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Flashcards in Diagnosis of effusions Deck (43):
1

What is an effusion?

increased amount of fluid (abdominal or thoracic cavity), not a disease but a sign of a pathologic process, may be the only cause of clinical signs

2

Why analyse an effusion?

-differentiate fluid types --> further diagnostics and management
-identify fluid types with a more specific aetiology
-definitive diagnosis

3

Into which tubes do you collect fluid?

-into EDTA for counts, cytology and protein
-into serum/plain tube for biochemistry or culture

4

What are the 3 most important things looked at on fluid analysis?

-total nucleated cell count (TNCC)
-cell identification and morphology
-protein concentration

5

What else can be looked at?

-enzymes (amylase, lipase)
-urea and creatinine
-cholesterol and Tg

6

Describe normal fluid (volume, colour, protein, nucleated cell count, other cells)

low volume
clear, straw colour
total protein: 25-30g/L
nucleated cell count <3*10^9/L
-mesothelial cells and macrophages

7

4 factors regulating fluid movement

-hydrostatic pressure
-collod osmotic pressure (albumin)
-capillary wall permeability
-lymphatic drainage

8

How are transfusions classified? 3

TNCC, total protein and cell morphology/size

9

3 types of effusion

transudate, modified transudate (less so), exudate.
Also haemorrage

10

Describe transudate (colour, protein, nucleated cell count, other cells)

low protein and cellularity
clear
S.G. < 25g/L
TNCC <0.5 * 10^9/L
mesothelial cells, macrophages, low numbers of non-degenerate neutrophils

11

Causes - transudates

Several theories:
-decreased colloid osmotic pressure - hypoalbuminaemia (classic simplest theory but rarely occurs as often alterations in hydrostatic pressure too). This may occur secondary to glomerular disease, hepatic disease or GI loss (e.g. PLE). Most animals with abdominal transudates have albumin in range of 15-25g/L so other factors are involved.
-RAAS activation

12

What exudate do hepatic cirrhosis and portal hypertension cause?

transudate

13

Describe pathogenesis of transudate formation secondary to hepatic fibrosis/cirrhosis

Prolonged portal hypertension and formation of secondary collateral circulation --> local production of local vasodilators (NO), leads to splanchnic vasodilation and decreased effective BF, compounded by renal secretion of sodium via RAAS and generalised hypertension --> expansion of plasma volume and leakage of low protein lymph from the intestines

14

Desribe modified transudate (colour, protein, nucleated cell count, other cells)

yellow to serosanguinois, cloudy
TNCC 0.3-5.5 * 10^9/L (up to 7*)
SG 1.018 to 1.030
protein variable 25-50g/L
mesothelial cells, macrophages, non-degenerate neutrophils, small lymphocytes

15

Causes of modified transudates? 3

Cardiac disease
chylous effusion
lymphatic obstruction (neoplasia)

16

Explain pathogenesis of how cardiac diseae leads to modified transudate formation

chronic passive congestion --> increased hydrostatis pressure, especially in hepatic sinuosids, leakage of protein rich lymph from liver, Na and fluid retention.

17

Desrcibe exudate (colour, protein, nucleated cell count, other cells)

high TNCC and protein
turbid -red, yellow, white
SG > 1.018
total protein >30g/L
TNCC >3.0 *10^9/L
neutrophils (Degenerate or not), macrophages, (lymphocytes and eosinophils)

18

Causes - exudates 3

-inflammation of pleural/abdominal cavities or their linings (septic vs non-septic)
-long-standing modified transudate
-neoplasia

19

Distinguish non-septic exudate from a septic exudate

NON-SEPTIC: non-degenerate neutrophils, no bacteria, FIP
SEPTIC: degenerate neutrophils and intracellular bacteira

20

Describe the fluid found in FIP

TNCC variable (0.2-23 * 10^9/L)
non-degenerate neutrophils and macrophages
high protein (35-80g/L)
albumin: globulin >0.81 on fluid - highly correlated
positive coronavirus (higher titres more suggestive in dry FIP (>640), may be 0->1280 with wet
alpha-1-acid glycoprotein (APP) elevation >1500microg/mL

FLUID MAY BE CLASSIFIED AS MODIFIED EXUDATE OR TRANSUDATE DEPENDING ON TNCC

21

Describe a healthy neutrophil

-dense chromatin fibres
-intact membrane
-nice cytoplasm

22

Describe a haemorrhagic effusion

turbid -red
SG 1.025-1.040
total protein >30g/L
TNCC 1.5-10*10^9/L (ccompare with peripheral blood)
cells present (WBC from peripheral blood, includes neutrophils), and macrophages

23

Types of haemorrhage and how to distinguish them - 3

IATROGENIC OR ONGOIN (eryhrocytes and platelet clumps)
ACUTE HAEMORRHAGE (erythrophagia)
CHRONIC (siderophages, haematoidin)

24

What might platelets in you fluid mean? 3

-you sampled actual blood
-animal still haemorrhaging (rare)
-iatrogenic haemorrahe

25

Describe a chylous effusion (colour, protein, nucleated cell count, other cells)

opaque, milky
SG >1.017
protein variable >30g/L
TNCC 1.5-20*10^9/L
Cytology:
ACUTE - small lymphocytes, macrophages, mature neutrophils, variable
CHRONIC: mixed population with increased neutrophils and macrophages but decreased lymphocyte % (although still many)

26

Describe levels of Tg in chylous effusion fluid

Tg in fluid greater than in serum (and cholesterol lower)

27

What is a 'cream top'?

the chylomicrons that form on the top of a chylous effusion if it is refridgerated

28

What can you use to stain lipid droplets?

sudan 3

29

Describe other features of a chylous effusion

-cholesterol:tg ratio of 100mg/dL (1.13mmol/L)

30

What are mesothelial cells? Why are they important?

Normal lining cells of the abdominal and thoracic cavities/ Show 'reactive change' with inflammation or effusions that can cause them to be confused with neoplastic cells. Requires biopsy and histopathology to confirm a diagnosis of a neoplasm.

31

Describe the appearance of mesothelial cells

they have a corona/cytoplasmic bleb that looks a bit like cilia. can have multiple nuclei and other features that make cells look like tumours (although they're not!)

32

Describe some ectopic sources of fluid

Urine --> uroabdomen
Bile - bile peritonitis
Pancreatitis
All of these can produce variable amounts of effusion and inflammation. TNCC and protein levels will vary.

33

Describe uroabdomen fluid - classification

transudate/modified transudate (if chonric)

34

Describe bile peritonitis fluid - classification

green colour, modified transudate/exudate

35

Describe pancreatitis fluid - classification

modified transudate/exudate

36

Describe biochemistry ratios of creatinine, lipase and bilirubin in fluid vs plasma

CREATININE - much higher in urine normally than plasma
LIPASE
BILIRUBIN (bile duct/gall bladder rupture) - much higher in blood normally. If higher in cavity fluid than in blood, then bilirubin has leaked.

37

Describe equine peritoneal fluid - volume

Normally find low volume in equine abdomen (100-300ml) so can collect 3-5ml from a normal horse. Increased volume = effusion

38

Describe equine peritoneal fluid (colour, protein, nucleated cell count, other cells)

pale yellow, clear
TNCC 0.5-9.0 * 10^9/L (usually < 4.0*)
protein <15g/L
specific gravity 1.000 - 1.010
Approximately 50% macrophages and 50% non-degenerate neutrophils

roughly equivalent to a modified transudate

39


Describe equine peritoneal fluid - NON-SEPTIC EXUDATE (colour, protein, nucleated cell count, other cells)

amber slightly turbid fluid
TNCC >10*10^9/L
protein >25g/L
neutrophils>macrophages

40


Describe equine peritoneal fluid - SEPTIC EXUDATE (colour, protein, nucleated cell count, other cells)

yellow, brown, turbid
TNCC > 10*10^9/L
protein > 34g/L
degenerate neutrophils, bacteria
loog for plant material = rupture of perforation of gut wall

41

What is enterocentesis?

tap into gut

42

What might you see on enterocentesis?

plant material, protozoa and bacteria (mixed population), very few cells

43

How can you tell apart tapping into the gut or if you have a peracute rupture of the gut with overwhelming inflammation?

with both will see plant material, bacteria and possibly protozoa, cell count will be low if rupture is peracute, clinical impression is important in these cases - horses with gut rupture will quickly develop CV collapse.