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relating to the esophagus

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/04/05 14:28:32」(JST)

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In medicine (gastroenterology), esophageal varices (or oesophageal varices) are extremely dilated sub-mucosal veins in the lower third^[1] of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.

Esophageal varices are diagnosed with endoscopy.^[2]

Pathogenesis

The upper two thirds of the esophagus is drained via the esophageal veins, which carry deoxygenated blood from the esophagus to the azygos vein, which in turn drains directly into the superior vena cava. These veins have no part in the development of esophageal varices. The lower one third of the esophagus is drained into the superficial veins lining the esophageal mucosa, which drain into the left gastric vein (coronary vein), which in turn drains directly into the portal vein. These superficial veins (normally only approximately 1 mm 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 12 mmHg, this gradient rises to 7-10 mmHg.^[3] A gradient greater than 5 mmHg is considered portal hypertension. At gradients greater than 10 mmHg, blood flow through 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 situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastomosis, leading to esophageal varices. Splenic vein thrombosis is a rare condition that causes esophageal varices without a raised portal pressure. Splenectomy can cure the variceal bleeding due to splenic vein thrombosis.

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. In some cases, schistosomiasis also leads to esophageal varices.

Prevention

In ideal circumstances, 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 (e.g. isosorbide mononitrate (IMN) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers like atenolol) are preferred because they decrease both cardiac output by β₁ blockade and splanchnic blood flow by blocking vasodilating β₂ receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.^[5]

However, non-selective β-blockers do not prevent the formation of esophageal varices.^[6]

When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then treatment with prophylactic endoscopic variceal ligation is often performed.^[7]

Treatment

Esophageal varices seven days after banding, showing ulceration at the site of banding

In emergency situations, care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics (usually a quinolone or ceftriaxone, as infection by Gram-negative strains is either concomitant or a precipitant).

Blood volume resuscitation should be done promptly and with caution. The goal should be hemodynamic stability and hemoglobin of over 8 g/dl. Resuscitation of all lost blood leads to increase in portal pressure leading to more bleeding. Volume resuscitation can also worsen ascites and increase portal pressure. (AASLD guidelines)

Therapeutic endoscopy is considered the mainstay of urgent treatment. The two main therapeutic approaches are variceal ligation or banding and sclerotherapy.

In cases of refractory bleeding, balloon tamponade with a Sengstaken-Blakemore tube may be necessary, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal hypertension). Esophageal devascularization operations such as the Sugiura procedure can also be used to stop complicated variceal bleeding. Methods of treating the portal hypertension include: transjugular intrahepatic portosystemic shunt, 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.^[8]

Terlipressin and octreotide for 1 to 5 days have also been used.^[9]

Histology

Axial CT showing esophageal varices in liver cirrhosis with portal hypertension

Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.

References

^ Rubin's Pathology: Clinicopathologic Foundations of Medicine edited by Raphael Rubin, David S. Strayer, Emanuel Rubin, page 612
^ Biecker E, Schepke M, Sauerbruch T (2005). "The role of endoscopy in portal hypertension". Dig Dis 23 (1): 11–7. doi:10.1159/000084721. PMID 15920321.
^ Arguedas M (2003). "The critically ill liver patient: the variceal bleeder". Semin Gastrointest Dis 14 (1): 34–8. PMID 12610853.
^ 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 (23): 1371–1374. doi:10.1056/NEJM198112033052302. PMID 7029276.
^ Talwalkar JA, Kamath PS (2004). "An evidence-based medicine approach to beta-blocker therapy in patients with cirrhosis". Am J Med 116 (11): 759–766. doi:10.1016/j.amjmed.2004.03.006. 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. doi:10.1056/NEJMoa044456. PMID 16306522.
^ Garcia-Tsao G, Sanyal AJ, Grace ND, Carey W; Practice Guidelines Committee of the American Association for the Study of Liver Diseases; Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922-938. PMID 17879356
^ 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. doi:10.1023/A:1018838808396. PMID 9073135.
^ Abid S, Jafri W, Hamid S, et al. (March 2009). "Terlipressin vs. octreotide in bleeding esophageal varices as an adjuvant therapy with endoscopic band ligation: a randomized double-blind placebo-controlled trial". Am. J. Gastroenterol. 104 (3): 617–23. doi:10.1038/ajg.2008.147. PMID 19223890.

External links

Treatment of Esophageal Varices - World Gastroenterology Organisation (WGO)

UpToDate Contents

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1. 肝硬変患者における静脈瘤出血に対する一次予防および静脈瘤形成予防 primary and pre primary prophylaxis against variceal hemorrhage in patients with cirrhosis
2. 静脈瘤出血のマネージメントの一般原則 general principles of the management of variceal hemorrhage
3. 急性静脈瘤出血患者における止血法 methods to achieve hemostasis in patients with acute variceal hemorrhage
4. 患者情報：食道静脈瘤（詳細） esophageal varices beyond the basics
5. 慢性C型肝炎ウイルス感染のマネージメントの概要 overview of the management of chronic hepatitis c virus infection

English Journal

Factors Associated with Aggravation of Esophageal Varices after B-RTO for Gastric Varices.

Jogo A, Nishida N, Yamamoto A, Matsui H, Takeshita T, Sakai Y, Matsuoka T, Nakamura K, Miki Y.SourceDepartment of Radiology, Osaka City University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan, duexg204@gmail.com.
Cardiovascular and interventional radiology.Cardiovasc Intervent Radiol.2013 Dec 10. [Epub ahead of print]
PURPOSE: To retrospectively evaluate risk factors for aggravation of esophageal varices (EV) within 1 year after balloon-occluded retrograde transvenous obliteration (B-RTO) of gastric varices (GV) and to clarify suitable timing for upper endoscopy to detect EV aggravation after B-RTO.METHODS: Part
PMID 24322305

Pathophysiology and recent findings of primary biliary cirrhosis complicated by systemic sclerosis.

Ohira H, Watanabe H.SourceDepartment of Gastroenterology and Rheumatology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Hepatology research : the official journal of the Japan Society of Hepatology.Hepatol Res.2013 Dec 6. doi: 10.1111/hepr.12285. [Epub ahead of print]
Primary biliary cirrhosis (PBC) can be complicated by systemic sclerosis (SSc) and more specifically, limited cutaneous SSc (lcSSc), which was previously called CREST syndrome. Moreover, combined PBC and SSc has been described in many case reports. Although neither the etiology of PBC nor that of SS
PMID 24308674

Chronologic changes of explanted liver volume and the use of ursodeoxycholic acid in patients with end-stage primary biliary cirrhosis.

Tanaka T, Yamashiki N, Sugawara Y, Tamura S, Nakamura M, Kaneko J, Aoki T, Sakamoto Y, Hasegawa K, Kokudo N.SourceOrgan Transplantation Service, The University of Tokyo Hospital.
Hepatology research : the official journal of the Japan Society of Hepatology.Hepatol Res.2013 Dec 2. doi: 10.1111/hepr.12283. [Epub ahead of print]
AIM: Primary Biliary Cirrhosis (PBC) is a common indication for liver transplantation (LT). The clinical presentation of PBC at the time of LT might have changed, due to the long-term use of ursodeoxycholic acid (UDCA). The aim of this retrospective study was to investigate whether the clinical char
PMID 24298893

Japanese Journal

生体肝移植術を含む3回の開腹術歴後に完全腹腔鏡下脾臓摘出術を施行し得た一例

矢野博子,池上徹,吉住朋晴,赤星朋比古,富川盛雅,内山秀昭,副島雄二,調憲,前原喜彦,Yano Hiroko,Ikegami Toru,Yoshizumi Tomoharu,Akahoshi Tomohiko,Tomikawa Morimasa,Uchiyama Hideaki,Soejima Yuji,Shirabe Ken,Maehara Yoshihiko,ヤノヒロコ,イケガミトオル,ヨシズミトモハル,アカホシトモヒコ,トミカワモリマサ,ウチヤマヒデアキ,ソエジマユウジ,シラベケン,マエハラヨシヒコ
福岡医学雑誌 104(3), 64-67, 2013-03-25
… She was hospitalized this time for decompensated liver cirrhosis due to recurrent cholangitis, with apparent hypersplenism and risky esophageal varices. … After a few session of endoscopic treatment for esophageal varices, we applied total laparoscopic splenectomy for hypersplenism in a patient with multiple surgical histories, for seeking better surgical field for safety. …
NAID 120005295633

食道静脈瘤に対する内視鏡下治療時の栄養療法の意義 (特集肝硬変患者の栄養マネージメント)

坂井良行,齋藤正紀,岩田恵典 [他]
消化器内科 55(6), 791-798, 2012-12-00
NAID 40019559785

食道静脈瘤出血に対する内視鏡治療の到達点 (特集上部消化管出血に対する緊急内視鏡の最前線)

中村真一,岸野真衣子,山本果奈 [他]
消化器内科 55(5), 539-544, 2012-11-00
NAID 40019527026

Related Pictures

★リンクテーブル★

リンク元	「食道静脈瘤」「esophageal and gastric varices」
拡張検索	「endoscopic injection sclerotherapy for esophageal varices」
関連記事	「esophageal」

「食道静脈瘤」

Esophageal varices
	Gastroscopy image of esophageal varices with prominent cherry-red spots
Classification and external resources
Specialty	Gastroenterology
ICD-10	I85
ICD-9-CM	456.0-456.2
DiseasesDB	9177
MedlinePlus	000268
eMedicine	med/745 radio/269
MeSH	D004932
	[edit on Wikidata]

　　[★]

英: esophageal varix, esophageal varices
関: 胃静脈瘤、variceal bleeding、門脈圧

病態

門脈圧亢進を背景として粘膜下層～粘膜固有層の静脈叢に静脈瘤が形成される。
好発部位：下部食道
静脈瘤の形成には左胃静脈、短胃静脈、後胃静脈が関与している。

検査

上部消化管内視鏡検査

日本では形態(form, F)F2以上や発赤所見(red color sign, RC)RC2以上が危険な静脈瘤として予防的治療の適応となっている(SSUR.645)
青色静脈瘤、連珠状静脈瘤(F2)以上、red color sign陽性は治療対象(QB.A-341)

内視鏡所見の分類

参考3

F:form 形態	F0 静脈瘤として認められないもの F1 直線的な細いもの F2 連珠状、中等度 F3 結節状、腫瘤状
C: color 色調	Cw (白色静脈) Cb (青色静脈)
RC:red color sign 発赤所見	Red color sign(RC) ミミズ腫れ所見 red wale marking (RWM) サクランボ様発赤 cherry red spot様所見 (CRS) 血マメ所見 hematocystic spot (HCS)

F3, red color sign [show details]

治療

SSUR.649-

バルーンタンポナーデ法

ゼングスターケン・ブレークモア管 Sengstaken-Blakemoreチューブ

薬物療法

(緊急出血)バソプレシン・ソマトスタチン：門脈の流入血流を減少させ、門脈圧を減少させる。肝機能悪化リスクあり。
(予防)プロプラノロール・ナドロール：非選択的βブロッカーを使うことで、β2受容体を介した血管拡張がblockされα1受容体を介した血管収縮が優位となり、腸管の細動脈の収縮により門脈の血流が減少、門脈圧が低下する。さらに多く用いれば、β1受容体を介した心拍出量の低下により脾動脈血流量が減少し、門脈圧がより低下する。(参考2)