Diagnosis of effusions Flashcards
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
Why analyse an effusion?
- differentiate fluid types –> further diagnostics and management
- identify fluid types with a more specific aetiology
- definitive diagnosis
Into which tubes do you collect fluid?
- into EDTA for counts, cytology and protein
- into serum/plain tube for biochemistry or culture
What are the 3 most important things looked at on fluid analysis?
- total nucleated cell count (TNCC)
- cell identification and morphology
- protein concentration
What else can be looked at?
- enzymes (amylase, lipase)
- urea and creatinine
- cholesterol and Tg
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
4 factors regulating fluid movement
- hydrostatic pressure
- collod osmotic pressure (albumin)
- capillary wall permeability
- lymphatic drainage
How are transfusions classified? 3
TNCC, total protein and cell morphology/size
3 types of effusion
transudate, modified transudate (less so), exudate.
Also haemorrage
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
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
What exudate do hepatic cirrhosis and portal hypertension cause?
transudate
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
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
Causes of modified transudates? 3
Cardiac disease
chylous effusion
lymphatic obstruction (neoplasia)
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.
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)
