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Alimentary > Effusion Dx > Flashcards

Effusion Dx Flashcards

1
Q

What is an effusion?

A
  • ^ amount fluid in thoracic/abdo cavity
  • not disease, indicates pathologic process
  • BUT fluid may be only cause of clinical signs
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2
Q

What sample tube should effusions be collected into?

A
  • EDTA for counts, cytology and protein

- Serum (plain) for biochem and culture

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3
Q

Give 4 main things that can be analysed in effusions

A
  • TNCC (total nucleated cell count)
  • Cell ID morphology
  • Protein concentration
  • Other (enzymes eg. amylase and lipase, urea and creatinine, cholesterol and TGs)
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4
Q

What should normal fluid be like in small animals>

A
  • 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
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5
Q

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

A
  • Hydrostatic pressure
  • Colloid osmostic pressure (albumen)
  • Permeability of capillary wall
  • Lymph drainage
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6
Q

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

A
  • Transudate (passive, due to hydrostatic:oncotic pressure imbalance)
  • Modified transudate
  • Exudate (active)
    > may also be haemorrhage
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7
Q

HOw may a transudate be identified?

A

> low protein and cellularity, clear like water

  • SG <0.5x10e9/l (difficult to find cells)
  • mesothelial cells/macrophages/low no.s non-degenerate neutrophils
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8
Q

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

A
  • 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
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9
Q

How may hepatic cirrhosis lead to transudate formation?

A
  • 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
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10
Q

What effusion occours with pre-hepatic congesttion?

A

Low protein

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11
Q

Describe a modified transudate

A
  • yellow - serosanginous, cloudy
  • TNCC 0.3-7x10e9/L
  • SG 1.018 - 1.030
  • protein variable 25-50g/l
  • mesothelial cells, macrohpages, non-degenerate neutrophils
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12
Q

What is true modified transudate usually seen due to?

A

> 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!

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13
Q

Describe exudate. Why does this occour?

A
  • 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
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14
Q

Give 3 causes of exudates

A
  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
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15
Q

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

A 
Non-Septic
- non-degenerate neutrophils
- no bacteria 
- eg. FIP (viral)
Septic
- degenerate neutrophils 
- intracellular bacteria
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16
Q

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

A
  • 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
17
Q

What is the treatment of FIP?

A

Euthanasia

18
Q

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

A
  • 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
19
Q

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

A
  • erythrocytes

- platelet clumps

20
Q

What will be seen in acute haemorrhage?

A

Erythrophages

21
Q

What will be seen in chronic haemorrhage?

A

Siderophages, haematoidin [Hbg breakdown product]

22
Q

When would erythrophages be seen?

A

1d after hamorrhage

23
Q

When would siderophages be seen?

A

> 3d post haemorrhage with hematoidin

24
Q

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

A

Multiple bleeds or chronic bleeding

25
Q

Describe a chylous effusion

A
  • 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 ^
26
Q

How big is the nucleus of a smalll lymphocyte?

A

== RBC

27
Q

Why may a chylous effusion look less milky sometimes?

A

Dependant on food intake - if anorexic may look less milky

28
Q

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

A

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

29
Q

What normal attribute of mesothelial cells may appear strange?

A

Cilia

30
Q

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)?

A
  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
31
Q

What occours when bile pigment is free in an effusion?

A

macrophages engulf

32
Q

How does equine peritoneal fluid differ to smallies?

A
  • 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
33
Q

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

A
  • A,ber slightly turbid
  • TNCC >10x10e9/L
  • Protein > 25g/L
  • Neutrophils > macrophages
34
Q

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

A
  • 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
35
Q

When is gut rupture in the horse easiest to detect?

A

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

36
Q

How can enterocentesis be distinguished from septic inflammation?

A

Clinical impression - if rupture -> CV collapse quite rapidly

Alimentary (30 decks)

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