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