Esophageal varices
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Overview
| Esophageal varices Classification and external resources | |
 | |
|---|---|
| Gastroscopy image of esophageal varices with prominent red wale spots | |
| ICD-10 | I85. |
| ICD-9 | 456.0-456.2 |
| DiseasesDB | 9177 |
| MedlinePlus | 000268 |
| eMedicine | med/745 radio/269 |
| MeSH | D004932 |
In medicine (gastroenterology), esophageal varices are extremely dilated sub-mucosal veins in the esophagus. They are most often a consequence of portal hypertension, such as may be seen with cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.
Esophageal varices are diagnosed with endoscopy.[1]
Pathogenesis
The majority of blood from the esophagus is drained away via the esophageal veins, which drain deoxygenated blood from the esophagus to the azygos vein which in turn, directly drains into the superior vena cava. These veins have no part in the development of esophageal varices. The remaining blood from the esophagus is drained away via the superficial veins lining the esophagus interior, which drain into the coronary vein (left gastric vein) which in turn, drains directly into the portal vein. These superficial veins lining the esophagus interior (normally only approximately 1mm in diameter) become distended up to 1-2 cm in diameter in association with portal hypertension.
Normal portal pressure is approximately 9 mmHg compared to an inferior vena cava pressure of 2-6 mmHg. This creates a normal pressure gradient of 3-7 mmHg. If the portal pressure rises above 12mmHg, this gradient rises to 7-10 mmHg.[2] A gradient greater than 10 mmHg is considered portal hypertension. At gradients greater than 10 mmHg, blood flow though the hepatic portal system is redirected from the liver into areas with lower venous pressures. This means that collateral circulation develops in the lower esophagus, abdominal wall, stomach and rectum. The small blood vessels in these areas become distended, becoming more thin-walled, and appear as varicosities. In addition, these vessels are poorly supported by other structures, as they are not designed for high pressures.
In situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastomosis, leading to esophageal varices.
Varices can also form in other areas of the body, including the stomach (gastric varices), duodenum (duodenal varices), and rectum (rectal varices). Treatment of these types of varices may differ.
Treatment and the role of endoscopy
In emergency situations, the care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics (as infection is either concomitant, or a precipitant).
Therapeutic endoscopy is considered the mainstay of urgent treatment. Two main therapeutic approaches exist:
- Variceal ligation, or banding
- sclerotherapy
In cases of refractory bleeding, balloon tamponade may be necessary, usually as a bridge to further endoscopy, a transjugular intrahepatic portosystemic shunt (TIPS), or a distal splenorenal shunt procedure or a liver transplantation.
Nutritional supplementation is not necessary if the patient is not eating for four days or less.[3]
 Esophageal varices seven days post banding, showing ulceration at the site of banding. |
Prevention
Ideally, patients with known varices should receive treatment to reduce their risk of bleeding.[4] The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates have been evaluated for secondary prophylaxis. The effectiveness of this treatment has been shown by a number of different studies.[5]
Unfortunately, non-selective β-blockers do not prevent the formation of esophageal varices.[6]
See also
References
- ↑ Biecker E, Schepke M, Sauerbruch T (2005). "The role of endoscopy in portal hypertension". Dig Dis 23 (1): 11-7. PMID 15920321.
- ↑ Arguedas M (2003). "The critically ill liver patient: the variceal bleeder". Semin Gastrointest Dis 14 (1): 34-8. PMID 12610853.
- ↑ de Lédinghen V, Beau P, Mannant PR, et al (1997). "Early feeding or enteral nutrition in patients with cirrhosis after bleeding from esophageal varices? A randomized controlled study". Dig. Dis. Sci. 42 (3): 536-41. PMID 9073135.
- ↑ Lebrec D, Poynard T, Hillon P, Benhamou J-P (1981). "Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study". N Engl J Med 305: 1371–1374. PMID 7029276.
- ↑ Talwalkar JA, Kamath PS (2004). "An evidence-based medicine approach to beta-blocker therapy in patients with cirrhosis". Am J Med 116: 759–766. PMID 15144913.
- ↑ Groszmann RJ, Garcia-Tsao G, Bosch J, et al. (2005). "Beta-Blockers to Prevent Gastroesophageal Varices in Patients with Cirrhosis". N Engl J Med 353 (21): 2254–2261. PMID 16306522.
See also
Circulatory system pathology (I, 390-459) | |
|---|---|
| Hypertension | Hypertensive heart disease - Hypertensive nephropathy - Secondary hypertension (Renovascular hypertension) |
| Ischaemic heart disease | Angina pectoris (Prinzmetal's angina) - Myocardial infarction (heart attack) - Dressler's syndrome |
| Pulmonary circulation | Pulmonary embolism - Cor pulmonale |
| Pericardium | Pericarditis - Pericardial effusion - Cardiac tamponade |
| Endocardium/heart valves | Endocarditis - mitral valve (regurgitation, prolapse, stenosis) - aortic valve (stenosis, insufficiency) - pulmonary valve (stenosis, insufficiency) - tricuspid valve (stenosis, insufficiency) |
| Myocardium | Myocarditis - Cardiomyopathy (Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Loeffler endocarditis, Restrictive cardiomyopathy) - Arrhythmogenic right ventricular dysplasia |
| Electrical conduction system of the heart | Heart block: AV block (First degree, Second degree, Third degree) - Bundle branch block (Left, Right) - Bifascicular block - Trifascicular block Pre-excitation syndrome (Wolff-Parkinson-White, Lown-Ganong-Levine) - Long QT syndrome - Adams-Stokes syndrome - Cardiac arrest - Sudden cardiac death Arrhythmia: Paroxysmal tachycardia (Supraventricular, AV nodal reentrant, Ventricular) - Atrial flutter - Atrial fibrillation (Familial) - Ventricular fibrillation - Premature contraction (Atrial, Ventricular) - Ectopic pacemaker - Sick sinus syndrome |
| Other heart conditions | Heart failure - Cardiovascular disease - Cardiomegaly - Ventricular hypertrophy (Left, Right) |
| Cerebrovascular diseases | Stroke - Transient ischemic attack - Intracranial hemorrhage/cerebral hemorrhage: Extra-axial hemorrhage (Epidural hemorrhage, Subdural hemorrhage, Subarachnoid hemorrhage) Intra-axial hematoma (Intraventricular hemorrhages, Intraparenchymal hemorrhage) - Anterior spinal artery syndrome - Binswanger's disease - Moyamoya disease |
| Arteries, arterioles and capillaries | Atherosclerosis (Renal artery stenosis) - Aortic dissection/Aortic aneurysm (Abdominal aortic aneurysm) - Aneurysm - Raynaud's phenomenon/Raynaud's disease - Buerger's disease - Vasculitis/Arteritis (Aortitis) - Intermittent claudication - Arteriovenous fistula - Hereditary hemorrhagic telangiectasia - Spider angioma - Dissection (Carotid artery, Vertebral artery) |
| Veins, lymphatic vessels and lymph nodes | Thrombosis/Phlebitis/Thrombophlebitis (Deep vein thrombosis, May-Thurner syndrome, Portal vein thrombosis, Venous thrombosis, Budd-Chiari syndrome, Renal vein thrombosis, Paget-Schroetter disease) - Varicose veins / Portacaval anastomosis (Hemorrhoid, Esophageal varices, Varicocele, Gastric varices, Caput medusae) - Superior vena cava syndrome - Lymph (Lymphadenitis, Lymphedema, Lymphangitis) |
| Other | Hypotension (Orthostatic hypotension) - Rheumatic fever |
| See also congenital (Q20-Q28, 745-747) | |
| ||||
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
