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28 Şubat 2017 Salı


The severity of hyponatremia in patients with cirrhosis is related to the severity of cirrhosis. In the pathogenesis, systemic vasodilatation plays a central role. These patients usually have a significant decrease in systemic vascular resection (SVR) and mean arterial pressure, and a significant increase in cardiac output. Blood tends to accumulate in the splanchnic area.

Factors that cause splanchnic vasodilatation may affect the kidneys, biphasic. In the early stages of the absence of ascites, dilating agents can also affect kidney vessels and cause increased GFR. As the disease progresses, the blood pooled in the splanchnic area decreases the blood supply to other areas and the mean arterial pressure decreases. As a result, renal blood flow is also reduced.
Increased Nitric Oxide (NO) and prostaglandin synthesis play an important role in vasodilatation in cirrhosis. NO synthesis may be stimulated by adsorbed endotoxins. Clearance of these endotoxins is impaired due to decrease in RES functions and portosystemic shunting.
The decrease in blood pressure detected by the baroreceptors activates the water and sodium-retaining neurohumoral mechanisms. These are RAAS, sympathetic nervous system and ADH.
The net effect is water and sodium retention. Despite extracellular sodium storage, the patient experiences a decrease in the effective arterial volume. Sodium retention will also result in ascites if salt restriction is not applied to the patient and diuretics are not given.
Water excretion of patients with cirrhosis before ascites development is usually normal. As the disease progresses, it gradually deteriorates. This is associated with increased secretion of ADH. A less important mechanism in the reduction of water excretion is the reduced renal blood flow.

The result is hypotonic hyponatremia.
Serum sodium level below 130 meq / L is associated with poor prognosis. If sodium falls below 125 meq / L, it may indicate a hepatorenal syndrome that will develop.

MELD scoring is used to predict mortality in patients who are waiting for transplantation. Adding serum sodium to this scoring (bilirubin, creatinine and INR) provides a better mortality prediction than MELD.

In fact, hyponatremia does not give clear clinical findings unless the serum sodium level drops below 120 meq / L, which is only 1% of cirrhotic patients.
Patients who are scheduled to undergo liver transplantation within a short time should be treated if their serum sodium level falls below 130 meq / L (especially to prevent posttransplant osmotic demyelination).
In cirrhotic patients, there is no data on the elevation of serum sodium concentration by treatment to improve morbidity and mortality. In other words, if a person is not a transplant candidate, it is doubtful that he will benefit from aggressive sodium correction therapy. Of course, if there is neurological symptoms that can be attributed to hyponatremia, or if serum sodium concentration is below 120 meq / L, treatment should be done.
Serum sodium should be corrected to 4-6 meq / L per day and should not exceed 9 meq / L.
Water restriction
Although water restriction is a commonly used treatment, there is no data to support it.
As ADH, which is increased by systemic vasodilatation, also increases thirst, it can be a challenge for fluid restriction.

The patient is allowed to drink less fluid from the fluid he or she removes, and ice extraction etc. may be recommended to relieve thirst.
Hipokaleminin düzeltilmesi
Hipokaleminin düzeltilmesi de serum sodyum konsantrasyonunun yükseltilmesine katkı yapacaktır.
Vasopressin receptor antagonists
V2 receptors control mainly the antidiuretic response. While V1a regulates vasoconstriction, V1b is associated with ACTH release.

V2 selective blockers are tolvaptan, satavaptan and lixivaptan. Conivaptan, in addition to v2, buffers V1a.
As a result, great care must be taken when using Conivaptan in cirrhosis.

Tolvaptan increases liver function tests by up to 2.5 fold and worsens liver disease. It should not be used in patients with cirrhosis.
Demoklosiklin has been tried to treat hyponatremia of cirrhotic patient, but was not included in the treatment due to nephrotoxicity. The main cause of this nephrotoxicity is thought to be increased drug levels due to hepatic insufficiency.

Serum sale
It is suitable for use in cirrhosis with deep hyponatremia or in patients who are scheduled to undergo transplantation soon.