Effusion Dx

Question 1

What is an effusion?

Answer 1

• ^ amount fluid in thoracic/abdo cavity
• not disease, indicates pathologic process
• BUT fluid may be only cause of clinical signs

Question 2

What sample tube should effusions be collected into?

Answer 2

• EDTA for counts, cytology and protein

- Serum (plain) for biochem and culture

Question 3

Give 4 main things that can be analysed in effusions

Answer 3

• TNCC (total nucleated cell count)
• Cell ID morphology
• Protein concentration
• Other (enzymes eg. amylase and lipase, urea and creatinine, cholesterol and TGs)

Question 4

What should normal fluid be like in small animals>

Answer 4

• 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

Question 5

What 4 factors affect movement of fluid in/out of pleural/peritoneal cavities? (ie. all pathologies -> effusion act via one of these)

Answer 5

• Hydrostatic pressure
• Colloid osmostic pressure (albumen)
• Permeability of capillary wall
• Lymph drainage

Question 6

What are the 3 classifications of effusions based on TNCC and TP? What else may an effusion be?

Answer 6

• Transudate (passive, due to hydrostatic:oncotic pressure imbalance)
• Modified transudate
• Exudate (active)
  > may also be haemorrhage

Question 7

HOw may a transudate be identified?

Answer 7

> low protein and cellularity, clear like water

• SG <0.5x10e9/l (difficult to find cells)
• mesothelial cells/macrophages/low no.s non-degenerate neutrophils

Question 8

What is the most common cause of transudate? what else may be involved?

Answer 8

• 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

Question 9

How may hepatic cirrhosis lead to transudate formation?

Answer 9

• 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

Question 10

What effusion occours with pre-hepatic congesttion?

Answer 10

Low protein

Question 11

Describe a modified transudate

Answer 11

• yellow - serosanginous, cloudy
• TNCC 0.3-7x10e9/L
• SG 1.018 - 1.030
• protein variable 25-50g/l
• mesothelial cells, macrohpages, non-degenerate neutrophils

Question 12

What is true modified transudate usually seen due to?

Answer 12

> 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!

Question 13

Describe exudate. Why does this occour?

Answer 13

• 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

Question 14

Give 3 causes of exudates

Answer 14

1. Inflammation of pleural/abdominal cavities or linings
   - septic OR non-septic
2. Long standing modified transudate becomes exudate as causes inflammation
3. Neoplasia - necrotic foci etc. -> inflammatino

Question 15

How would a septic exudate be distinguished from a non-septic exudate? Give an eg. of a non-septic exudate

Answer 15

Non-Septic
- non-degenerate neutrophils
- no bacteria 
- eg. FIP (viral)
Septic
- degenerate neutrophils 
- intracellular bacteria

Question 16

What are the characteristic results of diagnostics for FIP? How is the effusion asssociated with FIP usually clasified? Are these diagnositc of FIP?

Answer 16

• 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

Question 17

What is the treatment of FIP?

Answer 17

Euthanasia

Question 18

How can haemorrhage be identified? Why may other effusions be mistaken for frank blood?

Answer 18

• 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

Question 19

WHat will be seen in iatrogenic or ongoing haemorrhage? (sampled spleen etc.)

Answer 19

• erythrocytes

- platelet clumps

Question 20

What will be seen in acute haemorrhage?

Answer 20

Erythrophages

Question 21

What will be seen in chronic haemorrhage?

Answer 21

Siderophages, haematoidin [Hbg breakdown product]

Question 22

When would erythrophages be seen?

Answer 22

1d after hamorrhage

Question 23

When would siderophages be seen?

Answer 23

> 3d post haemorrhage with hematoidin

Question 24

What can you infer from the presence of both erythrophages and siderphages?

Answer 24

Multiple bleeds or chronic bleeding

Question 25

Describe a chylous effusion

Answer 25

- opaque, milky due to chylomicrons (forms "cream top" if refridgerated) - does not separate on centrifuging - TG in fluid ^ than in serum, cholesterol lower (cholesterol:TG ratio 100mg/dL - SG >1.017 - Protein variable >30g/L - TNCC variable 1.5-20x10e9/L - Cytology variable > acute: 80% small lymphocytes, macrophages, mature neutrophils > chronic/long standing effusion: mixed population - neutrophils ^

Question 26

How big is the nucleus of a smalll lymphocyte?

Answer 26

== RBC

Question 27

Why may a chylous effusion look less milky sometimes?

Answer 27

Dependant on food intake - if anorexic may look less milky

Question 28

Which cells may be mistaken for neoplastic cells? How can they be differentiated?

Answer 28

> Mesothelial cells - show reactive change with inflammation/effusions > otherwise normal cells lining abdo and thoracic cavities > requires biopsy and histopath

Question 29

What normal attribute of mesothelial cells may appear strange?

Answer 29

Cilia

Question 30

Give 3 ectopic sources of fluid in the abdomen. What type of effusion do these result in? What biochemical imbalances may be associated with each (higher in fluid than serum)?

Answer 30

1. Uroabdomen - transudate/modified transudate -creatinine (and urea but this equilibrates) 2. Bileperitonitis - green modified transudate/exudate - bilirubin 3. Pancreatitis - modified transudate/exudate - Lipase [rarely used nowadays] > inflam. TNCC and protein levels will vary

Question 31

What occours when bile pigment is free in an effusion?

Answer 31

macrophages engulf

Question 32

How does equine peritoneal fluid differ to smallies?

Answer 32

- 100-300ml always present (so can easily tap 3-5ml) - Only an effusion if increased - Normal composition == modified transudate > pale yellow, clear > TNCC 0.5-9x10e9/L, usually Protein SG 1 - 1.01 > approx 5-% macrophages 50% non-degenerate neutrophils

Question 33

How may a non-septic exudate be identified in horses?

Answer 33

- A,ber slightly turbid - TNCC >10x10e9/L - Protein > 25g/L - Neutrophils > macrophages

Question 34

How may a septic exudate be identified in horses? What may this be confused with?

Answer 34

- Yellow/brown, turbid - TNCC >10x10e9/L - Protein > 34g/L - Degenerate neutrophils, bacteria > look for plant material to indeicate gut rupture or perforation > Do not confuse with accidental enterocentesis -> protozoa, bacteria (mixed population), very few cells, plant material

Question 35

When is gut rupture in the horse easiest to detect?

Answer 35

After the acute phase when a chronic exudate has formed - in acute phase cell count will still be low (may confused with gut tap)

Question 36

How can enterocentesis be distinguished from septic inflammation?

Answer 36

Clinical impression - if rupture -> CV collapse quite rapidly