Liver cirrhosis is the final stage of chronic liver disease and can be divided into compensated and decompensated phases. Recent evidence reinforces the importance of preventing first decompensation in those patients with compensated cirrhosis or clinically significant liver disease.
With the advent of non-invasive measures of liver stiffness, new concepts gained momentum. The measurement of the porto-hepatic venous gradient is an invasive measure and not available in clinical practice. However, we know that there is clinically significant portal hypertension (HPCS) when this gradient is above 10 mmHg. This increases the risk of decompensation events such as ascites and formation of esophagogastric varices. In this situation, preventive treatment is indicated.
Liver elastography helps in the diagnosis of clinically significant portal hypertension and allows intervention with prophylaxis measures, such as the use of non-selective beta-blockers (BBNS). HPCS can be defined in patients with mean hepatic stiffness (HMR) > 25 kPa or between 20-25 with platelet counts <150,000/mm³. RHM values < 15 kPa + plaquetas > 150,000/mm³ has good negative predictive value to exclude HPCS.
A recently published review article, written by Guadalupe Garcia and Maria Diaz-Soto, brought what is new in the management of HPCS and esogagogastric varices.
Presence of esophageal varices:
- 50-60% – compensated cirrhosis;
- Up to 85% – decompensated cirrhosis.
First variceal upper gastrointestinal bleeding (HDAv) occurs at a rate of 10-15% per year and HDAv recurs at a rate of up to 60% per year.
Mortality from HDAv in six weeks
- 40% in the 1980s to 15 to 20% more recent.
ascites it’s usually the first clinical manifestation of decompensated liver cirrhosis. Thus, current evidence reinforces that the main objective in compensated cirrhosis is not only to prevent variceal bleeding, but to prevent any decompensation, including ascites, HDAv, and hepatic encephalopathy.
Portal hypertension occurs mainly by two mechanisms.
1. Increased intrahepatic resistance to portal flow:
- 70% related to structural component of fibrosis and regeneration nodules The It can be modified by treating the underlying disease.
- 30% for endothelial dysfunction and reduced nitric oxide leading to increased hepatic vascular tone
Statins are promising drugs being studied in the treatment of HPCS, with antifibrotic potential and also potential to improve endothelial dysfunction.
two. Increased portal venous flow
- Collateral circulation – eg. esophageal varices;
- splanchnic vasodilation The Reduction of effective circulating volume The RAAS activation The sodium and water retention The Increased cardiac output
The increase in portal venous flow is the target of therapies such as:
- BBNS (nadolol, propranolol and carvedilol):
- It is made β2 blocker The splanchnic vasoconstriction.
- It is made β1 blocker The reduction in cardiac output and portal flow.
Carvedilol should be the drug of choice when tolerated (in the absence of hypotension) due to its α1-blocking effect, which generates intrahepatic vasodilation.
- Parenteral splanchnic vasoconstrictors, such as somatostatin and its octreotide analogue, and vasopressin and its terlipressin analogue The used in HDAv
Other therapies used in the management of esophagogastric varices are transjugular intrahepatic portosystemic tshunt (TIPS) and elastic ligation of esophageal varices (LIGHT).
In TIPS, blood is diverted from the portal vein to the hepatic vein, reducing portal pressure, but this also diverts toxic metabolites, the main complication being hepatic encephalopathy.
LEVE is the main approach to control acute LV bleeding, obliterating them. sare local and transient therapies and do not improve portal hypertension.
Treatment of compensated cirrhosis with HPCS
Defined by CPS A liver cirrhosis with one of the following:
In case of intolerance to BBNS, perform EDA and adopt the conducts according to the findings.
- Absence of EV: New EDA in two years
- Fine-gauge EV: New EDA in one year
- Medium/Large Caliber VE: LIGHT
Treatment of decompensated liver cirrhosis
It is indicated to perform UDE for evaluation of esophagogastric varices.
In the presence of low-risk varicose veins, start BBNS.
In the presence of high-risk varicose veins, start BBNS preferably. If contraindication or intolerance, proceed with LEVE.
In the presence of recurrent ascites, requiring more than three large-volume paracentesis in 1 year, TIPS should be considered.
Treatment of HDAv
– PERVIA AIRWAY
– VOLUME REPLACEMENT, RESTRICTIVE TRANSFUSION POLICY – HB TARGET BETWEEN 7-9 G/DL. DO NOT MAKE FRESH FROZEN PLASMA ROUTINELY.
– SPLANCHNIC VASOCONSTRICORERS (TERLIPRESSIN, SOMATOSTIN, OCTREOTIDE)
– ANTIBIOTIC PROPHYLAXIS (PARENTERAL CEFTRIAXONE 5-7 days)
- Early UDE – first 12 hours with rubber band ligation in the following cases:
– ACTIVE BLEEDING IN VARIZATION;
– RECENT BLEEDING STIGMAS;
– VARICES WITHOUT SIGNS OF BLEEDING, IN THE ABSENCE OF ANOTHER FOCUS OF BLEEDING.
- Continue splanchnic vasoconstrictors for 2-5 days.
– IN THE ABSENCE OF BLEEDING: DISCONTINUE PARENTERAL DRUG AND START BBNS;
– IN CASE OF BLEEDING The TYPES OF REDEMPTION
- In the presence of uncontrolled bleeding The Balloon bridge or expandable prosthesis up to rescue TIPS.
- Consider preemptive TIPS within 72 hours in patients at high risk of rebleeding:
– CPS 10-13 POINTS;
– CPS B> 7 WITH ACTIVE BLEEDING AT ENDOSCOPY.
The prevention of recurrence of HDAv is made through the association of BBNS and LEVE. In patients undergoing TIPS, there is no need for additional therapy, as they have already undergone the definitive method of reducing portal pressure.
Guide on diagnosis, transmission and prevention of hepatitis D and E [e-book]
Treatment of gastric varices
|Esophageal varices that extend to the lesser curvature||
75% of gastric varices.
Management equal to EVs
|Esophageal varices extending to the greater curvature and gastric fundus||Management similar to IGV 1|
|Gastric varices isolated on a background||
|Gastric varices isolated elsewhere in the stomach||
The GOV2 and IGV1 varices are the cardia/fundus varices and have similar and more difficult management than the GOV1. Few studies of preventive treatment of rupture of these varicose veins. In the presence of acute bleeding, cyanoacrylate injection and, when necessary, placement of a balloon or self-expanding prosthesis can be continued.
In some cases, definitive interventional radiology procedures such as TIPS and retrograde transvenous venous obliteration are required.
In recent years, great advances have been made in understanding the pathophysiology of liver cirrhosis. We know that there is a big prognostic difference between compensated and decompensated cirrhosis and therefore, preventing decompensation events such as ascites and HDAv are very important goals. Non-selective beta-blockers should be the drug of choice not only to prevent variceal bleeding, but also the development of ascites in patients with HPCS. Statins are promising drugs in liver cirrhosis, but more studies are still needed to become a formal recommendation.
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