1. Approach to patient with Ascites -Osama Alzoubi -Amr Alomari -Mohamad Ghzawy -Basil Kaabneh -Basil Haddadin -Baraa

2. Definition and causes Historyand physical examination Investigations Treatment

3. What is Ascites ? - Ascites is abnormal accumulation of free fluid in the peritoneal cavity. -Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle. -Small amount are asymptomatic ( >1 liter) -Larger accumulation of fluid : -abdominal distension -fullness in the flanks - shifting dullness on percussion - fluid thrill ( when the ascites is marked) - Other features include eversion of the umbilicus, hernia, abdominal striae and scrotal edema.

5. Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 25 liters are possible. TransudateExudate result of increased pressure in the portal vein (>8 mmHg, usually around 20 mmHg) exudates are actively secreted fluid due to inflammation or malignancy low protein (<30g/L)high in protein low LDHhigh in lactate dehydrogenase high pHlow pH (<7.30) normal glucoselow glucose level Fewer WBCmore WBC

7. Pathophysiology Portal hypertension plays an important role in the production of ascites by  raising capillary hydrostatic pressure within the splanchnic bed  and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.

8. Regardless of the cause, sequestration of fluid within the abdomen leads to additional fluid retention by the kidneys due to stimulatory effect on blood pressure hormones, notably aldosterone. The sympathetic nervous system is also activated, and renin production is increased due to decreased perfusion of the kidney

10. HEPATIC  Cirrhosis  Cong.hepatic fibrosis  Fulminant hepatic failure  Budd-chiari syndrome  Lysomal storage ds. RENAL  Nephrotic synd.  Obst.uropathy  Perforation of urinary tract  Peritoneal cyst CARDIAC  Heart failure  Constrictive pericarditis  Inferior venacaval web

11. INFECTION  Tuberculosis  Abscess  chlamydia  Schistosomiasis GASTROINTESTINAL  Infected bowel  Perforation  NEOPLASM  Lymphoma  Neuroblastoma GYNAECOLOGIC  Ovarian tumor  ovarian torsion,rupture PANCREATIC  Pancreatitis  rupture pancreatic duct.

12. Historyand physical examination

13. History  Determine rapidity of onset. Abdominal obesity can masquerade as ascites, but generally develops over months to years, while ascites accumulates more rapidly.  Ask about alcohol consumption (The amount and duration ), as alcoholic hepatitis can cause ascites without cirrhosis.  History of possible toxins or drugs such as paracetamol should also be elicited.  Risk factors for infection with hepatitis C should be assessed; these include blood transfusion, needle-sharing during IV drug abuse and tattoos.  A history of autoimmune diseases may be present in patients with autoimmune hepatitis

14.  Family history of liver diseases such as haemochromatosis should be obtained  Ask if there is itching. Patients with primary biliary cirrhosis may complain of itching.  Joint pains and changes in skin colour may be found in patients with haemochromatosis.  Ask if there is shortness of breath on exertion or at rest with orthopnoea  CHF  Patients may have a history of heart disease (e.g., coronary heart disease, prior heart surgery, chest pain on exertion ).  Patients with gastrointestinal malignancies may have a known malignancy or symptoms suggestive of malignant disease (e.g., loss of weight/appetite).

15.  A history of acute pancreatitis may be found in pancreatic ascites and biliary ascites occurs following biliary surgery.  Sexual History : Multiple sexual partners, Homosexual activity with a male partner.  Obesity, hypercholesterolemia, and type 2 diabetes mellitus are recognized causes of nonalcoholic steatohepatitis, which can progress to cirrhosis.

16. Examination of ascites Patients with ascites, regardless of the etiology, will typically have abdominal distention, fullness of flanks and umbilicus eversion

17. Inspection -Abdominal distention. -Fullness of flanks. -Umbilicus Everterion. -Divarication of recti muscles. -Distended abdominals veins. -Skin is stretched and shiny.

18. Palpation -Fluid thrill  place the palm of your left hand flat against the left side of the abdomin and flick a finger of your right hand against the right side of the abdomin, if you feel a ripple against your left hand ask an assistant to place the edge of their hand on the midline of the abdomin. This prevents transmission of the impulse via the skin rather than through the ascites, if you still feel a ripple against your left hand, a fluid thrill is present. -Hepatosplenomegaly. -If there is any abdominal mass.

20. Percussion -Shifting dullness  when the patient is supine, percuss from the midline out to the flanks. Notice any change from resonant to dull. Keep your finger in the site of dullness in the flank and ask the patient to turn on to his opposite side. Pause for at least 10 seconds to allow any ascites to gravitate, then percuss again. If the area of dullness is now resonant, shifting dullness is present, indicating ascitis. Patient should be asked to evacuate his\her baldder before test for shifting dullness and fluid thrill.

22. -Puddle sign  It is useful for detecting small amounts of ascites -- as small as 120 mL ; shifting dullness typically requires 500 mL. Patient lies prone for 5 minutes then rises onto elbows and knees. Apply stethoscope diaphragm to most dependent part of the abdomen. Examiner repeatedly flicks near flank with finger. Continue to flick at same spot on abdomen then move stethoscope across abdomen away from examiner. A sharp increase in the intensity of the sound picked up by the stethoscope indicates the level of fluid.

24.  Auscultaion : Venous hum over the distended veins around umblicus in cirrhosis with portal hypertension.

25. Other signs :  Respiratory system -Hydrothorax ( commonly rt. Sided ). -Basal collapse.  Cardiovascular system -Diffuse pulsation over the precordium.

26. Investigations

27. GENERAL INVESTIGATIONS History and examination findings may reveal the underlying cause. General investigations can be used to confirm or indicate the possible etiology.

28. Urine dipstick: Positive for protein in nephrotic syndrome. If so, a 24-hour urine collection for protein should be undertaken; more than 3.5g/24h is indicative of nephrotic syndrome. CBC: A raised WBC count may indicate an infective etiology.

29. Urea & electrolytes: Elavated urea and creatinine implies severe renal impairment, and may occur as a component of hepatorenal syndrome, which is renal impairment secondary to liver failure. LFTs: May be deranged in the presence of liver disease. The serum albumin will be able to indicate hypoalbuminaemia but the underlying cause must still be investigated.

30. CXR: Findings suggestive of cardiac failure such as cardiomegaly, the presence of Kerley B lines, pulmonary edema and pleural effusions. Occasionally the presence of carcinoma may be suggested by a lesion in the lungs. Abdominal US: In addition to confirming the presence of ascites, US will detect any intra-abdominal masses that are not palpable on clinical examination, and visualize fatty deposits in the liver in the presence of cirrhosis. Dilated collateral veins may be seen in conditions that result in venous obstruction of the liver, such as Budd-Chiari syndrome.

33. Abdominal paracentesis: A procedure in which a needle or catheter is inserted into the peritoneal cavity, typically in the left lower quadrant, to obtain ascitic fluid for diagnostic or therapeutic purposes.

34. Ascitic fluid Appearance: ChylousThe milky white appearance of chylous ascites is due to obstruction of the lymphatic ducts. Bile-stainedis suggestive of bile peritonitis. HaemorrhagicCan occur in malignancy, trauma and TB. Straw-colouredThe usual appearance with most other causes.

35. Biochemistry: ProteinThe ascitic protein levels are often used to classify the ascites as a transudate or an exudate; however, this may not always be reliable. A transudate would be ascitic fluid with the protein concentration of less than 25g/L in the sample or 11g/L lower than the serum protein level, while an exudate is the opposite. AmylaseUsually elevated in pancreatic ascites. GlucoseLow in bacterial infection. TriglycerideElevated in chylous ascites, may indicate obstruction of drainage of the thoracic duct. BilirubinElevated in bile ascites.

36. Microbiology: Gram and Ziehl-Neelsen staining with cultures may be positive with a bacterial aetiology. Cytology: WCCNeutrophilia is suggestive of a bacterial peritonitis, while tuberculous peritonitis usually results in a lymphocytosis. Malignant cells may be identified and a primary source may possibly be located.

37. SPECIFIC INVESTIGATIONS Echocardiography: Cardiac failure will manifest as a dilated and poorly contracting ventricle with a reduced ejection fraction. A pericardial effusion is visible as an echo-free space between the left ventricle and the pericardium. Tricuspid regurgitation can be visualized with color-flow Doppler imaging.

38. Liver biopsy: Will be able to confirm and may be able to ascertain the underlying cause of liver cirrhosis. Renal biopsy: Reveals the underlying cause of nephrotic syndrome. Portal venography: Is indicated if obstruction to the venous outflow of the liver is suspected and can confirm Budd-Chiari syndrome and veno-occlusive disease.

39. “Ascites can result from abnormalities in a number of different systems and a detailed examination of all systems is required to avoid missing potentially treatable conditions, such as cardiac failure and TB.”

40. Treatment

41.  General care -Monitoring of input and output. -Diatery modifications : Soduim restriction up to 1 g/day. water restriction. - Bed rest : improves renal perfusion which leads to diuresis.

42. The treatment of ascites largely depends on the underlying cause. For example, peritoneal carcinomatosis or malignant ascites may be treated by surgical resection of the cancer and chemotherapy, while management of ascites related to heart failure is directed toward treating heart failure with medical management and dietary restrictions.  Medication Diuretics increase water and salt excretion from the kidneys. The recommended diuretic regimen in the setting of liver related ascites is a combination of spironolactone (Aldactone) and furosemide (Lasix).

43. Therapeutic paracentesis  Therapeutic paracentesis (a needle carefully is placed into the abdominal area, under sterile conditions) can be performed to remove large amounts of fluids. A few liters (up to 4 to 5 liters) of fluid can be removed safely with the replacement of salt free albumin. For patients with malignant ascites, this procedure may also be more effective than diuretic use. If done alone, it is associated with postparacentesis circulatory dysfunction (PPCD) in 20% cases. PPCD is found to be associated with increased risk of renal failure and mortality up to 30 days after large volume paracentesis.

45. Surgery  For more refractory cases, surgical procedures may be necessary to control the ascites. Transjugular intrahepatic portosystemic shunts (TIPS) is procedure done through the internal jugular vein (the main vein in the neck) under local anesthesia by an interventional radiologist. A shunt is placed between the portal venous system and the systemic venous system (veins returning blood back to the heart), thereby reducing the portal pressure. This procedure is reserved for patients who have minimal response to aggressive medical treatment. It has been shown to reduce ascites and either limit or eliminate the use of diuretics in a majority of cases performed. However, it is associated with significant complications such as hepatic encephalopathy (confusion) and even death.

46. Livertransplant  Liver transplantation for advanced cirrhosis may be considered a treatment for ascites due to liver failure. Liver transplant involves a very complicated and prolonged process and it requires very close monitoring and management by transplant specialists.

47. References: Macleod’s clinical examination, 12 th edition. Bailey and Love’s short practice of surgery. Davidson’s principles and practice of medicine, 21 st edition. Differential diagnosis, Third edition. http://emedicine.medscape.com

48. Thank You