58 ± 18.25 -30.43 0

One-month post-op 17 156 252 200.82 ± 24.11 -24.11 03-months post-op 17 180 233 199.94 ± 15.36 -31.71 0

RBC

Pre-op 17 3 5 4.264 ± 0.600Early post-op 17 4.5 5.9 5.170 ± 0.426 -5.097 0

One-month post-op 17 4.6 5.9 5.294 ± 0.432 4.191 03-months post-op 17 4.5 5.8 5.205 ± 0.456 -5.355 0

HB

(Pre-op 17 9.8 13.1 11.635 ± 1.179Early post-op 17 10.3 13.4 11.976 ± 0.747 -1.748 0.099

One-month post-op 17 11.2 14 12.111 ± 0.646 -1.885 0.0773-months post-op 17 11.3 13.6 12.176 ± 0.643 -1.931 0.071

WBC

Pre-op 17 1.9 8.2 4.858 ± 2.147Early post-op 17 4.8 13.5 9.747 ± 2.683 -5.944 0




Grade of esophageal varicesZ value P Value

I II III IV

Group I

Pre-operatively 5 7 4 1

No improvement recordedearly Post-operatively 5 7 4 1

1 month Post-operatively 5 7 4 13-months (Post-operatively 5 7 4 1

Group II

Pre-operatively 2 7 7 1-1 0.317

early Post-operatively 3 6 8 0Pre-operatively 2 7 7 1

-2.645 0.0081 month Post-operatively 5 7 5 0

Pre-operatively 2 7 7 1-2.645 0.008

3 months Post-operatively 5 7 5 0

Table 9. Changes in oesophageal variceal at different times of follow up comparing it to the preoperative one.

Liver function group follow-up in each group comparing each post-operative measure to the pre-operative one Normal Impaired Z CP

Group I Pre-operatively 15 (-88.2%) 2 (-11.8%)early Post-operatively 8 (-47%) 9 (-52%) -2.645 0.008

1 month Post-operatively 13 (-76.5%) 4 (-23.5%) -1.414 0.1573 month Post-operatively 16 (-94.1%) 1 (-5.9%) -1 0.317

Group II Pre-operatively 14 (-100%) 3 (0%)early Post-operatively 9% 8% -2.236 0.025

1 month Post-operatively 14 3 0 13 month Post-operatively 15 2 -0.58 0.563

Table 10. Liver functions conditions at different times of follow-up in each group comparing it to the pre-operative one.

Table 8. Preoperative oesophageal varices distribution in both groups of patients.

Esophageal Varices grade I II III IV Total X2 P

Group I 5 (-29.5%) 7 (-41.2%) 4 (-23.5%) 1 (-5.8%) 172.104 0.551Group II 2 (-11.8%) 7 (-41.2%) 7 (-41.20%) 1 (-5.8%) 17

Total 7 (-20.6%) 14 (-41.2%) 11 (-32.4%) 3 (-5.8%) 34

Post-operative complications Splenectomy alone Splenectomy plus vasoligation X2 Pfever 7 (41.2 %) 8 (47.1 %) 0.119 0.73

Chest infection 4 (23.5 %) 5 (29.4 %) 0.151 0.697Portal vein thrombosis 1 (5.8 %) 1 (5.8 %) 0 1Subphrenic collection 1 (5.8 %) 0 (0 %) 1.03 0.31

Wound infection 0 (0 %) 1 (5.8 %) 1.03 0.31Incisional hernia 1(5.8 %) 2 (11.8 %) 0.366 0.545

Table 11. Postoperative complications.

Post-operative hospital stayGroup N Mean ± SD t P

Splenectomy alone 17 4.53 ± 1.1788-0.298 0.383

Spleuectomy plus vasoligation 17 4.65 ± 1.1147

Table 12. Postoperative hospital stay.

portal pressure, without creating a portosystemic shunt [8].

Thirty-four patients with hypersplenism and asymptomatic esophageal varices were included in this study.

Patients were divided into two groups:

•• Group I: 17 patients were managed by splenectomy alone.

•• Group II: 17 patients were managed by splenectomy and vasoligation.

This study was conducted to evaluate the effect of vasoligation on esophageal varices grade by studying endoscopic variceal grading preoperatively, early postoperative during hospital stay, after one month and after 3 months; as well as study the effect of both procedures on patient morbidity and mortality.

In this study, there were 10 female patients (58.8%) and 7 (41.2%) male patients in group I while in group II there were 9 (52.9%) female and 8 (47.1) male patients. Patients’ age ranged from 26 to 60 years with the mean age 44.4 years in group I and 48.1 years old in group II. Portal hypertension affects many patients at young and middle ages which is considered an economic and health burden in our country.

In a study made by Lacerda et al. [9], they had 13 female patients (59%) and 9 male patients (41%) with overall patients (22 patients). This was matched to our study, where female patients were more prevailing.

In our study, the most common presenting symptoms was pain in the left hypochondrium 8 (47%) patients in each group then abdominal swelling in the left hypochondrium which was found in 5 (29.4%) in group I and in 6 (35.29%) in group II. Bleeding tendency in the form of easy bruisability and bleeding gums was found in 3 (17.6%) in each



group and none of our patients had history of hematemesis and/or melena.

Single patients in group I was referred to us to manage hypersplenism before the patient started antiviral therapy against HCV.

The prevalence of hepatitis C viral infection among patients in this study was 70.58% (12 patients) in group I and 82.35% (14 patients) in group II. HCV infection was found either alone [10 patients (58.8%) in group I and 8 patients (47.1%) in group II] or with co infection with HBV [1 patient (5.9%) in group I and 2 patients (11.8%) in group II] or Bilhasiasis [1 patient (5.9%) in group I and 4 patients (23.5%) in group II]. In Egypt, hepatitis C viral infection is considered a national health problem. HCV is the commonest cause of liver cirrhosis and portal hypertension nowadays in our country. In the past, bilhasiasis was the commonest cause of liver fibrosis and portal hypertension which had regressed due to mass treatment and snail control.

In a study carried out in India by Kedia et al. [5], they found the prevalence of hepatitis C viral infection among patients of their study was 10 (30%) patients among the whole patients who were 30 patients with pre-operative diagnosis of cirrhosis with hypersplenism. This may be due to the difference in the prevalence of hepatitis C viral infection between the two countries.

In our study, we found preoperatively that thrombocytopenia was found in 34 patients (100%) either in the form of single cell line affection, only the platelet count was decreased, in 7 (41.2 %) patients in group I and 6 (35.29%) patients in group II or in combination with either leucopenia 4 (23.5 %) patients in group I and 3 (17.6 %) patients in group II, erythropenia 3 (17.6 %) patients in group I and 4(23.5 %) patients in group II or both 3 (17.6 %) patients in group I and 4 (23.5 %) patients in group II. There was no significant difference between both groups preoperatively.

We found that thrombocytopenia and other blood cell impairment were corrected in all patients in both groups. But there was no significant improvement in the hemoglobin (HB) level which might be contributed to a persistent cause of anemia as iron deficiency anemia which is common in our country or occult gastro intestinal blood loss due to congestive gastropathy.

Lu et al. [10], in a study for evaluation of hypersplenism in 322 with portal hypertension, found simultaneous decreases in WBC, RBC and PLT occurred in 89 cases (27.6%), WBC + PLT decreases in 52 cases (16.1%), RBC + PLT decreases in 29 cases (9.0%), and WBC + RBC decreases in 36 cases (11.2%) single type PLT decreases occurred in 31 cases (9.6%), single type WBC decreases in 29 cases (9.0%), and single type RBC decreases in 56 cases (17.4%).

In this study, we had different grades of esophageal varices. In group I there were 5(29.5 %) patients with esophageal varices grade I, 7 (41.2 %) patients with grade II, 4 (23.5 %) patients with varices grade III and 1 (5.8 %) patient with varices grade IV. None of the patients in group I showed either improvement or worsening in the grade of varices postoperatively. In group II, we had 2 (11.8 %) patients with esophageal varices grade I, 7 (41.2 %) patients with varices grade II, and 7(41.2 %) patients grade III and 1 (5.8 %) patient with varices grade IV.

There were improvements in the grade of varices postoperatively in 7 patients (41%) of them 3 patients had varices grade II improved to grade I postoperatively and 3 patients with varices grade III improved to grade II as well as 1 patient with esophageal varices grad IV improved to grade III. There was no improvement in patients with varices in grade I.

The improvement of varices in group II of patients was statistically significant with p value <0.05. But, disappearance of varices couldn't be detected in this group.

Lacerda et al. [9], found improvement in the grade of varices in 4 (20%) of 20 patients after splenectomy and left gastric vein ligation. This difference from our study may be due to the use of a grading system for varices differed from that we used.

We found in this study that the portal vein diameter preoperatively was dilated (>12 mm in diameter) and ranged from 12 to 19 mm with mean values 13.94 ± 2.304 and 14.64 ± 2.059 in group I and II respectively. But there was no correlation between portal vein diameter and the degree of esophageal varices. The portal vein diameter was decreased significantly in both groups of patients. In group I, the mean 3 months postoperative portal vein diameter was 12.94 ± 1.390 compared to 13.94 ± 2.304 preoperatively with P value = 0.001. In group II, the mean postoperative portal vein diameter was 13.70 ± 1.424 compared to 14.64 ± 2.059 preoperatively with P value = 0.002.

Rani et al. [11], reported that the diameter of portal vein on US examination is an indirect indicator of portal pressure which is responsible for development of varices. Portal vein of a diameter greater 13 mm can be considered as a non-invasive predictor of esophageal varices.

From this study, although the was no co-relation between the portal vein diameter and the grade of varices but all of our patients had a portal vein diameter more than12 mm. So, we can predict the presence of varices if the portal vein diameter is more than 12mm. Decreased portal vein diameter after splenectomy or splenectomy and vasoligation might reflect the decrease in the portal pressure and improved hemodynamics of the portal circulation.

Liu et al. [12], found that there is reduction of the portal vein diameter after a modified Hassab's procedure from 14.5 ± 2.2 preoperatively to 12.9 ± 1.6 postoperatively which was found statistically significant with P value >0.0001.

With the regard to the effect of splenectomy or splenectomy and vasoligation the liver functions, we found that there was no significant change between the preoperative liver function and 3-month postoperative liver functions. We also found statistically significant impairment of the liver functions early postoperative in both groups may be because of anesthesia and surgery. This impairment of the liver functions was mild without clinical decompensation which improved to the basal preoperative liver functions in 3 months.

Elsebae et al. [13], reported that the mean value of serum albumin was not of a statistically significant difference before surgery and at the 2nd postoperative day (P=0.608). However, those results may be biased by the intensive parenteral infusions of human albumin and fresh frozen plasma given to patients at the perioperative period. Mean value of serum albumin on the 60th postoperative day was significantly higher than preoperative value. Mean values of serum AST and ALT were higher in the preoperative than the 60th postoperative day they were significantly lower than preoperative values. These results disagreed with our results most probably because all our patients were in Child A with the original levels of the studied parameters were nearly normal.

In this work, postoperative fever was found in 7 (41.2%) patients in group I and in 8 (47.1%) patients in group II. The cause of fever was attributed to chest infection, wound infection and sub phrenic collection.



There were 4 (23.5%) patients with chest infection in Group I and patients 5 (29.4%) in group II. Those patients were managed by antibiotics, mucolytics and chest physiotherapy. One patient with wound infection in group II was managed by repeated wound dressing, removal of some sutures and antibiotics. A patient in group I with sub phrenic collection was managed conservatively with no need for surgical or image guided drainage. 2 patients in each group had no apparent cause of fever with complete resolution within a week.

Kedia et al. [5], found that 10 (30%) patients in their study had postoperative fever which was attributed to chest infection (the commonest cause of post-operative fever); wound infection, sub phrenic collection and fever can't be attributed to apparent cause.

In this study, portal vein thrombosis was detected in one patient (5.8) in group I and one patient (5.8) in group II. Both cases were asymptomatic and discovered accidentally by portal vein Doppler during the follow-up period. The patient in group II was discover early postoperative during the hospital stay. It was partial portal vein thrombosis and there was no change in the degree of varices compared to the preoperative grade, and the patient received anticoagulant in the form of low molecular weight heparin (clexan® 40 units twice daily for 10 days) and marevan 3 mg/day for 3 months. Complete recanalization was achieved in 3 months which is documented by Doppler US. The patient of group I was discovered during the follow up period after a month of surgery it was asymptomatic with no risky varices on endoscopic follow up and the patient received anticoagulants in the form of low molecular weight heparin (clexan® 40 units twice daily for 10 days) and marevan 3 mg/day for 3 months with complete recanalization in 2 months.

Liu et al. [12], found that 26 (5.5%) of 476 patients had portal venous thrombosis after modified Hassb's procedure. Portal vein thrombosis in cirrhotic patients is highly challenging. It carries the risk for venous gangrene of the bowel as well as the risk of bleeding varices. The optimal management of PVT in individuals with cirrhosis is currently not addressed in any practice guidelines.

In our study, hematemesis and/or melena didn't occur to any patient of both, either early postoperative or during the follow up period.

Liu et al. [12], had 17 (3%) patients of 562 patients experienced upper GI bleeding during the postoperative period. This differed from our study which might be contributed to the larger number of patients in the study conducted by Liu et al. [12], who reported significant improvement in the cytopenia’s after splenectomy.

We also found that there were no mortalities in both groups of patients. This may be reserved to the good liver reserve of our patients.

Kedia et al. [5], reported no splenectomy related mortality in a study including 39 splenectomies for cirrhotic patients with Child A and B scores.

Conclusion•• Hypersplenism was corrected significantly after both types of

surgical procedures.

•• No significant correlation was found between the portal vein diameter and the grade of varices but, we can predict the presences of esophageal varices in patients with portal vein diameter greater than 12 mm.

•• Portal vein diameter was significantly reduced after both types of surgical procedures.

•• Splenectomy alone has no effect on the degree or eradication of the varices.

•• Vasoligation when added to splenectomy has a significant effect on decreasing the grade of varices, but unfortunately it doesn't eradicate it.

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4. Hayashi H, Takamura H, Yamaguchi Y, Shoji Y, Nakagawara H, et al. (2012) Recent role of Hassab’s operation for cirrhotic patients: Combination with endoscopic procedure for varices. Asian J Surg 35: 57-61. [Crossref]

5. Kedia S, Goyla R, Mangla V, Kumar A, Daa P, et al. (2012) Splenectomy in cirrhosis with hypersplenism: improvement of cytopenias, Child's status and institution of specific treatment of hepatitis C with success. Ann Hepatol 11: 921-929. [Crossref]

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10. Lu Y, Li X, Han X, Gong X, Chang S (2013) Peripheral blood cell variations in cirrhotic portal hypertension patients with hypersplenism. Asian Pac J Trop Med 6: 663-666. [Crossref]

11. Rani S, Sudarsi B, Siddeswari R, Manohar S (2015) Correlation of portal vein size with esophageal varices severity in patients with cirrhosis of liver with portal hypertension. Int J Scie Res Pub 5: 1-5.

12. Liu Y, Li Y, Ma J, Lu L, Zhang L (2013) A modified Hassab’s operation for portal hypertension: experience with 562 cases. J Surg Res 185: 463-468. [Crossref]

13. Elsebae M, Abu-Zekri N (2008) A study of the effect of splenectomy on hepatic functional reserve and structural damage in patients with chronic hepatitis C virus infection by non-invasive serum markers. A prospective study. Int J Surg 6: 362-366. [Crossref]

Copyright: ©2018 Hammad A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

https://www.ncbi.nlm.nih.gov/pubmed/19493387









Concurrent devascularization and splenectomy …of a pathological increase in portal vein pressure...

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