Evaluation of ascites

1,317 views 86 slides Jul 31, 2020
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About This Presentation

Evaluation of ascites - tapping diagnosis evaluation management SAAG Ratio and physician and updates and guidelines


Slide Content

EVALUATION OF ASCITES DR.CHETHAN Y DR.PRAVEEN KUSUBI

DEFINITION Greek word ‘ ASKOS’ –Bag or sac Accumulation of fluid with in the peritoneal cavity

PATHOGENESIS

NON CIRRHOTIC ASCITES P roduction of proteinaceous fluid Stenosis or occlusion of portal vein by tumour nodules Portal vein thrombosis lymph node obstruction by tumor H ypoalbuminaemia secondary to proteinuria High output or low output heart failure

Leakage of pancreatic or bile fluid Extensive retroperitoneal dissection

CAUSES OF ASCITES PARENCHYMAL LIVER DISEASE (78%) Cirrhosis of liver Fulminant hepatic failure MALIGNANCY(12%) CARDIOVASCULAR CAUSES(5%) CCF Constrictive pericarditis Cardiomyopathy Thrombosis of IVC Budd chiari syndrome Veno occlusive diseases

INFECTIONS(2%) TB Coccidioidomycosis Fitz hugh curtis syndrome Renal(1.5%) Nephrotic syndrome Uremia Hemodialysis OTHERS(1.5%) Pancreatitis Severe hypothyroidsm Collagen vascular disease Trauma

CLINICAL FEATURES HISTORY Alcohol abuse Injection Drug use Blood transfusion Multiple sexual partners Homosexuality Tattos Life time maximum body weight

History of heart failure Onset of ascites pain abdomen Fever Vaginal discharge

PHYSICAL EXAMINATION Abdominal distension Check for Flank dullness, if present check shifting (Rule out D/D for distension of abdomen by percussion) Check for the signs of liver cell failure Sister mary joseph nodule JVP

DIAGNOSIS Diagnosis of ascites: abdominal paracentesis /USG Evaluation of cause of Ascites = HISTORY +PHYSICAL EXAMINATION+ ACSITIC FLUID ANALYSIS

ABDOMINAL PARACENTESIS Indications : New onset ascites for evaluation of cause All in-patient with ascites Repeat the paracentesis if signs of infection appears

CONTR-INDICATIONS: Coagulopathy: only when clinically evident DIC or fibrinolysis is present PATIENT POSITION Supine or lateral decubitus position INSERTION SITE Left lower quadrant> right lower quadrant 2 finger breadth cephalad and 2 finger breadth medial Careful in the case of surgical scar

CHOICE OF NEEDLE 1.5 inch, 22 guage needle 3.5inch ,22 guage needle Steel needles preferredto plastic sheathed canula TECHNIQUE DIAGNOSTIC PARACENTESIS: Sterile aseptic measures local anesthesia infiltrated Z technique

Slow insertion with Intermittent Aspirations Approx. 30ml of fluid Discard the needle and attach another sterile needle to the syringe Inoculate in to 2 blood culture bottles( 5- 10ml in 50ml bottle and 10-20ml in 100ml culture bottle) EDTA tube for cell count and red top tube for biochemistry

THERAPEUTIC PARACENTESIS 1.5 inch 18 guage or 3.5 inch 18 guage needle 15 guage 5 holed needle has been produced specifically for this purpose Use of vaccum bottles or pump for faster collection 2-4 litres of fluid is removed in diuretic sensitive ascites Total tap is done for diuretic resistant

Indications for therapeutic paracentesis Tense ascites (first line management) Diuretic resistant ascites (second line management ) Childs grade B Selection of patients S. Biilrubin <10mg/dl Plt >40,000/mm3 S.Cr <3mg/dl

ASCITIC fluid Analysis Routine optional Unusual Unhelpful Cell count Amylase Bilirubin Cholesterol Albumin Culture in blood culture bottles Cytology Fibronectin Total protein Glucose MTB smear, culture and PCR Lactate Gram stain, LDH TG ph

GROSS APPEARANCE Normal Transparent and slightly yellow Absolute neutrophil count <1000/mm3 Nearly clear Counts >5000/mm3 Cloudy and shimmering effect Counts >50,000/mm3 Resembles mayonnaise RBC count of 10,000/mm3 Pink appearance RBC count of >20,000/mm3 Distictly red Traumatic Tap Blood clots Milky fluid TG >200mg/dl ( without shimmering effect) and layers out if placed in refrigerator Dilute Skim milk TG 100-200mg/dl Jet black or Tea coloured Pancreatic Ascites and Malignant melanoma Dark brown fluid Biliary perforation

CELL COUNT WBC < 500 cells/mm3 PMN <250 cells/mm3 Corrected WBC count in traumatic tap- 1PMN subtacted for every 250 RBC SBP- neutrophilic predominance TB peritonitis and peritoneal carcinomatosis - Lmphocytic predominance Diuresis related elevation of total counts

SAAG(serum ascites albumin gradient) Based on oncotic-hydrostatic balance Calculated by subtracting the albumin values of both serum and ascitic fluid Correlates directly with portal pressure SAAG of > 1.1gm/dl considered to have portal HTN (97% accuracy) Converse is also true

After diuretics SAAG narrows down in cardiac ascites and never in cirrhosis of liver Help ful in management

Draw backs- D oesn’t explain pathogenesis SAAG falsely low if S.Albumin is less than 1.1gm/dl Both serum and acsitic sample are obtained simultaneously Lipid interferes in albumin assay Arterial hypotension narrow SAAG

Corrected SAAG in hyperglobulinaemia =uncorrected SAAG*0.16*serum globulin +2.5 Approx 5% cases of ascites have mixed ascites (TB peritonitis and cirrhosis) and SAAG will be >1.1gm/dl of

High gradient >1.1gm/dl Alcoholic hepatitis Budd chiari syndrome Cardiac ascites Fulminant hepatic failure Massive liver mets Mixed ascites Myxedema Portal vein thrombosis Sinusoidal obstructive syndrome

LOW GRADIENT <1.1GM/DL Biliary ascitis Bowel obstruction or infarction Nephrotic syndrome Pancreatic ascites Peritoneal carcinomatosis Post operative lymphatic leak Serositis in connective tissue disorder Tubercular Peritonitis

CULTURE Done with blood culture bottles with high sensitivity Sensitivity was approx. around 50% in agar plates and 80% in blood culture bottle method

TOTAL PROTEIN Depends on S erum protein concentration and Almost 20% cases of cirrhosis with relatively high serum protein will have ascitic fliuid protein >2.5gm/dl Total protein doesn’t increase during SBP Cardiac ascites > 2.5gm/dl HCC, massive liver metastasis <2.5gm/dl Old transudate/ exudate classification is obsolete now

Combination of total protein , glucose and LDH helps in distinguishing SBP from secondary peritonitis Total protein> 1gm/dl Glucose less than 50mg/dl LDH > upper limit of normal for serum

GLUCOSE APPROX equal to serum glucose In SBP detected late almost drops to 0mg/dl LDH Uncomplicated ascites- half of the serum level SBP and secondary peritonitis – concentration is more than serum AMYLASE Normal-<50u/l Acute pancreatitis and intestinal perforation- >2000u/l(5 folds of serum)

GRAM STAIN of ASCITIC FLUID Detects only if >10,000 bacteria/ml In SBP concentration usually 1/ml (sensitivity of 10% in centrifuged sample) Helpful in diagnosis of secondary peritonitis

Zn STAIN and CULTURE FOR TB Stain is Rarely positive Sensitivity of culture is 50% and 100% in laproscopy with histology and culture of peritoneal biopsy CYTOLOGICAL EXAMINATION It wil not detect unless peritoneal in involved sensitivity is 100% in peritoneal carcinomatosis and 20-30% in malignancy related ascited Serum AFP is more sensitive than ascitic fluid cytology in HCC

TRIGLYCERIDES Chylous ascites- > 200mg/dl (usually greater than 1000mg/dl) Sterile but cloudy ascites in the setting of cirrhosis : 60+/- 40mg/dl Clear acsites :18+/- 9mg/dl BILIRUBIN >6mg/dl or greater than serum bilirubin suggestive of biliary or proximal SI perforation

A lgorithm for the approach to Ascites ABDOMINAL PARACENTESIS DARK BROWN BLOODY MILKY CORRECTED WBC COUNT BILIRUBIN CONCENTRATION TG LEVELS CELL COUNT

WBC PMN SAAG >50% PMN <50%PMN CELL COUNT <500 >500 <250 >250 >1.1 <1.1 >1.1 <1.1 >1.1 <1.1 TP<2.5gm TP>2.5gm TP<2.5gm SBP Secondary bacterial peritonitis Pancreatic ascitis Positive cytology TB testing

Approach for differentiating SBP from secondary Bacterial pancreatitis PMN >250/mm3 Bile stained TP->1gm Glu -<50mg LDH raised BIL >6mg and bil concentration more in ascitis Free air extravasation perf . peritonitis PMN <baseline after antibiotic Non perf . Sec. Bacterial peritonitis BIL perf SBP surgery u/s for loculated infection surgery

COMPLICATIONS ASCITIC FLUID INFECTION 1.Classification Spontaneous bacterial peritonitis Monomicrobial non neutrocytic bacterascites spontaneous ascitic infection Culture negative neutrocytic ascites Secondary bacterial peritonitis Polymicrobial bacterascites

2.CRITERIA SBP MNB CNNA SEC. BACTERIAL PERITONITIS POLYMICROBIAL BACTERASCITES Positive ascitic fluid culture( monomicrobial ) Positive ascitic fluid culture( monomicrobial ) NEGATIVE culture Positive ascitic fluid culture( polymicrobial ) Positive ascitic fluid culture( polymicrobial ) PMN>250/mm3 PMN<250/mm3 PMN >250/mm3 PMN >250/mm3 PMN <250/mm3 No evidence of intraabdominal surgically treatable source of infection No evidence of intraabdominal surgically treatable source of infection NO antibiotic given and no other explanation of elevated counts Evidence of intraabdominal surgically treatable source of infection Previous Traumatic tap (diagnostic of perforation by paracentesis needle)

2. PATHOGENESIS ALTERED BOWEL FLORA BACTERIA IN MESENTRIC NODES BACTERIA IN ABD LYMPHATICS BACTERIA IN THORACIC DUCT

BACTERAEMIA BACTERIA IN HEPATIC LYMPH BACTERASCITES POOR OPSONIC ACTIVITY MODERATE OPSONIC ACTIVITY GOOD OPSONIC ACTIVITY SBP CNNA STERILE NON NEUTROCYTIC ASCITES

For spontaneous infections : ascites is prerequesite Liver disease can be chronic, acute or subacute For secondary infections Ascites and intra abdominal surgical source of infection are prerequesite

Asctic fluid protein concentration < 1gm/dl is a risk factor for SBP MNB probably represents the early stage of ascitic infection CNNA probably results from previous antibiotic injection inadequete inoculation of fluid spontaneously resolving SBP

3.SYMPTOMS AND SIGNS OF ASCITIC FLUID INFECTION Symptom or sign SBP (%) MNB CNNA Sec. peritonitis Polymicrobial bacterascites Fever 68 57 50 33 10 Abdominal pain 49 32 72 67 10 Abdominal tenderness 39 32 44 50 10 Rebound tenderness 10 5 17 Altered mental status 54 50 61 33

4.FREQUENCY OF OCCURANCE In 1980,s frequency was- 10% Recently – 5-6% Of culture positive ascites- 2/3 rd will be SBP and 1/3 rd MNB Polymicrobial bacterascites I in 1000 paracentesis Secondary peritonits 0-2% of those admitted with ascites

5.PATHOGENS IN ASCITIC FLUID INFECTION Organism SBP(%) MNB Sec. bacterial peritonitis SBP with SID Monomicrobial E.Coli 37 27 20 K.Pneumoniae 17 11 7 7 S.Pneumoniae 12 9 29 S.Viridans 9 2 S.Aureus 7 13 Miscellaneous Gram positive 14 30 50 Miscellaneous Gram negative 10 14 7 7 Polymicrobial 1 53 7

6.RISK FACTORS T. Protein<1gm/dl Paracentesis (1 in 1000 taps) GI hemorrhage UTI

7.DIAGNOSIS Ascitic fluid analysis Elevated absolute PMN with a predominance of neutrophils in a clinical setting compatible with infection should prompt emperical therapy Differentiate it from secondary peritonitis Patient with sec peritonitis unrelated to perforation do not have diagnostic initial ascitic fluid analysis

Repeat the paracentesis after 48 hours to asses the response to treatment

TREATMENT WHEN TO START ??? PMN >250cells/mm3 MNB CNNA Wbc >500 cells/mm3 PMN<250 cells/mm3

WHAT TO START?? WHENT TO REPEAT PARACENTESIS??

8. TREATMENT OF ASCITIC FLUID INFECTION DIAGNOSIS TREATMENT SBP 5 days of IV antibiotic Cefotaxime 2gm 8 th hourly Switch over to more specific therapy after suceptability results are available MNB Treatment is mainly individualised 5 days of IV antibiotic to which organism is susceptable , if the patient is symptomatic or persistently culture positive Assymptomatic people might not require treatment (repeat paracentesis and act accordingly)

CNNA 5 days of IV third generation cephalosporin ( cefotaxime 2gm 8 th hourly) Repeat paracentesis after 48 hours Stable ascitic PMN count with predominant lymphocytes consider TB Secondary bacterial peritonitis Surgical intervention plus 2 weeks of IV cefotaxime 2gm 8 th hourly plus Metronidazole (until sensitivity report) If S.cr >3mg- 12 th hourly

Polymicrobial bacterascites IV 3 rd GEN cefhalosporins plus antianerobes Peritonitis develops in 1 in 10 of needle perforation (if ascitic protein < 1gm/ dl) Duration of treatment determined by clinical response and serial ascitic fluid PMN and cultures

Amoxicillin- clavulanic acid is also effective Avoid fluroquinolones as emperical therapy to treat SBP Avoid nephrotoxic antibiotics

IV ALBUMIN 1.5GM/KG/BD.WT at the time of infection detected 1gm/kg/BD.WT on day 3 ORAL ANTIBIOTICS Oral ofloxacin 400mg BD has been tried for 8 days But usually avoided FOLLOW UP PARACENTESIS In atypical cases, when symptomatic response is not there after 48 hrs MNB, CNNA, polymicrbial bacterascites

9. PROGNOSIS In the past mortality was 48-95% By 1991 reduced to <10 % by early detection and treatment No survivors till now with when diagnosis has been made after s.cr level had risen to 4mg/dl Secondary peritonitis- 100% mortality without surgical intervention With emergency laprotomy 50-67% mortality

10.PREVENTION OF SBP Indication Drug Result Prior SBP Norfloxacin 400mg oral OD until death or liver transplantation 66%reduction of recurrence Cirrhosis with GI hemorrhage Norfloxacin 400mg BD for 1 week Or Ceftriaxone 1gm iv BD for 1 week 73 % reduction in infection 67% reduction in infection

Cirrhosis with ascitic fluid toal protein <1.5gm/dl And either CTP >9 plus T.Bil >3 mg/dl Or S.Creatinie >1.2mg/dl Or BUN>25mg/dl Or S.sodium <130 meq /l Norflox 400mg OD for 1 year 89% reduction in SBP 32% reduction in HRS 52% increase in 3-month survival 25% increase in 1 year survival Cirrhosis with ascitic fluid toal protein <1.5gm/dl Ciplrofoxacin 500mg daily for 1 year 31% reduction in infection 30% improvement in survival

OTHER COMPLICATIONS Cellulitis of lower limb and abdominal wall Tense ascitis Hepatic hydrothorax Abdominal wall hernias

TREATMENT OF ASCITES The SAAG is helpful diagnostically and for therapeutic decision making Diuretics and salt restriction is helpful in high gardient SAAG

LOW GRADIENT ASCITES Peritoneal carcinomatosis (m/c)- Repeated paracentesis TB peritonitis - ATT Pancreatic ascites - spontaneous resolution/ stent chlamydia - Doxycycline Lupus serositis - glucocorticoids

HIGH GRADIENT ASCITES Abstinence from alcohol 1) DIET EDUCATION Salt restriction 2gm/day Fluid restriction is warranted only in hyponatremia of <120mmol

Monitoring urinary sodium excretion Role of urine sodium to pottassium ratio in management Avoid urinary catheterisation

2) ROLE OF DIURETICS Spironolactone is the mainstay of treatment for patients with cirrhosis and ascites Started with both spironolactone and frusemide with initail doses (100mg/ 40mg) Amiloride , 10 mg/day, can be substituted for spironolactone. Frequent dosing is not needed. Titrate both the drugs simultaneously (max of 400mg/160mg)

The 100 : 40 ratio of the daily doses of spironolactone and furosemide usually maintains normokalemia Alcoholic patient who has not had recent food- with hold frusemide for some time (risk of hypokalemia) Prefer oral diuretics over IV diuretics (diuretic induced azotemia)

No limit has been identified for acceptable daily weight loss in patients who have massive edema As soon as the edema has resolved, a reasonable maximum weight loss is probably 0.5 kg/day Avoid NSAIDS

when to stop diuretics? Encephalopathy serum sodium concentration less than 120 mmol /L despite fluid restriction, and serum creatinine level > 2.0 mg/ dL (180 mmol /L ) Potassium abnormality donot stop diuretics adjust the dosage of two diuretics

3 ) BLOOD PRESSURE whether diuretics should be withheld when a patient’s blood pressure is low?? Moniter the baseline BP, consciousness of patient and sr. creatinine baseline blood pressure is usually low (e.g., 60 to 100 mm Hg systolic) in a patient with cirrhosis and ascites

Unless it has dropped rapidly or the patient has confusion or azotemia , diuretics should be given . Blood pressure correlates with survival in cirrhosis. if mean arterial pressure is 82 mm Hg or less, 2-year survival is only 20 % Beta blockers should be stopped if blood pressure is less than 100 mg Hg systolic .

Midodrine can be started at 5 mg orally 3 times daily and titrated up to achieve an increase in blood pressure of approximately 10 mm Hg,

5) THERAPEUTIC PARACENTESIS What is the role of therapeutic paracentesis ? When to do A scitic tap? How frequently to do? How much fluid has to be removed at a time? Role of

4) Role of vaptans Increase urinary water excretion largest randomized trial that included only patients with cirrhosis demonstrated that the vaptan was not clinically beneficial Increase mortality

5.OUT PATIENT MANAGEMENT OF ASCITES Moniter BP, orthostatic hypotension, urea, creat , once in every 2-4 weeks until they are clearly responding to treatment Diuretic doses and dietary sodium intake are adjusted to achieve weight loss and negative sodium balance Spot urine sample for Na/K ratio will guide you in deciding the diuretic dosage

Diet education is crucial to the successful management of such patients Patients with truly diuretic-resistant ascites excrete nearly sodium-free urine despite maximal doses of diuretics.

Low sodium diet (2000 mg/d) and carefully titrated doses of diuretics (spironolactone and furosemide Urine Na/K >1 urine Na/K <1 Further diet education Discontinue NSAID, ACEI, ARB, and beta blocker Continue same treatment

Discontinue NSAID, ACEI, ARB, and beta blocker Ascites persists Add midodrine (if BP<90) Ascites persists Therapeutic paracentesis every 2 weeks and consider TIPS Ascites improves Peritoneovenous shunt if TIPS CI

Refractory ascites Refractory ascites is defined as ascites unresponsive to a sodium-restricted diet and high-dose diuretic treatment 10% patients liver transplantation, serial therapeutic paracentesis , TIPS, and peritoneovenous shunts are the options

COLLOID REPLACEMENT A controversial issue regarding therapeutic paracentesis is the role of colloid replacement Currently A void serial large-volume paracentesis n patients with diuretic-sensitive ascites Withhold albumin after taps of 5 L or less, and consider albumin infusion (6 to 8 g/L of fluid removed) after taps of larger volume in patients with diuretic-resistant ascites

TIPS ( TRANSJUGULAR INTRAHEPATIC PORTO SYSTEMIC SHUNT) TIPS is a side-to-side portacaval shunt TIPS placement was first used for the treatment of refractory variceal bleeding, but it also has been advocated for diuretic-resistant ascites

Indications : Cirrhosis with diuretic resistant ascites Varices Hepatic hydrothorax

PERITONEOVENOUS SHUNT

LIVER TRANSPLANTATION

References Sleisenger and Fordtran’s gastrointestinal and liver disease 10 th edition Diseases of liver and biliary system- SHIELA SHERLOCK 11 th edition HARRISONs principles of internal medicine-19 th edition