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ascites.pptx
- 1. ASCITES AND OTHER PERITONEAL AFFECTIONSIN DOGS K.MADHUMATHI BVT18031
- 2. ASCITES ■ Accumulation ofnon-inflammatory fluid ( mostly transudate in the peritoneal cavity characterized by bilateral distension of lower abdomen. ■ Transudate - sg <1.016, protein < 3 g/dl
- 3. CAUSES ■ Primary causes: ■Fall in osmotic pressure of blood ■ Obstruction of lymphatic vessels ■ Increased hydrostatic pressure in capillaries due to cardiac insufficiency & congestive heart failure
- 4. Contd... ■ Renal retentionof sodium – Renal insufficiency and liver damage. ■ Hypoproteinaemia – -Protein deficiency diet -Lower protein synthesis in liver damage -Loss of protein in heavy parasitic infections like haemonchosis , strongylosis.
- 5. PATHOGENESIS ■ Hypoproteinaemia ■ Plasmacolloidal osmotic pressure is decreased ■ Increase in hydrostatic pressure ■ Fluid escaped from circulation accumulated in body cavity
- 6. Liver Cirrhosis orRenal damage Less kidney perfusion Renin –angiotensin –aldosterone mechanism Retention of more sodium in circulation Ascites
- 7. CLINICAL FINDINGS ■ Bilateraldistension of lower abdomen-‘Pear shaped appearance ■ Linea alba-distended downward ■ Reduction in tone of abdominal muscles ■ Dyspnoea ■ Constipation ■ inappetance ■ Palpation-undulating movement of fluid
- 8. EXCESSIVE DISTENSION ■ Distensionmay reach up to costal margins and lower abdominal border may touch ground suface ■ Barrel shaped ■ Increased respiration and heart rate ■ Lie down as they have little tendency to walk ■ Engorged and prominently visible blood vessels in abdominal area
- 9. DIAGNOSIS ■ History oflow protein diet ■ Clinical signs ■ Radiography - Ground glass appearance - abdominal organs may not be visible ■ USG
- 10. ABDOMINOCENTESIS ■ Protein contentbelow 3.5 g/dl and Specific gravity less than 1.016 ■ Greenish yellow-presence of bile ■ Reddish- presence of erythrocytes ■ Inflammatory >500 total nucleated cells/ml of fluid, Presence of macrophages
- 11. DIFFERENTIAL DIAGNOSIS ■ Urethralobstruction with enlarged bladder ■ Gastric torsion and intestinal obstruction ■ Fat deposition ■ Septic Peritonitis or secondary peritonitis -exudate May be due to GIT perforation,intestinal suture dehiscence high temperature and vomition
- 12. CHYLOABDOMEN ■ Presence ofchyle ■ made up of lymph and triglycerids ■ Milky white in colour ■ CAUSES - Abdominal lymphatic obstruction - rupture of lymphatic.
- 13. PRIMARY PERITONEAL TUMOUR ■Rare in animals. ■ Occurs when the peritoneal lining cells grows abnormally. ■ Does not spread there from other Parts of body. ■ Peritoneal carcinomatosis ■ Spreads from carcinoma of GIT
- 14. ABDOMINOCENTESIS ■ Two methods, Simpleabdominocentesis – left lateral recumbency Four quadrant abdominocentesis – dorsal or left lateral ■ 20 gauge scalp vein can be used ■ Should not drain all the fluid.
- 15.
- 16. MEDICAL MANAGEMENT ■ Toprevent the hypovolaemic shock Fluid therapy -10ml/kg iv, ■ Diuretics Frusemide 2-4 mg /kg iv ■ In hypoproteinaemia associated with parasitic infection (PLE) Broad spectrum antihelmintic ■ Protein rich diet,sodium free diet ■ Broad spectrum antibiotics (SBP)
- 17. HEMOPERITONEUM ■ Most redeffusions – blood- tinged transudate ■ Hemoabdomen Indicated by fluid with hematocrit of 10-15 %
- 18. CAUSES ■ Trauma Automobile accidents Splenictorsion and splenic hematoma ■ Coagulopathy ■ Thrombocytopenia ■ Iatrogenic ■ In older dogs, Hemangiosarcoma,hepatocellular carcinoma
- 19. Diagnosis ■ Physical examination ■Coagulopathy studies ■ Abdominal radiography ■ USG ■ Cytology and HP – neoplastic cells
- 20. TREATMENT ■ Intravenous fluidtherapy ■ Blood transfusion ■ Oxygen therapy ■ Analgesic therapy (pain medication) ■ Vitamin K administration ■ Emergency exploratory surgery ■ PROGNOSIS : POOR