​Kembara Xtra - Medicine - Esophageal Varices

​Kembara Xtra - Medicine - Esophageal Varices 

Variceal rupture is the most common fatal complication of cirrhosis; the severity of liver disease correlates with the presence of varices and the risk of bleeding. Varices are dilated submucosal esophageal veins that connect the portal and systemic circulations. Varices most commonly result from portal hypertension, which is typically the result of cirrhosis. Varices are connected to the portal and systemic circulations.

Epidemiology 

Incidence

 Thirty percent of patients with cirrhosis have varices at the time of diagnosis, and this number rises to ninety percent after ten years. The risk of initial variceal bleeding after one year is five percent for small varices and fifteen percent for large varices.
Prevalence
Bleeding occurs in almost half of individuals who have esophageal varices at some time in their treatment.
Variceal hemorrhage has been linked to a mortality rate ranging from 10 to 20 percent in the six weeks that follow an episode.


Causes and effects: etiology and pathophysiology 
The establishment of portacaval anastomoses is what leads to the decompression of the portal circulation when portal hypertension is present. This results in a clogged submucosal venous plexus that has dilated and convoluted veins, most noticeably in the distal portion of the esophagus. When a variceal sac ruptures, bleeding will occur.
Pathophysiology of portal hypertension, including but not limited to:
— An increase in the resistance to portal flow at the level of hepatic sinusoids as a result of intrahepatic vasoconstriction, which is induced by a decrease in the synthesis of nitric oxide and an increase in the release of endothelin-1 (ET-1), angiotensinogen, and eicosanoids.
a disturbance in blood flow is brought on by sinusoidal remodeling.
- An increase in portal flow as a result of hyperdynamic circulation brought on by splanchnic arterial vasodilation brought about by the action of mediators like nitric oxide, prostacyclin, and tumor necrosis factor.
Extrahepatic portal vein obstruction (EHPVO) is one of the prehepatic and extrahepatic causes of portal hypertension.
Massive splenomegaly with an increase in blood flow through the splenic veins
Posthepatic symptoms include severe right-sided heart failure, constrictive pericarditis, and hepatic vein obstruction (also known as Budd-Chiari syndrome).
- Cirrhosis, which is responsible for the majority of cases of portal hypertension, is an intrahepatic condition. Schistosomiasis, significant fatty change, disorders that disrupt portal microcirculation such as nodular regenerative hyperplasia, and diffuse fibrosing granulomatous diseases such as sarcoidosis are among the less common causes of this condition.
Genetics
Cirrhosis is not an inherited condition very often.

Risk Factors 
Cirrhosis Patients with cirrhosis are more likely to have esophageal varices, and thrombocytopenia and splenomegaly are also independent predictors of this condition.
Hypertension of the portal vein in the absence of cirrhosis

Varix size, endoscopic symptoms (red wale markings, cherryred patches), vessel wall thickness, and a rapid increase in variceal pressure (i.e., the Valsalva maneuver) are all factors that are associated with an increased risk of bleeding in patients who are known to have varices.
a high MELD/Child-Pugh score, the presence of portal vein thrombosis, and an elevated hepatic venous pressure gradient (HVPG).
GENERAL PREVENTION
Take measures to avert the underlying causes: Abuse of alcohol should be prevented, along with the administration of the hepatitis B vaccine, proper needle hygiene, and intravenous (IV) drug use (needle exchange programs minimize the incidence of hepatitis); specific screening and treatment for hepatitis B and C, as well as hemochromatosis, should also be performed.


Conditions That Often Occur Together 

 Portal hypertensive gastropathy; varices in the stomach, duodenum, colon, or rectum (which produces significant bleeding, in contrast to hemorrhoids); infrequently at the umbilicus (caput medusae) or ostomy sites.

Isolated gastric varices might manifest themselves as a consequence of splenic vein thrombosis or stenosis brought on by hypercoagulability or continuous inflammation (most frequently, chronic pancreatitis).
Other consequences associated with cirrhosis include hepatic encephalopathy, ascites, hepatorenal syndrome, spontaneous bacterial peritonitis, and hepatocellular cancer.

The first sign of varices is typically bleeding in the gastrointestinal tract, which can manifest as hematemesis, hematochezia, and/or melena.
Occult bleeding (anemia): a rather rare occurrence

History of the Present Cirrhosis and Liver Disease has been present for a very long time. Variceal bleeding is one of the potential early presentations of cirrhosis that has not yet been detected.

 The consumption of alcohol, the transmission of blood-borne infections through the use of intravenous drugs or sexual behaviors
● Hematemesis, melena, or hematochezia
Rectal bleeding is a possible symptom of a rapid bleed in the upper GI tract.

The Patient's Clinical Examination 
Determine whether or not the patient's hemodynamic stability is stable by checking for hypotension and tachycardia (active bleeding).
Liver palpation and percussion during the abdominal exam (with cirrhosis, the liver is frequently rather tiny and firm).
Splenomegaly and ascites (varying degrees of dullness; fluid shift; puddle splash—physical maneuvers have limited sensitivity)

● Visible abdominal periumbilical collateral circulation (caput medusae)
Alcoholism's peripheral stigmata include spider angiomata on the chest and back, palmar erythema, testicular shrinkage, and gynecomastia.
● Rectal varices
encephalopathy caused by hepatitis; asterixis; seeing blood on the rectal exam


Differential Diagnosis Upper gastrointestinal bleeding: varices account for 10–30% of cases.
Up to fifty percent of individuals with documented varices experience bleeding from causes other than varices.
– Cancer of the stomach or esophagus – Gastritis – Ulcer of the peptic tract
- The congestive gastropathy that is associated with portal hypertension
— Malformation of the arteriovenous system
Hemoptysis; bleeding from the nose and eyes; Mallory-Weiss tears; aortoenteric fistula

• Bleeding in the lower gastrointestinal tract: rectal varices; hemorrhoids: colonic neoplasia
- Diverticulitis in addition to arteriovenous malformation
- A location in the upper GI that is actively bleeding
Risk of ongoing or recurring bleeding: actively bleeding or a large varix, a high Child-Pugh severity score, infection, or renal failure


Results From the Laboratory Initial Examinations (lab, imaging)

 Anemia: Hemoglobin levels may be normal during active bleeding; it may take anywhere from six to twenty-four hours for levels to equilibrate; people with cirrhosis frequently have various causes of anemia.
Thrombocytopenia is the most sensitive and specific criterion, and it correlates with portal hypertension, as well as big esophageal varices.

Cirrhosis may be present if aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and bilirubin are abnormal, as well as if the prothrombin time is prolonged and the albumin level is low.
BUN, creatinine (BUN is typically increased in the presence of GI bleeding)

 Patients who are being treated with terlipressin may see a decrease in their sodium level. Noninvasive tests are used to screen out high-risk varices (HRVs) in patients who have compensated for their cirrhosis.

 Esophagogastroduodenoscopy – Capable of identifying actively bleeding varices as well as large varices and stigmata of recent bleeding – Can be used to treat bleeding with esophageal band ligation (preferred to sclerotherapy); prevent rebleeding; detect gastric varices, portal hypertensive gastropathy; diagnose alternative bleeding sites Esophagogastroduodenoscopy – Capable of identifying alternative bleeding
- Capable of locating and treating varices that do not cause bleeding. Varices are bulging submucosal veins that are seen in the distal part of the esophagus.


Diagnostic Methods and Other Procedures
CLD patients who are at risk for developing clinically significant portal hypertension (CSPH) can be identified using a technique called transient elastography (TE).
● HVPG >10 mm Hg: gold standard to diagnose CSPH (normal: 1 to 5 mm Hg) 
Responders to nonselective beta-blockers (NSBB) can be identified by an HVPG response of less than 10% or of less than 12 mm Hg to IV propranolol. This response is associated with a reduced risk of variceal bleeding.
The use of video capsule endoscopy for screening purposes as an alternative to conventional endoscopy

 Doppler sonography (second line): reveals patency, diameter, and flow in portal and splenic veins, as well as collaterals; is sensitive for stomach varices; verifies patency following ligation or transjugular intrahepatic portosystemic shunt (TIPS);
Venous-phase celiac arteriography: demonstrates portal vein and collaterals; hepatic vein occlusion Portal pressure measurement using retrograde catheter in hepatic vein CT- or MRI-angiography (second line, not routine): demonstrates large vascular channels in abdomen, mediastinum; demonstrates patency of intrahepatic portal and splenic vein 


Management 
Variceal bleeding is frequently made more difficult by hepatic encephalopathy and infection. Ensure that any underlying cirrhotic comorbidities are properly treated.

 Active bleeding (2) – intravenous access, hemodynamic resuscitation – kind and crossmatch packed RBCs. An excessive amount of blood is being given, which raises the portal pressure and the danger of further bleeding.
- Coagulopathy should be treated if it occurs. The risk of rebleeding and an increase in blood volume may be associated with the use of fresh frozen plasma.
– Acutely, you should avoid nephrotoxic medicines and beta-blockers as well as sedatives and monitor the patient's mental status.
IV octreotide to lower portal venous pressure as an adjunct to endoscopic management; IV bolus of 50 g followed by drip of 50 g/hr IV terlipressin (alternative): 2 mg q4h IV for 24 to 48 hours and then 1 mg q4h IV erythromycin 250 mg IV 30 to 120 minutes before endoscopy (1) IV octreotide to lower portal venous pressure as an[A]
- Immediate upper gastrointestinal endoscopy for the purpose of diagnosis and therapy
Variceal band ligation is favored over sclerotherapy for bleeding varices; it is also recommended for nonbleeding medium-to-large varices in order to lower the risk of bleeding.
 Ligation has greater rates of variceal eradication, lower rates of rebleeding, and less problems than other methods. It also stops bleeding more quickly.
rebleeding requires a second round of ligation and sclerosant treatment.
If endoscopic treatment is unsuccessful, you may wish to explore self-expanding esophageal metal stents or the implantation of a Sengstaken-Blakemore–type tube orally for up to twenty-four hours in order to stabilize the patient in preparation for TIPS.

Antibiotic prophylaxis with oral norfloxacin 400 mg or IV ceftriaxone 1 g q24h for up to a week is recommended for patients who have variceal bleeding. Up to two-thirds of patients with variceal bleeding acquire an infection, most commonly spontaneous bacterial peritonitis, urinary tract infection, or pneumonia.
Do not take beta-blockers if you are experiencing active bleeding since they lower blood pressure (BP) and diminish the normal increase in heart rate that occurs with acute hemorrhage.
Take measures to prevent future episodes of acute bleeding.
- Vasoconstrictor medications such as terlipressin and octreotide, which lower portal blood pressure.
– Endoscopic band ligation (EBL): if bleeding recurs or portal pressure monitoring shows portal pressure stays greater than 12 mm Hg. – TIPS: second-line therapy if the preceding methods fail; TIPS decreases portal pressure by developing communication between a hepatic vein and an intrahepatic portal vein branch.

Medication
Primary prevention of variceal bleeding includes endoscopy, which evaluates variceal size and determines risk stratification based on the presence or absence of a red wale sign (a longitudinal variceal crimson streak that indicates either a recent bleed or an impending bleed). F1 varices are short and straight, whereas F2 varices are larger and tortuous, occupying less than one third of the esophagus lumen. F3 varices are larger, appear to be coiled, and take up more than one third of the esophageal lumen. Both F2 and F3 varices are treated in the same manner.
– Primary prophylaxis: (i) NSBB; (ii) endoscopic variceal ligation (EVL) – Endoscopy every 1 to 2 years if tiny varices and not getting -blockers; every 2 years if cirrhosis and no varices. – Endoscopy every 2 to 3 years if cirrhosis and no varices.

First Line
They are not now actively bleeding. NSBB are effective in cirrhosis with minor varices and increased hemorrhage risk as well as cirrhosis with medium-to-large varices because they lower portal pressure and reduce the risk of first bleeding from 25% to 15% when used as primary prophylaxis. NSBB are also beneficial in patients with cirrhosis who have medium-to-large varices.
● Carvedilol: 6.25 mg daily (3)When it comes to lowering HVPG, [A] is more successful than NSBB.
- Propranolol: 20 mg BID increase until the patient's heart rate has lowered by 25% compared to baseline.
- Nadolol 80 mg once daily; increase dosage as described earlier
- Severe asthma should not be used in patients
Chronic prevention of rebleeding (secondary prevention): NSBBs and EBL lower the rate of rebleeding to a comparable level; however, beta-blockers reduce mortality, whereas ligation does not (5)[A].
Second in Rank
In patients who are unable to take medicine for the prevention of varices, esophageal ligation can be used to eradicate the condition.
Treatment for Budd-Chiari syndrome includes anticoagulation, angioplasty/thrombolysis, TIPS, and orthotopic liver transplantation. Treatment for EHPVO includes anticoagulation as well as mesenteric-left portal vein bypass (meso-Rex procedure).


Referral For endoscopy, liver transplantation, and interventional radiology, refer patients who have symptoms of TIPS.


Pneumococcal and hepatitis A/B vaccines (HAV/HBV) are additional treatments that may be administered.


Surgical Procedures Esophageal transection: used only in extremely rare instances of uncontrollable, life-threatening bleeding Liver transplantation: performed when all other options have been exhausted

Continued Patient Observation and Monitoring
Endoscopic variceal ligation, performed once every one to four weeks, until the varices are eliminated. If TIPS is present, a repeat endoscopy should be performed to evaluate rebleeding.
Endoscopic screening in patients with known cirrhosis every 2 to 3 years; yearly in patients with decompensated cirrhosis Patients with a liver stiffness 20 kPa and with platelets >150,000 can avoid endoscopic screening (1)[A] and may follow up by annual TE and platelet count Patients with a liver stiffness 20 kPa and with platelets >150,000 can avoid endoscopic screening Patients with a liver 

In cirrhosis, the 1-year survival rate is 50% for those who survive at least 2 weeks following a variceal bleed. In-hospital mortality remains high and is related to the severity of underlying cirrhosis, ranging from 0% in Child- Pugh class A disease to 32% in Child-Pugh class C disease. The prognosis for noncirrhotic portal fibrosis is better than for cirrhotic portal fibrosis.

Complications 
The development of gastric varices following the successful treatment of esophageal varices

● Esophageal varices might reoccur.
encephalopathy caused by damage to the liver, failure of the kidneys, and hepatorenal syndrome
Infections that occur following the banding or ligation of varices

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