HYPONATREMIA IN CIRRHOTIC PATIENT

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.

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.

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.

1. Treatment of hypercalcemia,
2. Metformin and renal impirment, 
3. PBC - Primary biliary cirrhosis, 
4. Giant cell arteridis:Clinical features,  
5. Vancomycin Resistant Enterococcus: a current overview of diagnosis, prevention and treatment, 
6. PAN -Diagnosis, 
7. Cateter Releated Bloodstream Infections-diagnosis,
8. Exercise-induced hematuria
9. Serratia Infections-Brief

SERRATIA INFECTIONS -Brief

Serratia are gram-negative bacilli belonging to the enterobacter group. There are at least 15 species. The genus is composed of facultative anaerobic gram-negative rods. It is painted red. The strains obtained from the hospital are usually white-creamy stained and multiply well in standard incubators (35-37 ° C).

S. marcescens and other Serratia species do not secrete too many virulence factors and are considered opportunistic. They are mobile and can become adherents to the cell through the fimbrial exchange. S. marcescens can secrete several different hemolysins that are toxic to different cell types.

Serratia infections in humans are generally acquired from exogenous environment. People do not get infected from animals etc.  serratia are, in general, is directly gained from contacts with sources such as soil or water. Although serratia species are often associated with hospital outbreaks, epidemics outside the hospital are not very common. Outbreaks are defined as contamination of ready-made solutions that must be sterile as a fabrication defect.

Individually, hospital-acquired Serratia infection is not very common. The presence of an invasive device in the patient is an important risk factor for Serratia species acquired from the hospital. However, surveillance data indicate that Serratia is not predominant as device-associated infection pathogens. More often, it is necessary to focus on common resource outbreaks.

S. marcescens is a demonstrated human pathogen that can cause urinary tract infection, pneumonia and bloodstream infections. It may cause infective endocarditis in patients using intravenous drug. Rarely, skin and soft tissue infections, surgical site infections, even necrotizing fasciitis, osteomyelitis, septic arthritis have been described.

CNS infections are usually associated with ventriculoperitoneal shunting, lumbar puncture, or spinal injections. Meningoencephalitis has been reported in newborns.

Serratia species affect the eye more often than other regions. According to some studies, Serratia is the most common cause of hospital-acquired ocular infection following P. aeruginosa. Ocular involvement may be in the form of conjunctivitis, keratoconjunctivitis, corneal ulcers and keratitis. Serratia-induced endophthalmitis is uncommon, but its long-term outcome may be poor.

Serratia species are naturally resistant to ampicillin, amoxicillin, ampicillin-sulbactam, amoxicillin clavulanate. Likewise, it is resistant to narrow spectrum cephalosporins (such as cefazolin), cephamycin, macrolides, tetracyclines and nitrofurantoin. AmpC can also produce broad-spectrum beta-lactam resistance by producing beta lactamase. ESBL production and carbapenemase production are also described.

Serratia species are susceptible to a series of antibiotics such as fluoroquinolones, aminoglycosides, trimotoprim-sulfamethoxazole, piperacillin-tazobactam, ticarcillin-clavulanate, 3rd and 4th generation cephalosporins, aztreonam and carbapenems.

Internalism English content

1. Treatment of hypercalcemia,
2. Metformin and renal impirment, 
3. PBC - Primary biliary cirrhosis, 
4. Giant cell arteridis:Clinical features,  
5. Vancomycin Resistant Enterococcus: a current overview of diagnosis, prevention and treatment, 
6. PAN -Diagnosis, 
7. Cateter Releated Bloodstream Infections-diagnosis,
8. Exercise-induced hematuria

Vancomycin Resistant Enterococcus: a current overview of diagnosis, prevention and treatment

Although many enterococcus species can be held responsible for VRE, Enterococcus faecum and Enterococcus faecalis constitute 95% of VRE infections.

We can add vancomycin resistant strains such as E. gallinarus and E.casselflavius ​​to these, but these two organisms are more or less related to colonization. Their pathogens are low and they can live in nature for years.

Vancomycin inhibits enterococci by binding to the D-alanyl-D-alanine (D-Ala-D-Ala) terminal of cell wall precursors.

In the case of residence, the D-Ala-D-Ala terminus is replaced by the D-Ala-D-lactate termination. Vancomycin binds to this end with low affinity. As a result, the MIC value for vancomycin is almost 1000 fold.

The accepted MIC value for vancomycin susceptibility is ≤4 mcg / mL, while the value that is resistant is considered to be ≥32 mcg / mL. Values ​​between 8-16 mcg / mL Vancomycin is considered to be intermediate, at which Vancomycin is not preferred.

Pulse-field gel electrophoresis (PFGE) is used in the analysis of both endemic and epidemic clusters of VRE infection and colonization.

The vast majority of VREs are Enterococcus faecum.

Risk factors

• Previous antibiotic therapy history is the most common risk factor for VRE. Vancomycin and cephaloporins are prominent antibiotics. Ceftazidime has been found one of the most prominent in a study.
• Administration of antibiotics for anaerobic treatment is known to increase the intensity of the fecal colonization of VRE, which decreases after the antibiotic is discontinued.

Patient characteristics

• More than 72 hours of hospital stay, important underlying medical conditions, need for ICU and invasive devices.
• Colonization pressure
• Exposure to contaminating surfaces
• Patient from care centers

The patient known to be colonized with VRE is estimated to have been colonized for at least 1 year.

The percentage of VRE infection development in patients who are contaminating with VRE is about 8%. This rate is higher in severely ill patients and those with immunodeficiencies.

Routine surveillance cultures are not recommended to detect colonized patients with VRE in non-epidemic centers. Active surveillance cultures are recommended for high-risk patients and are recommended for centers with increased frequency of VRE.

The most important method of protection is hand washing. In particular, it should be ensured that health personnel take into account contact measures.

VRE hasta odasındaki yüzeylerde saatlerce-günlerce kalabilmektedir.

VRE description: Vancomycin resistance is defined as ≤ 16 mm by disc diffusion method or 8 μg / ml by agar dilution method (MIC) or automated methods.

To say that there is an epidemic; We need to show that in the healthcare facility, 3 or more infections with clinical significance have been acquired within 7 days.

Optimal antibiotic treatment in infected patients with VRE has not been definitively identified. Linezolid is FDA approved. While quinopristin-dalfopristin has been FDA approved in the past, this approval has been lifted due to ineffectiveness.

aminoglycosides.

E.faecalis, like E. gallinarus and E.casselflavius, are generally susceptible to beta-lactams.

Linezolid, daptomycin and tigecycline have activity against both E. faecium and E. faecalis.

The effect of quinopristin-dalfopristin is only against E. faecum, not against E. faecalis.
Türkçe 

1. Treatment of hypercalcemia,
2. Metformin and renal impirment, 
3. PBC - Primary biliary cirrhosis, 
4. Giant cell arteridis:Clinical features,  
5. PAN -Diagnosis, 
6. Cateter Releated Bloodstream Infections-diagnosis,
7. Exercise-induced hematuria
8. Serratia Infections-Brief