​Kembara Xtra - Medicine - Ascites

​Kembara Xtra - Medicine - Ascites 
ESSENTIAL DESCRIPTION
Fluid buildup in the peritoneal cavity, which can happen in circumstances that result in widespread edema
Refractory ascites, often known as ascitic fluid that recurs after paracentesis or that cannot be treated,
Men typically have no peritoneal fluid, however women may have up to 20 mL, depending on their menstrual cycle.

EPIDEMIOLOGY
Children are most frequently linked to malignancy and nephrotic syndrome.
Adults: 81% have cirrhosis, 10% have cancer, 3% have heart failure, and 6% have another disease. 50–60% of cirrhotic individuals will develop ascites within 10 years. With a 50% 2-year survival rate, ascites is a poor prognostic sign in cirrhotic patients.
Ascites is present in 10% of cirrhotic patients.

PATHOPHYSIOLOGY AND ETIOLOGY
Serum-ascites albumin gradient (SAAG): (serum albumin level: ascites albumin level) helps to discriminate between portal hypertension and nonportal hypertension, which cannot be consistently established or confirmed without paracentesis.
In the United States, cirrhosis is the most frequent cause of ascites (high portal pressure, SAAG 1.1).
Acute liver failure, liver cancer, either primary or metastatic, elevated right-sided filling pressures from heart failure or constrictive pericarditis, hepatic venous thrombosis (Budd-Chiari syndrome), and portal vein thrombosis are among conditions that can cause hepatitis.
Meigs syndrome (ovarian cancer), Lymphatic leak (chylous ascites), Pancreatitis, Inflammatory (vasculitis, lupus serositis, sarcoidosis), Other Infections (Parasitic, Fungal), Hemoperitoneum (trauma or ectopic pregnancy), Peritoneal carcinomatosis, Tuberculosis (TB), Severe Hypoalbuminemia (nephrotic
Pathogenesis of ascites in the presence of portal hypertension (cirrhotic ascites) - The majority of ascites is brought on by portal hypertension, which causes the visceral capillary bed to swell and leak fluid into the peritoneal cavity. This dilatation causes systemic blood volume to decrease and portal pressures to rise even higher, leading to hypotension. In an effort to make up for decreased systemic volume and pressure, systemic hypovolemia promotes neurohormonal mechanisms (renin-angiotensin system and antidiuretic hormone) for sodium retention.

RISK ELEMENTS
Hepatitis B and C, alcoholism, and cirrhosis
Advanced kidney disease, cancer, and congestive heart failure (CHF)
● TB

DURATIONAL PREVENTION
Adopt a healthy lifestyle that includes a balanced diet, regular exercise, safe sexual behavior, and abstinence from hepatotoxic drugs.

DISEASE HISTORY
Address risk factors, including as the use of ethanol, exposure to TB, prior cancers, sexual partners, transfusion history, metabolic syndrome, and a higher risk of non-alcoholic steatohepatitis developing into cirrhosis.
Look for signs of an underlying illness, such as chest pain, orthopnea, dyspnea, peripheral edema, asterixis, weight loss, night sweats, and a persistent cough.
Check for consequences (progressive dyspnea caused by increasing belly circumference, fever/abdominal discomfort indicative of spontaneous bacterial peritonitis [SBP]).
Abdominal distention that occurs over time could hurt.

MEDICAL ANALYSIS
The most sensitive (83%) and specific (56%) exam finding is abdominal distention with flank/shifting dullness, which needs more than 1,500 mL of fluid to be detected.
Right-sided heart failure symptoms that could be due to cardiac cirrhosis
Penile/scrotal and pedal edema, elevated jugular venous pressure
Palmar erythema, spider angiomata, and dilated collateral veins in the abdomen wall are symptoms of chronic liver cirrhosis.
Other symptoms of severe liver disease include asterixis, gynecomastia, leukonychia, and muscle atrophy.
Cachexia is a symptom of underlying cancer, and the supraclavicular (Virchow) node points to upper abdominal cancer.

DISTINCTIVE DIAGNOSIS
Weight gain
Large tumors in the ovary
Intestinal blockage
Significant splenomegaly

DETECTION & INTERPRETATION OF DIAGNOSIS
Initial examinations (lab, imaging)
Ultrasound (100 mL or less of ascitic fluid can be detected by ultrasound).
All inpatients and outpatients with clinically new-onset ascites undergo diagnostic paracentesis for fluid analysis to ascertain the cause and rule out infection; the complication rate for this procedure is 1%. Unless there is proof of primary fibrinolysis or disseminated intravascular coagulopathy, coagulation abnormalities do not prevent paracentesis.
Prior to paracentesis, routine efforts to treat platelet or coagulation abnormalities are not necessary. Ascitic fluid analysis: Cell count and differential: Polymorphonuclear (PMN) leukocytes 250 cells/mm3 are diagnostic of SBP.
A low portal pressure exudative process, such as inflammation, biliary/pancreatic, carcinomatosis, or tuberculosis, is indicated by an albumin value of 1.1 g (obtained by deducting ascitic fluid albumin from serum albumin measured on the SAME day).
Indicators of a portal hypertension or transudative process include cirrhosis, CHF, constrictive pericarditis, and thrombosis.
Total protein levels 10 g/dL in cirrhotic individuals without SBP indicate elevated risk and call for antimicrobial prophylaxis (low in cirrhosis, nephrotic disease, and high in cardiac ascites).
Other investigations (depending on the clinical scenario to rule out causes other than cirrhosis) include the following: Bacterial Gram stain/culture if infection is suspected (Cirrhotic individuals with ascites can fail to mount fever or leukocytosis). Fluid cultures are often positive in 50-90% of instances of SBP.
If fluid is acquired before to the first dosage of antibiotics and blood culture flasks are inoculated at the bedside, yield is improved.
Amylase (possibility of bowel perforation, choledocholithiasis, or pancreatitis); Triglyceride (milky fluid); Cytology (less sensitive in the absence of carcinomatosis); Lactate dehydrogenase (LDH): An ascitic fluid-to-serum LDH ratio >1.0 can suggest infection, perforation, or tumor.
Alkaline phosphatase and carcinoembryonic antigen (both high in viscous perforation)
Polymerase chain reaction and mycobacterial culture for TB suspicion
Liver function tests and hepatitis serologies (hepatitis) Blood urea nitrogen/creatinine, electrolytes, and brain natriuretic peptide (renal function)
Abdominal ultrasound (US) can confirm ascites; it is very sensitive, economical, and radiation-free.
Thrombosis or cirrhosis can be identified with portal US Doppler.

 CT scan for cancer in the intra-abdominal pathology
MRI is preferred for diagnosing portal vein thrombosis or evaluating liver dysfunction.

Other/Diagnostic Procedures
If imaging and paracentesis are not diagnostic, consider laparoscopy.
Enables direct peritoneal, liver, and intra-abdominal lymph node imaging and biopsy.
Test Interpretation Cytology may detect malignant cells, such as primary peritoneal carcinoma (most frequently associated with ascites) or adenocarcinoma (ovary, breast, GI tract). It is preferred for evaluating suspected peritoneal TB or malignancies.


TREATMENT
First-line treatment for all patients includes: Daily weight monitoring
If portal hypertension (high SAAG) is the culprit, limit your daily sodium intake to no more than 2 grams.
Only if serum sodium is less than 120 to 125 mEq/L is water restriction (1.0 to 1.5 L/day) necessary.
If you have liver disease, stay away from alcohol and eat a healthy diet.
In EtOH cirrhosis, baclofen may be administered to lessen alcohol cravings and consumption.

MEDICATION /ALERT
Exercise caution when diuring; excessive diuring can result in encephalopathy, hyponatremia, and prerenal acute kidney damage (AKI). Electrolytes and creatinine should be closely watched. Diaphoresis should be stopped if serum sodium or creatinine levels are below 120 mmol/L or 2, respectively.
Avoid using nonsteroidal anti-inflammatory medications, which can make oliguria and azotemia worse.
Due to an increased risk of hypotension and renal failure, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) may be hazardous in individuals with cirrhosis/ascites. Keep away from refractory ascites.
In patients with refractory ascites, SBP, increasing hypotension (SBP 90 mm Hg), AKI, hyponatremia 130 mEq/L, or azotemia, stopping -blockers may be an option.

Initial Line
For patients with increased portal pressures, sodium restriction and diuretics are the backbone of treatment; alternative reasons (such as carcinomatosis) are less likely to respond to medical therapy.
- Spironolactone, 100 to 400 mg daily PO; the initial dose is typically administered at 100 to 200 mg in the AM.
 The preferred diuretic because of its antialdosterone properties; it can be taken alone in ascites with little fluid retention. Be aware of hyperkalemia.
- Furosemide 40 to 160 mg PO daily; the initial dose is typically 40 mg administered in the morning.
The antinatriuretic action contributes to a sodium balance that is negative.
It is preferred to use furosemide in conjunction with spironolactone rather than as a monotherapy for optimum effectiveness and to maintain potassium homeostasis. This is the most typical (and preferred) regimen.
 Adjust the dosage to achieve the desired effects ([i] daily weight loss of no more than 0.5 kg/day in patients without peripheral edema and 1 kg/day in patients with peripheral edema; [ii] urinary sodium output more than the sodium intake) and regularly check the kidneys for function.
Observe your daily weight.
 Modify the ratio to keep the potassium level normal.

Diuretic-intractable/refractory ascites (10% of patients—50% mortality in 6 months) is defined as: (i) Persistent or worsening ascites despite maximum doses of spironolactone (400 mg/day) and furosemide (160 mg/day) for at least 1 week (ii) Recurrence of grade 2 or 3 ascites within 4 weeks of achieving minimal ascites (iii) Diuretic
Treatment: Use 24-hour urine sodium excretion to monitor adherence to dietary sodium reduction.
- Stop using diuretics if your daily urine sodium excretion is less than 30 mmol.
- Serial large-volume paracentesis (LVP) or therapeutic paracentesis (see "Surgery/Other Procedures") - IV furosemide significantly lowers eGFR in ascitic patients and is best avoided.

Next Line
For patients with intractable ascites or hypotension, midodrine 7.5 mg TID has been shown to improve hyponatremia, mean arterial pressure, and response to diuretics (1)[B]. It may also increase survival. Follow the response of the blood pressure.
Amiloride up to 40 mg/day and triamterene up to 200 mg/day in divided dosages are substitutes for spironolactone.
Furosemide substitutes include torsemide up to 100 mg/day and bumetanide up to 4 mg/day.
Vaptans may help treat hyponatremia and ascites, although routine usage in this condition is not yet recommended. Due to the potential to cause substantial liver harm, the FDA has advised against use in chronic liver disease.


QUESTIONS FOR REFERENCE
The only effective treatment for portal hypertension is liver transplantation. Whether or not ascites is evident or under control, individuals with decompensated liver disease should be referred for transplant.

SURGICAL AND OTHER PROCEDURE
Therapeutic paracentesis is the first line of treatment if tight ascites is present. Serial paracenteses, typically performed every two weeks, are the second line of treatment for patients with increased portal pressures after diuretics.
Similar complication rate to diuretics; replace albumin when removing more than 5 L of ascites; 5.5 to 8.0 g albumin for each liter removed; complications include infection, hemodynamic collapse, and acute renal failure. Albumin replacement reduces renal dysfunction, postparacentesis hyponatremia, and overall morbidity; it is probably not necessary for malignant ascites. If patients are undergoing recurrent paracentesis because they are not responding to diuretic monotherapy, diuretics should be continued at 50% of the prior dose.

TIPS is a fluoroscopically placed conduit from the portal vein to the hepatic vein for intractable ascites. At the time of placement, the portal pressure should drop by 20 mm Hg (or to 12 mm Hg), and the ascites should be under control with diuretics. TIPS is only used for patients with elevated portal pressures and refractory ascites.
4 weeks after TIPS, urinary salt and serum creatinine greatly improve and can normalize after 6 to 12 months when combined with diuretics. Annual US to establish shunt function.
After two years, shunt dilatation and/or replacement may be necessary.
TIPS is preferable to paracentesis for managing ascites; there is no mortality difference.
Automated low-flow ascites pumps remove ascitic fluid from the peritoneal cavity and into the bladder for elimination; they are typically employed in patients who cannot have liver transplants or TIPS placed.
Reinfusion of cell-free, concentrated ascites is used to treat malignant ascites. Reinfused intravenously is protein that has been recovered through the filtration and concentration of ascitic fluid.
The peritoneovenous shunt (LeVeen or Denver shunt), which drains ascites into the inferior vena cava, has not been shown to be superior to conventional therapy in terms of survival.
- Bacteremia, intestinal blockage, and variceal bleed are complications.
- Reserved for individuals with refractory ascites who cannot tolerate repeat paracentesis and are not candidates for TIPS or liver transplants.
Indwelling catheters with external drainage are most helpful as a palliative measure for malignant ascites (may be drained at home) and have a generally low infection rate.
Due to the high postoperative mortality rate, percutaneous endoscopic gastrostomy (PEG) tube installation should be avoided in patients with ascites.

CONTINUING CARE/DIAGNOSIS
Depending on the underlying cause, the prognosis changes.
Although ascites alone is rarely fatal, it might be an indication of a fatal underlying condition (such as cancer or end-stage liver disease).

COMPLICATIONS
SBP: Ascitic fluid PMN leukocyte count 250 cells/mm3 or positive culture. Broad-spectrum antibiotics include the following: Cefotaxime 2 g q8h or similar 3rd-generation cephalosporin is the treatment of choice for suspected SBP; covers 95% of flora (including Escherichia coli, Klebsiella, and pneumococci). Levofloxacin is an alternative for patients who are
Consider SBP prophylaxis in cases of GI bleeding, past SBP episodes, or ascitic fluid protein levels below 10 g in patients who are hospitalized for conditions other than SBP.
Hepatorenal syndrome: Type 1 is characterized by rapid acute worsening of renal function developing in the presence of a known precipitating factor. Type 2 is characterized by slow acute worsening of renal function evolving in the absence of a known precipitating factor. Refractory ascites causes type 2 to progress more slowly.
Patients with brawny edema who are obese frequently develop cellulitis. Use antibiotics and diuretics as treatment.