Effusion Dx Flashcards
What is an effusion?
- ^ amount fluid in thoracic/abdo cavity
- not disease, indicates pathologic process
- BUT fluid may be only cause of clinical signs
What sample tube should effusions be collected into?
- EDTA for counts, cytology and protein
- Serum (plain) for biochem and culture
Give 4 main things that can be analysed in effusions
- TNCC (total nucleated cell count)
- Cell ID morphology
- Protein concentration
- Other (enzymes eg. amylase and lipase, urea and creatinine, cholesterol and TGs)
What should normal fluid be like in small animals>
- Low volume (2ml) - cannot tap if healthy animal
- clear, straw coloured
- TP: 25-30g/l
- TNCC: <3x10e9/l (very difficult to find cells under microscope)
- mesothelial cells/macrophages
What 4 factors affect movement of fluid in/out of pleural/peritoneal cavities? (ie. all pathologies -> effusion act via one of these)
- Hydrostatic pressure
- Colloid osmostic pressure (albumen)
- Permeability of capillary wall
- Lymph drainage
What are the 3 classifications of effusions based on TNCC and TP? What else may an effusion be?
- Transudate (passive, due to hydrostatic:oncotic pressure imbalance)
- Modified transudate
- Exudate (active)
> may also be haemorrhage
HOw may a transudate be identified?
> low protein and cellularity, clear like water
- SG <0.5x10e9/l (difficult to find cells)
- mesothelial cells/macrophages/low no.s non-degenerate neutrophils
What is the most common cause of transudate? what else may be involved?
- v colloid osmotic pressure (hypoalbumenaemia) 2* to glomerular disease, hepatic disease, GI loss (usually also v globulins)
- hypoalbumenaemia alone ONLY able to cause transudate if extremely severe ( ^ water retention RAAS system
How may hepatic cirrhosis lead to transudate formation?
- Portal hypertension 2* to hepatic fibrosis/cirrhosis
- 2* collateral circulation forms
- local production of vasodilators (NO)
- splanchnic casodilation, v blood flow
- compounded by renal retention of Na [RAAS] and hypertension generally
=> end result: expansion of plasma volume, leakage of low protein lymph from intestines
What effusion occours with pre-hepatic congesttion?
Low protein
Describe a modified transudate
- yellow - serosanginous, cloudy
- TNCC 0.3-7x10e9/L
- SG 1.018 - 1.030
- protein variable 25-50g/l
- mesothelial cells, macrohpages, non-degenerate neutrophils
What is true modified transudate usually seen due to?
> chronic heart failure/ cardiac disease -> ^ hydrostatic pressure (esp in hepatic sinusoids) -> leakage of protein rich lymph from liver. Also Na+ and fluid retention.
chylous effusion
lymphatic obstruction - neoplasia
chronic hepatic venous obstruction
- though other fluids may be lumped into this group!
Describe exudate. Why does this occour?
- due to inflammation (High TNCC and protein)
- Turbid - red/yellow/white, PUSS
- SG >1.018
- TP >30g/L
- TNCC >3x10e9g/L
- DOminance of neutrophils (degenerate/normal), macrophages, some lymphocytes and easinophils possibly
Give 3 causes of exudates
- Inflammation of pleural/abdominal cavities or linings
- septic OR non-septic - Long standing modified transudate becomes exudate as causes inflammation
- Neoplasia - necrotic foci etc. -> inflammatino
How would a septic exudate be distinguished from a non-septic exudate? Give an eg. of a non-septic exudate
Non-Septic - non-degenerate neutrophils - no bacteria - eg. FIP (viral) Septic - degenerate neutrophils - intracellular bacteria
What are the characteristic results of diagnostics for FIP? How is the effusion asssociated with FIP usually clasified? Are these diagnositc of FIP?
- TNCC variable(0.2-22x10e9g/l)
- Non-degenerate neutrophils, macrophages
- High protein (35-80g/L) - protein precipitate, not necessarily high cell count
- Albumin:globulin (ratio?) >0.81 on fluid - highly correlated
- test + coronavirus - higher titres more suggestive in dry FIP(>640), in wet may be 0 - >1280
- a1 acute phase protein elevation >1500microg/mL
> classified as modified transudate or exudate depending on cell count - characteristic but NOT DIAGNOSTIC! Other things can cause all of this
What is the treatment of FIP?
Euthanasia
How can haemorrhage be identified? Why may other effusions be mistaken for frank blood?
- Turbid and red
- SG 1.025 - 1.040
- TP >30g/L
- TNCC 1.5-10x10e9/L : compare with peripheral blood
- cells include WBCs from peripheral blood inc neutrophils and macrophages
> any fluid with PCV >2/3 appears as frank blood to naked eye
WHat will be seen in iatrogenic or ongoing haemorrhage? (sampled spleen etc.)
- erythrocytes
- platelet clumps
What will be seen in acute haemorrhage?
Erythrophages
What will be seen in chronic haemorrhage?
Siderophages, haematoidin [Hbg breakdown product]
When would erythrophages be seen?
1d after hamorrhage
When would siderophages be seen?
> 3d post haemorrhage with hematoidin
What can you infer from the presence of both erythrophages and siderphages?
Multiple bleeds or chronic bleeding
