Gastrointestinal varices natural history, complications and prognosis: Difference between revisions
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==Natural History== | ==Natural History== | ||
Gastrointestinal varices are an indication of increased portal venous pressure, especially in cirrhotic patients. The progressive increase in portal pressure leads to a progressive increase in size of the varices and an increased vascular wall tension. Variceal hemorrhage resulting from rupture occurs when the expanding force exceeds the maximal wall tension. The following sequence of events typically summarizes the natural history of gastrointestinal varices: | |||
=== (i) No varices === | |||
* Early stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is less than 10 mmHg (normal) | |||
=== (ii) Small varices - No hemorrhage === | |||
* Middle to late stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is greater than equal to 10 mmHg | |||
* Development rate is 8 % per year | |||
=== (iii) Large varices - No hemorrhage === | |||
* The size increases with progression of cirrhosis and due to hyperdynamic circulation | |||
* Progression from small to large varices is 8 % per year | |||
=== (iv) Variceal hemorrhage === | |||
* Intravascular pressure in varices greater than the variceal wall tension leads to variceal rupture | |||
* Rate of rupture of esophageal varices is 5 - 15 % per year | |||
* Rate of rupture of gastric varices is 25 % (greater in IGV1 and GOV2) | |||
=== (v) Recurrent hemorrhage === | |||
* Persistent increase in portal pressure leads to recurrence after treatement if the underlying cause is not addressed | |||
==Complications== | ==Complications== |
Revision as of 03:15, 27 November 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Natural History
Gastrointestinal varices are an indication of increased portal venous pressure, especially in cirrhotic patients. The progressive increase in portal pressure leads to a progressive increase in size of the varices and an increased vascular wall tension. Variceal hemorrhage resulting from rupture occurs when the expanding force exceeds the maximal wall tension. The following sequence of events typically summarizes the natural history of gastrointestinal varices:
(i) No varices
- Early stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is less than 10 mmHg (normal)
(ii) Small varices - No hemorrhage
- Middle to late stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is greater than equal to 10 mmHg
- Development rate is 8 % per year
(iii) Large varices - No hemorrhage
- The size increases with progression of cirrhosis and due to hyperdynamic circulation
- Progression from small to large varices is 8 % per year
(iv) Variceal hemorrhage
- Intravascular pressure in varices greater than the variceal wall tension leads to variceal rupture
- Rate of rupture of esophageal varices is 5 - 15 % per year
- Rate of rupture of gastric varices is 25 % (greater in IGV1 and GOV2)
(v) Recurrent hemorrhage
- Persistent increase in portal pressure leads to recurrence after treatement if the underlying cause is not addressed
Complications
Prognosis
The AIMS65 score is best predictor of mortality in patients with variceal bleeding. The score is calculated as follows:
Variable | Score |
---|---|
Albumin | 1 |
INR | 1 |
Systolic blood pressure | 1 |
Altered mental status | 1 |
Age > 65 years | 1 |
Interpretation of AIMS65 score
Score 0 = No risk
Score 1-2 = Moderate risk
Score > 2 = High risk