الفهرس 
Anatomy of the Esophagus, stomach and portal venousOnly 14 pages are availabe for public view
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Abstract
Summary
ortal hypertension is characterized by increase in portal
pressure >10mmHg and could be a result of liver cirrhosis
or of non-cirrhotic diseases. When portal hypertension occurs
in absence of liver cirrhosis, non-cirrhotic portal hypertension
(NCPH) must be considered. Portal hypertension is a serious
complication of liver cirrhosis .The development of varices as a
consequence of portal hypertension is a common and dangerous
complication. Bleeding from these varices is a life threating
condition.
The current study was designed to asses different
clinical, laboratory, Doppler/ultrasonographic and endoscopic
parameters which might predict initial variceal bleeding and
rebleeding in patients with NCPH.This study was conducted on
60 patients with NCPH who were admitted to Ain Shams
University hospital, Tropical Medicine Department or attending
the outpatient clinics during the period from October 2011 to
October 2013.
According to variceal bleeding, the patients were
classified into two groups. Group (1) included 26 patients with
variceal bleeding and Group (2) included 34 patients without
variceal bleeding.
In the present study we made a comparison between
patients with variceal bleeding (Group 1: n = 26) and those
P
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without (Group 2: n= 34) first by using univariate analysis of
different variables then significant variables in univariate
analysis were subjected to multivariate logistic regression
analysis.
Budd-Chiari syndrome was the commenest cause of
NCPH among the patients of the current study (68.3%)
followed by extra-hepatic portal vein thrombosis(13.3%),
idiopathic non cirrhotic portal hypertension (8%) and
schistosomiasis (5%).
Regarding the clinical data of the studied patients in the
present study, it was found that palpable spleen was more
evident (84.6%) in patients with variceal bleeding than in those
without variceal bleeding (61.8%) with highly statistically
significant difference between two groups. However, other
clinical data in the present study as ascites, lower limb oedema
and encephalopathy they did not show positive correlation with
variceal bleeding.
On analyzing laboratory data of our patients we found
that patients with variceal bleeding had more frequent
thrombocytopenia than those patients without variceal bleeding
with highly statistically significant difference between the two
groups. We found that Platelet count / spleen diameter ratio was
lower in patient with variceal bleeding than in those without
variceal bleeding with a highly statistically significant
difference between the two groups by univariate analysis.
Receiver operator curve (ROC) shows that the best cut off point
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for platelet count/ spleen ratio between both groups was < 1000
with sensitivity 92% and specificity 73.5% and negative
predictive value 92.6% and positive predictive value 71.9%.
Regarding abdominal ultrasonographic findings in the
studied patients, we found that the size of spleen (cm) was
highly statistically significant increased in patients with
variceal bleeding in comparison to those without variceal
bleeding. Moderate and huge splenomegaly were observed
more common in bleeders group while average and mild
splenomegaly were observed more common in non bleeders
group. We found that portal vein diameter was highly
statistically significant increased in patients with variceal
bleeding in comparison to those without. Splenic vein diameter
(mm) was highly statistically significant increased in patients
with variceal bleeding in comparison to the other group.
The results of Doppler abdominal examination of our
studied groups, the mean portal vein flow velocity was lower in
patients with variceal bleeding than in those without variceal
bleeding with a statistically significant difference. Portal vein
flow direction was non hepatopetal in 56.7% of bleeder patients
(hepatofugal in 38.8% and portal vein thrombosed in 26.9%)
while portal vein flow direction was hepatopetal in 76.5% of
non bleeder patients with statistically significant difference
between both groups.
Endoscopy was proved to be a powerful tool for
determination of bleeding risks. The current study had shown
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that large varices are more likely to bleed than small ones.
Another significant endoscopic predictor of bleeding from
oesophageal varices noted in the current study is presence of
risk signs (cherry spots, hemocystic and red wale markings).
Varices with risk signs were observed in 88.5% of patients with
variceal bleeding while it was absent in patients without
variceal bleeding with highly statistically significant difference
between both groups. Regarding the number of variceal
columns, we observed that as number of columns increases, the
risk of bleeding from varices increases.
Isolated gastric varices is found in 30.8% of studied
patients in bleeders group while it is found in 2.9% of studied
patients in non bleeders group. The presence of varices in
gastric fundus indicates a particularly high venous blood
pressure in that area which increase bleeding risk. Another
criterion in predicting bleeding from esophageal varices in the
current study is the presence of severe portal hypertensive
gastropathy on endoscopy. Severe PHG had been observed in
10 patients (38.5%) of the bleeders group. However, none of
the patients in non bleeder group had severe PHG.
Starting anticoagulation treatment for the patients of the
present study when anticoagulation was indicated did not cause
a significant increase in GI bleeding rate in those patients.
Appropriate prophylaxis against GIT bleeding from esophageal
and/or gastric varices by endoscopic band ligation for
esophageal varices or endoscopic obturation for gastric varices
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should be performed before staring anticoagulation for
treatment of patients with Budd-Chiari syndrome and portal
vein thrombosis.
In the present study, the frequency of rebleeding in our
patients was 30.8% (8 patients out of 24 patients). It was once
in 11.5% and two times in 11.5% and three times in 7.7% of
our studied patients. Approximately one quarter of the patients
had rebleeding within the first six weeks while 75% the patients
had rebleeding after six weeks from the initial bleeding
episode. These results were different from what was reported
by Benedeto-Stojanov (2006) who studied predictive factors of
rebleeding from esophageal varices in cirrhotic patients. The
risk of rebleeding was 86.3% and one-half of all rebleeding
attacks occurred within the first six weeks. This is might be
attributed to the fact that the patients in Benedeto-Stojanov s
study were cirrhotic and 85% of them had large varices.
In the present study we compared between patients with
initial variceal bleeding and those with reccurent variceal
bleeding by using univariate analysis of different variables to
identify risk factors of variceal rebleeding, we observed that
there was no statistically significant difference between. This is
different from Benedeto-Stojanov (2006) who observed that the
most effective indicators of risk of rebleeding was hepatocllular
dysfunction (Child Pugh class c). Mei-Tang et al. (2011)
concluded that rebleeding after initial variceal bleeding in
cirrhotic patients is correlated with more blood transfusions.
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Presence of ascites and prophylactic antibiotics was protective
against rebleeding.
In the present study, we used the significant
variables in univariate analysis and included them into
multivariate analysis by the logistic regression stepwise
method. from this multivariate analysis, we found that the
splenic vein diameter (mm), platelet count/spleen diameter
(mm) ratio and number of columns of esophageal varices were
independent risk factors for variceal bleeding in non cirrhotic
portal hypertension. The risk of the variceal bleeding increased
with increased splenic vein diameter, increased number of
columns of esophageal varices and decreased platelet/spleen
diameter ratio. Other variables in our study which were
significant by univariate analysis failed to reach statistical
significance when they were submitted to the multivariate
analysis.
The performance of our prediction model was displayed
by the Receiver Operating characteristic (ROC) curve. The
Area under the Curve (AUC) was 0.952 95% CI 0.901 –
1.002).This denotes that this model gives a good discrimination
between patients with risk of variceal bleeding and those
without. from this proposed model, a prediction scoring system
was generated. A scoring point is given to each parameter in
the model: As regards number of columns: presence of 3 or
more columns by endoscopy take 1 point and presence of less
than 3 columns take 0 point then multiply by 3.3, the patient
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splenic vein diameter in mm is multiplied by 0.97 and the
patient platelet count/spleen diameter in mm ratio is multiplied
by -0.001. Then the total score of the patient is the product of
summation of all these points.
We found a high performance of both the prediction
score and the regression model probability by the Receiver
Operating characteristic (ROC) curve. The Area under the
curve (AUC) for prediction score = 0.952 95% CI 0.901 –
1.002) and for regression model probability = 0.952 95% CI
0.901-1.002). Our prediction score had a high sensitivity and
specificity at cutoff point 9.17. So, this cutoff point was
considered the most practical one. At cutoff 9.17, sensitivity was
96%, specificity was 88.2%. Thus, above this cutoff value, the
risk of variceal bleeding in non cirrhotic portal hypertension
increased.
According to our knowledge, no previous studies had
proposed a prediction scoring system for the risk of variceal
bleeding among patients with non cirrhotic portal hypertension.
However, many investigators tried to find scoring system and
independent risk factors for the variceal bleeding in cirrhotic
patients.
Sarangapani et al. (2010) studied predictors of presence
of large oesophageal varices and found that platelet count,
spleen size, portal vein diameter, splenic vein diameter and
platelet count/spleen diameter ratio were independent risk
factors for variceal bleeding in cirrhotic patients by multivariate
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logistic regression. The present study had demonstrated that
platelet count <122.000 platelet count/ spleen diameter ratio cut
off <1000, portal vein diameter >12mm. splenic vein diameter
>10mm and spleen size> 17mm are predictors of variceal
bleeding in non-cirrhotic portal hypertension because they
represent the median values and offered the best discrimination.
This is partially in agreement with Sarangapani et al. (2010).
Who found that platelet count/spleen diameter ratio cut off 909,
platelet count <120.000 PVdiameter>13mm and splenic vein
diameter >13.8 mm were predictors for large oesophageal
varices.
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Conclusion
1) Budd-Chiari syndrome was the commenest cause of NCPH
among the patients of the current study (68.3%) followed by
extra-hepatic portal vein thrombosis (13.3%), idiopathic non
cirrhotic portal hypertension (8%) and schistosomiasis (5%).
2) Platelet count / spleen diameter ratio < 1000 proved to be a
predictor of bleeding from esophageal varices due to NCPH
with sensitivity 92%, specificity 73.5%, negative predictive
value 92.6% and positive predictive value 71.9%.
3) Splenic vein diameter (mm), platelet count/spleen diameter
(mm) ratio and number of columns of esophageal varices were
independent risk factors for variceal bleeding in NCPH by
multivariate analysis. These parameters were included into
model that can predict the risk of variceal bleeding with good
performance.
4) The suggested prediction score has a high sensitivity and
specificity at cutoff point 9.17 (sensitivity is 96% and
specificity is 88.2%).
5) Anticoagulation if indicated did not increase the risk of GIT
bleeding in patients with NCPH.