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done by Al Yaqdhan Al Atbi
Senior clerkship medical student SQUH - Oman

Published in: Health & Medicine
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  1. 1.  Case scenario  Definition of ascites  Causes of ascites  Diagnosis of ascites:  History, physical examination, investigations, and procedures  Management of ascites
  2. 2.  A 42 years gentleman k/c/o:  HTN since 3 years on medication  Liver cirrhosis secondary to chronic HBV infection  Oesophageal varices treated with sclerotherapy and banding  Presented to the A&E complaining of headache since one day and abdominal distension since four days.  The headache is in the frontal area, dull in nature, scored by 8, not radiating. It is associated with drowsiness and slurred speech.
  3. 3.  He denied any Hx of nausea/ vomniting, weakness, fever, or trauma to head. He complain of tremor of both hands to the extend that he can't hold any thing. He gave Hx of two days constipation.  Medication:  Fursmide 40 mg OD  Spironolacton 100 mg OD  Propranolo 100 mg TID  Omeprazol  Lactelose  Entacavir 0.5 mg OD  He is not smoker or alcohol consumer.  Rest of Hx: unremarkable.
  4. 4.  Young gentleman alert oriented not in pain or distress GCS 15/15, MMSE 27  Vitals: BP 161/102 mmHg; PR 75 bpm; RR 18; temp 36.7; saturation 99%  General assessment: jaundice, pallor, pitting edema in both legs up to the knee, dehydrated, JVP 5cm rised, no cynosis or LN enlargement. Have mild flapping tremor. No other sings of chronic liver disease.
  5. 5.  Abdominal examination:  Distended, everted umbilicus , no dilated viens  Tens, non tender, no organomegaly.  Massive ascites +4  I couldn’t appreciate bowel sounds  DRE: pt refused  Chest bilateral inspiratory basal crepitation
  6. 6. Investigations:  CBC: Hb9.7; hemtocrits n; plt 99; WBC 6.6  Coagulation: all are abnormal; INR 2.11  NH3: 386 on admission; on discharge 87  LFT: AST 220; ALT 81; ALP normal; albumin39 low; total bilirobin 122 high  Lipid profile : normal  U&E: AG16; urea 8.7; rest WNL  AFP: 5509  CT chest and abdomen: Liver cirrhosis with mass in segment 3 suggstive of HCC; gross ascites; chest normal  CT brain: no lesion
  7. 7.  Lactulose enema 50 ml  Continue oral lactulose  Start ciftrixione  Follow up in gastro OPD after 1 month
  8. 8.  Ascites is defined as the accumulation of free fluid in the peritoneal cavity.  It is a common clinical finding with a variety of both extraperitoneal and peritoneal etiologies.  It is most often caused by: -liver cirrhosis 75% of patients -malignancy (10%) heart failure (3%) pancreatitis (1%) TB (2%)
  9. 9. Non-peritoneal causes Examples Intrahepatic portal hypertension Cirrhosis Fulminant hepatic failure Veno-occlusive disease Extrahepatic portal hypertension Hepatic vein obstruction (ie, Budd-Chiari syndrome) Congestive heart failure Hypoalbuminemia Nephrotic syndrome Protein-losing enteropathy Malnutrition Miscellaneous disorders Myxedema Ovarian tumors Pancreatic & Biliary ascites Chylous Secondary to malignancy, trauma
  10. 10. Peritoneal Causes Examples Malignant ascites Primary peritoneal mesothelioma Secondary peritoneal carcinomatosis Granulomatous peritonitis Tuberculous peritonitis Fungal and parasitic infections Sarcoidosis Foreign bodies (cotton ,starch, barium) Vasculitis Systemic lupus erythematosus Henoch-Schönlein purpura Miscellaneous disorders Eosinophilic gastroenteritis Whipple disease Endometriosis
  11. 11.  Approximately 85% of patients with ascites have cirrhosis, Past history of cancer, heart failure, or TB.  Symptoms:  abdominal distension:  painless or associated with abdominal discomfort  course of days (eg, bloody ascites due to trauma) or months (eg, malignant ascites)
  12. 12.  Weight gain, shortness of breath, early satiety, and dyspnea due to fluid accumulation and increased abdominal pressure.  Spontaneous bacterial peritonitis  fever, abdominal tenderness, and altered mental status.
  13. 13.  Cirrhosis: confusion and GI bleeding  Malignant ascites: weight loss  Heart failure: dyspnea, orthopnea, and peripheral edema  Chylous ascites: diarrhea and steatorrhea, malnutrition, edema, nausea, enlarged lymph nodes, early satiety, fevers, and night sweats
  14. 14.  Approximately 1.5 L must be present before flank dullness is detected.  If no flank dullness is present, the patient has less than 10% chance of having ascites.  Shifting dullness & fluid thrill mean that more fluid is present.  Abdominal ultrasound to determine with certainty if fluid is present and in obese.
  15. 15.  Signs:  flank dullness; shifting dullness; fluid wave; evidence of pleural effusion  PE findings related to the underlying cause of the ascites, such as:  Stigmata of cirrhosis.  HF  Other causes
  16. 16.  Two grading systems for ascites have been used in the literature.  An old system which grades ascites from 1+ to 4+, depending on the detectability of fluid on physical examination.  More recently, the International Ascites Club has proposed a system of grading from 1 to 3.
  17. 17.  The older system  1+ is minimal and barely detectable.  2+ is moderate.  3+ is massive but not tense.  4+ is massive and tense.  The International Ascites Club grading (2003)  Grade 1: mild ascites detectable only by US.  Grade 2: moderate ascites manifested by moderate symmetrical abdominal distension.  Grade 3: large or gross ascites with marked abdominal distension.
  18. 18.  Patients suspected of having ascites based on history and physical examination should undergo radiographic imaging.  Ultrasound is probably the most cost-effective modality.  In cirrhotic pt, US, CT, or MRI may reveal evidence of a nodular liver.  US findings in patients with portal HTN may include:  Dilation of the portal vein to ≥13 mm  Dilation of the splenic and superior mesenteric veins to ≥11 mm
  19. 19.  Abdominal paracentesis is mainly to identify the cause of ascites.  Abdominal paracentesis is indicated for all patients with new onset ascites
  20. 20. - New onset ascites - Hospitalization of a patient with ascites - Clinical deterioration of an inpatient or outpatient with ascites - Fever - Abdominal pain - Abdominal tenderness - Hepatic encephalopathy - Peripheral leukocytosis - Deterioration in renal function 25 1/25/2014
  21. 21.  Patients with disseminated intravascular coagulation.  Primary fibrinolysis.  Patients with a massive ileus with bowel distension.  The location of the paracentesis should be modified in patients with surgical scars so that the needle is inserted several centimeters away from the scar.  Relative contraindications:  Pregnancy  Distended urinary bladder  Abdominal wall cellulitis  Distended bowel  Intra-abdominal adhesions 26 1/25/2014
  22. 22.  Initial tests that should be performed on the ascitic fluid:  Appearance assessment  Serum-to-ascites albumin gradient determination (SAAG)  Cell count and differential; culture  Total protein concentration  Additional tests that may be performed to aid in confirming a diagnosis include:  Culture with bedside inoculation of aerobic and anaerobic blood culture bottles  Glucose concentration (malignancy, infection, bowel perforation)  Lactate dehydrogenase concentration (malignancy, infection, or bowel perforation)  Gram stain (suspected bowel perforation)  Amylase concentration (pancreatic ascites or bowel perforation)  Tuberculosis smear, culture, and adenosine deaminase activity (tuberculous peritonitis)  Cytology and possibly carcinoembryonic antigen level (malignancy)  Triglyceride concentration (chylous ascites)  Bilirubin concentration (bowel or biliary perforation)
  23. 23. Ascitic Fluid Testing Routine Sometimes useful Rarely helpful Cell count & differential Total protein pH Albumin Culture LDH Glucose Lactate Gram stain Amylase Triglycerides Bilirubin Cytology TB smear and culture
  24. 24. Color Appearance Translucent or yellow Normal/sterile Brown Hyperbilirubinemia GB or biliary perforation Cloudy or turbid Infection Pink or blood tinged Mild Trauma Grossly bloody traumatic tap; Malignancy Abdominal trauma Cirrhosis Thoracic duct injury Lymphoma Milky ("chylous")
  25. 25.  Smear & culture for mycobacteria.  Cytology : in peritoneal carcinomatosis (sensitivity increased by centrifuging large volume).  Elevated bilirubin level suggest  biliary or gut perforation. LDH >225mU/L, glucose <50mg/dL, total protein >1g/dL and multiple organisms on gram stain suggest secondary bacterial peritonitis.  High level of TG's confirms chylous ascites.  Elevated amylase level suggest perforation. pancreatitis or gut
  26. 26.  The Serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.  A high gradient (> 1.1 g/dL) >>>portal hypertension.  A low gradient (< 1.1 g/dL) >>>non-portal hypertensive etiology.
  27. 27.  Ascitic fluid leak  Bleeding  Infection  Mortality 34 1/25/2014
  28. 28.  Bed rest  Diet  Diuretics  Fluid Restriction  Paracentesis  TIPSS  Shunts  Transplant
  29. 29.  Bed rest : No clinical trials  Upright posture activates sodium retaining mechanisms , impairs renal perfusion and sodium excretion.
  30. 30.  Sodium restriction :  Aim for 2000mg (88 mmol) per day  Studies show severe restriction (22mmol/day) compared with less restricted is associated with longer duration of evolution of ascites, but higher incidence of diuretic induced renal impairment and hyponatraemia
  31. 31.  One controlled study, showed slightly reduced salt diet (120mmol/day) was equally effective when compared to a low salt diet ( 50mmol/day).  No significant survival difference, although low salt diet (50mmol/day ) improved survival in those with previous GI bleed
  32. 32.  Central hypovolaemia stimulates ADH receptors decreases free water clearance  dilutional hyponatraemia.  Therefore, treat by water restriction –  no trials to assess effect of water restriction in patients with cirrhosis and dilutional hyponatraemia.  Restriction may worsen central hypovolaemia.
  33. 33.  Antimineralocorticoids – Secondary hyperaldosteronism promotes sodium retention in distal tubules and collecting ducts • Controlled and uncontrolled trials Spironolactone effective antimineralocorticoid • S.E gynaecomastia, renal impairment, hyperkalaemia • Other K sparing diuretics: amiloride, triamterene • Loop Diuretics : Frusemide • S.E : hyponatraemia, hypokalaemia, hypovolemia, renal impairment of prerenal origin
  34. 34.  Diuretics are administered intially fluid loss from the Intravascular space decrease hydrostatic pressure fluid move from interstitial space to intravascular space  In patients with generalized edema due to heart failure, the nephrotic syndrome, or primary sodium retention, the edema fluid can be mobilized rapidly, since most capillary beds are involved.  In patients with cirrhosis and ascites but no peripheral edema  300 to 500 mL/day is the maximum amount that can be mobilized  In patients with anasarca, removal of 2 to 3 liters of edema fluid or more in 24 hours can usually be accomplished without a clinically significant reduction in plasma volume
  35. 35.  Weight loss of 0.5kg/day in absence of oedema and 1kg/day when oedema present  Use Spironolactone & Frusemide 100mg/40mg ratio  Medical treatment based on sodium restricted diet, diuretics – response in 90 % without renal failure.
  36. 36.  Ascites that does not recede or that recurs shortly after therapeutic paracentesis, despite sodium restriction and diuretic treatment.  To date, there is no approved medical therapy specifically for refractory ascites.  Management of these patients is based upon procedures such as large- volume paracentesis and transjugular intrahepatic portosystemic shunts (TIPS), which temporarily alleviate symptoms but are not curative.
  37. 37.  These patients have a poor prognosis and are at risk for a series of complications:  pontaneous bacterial peritonitis, hepatic hydrothorax, spontaneous bacterial empyema, and umbilical hernia.  The predicted survival rate is as low as 50% at 1 year, and prognosis worsens as patients present with comorbidities such as hepatorenal syndrome, renal failure, and hepatocellular carcinoma.  The only curative treatment is liver transplantation, though current studies have shown that TIPS also increases survival.
  38. 38.  ascites?detectedLanguage=en&source=search_result&search=ascites& selectedTitle=1~150&provider=noProvider#H56451750  initialtherapy?detectedLanguage=en&source=search_result&search=ascites &selectedTitle=2~150&provider=noProvider   o Davidson o Oxford handbook of clinical medicine. o Macleod’s clinical examination,12th edition