Portal hypertension occurs as a complication of liver cirrhosis and complications such as variceal bleeding lead to significant demands on resources. Endoscopy is the gold standard method for screening cirrhotic patients however universal endoscopic screening may mean a lot of unnecessary procedures as the presence of oesophageal varices is variable hence a large time and cost burden on endoscopy units to carry out both screening and subsequent follow up of variceal bleeds. A less invasive method to identify those at high risk of bleeding would allow earlier prophylactic measures to be applied. Hepatic venous pressure gradient (HVPG) is an acceptable indirect measurement of portal hypertension and predictor of the complications of portal hypertension in adult cirrhotics. Varices develop at a HVPG of 10-12 mmHg with the appearance of other complications with HPVG > 12 mmHg. Variceal bleeding does not occur in pressures under 12 mmHg. HPVG > 20 mmHg measured early after admission is a significant prognostic indicator of failure to control bleeding varices, indeed early transjugular intrahepatic portosystemic shunt (TIPS) in such circumstances reduces mortality significantly. HVPG can be used to identify responders to medical therapy. Patients who do not achieve the suggested reduction targets in HVPG have a high risk of rebleeding despite endoscopic ligation and may not derive significant overall mortality benefit from endoscopic intervention alone, ultimately requiring TIPS or liver transplantation. Early HVPG measurements following a variceal bleed can help to identify those at risk of treatment failure who may benefit from early intervention with TIPS. Therefore, we suggest using HVPG measurement as the investigation of choice in those with confirmed cirrhosis in place of endoscopy for intitial variceal screening and, where indicated, a trial of B-blockade, either intravenously during the initial pressure study with assessment of response or oral therapy with repeat HVPG six weeks later. In those with elevated pressures, primary medical prophylaxis could be commenced with subsequent close monitoring of HVPG thus negating the need for endoscopy at this point. All patients presenting with variceal haemorrhage should undergo HVPG measurement and those with a gradient greater than 20 mmHg should be considered for early TIPS. By introducing portal pressure studies into a management algorithm for variceal bleeding, the number of endoscopies required for further intervention and follow up can be reduced leading to significant savings in terms of cost and demand on resources.
Variceal haemorrhage; Portal hypertension; Portal pressure; Varices; Hepatic venous pressure gradient
The value of emergency upper gastrointestinal fibre-endoscopy, followed where required by the use of a modified Sengstaken tube, was studied during 84 episodes of acute bleeding in 75 patients who had evidence of portal hypertension with varices. The portal hypertension was due to alcoholic cirrhosis in 80% and to cryptogenic cirrhosis in 9% of the patients. By definition, varices were present in all patients, but in only 66% of episodes were the varices the cause of the bleed. The correct diagnosis of the source of bleeding was made at endoscopy in 89%. A Boyce modification of the Sengstaken-Blakemore tube was passed in 73% of the episodes of variceal bleeding. It effectively stopped the bleeding primarily in 85% of patients but was successful as a final definitive measure only in 46%. Furthermore, only 40% of the patients in whom the tube was passed, survived. Mortality rate could be related to the severity of the bleed and to hepatocellular dysfunction. Survival increased from 23% in those patients with jaundice, ascites, and encephalopathy on admission to 92% in those without these manifestations. The in-hospital survival rate was 52% in patients bleeding from varices and 64% in those bleeding from other causes, with an overall survival rate of 56%, indicating the poor prognosis in cirrhotic patients with gastrointestinal bleeding, irrespective of the cause.
Injection sclerotherapy is now the accepted first line treatment for bleeding oesophageal varices, although it is associated with an impressive list of rare complications. The main problem concerns the strategy for uncontrollable or recurrent bleeding. Patients with uncontrolled bleeding may be referred for surgery after considerable blood loss and are then extremely difficult to assess. The effects of blood loss on liver function can lead to an unduly pessimistic assessment of liver status. An effective choice of emergency surgical procedure may require considerable surgical expertise. Oesophageal transection and devascularisation are satisfactory for many patients with oesophageal varices secondary to cirrhosis and should nearly always control bleeding. Difficulties arise in patients who are grossly obese and in those who have undergone extensive surgery in the upper abdomen. Problems may also be encountered in those treated by repeated sclerotherapy, which may have caused severe inflammatory change and thickening around the lower oesophagus and upper stomach. We believe that an emergency mesocaval shunt using either a vein graft or a synthetic material such as polytetrafluoroethylene is the procedure of choice for this difficult group of very sick patients. The surgical exposure is satisfactory and not unduly prolonged in even the largest patients and the technique does not interfere with any subsequent transplant operation. There is a greater choice in the management of the patient with less urgent bleeding from recurrent varices after sclerotherapy. Repeat sclerotherapy may be effective for small oesophageal varices while liver transplantation may be indicated in the patient with deteriorating liver function. A selective distal splenorenal shunt should be considered for patients with intact splenic and left renal veins and a mesocaval vein graft for the remainder. We would therefore suggest that surgery should still be considered for the management of portal hypertension, particularly in the following circumstances: (1) Uncontrollable bleeding during the initial course of sclerotherapy; (2) Life threatening haemorrhage from recurrent varices; (3) Bleeding from ectopic varices not accessible to sclerotherapy; (4) Uncontrollable bleeding from oesophageal ulceration secondary to injection sclerotherapy; (5) Severe, symptomatic hypersplenism; (6) For patients who live in communities remote from blood transfusion facilities and adequate medical care. The management of the complications of portal hypertension continues to pose problems. We believe that the best results should come from a combined management approach using injection sclerotherapy as primary treatment and surgery for complications and for haemorrhage from unusual anatomical sites.
AIM: To propose a less invasive surgical treatment for schistosomal portal hypertension.
METHODS: Ten consecutive patients with hepatosplenic schistosomiasis and portal hypertension with a history of upper gastrointestinal hemorrhage from esophageal varices rupture were evaluated in this study. Patients were subjected to a small supraumbilical laparotomy with the ligature of the splenic artery and left gastric vein. During the procedure, direct portal vein pressure before and after the ligatures was measured. Upper gastrointestinal endoscopy was performed at the 30th postoperative day, when esophageal varices diameter were measured and band ligature performed. During follow-up, other endoscopic procedures were performed according to endoscopy findings.
RESULTS: There was no intra-operative mortality and all patients had confirmed histologic diagnoses of schistosomal portal hypertension. During the immediate postoperative period, two of the ten patients had complications, one characterized by a splenic infarction, and the other by an incision hematoma. Mean hospitalization time was 4.1 d (range: 2-7 d). Pre- and post-operative liver function tests did not show any significant changes. During endoscopy thirty days after surgery, a decrease in variceal diameters was observed in seven patients. During the follow-up period (57-72 mo), endoscopic therapy was performed and seven patients had their varices eradicated. Considering the late postoperative evaluation, nine patients had a decrease in variceal diameters. A mean of 3.9 endoscopic banding sessions were performed per patient. Two patients presented bleeding recurrence at the late postoperative period, which was controlled with endoscopic banding in one patient due to variceal rupture and presented as secondary to congestive gastropathy in the other patient. Both bleeding episodes were of minor degree with no hemodynamic consequences or need for blood transfusion.
CONCLUSION: Ligature of the splenic artery and left gastric vein with supraumbilical laparotomy is a promising and less invasive method for treating presinusoidal schistosomiasis portal hypertension.
Endoscopic banding; Esophageal varices; Portal hypertension; Schistosomiasis; Variceal bleeding
A simple and safe procedure providing sensitive and reproducible direct measurement of intravascular oesophageal variceal pressure (IOVP) during routine oesophagoscopy is described. The method requires only commercially available equipment. First results were obtained in 16 patients with oesophageal varices caused by liver cirrhosis (Child's A) can be summarised as follows: intravascular oesophageal variceal pressure was nearly identical in different varices of the single patient. Varices grade III exhibited a significantly higher intravascular oesophageal variceal pressure than varices grade II (22.7 +/- 2.5 vs 15.7 +/- 0.6 mmHg, p less than 0.05). After Valsalva's manoeuvre there was a remarkable increase in intravascular oesophageal variceal pressure by 13.6 +/- 1.0 mmHg irrespective of the variceal size. The high intravascular oesophageal variceal pressure values observed in grade III varices during the rise of the intraabdominal pressure may indicate an important risk factor for variceal haemorrhage. Glyceryltrinitrate (1.2 mg sprayed onto the tongues of 14 patients) very effectively lowered the intravascular oesophageal variceal pressure from 22.8 +/- 2.0 to 12.0 +/- 0.4 mmHg in grade III varices, and from 16.3 +/- 0.4 to 10.0 +/- 0.4 mmHg in grade II varices (p less than 0.005 in both groups). We conclude that this method provides a suitable tool to study the effect of drugs with presumed influence on the oesophageal variceal pressure and that the impressive effect of glyceryltrinitrate in lowering intravascular oesophageal variceal pressure warrants further study on the effect of longer acting nitrates on intravascular oesophageal variceal pressure, and the rebleeding rate after oesophageal variceal haemorrhage.
anti-inflammatory drugs (NSAIDs) can have severe gastrointestinal
effects and cause peptic ulcers to bleed. Acute bleeding from
oesophageal varices is a major complication of cirrhosis of the liver.
investigate the role, using a case-control study, of NSAIDs in first
bleeding episodes associated with oesophageal or cardial varices in
structured interview was conducted of 125cirrhotic patients with
bleeding mainly related to oesophageal varices and 75 cirrhotic
controls with oesophageal varices who had never bled.
patients who were admitted for bleeding related to portal hypertension
were more likely to have used NSAIDs during the week before the index
day (31 of 125 (25%)) than the cirrhotic controls (eight of 75 (11%);
odds ratio = 2.8, p = 0.016). Use of aspirin alone or combined with
other NSAIDs was also more prevalent in the cases (21 of 125 (17%))
than in the controls (three of 75 (4%); odds ratio = 4.9, p = 0.007).
Logistic regression analysis showed that NSAID use (p = 0.022, odds
ratio = 2.9, 95% confidence interval = 1.8 to 4.7) and variceal size
(p<0.001, odds ratio = 4.0, 95% confidence interval = 1.4 to 11.5)
were the only variables independently associated with the risk of bleeding.
used alone or combined with other NSAIDs, was associated with a first
variceal bleeding episode in patients with cirrhosis. Given the life
threatening nature of this complication, the possible benefit of this
treatment should be weighed against the risk shown here. No firm
conclusions could be drawn on non-aspirin NSAIDs used alone.
portal hypertension; non-steroidal anti-inflammatory
drugs; variceal bleeding; aspirin; cirrhosis
Patients with liver cirrhosis may develop upper gastrointestinal hemorrhage from a variety of lesions, which include those that arise by virtue of portal hypertension, namely gastroesophageal varices and portal hypertensive gastropathy and other lesions seen in the general population. Do patients with liver cirrhosis, hemorrhage from varices and other lesions equally, or are they more likely to bleed from varices? The aim of this study is to determine predominant causes of bleeding in patients with liver cirrhosis and upper gastrointestinal bleeding. PATIENTS AND METHODS: A retrospective review of 40 patients with liver cirrhosis based on the clinical and biochemical parameters of the Child-Pugh score, and upper gastrointestinal bleeding was carried out at an inner city hospital. Endoscopy diagnoses were documented. RESULTS: Of 40 patients, 38 patients had cirrhosis associated with alcohol consumption. Twelve of the above 38 patients who consumed alcohol also had hepatitis C virus (HCV) infection. Eleven patients had only varices on endoscopic examination, 17 had varices plus coexisting lesions. From these 17 patients, nine were found to have bled from varices, and eight were found to have bled from coexisting lesions. Twelve patients who had no varices bled from other lesions. Of 40 patients, 28 had varices, and 20 actually bled from varices. In this study there was no correlation between severity of liver cirrhosis as determined by the Child-Pugh score and the absence or presence of varices. CONCLUSION: Patients with liver cirrhosis and upper gastrointestinal bleeding hemorrhage from a variety of lesions. In this study of 40 patients, (70%) had gastroesophageal varices diagnosed at upper endoscopy, while 50% actually bled from varices.
Acute upper gastrointestinal haemorrhage remains the most common medical emergency managed by gastroenterologists. Causes of upper gastrointestinal bleeding (UGIB) in patients with liver cirrhosis can be grouped into two categories: the first includes lesions that arise by virtue of portal hypertension, namely gastroesophageal varices and portal hypertensive gastropathy; and the second includes lesions seen in the general population (peptic ulcer, erosive gastritis, reflux esophagitis, Mallory–Weiss syndrome, tumors, etc.).
Emergency upper gastrointestinal endoscopy is the standard procedure recommended for both diagnosis and treatment of UGIB. The endoscopic treatment of choice for esophageal variceal bleeding is band ligation of varices. Bleeding from gastric varices is treated by injection with cyanoacrylate. Treatment with vasoactive drugs as well as antibiotic treatment is started before or at the same time as endoscopy. Bleeding from portal hypertensive gastropathy is less frequent, usually chronic and treatment options include β-blocker therapy, injection therapy and interventional radiology.
The standard of care of UGIB in patients with cirrhosis includes careful resuscitation, preferably in an intensive care setting, medical and endoscopic therapy, early consideration for placement of transjugular intrahepatic portosystemic shunt and, sometimes, surgical therapy or hepatic transplant.
cirrhosis; upper gastrointestinal bleeding; management
BACKGROUND—Variceal pressure is a strong predictor for a first variceal bleed in patients with cirrhosis.
AIMS—To evaluate whether variceal pressure is also a determinant of the risk of a first variceal bleed in patients with non-cirrhotic portal hypertension.
METHODS—Variceal pressure was measured non-invasively in 25 patients with non-cirrhotic portal hypertension and large varices while receiving a stable therapeutic regimen. Factors predictive of bleeding were compared with those observed in 87 cirrhotics.
RESULTS—The one year incidence of variceal bleeding was 32% (n=28) for the cirrhotic and 20% (n=5) for the non-cirrhotic patients. There was no difference in factors predicting the risk of bleeding between the groups, except for variceal pressure. For the same level of variceal pressure, the risk of variceal bleeding was lower in patients with non-cirrhotic portal hypertension. Multiple logistic regression analysis revealed the following variables as having a significant predictive power: variceal pressure (p=0.0001), red spots (p=0.004), and the time interval between the first observation of the varices and the moment of variceal pressure measurement (p=0.0046). For the non-cirrhotics the risk of bleeding increased with higher Child-Pugh score (p=0.0024); this was not the case for the cirrhotic patients (p=0.9521).
CONCLUSION—Variceal pressure is a major predictor of variceal bleeding in patients with cirrhosis as well as in patients with non-cirrhotic portal hypertension. The risk of bleeding in non-cirrhotics is less than in cirrhotics for the same level of variceal pressure. In patients with non-cirrhotic portal hypertension the risk of variceal bleeding increases more with advancing disease.
Keywords: variceal haemorrhage; variceal pressure; non-cirrhotic portal hypertension
Twenty patients with liver cirrhosis were treated by surgery for bleeding from isolated gastric varices.
The presence of tortuous and engorged gastric veins connecting with a large splenorenal shunt was
demonstrated by transhepatic portography in all patients. The surgical procedures consisted of
splenectomy, proximal gastrectomy, paragastric devascularization, and ligation of the splenorenal
shunt. Sixteen patients survived the surgery. Four deaths were caused by emergency operation for
uncontrollable hemorrhage in extremely poor risk patients. Of the 16 survivors, 15 had been followed
wth endoscopy and portography for a mean period of 42 months. The other one died of hepatocellular
carcinoma three years after surgery. There was no bleeding episode during the period of follow-up in
these patients. Recurrent esophageal varices of mild degree were documented by endoscopy and
portography in three patients. Portography demonstrated that several newly formed retroperitoneal
veins arising from the junction of the portal and superior mesenteric veins joined to form recurrent
varices in these three patients. There was no significant change of the mean portal venous pressure
before and after surgery. Our data reveals that elective surgery may provide satisfactory results in
patients with isolated gastric varices. Transhepatic portography is the method of choice in radiologic
investigation for prominent gastric varices.
Non-variceal upper-gastrointestinal bleeding (NVUGIB) refractory to therapeutic endoscopy is a challenging situation. The following details a novel use for the Sengstaken-Blakemore tube in a case of severe ulcerative esophagitis after failure of conventional medical and endoscopic treatment. A 77-year-old man with a history of peptic ulcer disease developed massive hematemesis during a hospital admission. Initial gastroscopy revealed an adherent blood clot occupying the distal esophagus, extending to the gastric cardia and proximal fundus. Epinephrine was injected into and surrounding the clot; however, following the endoscopy the patient was hemodynamically unstable, requiring aggressive resuscitation. Repeat gastroscopy, following saline lavage, revealed active bleeding within severely ulcerated esophageal mucosa, immediately proximal to the gastro-esophageal (GE) junction. Despite apparent hemostasis following injection of epinephrine and electrocautery, the patient displayed clinical signs of continued bleeding. Furthermore, surgical and radiological interventions were precluded by the patient's hemodynamic instability. In an attempt to tamponade blood supply to the GE junction, a Sengstaken-Blakemore tube was inserted and placed under tension. Successful hemostasis was subsequently achieved and the patient remained stable. This is the first case to describe use of a Sengstaken-Blakemore tube in severe ulcerative esophagitis refractory to standard endoscopic management.
Esophagus; therapeutics; endoscopy; gastrointestinal hemorrhage
Portal hypertension is an unusual complication of liver metastases, which is frequently occurring in malignant disease. Portal hypertension may cause oesophageal varices and also stoma varices (colostomy and ileostomy). Oesophageal varices and bleeding from these varices have been frequently reported in literature. Stomal varices have also been reported in literature mostly associated with liver cirrhosis. These stomal varices lead to the massive bleeding causing morbidity and mortality.
Portal hypertension is a pathological increase in portal pressure gradient (the difference between pressure in the portal and inferior vena cava veins). It is either due to an increase in portal blood flow or an increase in vascular resistance or combination of both. In liver cirrhosis, the primary factor leading to portal hypertension is increase in portal blood flow resistance and later on development of increased portal blood flow. It has been postulated that in liver metastasis the increase in portal flow resistance occurs at any site within portal venous system as a consequence of mechanical architectural disturbance.
PRESENTATION OF CASE
We report a case of a 64 year old gentleman who developed portal hypertension due to secondary metastases from colorectal cancer. He subsequently developed bleeding varices in his end colostomy.
We believe that the combination of extensive metastases and chemotherapy induced portal hypertension in our patient.
Our case and other literature review highlight that the recurrent bleeding stoma associated with colorectal cancer should be investigated for portal hypertension.
Stoma varices; Portal hypertension; Liver metastases
Duodenal varices are a rare complication in patients with portal hypertension. Bleeding from duodenal varices often results in a severe prognosis. Diagnosis of the disease is usually based on findings obtained by endoscopy or angiography. However, it occasionally fails to detect the lesion and demonstrate its porto-systemic shunt vessels which are necessary information to decide an appropriate treatment. Recent advances in CT may make it possible for us to reveal duodenal varices with complicated porto-systemic shunt vessels. We report the case of a 58-year-old man with liver cirrhosis with repeated bleeding from duodenal varices. Esophagogastroduodenoscopy (EGD) revealed multinodular varices in the third portion of the duodenum. Then we conducted a capsule endoscopy (CE) and found fresh blood in the duodenum, suggesting duodenal variceal hemorrhage. Angiography depicted the varices with one afferent and two efferent vessels. Abdominal CT examination was conducted using a four-channel multi-detector row CT scanner. The multiplanar reconstructed images revealed not only the varices, but also three afferent and two efferent vessels. The patient was treated by surgical ligation and sclerotherapy, because of its complicated porto-systemic shunt and reserved liver function. No gastrointestinal bleeding has been seen after the surgery. Our case suggests the usefulness of multi-detector CT with multiplanar reconstruction (MPR) for the diagnosis and therapeutic decision of duodenal varices.
Varices; Computed tomography; Duodenum; Surgical hemostasis
Because several studies have suggested that beta blockers are effective in the prophylaxis of first variceal bleeding in cirrhosis, screening for oesophageal varices might be appropriate. We prospectively studied 84 cirrhotic patients without obvious evidence of large oesophageal varices and previous bleeding during a mean follow up of 16 months. At entry to the study 41 patients had no oesophageal varices and in 43 these were grade 1. The subsequent percentages of patients without large oesophageal varices were 74% at one year and 52% at two years. Univariate analysis showed that a longer duration of cirrhosis (p less than 0.05) and grade 1 oesophageal varices at entry (p less than 0.001) were predictive factors for the occurrence of large oesophageal varices, whereas, multivariate analysis showed that the initial size of the oesophageal varices (p less than 0.001), a high initial Child-Pugh score, and a smaller improvement in Child-Pugh score during the study were independent risk factors. Among patients with grades 0 and 1 oesophageal varices at the start of the study the proportions with large oesophageal varices at two years were 31% and 70% respectively. We have calculated that, accepting a maximum risk of first bleeding of 10% without prophylactic treatment, a patient without oesophageal varices should be screened endoscopically every other year, while a patient with grade 1 disease should benefit from one annual upper gastrointestinal endoscopy.
Isolated ectopic varices located in the small bowel are uncommon. Portal hypertension caused by liver cirrhosis is the most common predisposing risk factor.
PRESENTATION OF CASE
We present an unusual case of massive gastrointestinal bleeding from idiopathic jejunal varices in a 73-year-old Caucasian male without portal hypertension. Exploratory laparotomy disclosed ectopic varices located in the small intestine. Segmental resection of the jejunum with end to end anastomosis resulted in a complete resolution of the haemorrhage. During a 5 year follow up, the patient is stable with no bleeding recurrence.
Information on aetiology, diagnosis and management of jejunal varices is reviewed.
Diagnosis and management of isolated jejunal varices is challenging. Surgeons as well as acute care physicians have to consider idiopatic form of jejunal varices as a potential cause of gastrointestinal bleeding when gastroduodenoscopy and colonoscopy are negative.
Jejunal varices; Gastrointestinal haemorrhage; Diagnosis; Management
While esophagogastric varices are common manifestations of portal hypertension, variceal bleeding from the jejunum is a rare complication of liver cirrhosis. In addition, ectopic variceal bleeding occurs in the duodenum and at sites of previous bowel surgery in most cases, including of stomas. We report a case of obscure overt gastrointestinal bleeding from jejunal varices in a 55-year-old woman who had not previously undergone abdominal surgery, who had liver cirrhosis induced by the hepatitis C virus. Emergency endoscopy revealed the presence of esophageal varices without stigmata of recent bleeding, and no bleeding focus was found at colonoscopy. She continued to produce recurrent melena with hematochezia and received up to 21 units of packed red blood cells. CT angiography revealed the presence of jejunal varices, but no active bleeding was found. Capsule endoscopy revealed fresh blood in the jejunum. The patient submitted to embolization of the jejunal varices via the portal vein, after which she had a stable hemoglobin level and no recurrence of the melena. This is a case of variceal bleeding from the jejunum in a liver cirrhosis patient without a prior history of abdominal surgery.
Jejunal varices; Liver cirrhosis; Portal hypertension
Oesophageal varices and gastrointestinal bleeding are common complications of liver cirrhosis. More rarely, oesophageal varices occur in patients with non-cirrhotic portal hypertension that results from thromboses of portal or splanchnic veins.
We describe 2 young men who initially presented with varices as a result of portal vein thromboses. In the clinical follow-up, both were tested positive for a JAK2 mutation and consequently diagnosed with myeloproliferative neoplasms (MPNs). In an attempt to characterise the frequency of gastrointestinal complications in patients with JAK2-positive MPNs, we retrospectively analysed all known affected patients from our clinic for the diagnosis of portal vein thromboses and oesophageal varices. Strikingly, 48% of those who had received an oesophagogastroduodenoscopy had detectable oesophageal or gastric varices, and 82% of those suffered from portal or splanchnic vein thromboses.
While the association between JAK2, myeloproliferative disease and thrombotic events is well established, patients with idiopathic oesophageal varices are not regularly tested for JAK2 mutations. However, the occurrence of oesophageal varices may be the first presenting symptom of a MPN with a JAK2 mutation, and affected patients may profit from a close haematological monitoring to assure the early detection of developing MPN.
Oesophageal varices; Variceal bleeding; Splanchnic vein thrombosis; Portal vein thrombosis; JAK2; Myeloproliferative neoplasms
Gastric varices are less common than esophagogastric varices in patients with portal hypertension, occurring in up to 33% of patients. Gastric varices are more common in patients with noncirrhotic portal hypertension and extrahepatic portal vein thrombosis, are associated with a lower incidence of bleeding, and have a higher mortality rate than esophageal varices. Optimal management of gastric variceal bleeding is debatable. We present a case of gastric variceal bleeding caused by pre-hepatic venous thrombosis from essential thrombocythemia which was successfully treated by therapeutic splenectomy.
A 59-year-old woman with history of thrombocytosis presented with progressive abdominal pain, decreased appetite, and vomiting. Initial laboratory results showed a white blood cell count of 10.6 (x10∧9/L), hemoglobin of 14.6 (g/dL), platelet count of 279 (x10∧9/L) and normal PT/PTT. Triphasic liver computed tomography (CT) revealed splenomegaly and extensive portal, superior mesenteric, and splenic vein thrombosis with no collateral vascularity. Trans-abdominal catheter directed thrombolysis with continuous tissue plasminogen activator (tPA) infusion was unsuccessful. She was anticoagluated with heparin and then warfarin. A hypercoagulation workup showed positive heterozygous prothrombin gene mutation and JAK2 V617F gene mutation. Bone marrow biopsy was diagnostic of essential thrombocythemia. Two months later at an outside facility she had an evaluation for gastric cancer with esophagogastroduodenoscopy (EGD) and biopsy. She subsequently complained of epigastric pain, melenic stools, and fatigue. Hemoblobin was 10.4 (x10∧9/L) and INR was 3.2. Abdominal CT showed reduced clot burden but new periportal collateral veins and gastric varices. EGD showed an erosion over a gastric varix with stigmata of a recent bleeding. Anticoagulation was reversed and octreotide and propranolol were started. The patient continued to bleed with a drop in hemoglobin to 7.1(x10∧9/L) and splenectomy was performed. Post-operative EGD demonstrated complete resolution of gastric varices. Three months after discharge on warfarin, there has been no recurrence of hemorrhage.
Gastric variceal bleeding is usually caused by left-sided portal hypertension, most commonly from extrahepatic venous thrombosis. Optimal management of gastric varices remains controversial. In this case, traditional treatment of multivessel thrombosis (portal, mesenteric, and splenic veins) failed. Splenectomy is often reserved for patients with isolated splenic vein thrombosis, however, splenectomy was a successful treatment for this patient with gastric varices from multivessel extrahepatic thrombosis and essential thrombocythemia.
AIM: To evaluate the efficacy of human thrombin in the treatment of bleeding gastric and ectopic varices.
METHODS: Retrospective observational study in a Tertiary Referral Centre. Between January 1999-October 2005, we identified 37 patients who were endoscopically treated with human thrombin injection therapy for bleeding gastric and ectopic varices. Patient details including age, gender and aetiology of liver disease/segmental portal hypertension were documented. The thrombin was obtained from the Scottish National Blood Transfusion Service and prepared to give a solution of 250 IU/mL which was injected via a standard injection needle. All patient case notes were reviewed and the total dose of thrombin given along with the number of endoscopy sessions was recorded. Initial haemostasis rates, rebleeding rates and mortality were catalogued along with the incidence of any immediate complications which could be attributable to the thrombin therapy. The duration of follow up was also listed. The study was conducted according to the United Kingdom research ethics guidelines.
RESULTS: Thirty-seven patients were included. 33 patients (89%) had thrombin (250 U/mL) for gastric varices, 2 (5.4%) for duodenal varices, 1 for rectal varices and 1 for gastric and rectal varices. (1) Gastric varices, an average of 15.2 mL of thrombin was used per patient. Re-bleeding occurred in 4 patients (10.8%), managed in 2 by a transjugular intrahepatic portosystemic shunt (TIPSS) (one unsuccessfully who died) and in other 2 by a distal splenorenal shunt; (2) Duodenal varices (or type 2 isolated gastric varices), an average of 12.5 mL was used per patient over 2-3 endoscopy sessions. Re-bleeding occurred in one patient, which was treated by TIPSS; and (3) Rectal varices, an average of 18.3 mL was used per patient over 3 endoscopy sessions. No re-bleeding occurred in this group.
CONCLUSION: Human thrombin is a safe, easy to use and effective therapeutic option to control haemorrhage from gastric and ectopic varices.
Variceal haemorrhage; Ectopic Varices; Gastric varices; Portal hypertension; Thrombin
Bleeding from oesophageal varices, oesophageal ulcers or oesophagitis is occasionally massive and difficult to control. Octreotide, a synthetic analogue of somatostin lowers portal pressure and collateral blood flow including that through varices, increases lower oesophageal sphincter pressure, and inhibits the gastric secretion of acid as well as pepsin. Our current experience suggests it is effective in controlling acute variceal haemorrhage. Therefore we have examined the efficacy of octreotide in the control of postsclerotherapy bleeding from oesophageal varices, oesophageal ulcers and oesophagitis. During the study period 77 patients experienced a significant gastrointestinal bleed (blood pressure < 100 mm Hg, pulse >
100 beats per min or the need to transfuse 2 or more units of blood to restore the haemoglobin level) following injection sclerotherapy of oesophageal varices. The source of bleeding was varices in 42 patients, oesophageal ulcers in 31 and oesophagitis in 4. All patients received a continuous intravenous infusion of octreotide (50 μg/h) for between 40–140h. If bleeding was not controlled in the first 12h after commencing octreotide hourly bolus doses (50 μg) for 24h were superimposed on the continuous infusion. Haemorrhage was successfully controlled by an infusion of octreotide in 38 of the 42 patients with bleeding from varices, in 30 of 31 patients with oesophageal ulceration, and all patients with oesophagitis. In the 1 patient with persistent bleeding from oesophageal ulceration and in 2 of the 4 with continued haemorrhage from varices, haemostasis was achieved by hourly boluses of 50 μg octreotide for 24h in addition to the continuous infusion. No major complications were associated with octreotide administration. The results of this study clearly indicate that octreotide is a safe and effective treatment for the control of severe haemorrhage after technically successful injection sclerotherapy.
AIM: To identify clinical parameters, and develop an Upper Gastrointesinal Bleeding (UGIB) Etiology Score for predicting the types of UGIB and validate the score.
METHODS: Patients with UGIB who underwent endoscopy within 72 h were enrolled. Clinical and basic laboratory parameters were prospectively collected. Predictive factors for the types of UGIB were identified by univariate and multivariate analyses and were used to generate the UGIB Etiology Score. The best cutoff of the score was defined from the receiver operating curve and prospectively validated in another set of patients with UGIB.
RESULTS: Among 261 patients with UGIB, 47 (18%) had variceal and 214 (82%) had non-variceal bleeding. Univariate analysis identified 27 distinct parameters significantly associated with the types of UGIB. Logistic regression analysis identified only 3 independent factors for predicting variceal bleeding; previous diagnosis of cirrhosis or signs of chronic liver disease (OR 22.4, 95% CI 8.3-60.4, P < 0.001), red vomitus (OR 4.6, 95% CI 1.8-11.9, P = 0.02), and red nasogastric (NG) aspirate (OR 3.3, 95% CI 1.3-8.3, P = 0.011). The UGIB Etiology Score was calculated from (3.1 × previous diagnosis of cirrhosis or signs of chronic liver disease) + (1.5 × red vomitus) + (1.2 × red NG aspirate), when 1 and 0 are used for the presence and absence of each factor, respectively. Using a cutoff ≥ 3.1, the sensitivity, specificity, accuracy, positive predictive value (PPV), and negative predictive value (NPV) in predicting variceal bleeding were 85%, 81%, 82%, 50%, and 96%, respectively. The score was prospectively validated in another set of 195 UGIB cases (46 variceal and 149 non-variceal bleeding). The PPV and NPV of a score ≥ 3.1 for variceal bleeding were 79% and 97%, respectively.
CONCLUSION: The UGIB Etiology Score, composed of 3 parameters, using a cutoff ≥ 3.1 accurately predicted variceal bleeding and may help to guide the choice of initial therapy for UGIB before endoscopy.
Non-variceal bleeding; Predictor; Score; Upper gastrointestinal bleeding; Upper gastrointestinal hemorrhage; Variceal bleeding
A patient is described presenting with an acute lower gastrointestinal haemorrhage as a result of extensive colonic varices. Further investigation revealed that there were no oesophageal varices or splenomegaly. Liver biopsy showed grade II fatty change only, with no other specific or significant pathological features. Transhepatic portography showed a raised portal pressure (20 mm/Hg) but the portal system was patent throughout. There was an abnormal leash of vessels in the caecum thought to represent a variceal plexus. This patient was diagnosed as having idiopathic colonic varices. This case is discussed together with nine other reports of idiopathic colonic varices from the published literature. Four of these reports describe idiopathic colonic varices in more than one member of the same family. Possible modes of inheritance, aetiology of variceal change, natural history, and prognosis are discussed.
A 68-year-old man with hemophilia A and liver cirrhosis caused by hepatitis C virus was referred to our hospital to receive prophylactic endoscopic treatment for gastroesophageal varices (GOV). He had large, tense, and winding esophageal varices (EV) with cherry red spots extending down to lesser curve, predicting the likelihood of bleeding. Esophageal endoscopic injection sclerotherapy (EIS) was performed with a total 15 mL of 5% ethanolamine oleate with iopamidol (EOI). Radiographic imaging during EIS demonstrated that 5% EOI reached the afferent vein of the varices. He was administered sufficient factor VIII concentrate before and after EIS to prevent massive bleeding from the varices. Seven days after EIS, upper gastrointestinal endoscopy (UGIE) showed that the varices were eradicated almost completely. Eighteen months after EIS, the varices continued to diminish. We report a successful case of safe and effective EIS for GOV in a high-risk cirrhotic patient with hemophilia A.
Duodenal varices are a rare complication of portal hypertension secondary to liver cirrhosis. Compared to oesophageal varices, they bleed less often but are also more difficult to diagnose and treat. There is no established treatment for bleeding duodenal varices and different treatment strategies have been employed with variable results. The authors present a case of 52-year-old male who was admitted with melaena. Upper gastrointestinal endoscopy was performed which identified bleeding varices in the second part of duodenum. The varices were injected with cyanoacrylate and the outcome was favourable. Subsequent endoscopies showed complete resolution of the varices. The authors conclude that cyanoacrylate injection is an effective first-line treatment for bleeding duodenal varices.
Long-term results of surgical treatment were analysed in 42 patients with extrahepatic portal hypertension treated in the Department of Surgery, Institute of Haematology in Warsaw in the period 1971-1987. In all, 71 operations were carried out, and 20 patients were treated by endoscopic sclerotherapy of oesophageal varices. Recurrence of haemorrhage was found in 6 out of 11 patients 54% after venous shunting, in 13 out of 17 patients (76%) after treatment by ligation of oesophageal varices and in 32 out of 35 patients (91%) after splenectomy. Following repeated sclerotherapy of oesophageal varices, recurrence of haemorrhage occurred in 3 out of 20 patients (15%). During 17 years four deaths occurred (10%) none of which was due to haemorrhage from oesophageal varices. The authors conclude that the method of repeated sclerotherapy is presently the most effective way of preventing haemorrhage from oesophageal varices and consider this form of management as the treatment of choice in patients with extrahepatic portal hypertension.