Effusions Lecture 21 Flashcards
In Health what are the body cavities that contain fluid and what does the normal body cavity fluid consist of? Function?
The thoracic (pleural), abdominal (peritoneal), and pericardial cavities contain a small volume of
clear, watery (serous) fluid. This fluid functions to provide lubrication between organs and the body
wall and for diffusion of substances such as electrolytes.
What are the forces involved in body cavity fluid formation?
Rate of fluid formation is dependent on the balance between the opposing oncotic and hydraulic pressures.
Oncotic: water follows solid
Hydraulic: force of flow when fluid encounters resistance IE force your bloodflow is putting on vessels
How is normal cavity fluid formed?
Cavity fluid is formed when plasma exits the arterial capillary bed and enters the interstitial space.
The majority of this fluid is rapidly reabsorbed by venous capillaries and lymphatic vessels. Since
these arterial capillaries are relatively impermeable to proteins, serous fluid in body cavities has a
very low total protein concentration and contains very few cells.
When does effusion occur?
occur when there are changes that promote excess fluid formation or decreased fluid
removal
What are the 4 major mechanisms for effusion formation?
(1) disturbances of fluid circulation: changes in plasma oncotic pressure, hydraulic pressure, lymphatic drainage, or a combination of these factors (These processes generally result in
transudates)
(2) inflammation in a body cavity (This typically results in exudates)
(3) organ rupture (which usually leads to inflammation and/or hemorrhage)
(4) neoplasia
What is the clinical presentation of abdominal (peritoneal) effusions?
- Distended abdomen (+/- palpable fluid wave)
- Exercise intolerance
- +/- respritory difficulty due to pressure on the diaphragm
What is the clinical presentation of thoracic (pleural) effusions?
- increased respiratory rate
- Difficulty breathing esp on inspiration
- Exercise intolerance, weakness
What is the clinical presentation of Pericardial effusions?
- Exercise intolerance, weakness +/- collapse
- Respiratory difficulty
- Muffled heart sounds, weak pulses, jugular distention
- ECG abnormalities
- Usually also abdominal effusion
When collecting fluid samples you must:
be sterile and careful
- sternal recumbency
- Field clipped and prepped
- Sterile gloves
- U/S guidance is often used to help sample fluid
I have done a centesis…now what?
EDTA Tube –> clin path lab and order “Fluid analysis”. you will get TP, Total Nucleated cell count and cytology
Clot (red top) tube–> Clinical bacti and mycology lab, order a bacterial culture. You will get gram stain, culture and susceptibility testing
Heparin Tube–> Clin path lab, Biochemical testing (usually K+, creat, billirubin, triglyceridesm glucose or lactate depending on ddx). Always check with the lab before submitting your sample to make sure you submit
the correct specimen type!
T/F EDTA
results in the best preservation of cells for cytology and prevents clotting of the sample if it has a
high fibrinogen concentration or contains any blood.
True
What if I have to ship the sample to the laboratory?
- Make a direct smear of the fresh fluid, air dry it, &
place in slide holder (do NOT refrigerate)
– Feel free to make a direct smear for yourself to stain and
evaluate! After review, submit with the unstained slide. - Put fluid in EDTA tube ± red-top or heparin tubes
(depending on which assays you will be requesting)
& refrigerate until ship overnight on a cool pack
– EDTA anticoagulant results in best preservation of cellular
morphology for delayed microscopic evaluation
What are the two cytologic analysis options at UTCVM?
Fluid analysis: requireds a tube of fluid and gives you TP refractometry, TNCC, and microscopic evaluation
Cytology: microscopic evaluation only
Microscopic examination should occur ASAP after fluid collection. Cells will degrade and acquire
artifactual changes with storage time, even in EDTA. Also, phagocytic cells (neutrophils and
macrophages) continue “eating” even after they leave the body. Interpretation of intracellular
bacteria or phagocytized cells (erythrophagia, leukophagia) should be done cautiously when
fluid analysis is delayed >24 hours.
**Look at the Routine Fluid Analysis Section of Notes for More info on each
Why do we classify effusions?
- Help you think about mechanisms!
– Altered fluid circulation
– Inflammation
– Rupture of an organ
– Neoplastic - Mechanisms help narrow differential diagnoses!
- A few caveats:
– Interpret fluid data in light of entire clinical picture
– Some fluids can’t be neatly classified
– Fluid characteristics may change over time - The more chronic –> the more inflammatory
What 2 laboratory parameters are used to classify effusions?
Protein levels and cellularity
Describe the mechanisms for transudate formation.
Decreased oncotic pressure due to hypoalbuminemia
- Usually needs to be severe (<1.5 g/dL)
- EX: Protein losing nephropathy
Increased hydraulic pressure due to venous congestion, or venous obstruction (e.g., space-occupying lesion [tumor, granuloma], thrombus, organ
torsion).
- When the hydraulic pressure gradient exceeds the oncotic pressure gradient fluid is pushed out of the capillary lumen and into the interstitium at a rate that
exceeds lymphatic drainage, leading to fluid accumulation in tissues and body cavities. Another EX is R Sided HF.
Lymphatic Obstruction due to blockage or dysfunction of lymphatic vessels.
- If fluid formation outpaces fluid removal, effusion results
- Space occupying mass like a tumor
although in most cases
hypoalbuminemia alone will not cause transudation
Are the mechanisms of transudate formation mutually exclusive?
NO, often more than one
mechanism is at work in the same patient.
Why do some transudates have higher protein concentrations than other transudates?
Transudates are divided into low or high protein categories.
Not all capillaries are created equal! Some capillaries have large fenestrations, and some have
small fenestrations.
- Low protein transudate –> capillaries with small fenestrations. Typically very low cell counts and TP.
- High protein transudate –> capillaries with large fenestrations (hepatic sinusoids, lung)
Examples of Low protein transudate causes.
- End-stage liver failure (hepatic cirrhosis): this forms due to decreased albumin production by
the liver (decreased plasma oncotic pressure) and portal hypertension secondary to hepatic
fibrosis and high-resistance blood flow (increased plasma hydraulic pressure). There will
often be other biochemical evidence of hepatic insufficiency (hypoglycemia, low urea,
hypocholesterolemia)
Protein-losing disorders:
- Protein-losing nephropathy: Glomerular disease can result in the loss of large
amounts of albumin in the urine (decreased plasma oncotic pressure) and sodium
retention in the kidney (increased hydraulic pressure)
- Protein-losing enteropathy: Albumin loss through the gut can result in marked and
chronic hypoalbuminemia. Impaired lymphatic drainage (lymphangiectasia) is also
often present in protein-losing enteropathies.
Examples of High protein transudate causes
- High-protein transudates develop due to increased plasma hydraulic pressure within capillary beds
that are more permeable to protein loss (hepatic sinusoids, lungs) - Most common pathologies resulting in high-protein transudates are:
- Congestive heart failure: Decreased cardiac output can lead to venous congestion in
multiple organs, including liver and lungs - Portal hypertension can result in increased hydraulic pressure within the hepatic sinusoids, a
highly fenestrated capillary bed
What is the expected predominant cell type(s) in transudates?
All transudates have low cell counts. But depending on protein content, they are subclassified as either low-protein transudates or high-protein transudates
mostly mononuclear cells (macrophages and mesothelial cells with fewer lymphocytes), low
numbers of neutrophils. Variable amount of hemodilution.
Gross appearance: colorless to pale yellow
Difference between high and low protein transudate?
Low:
- Color: colorless, clear
- TP<2.5
- TNCC<1500
- Predominant cell type: Mononuclear cells
(macrophages, small
lymphocytes)
- May also see: Mesothelial cells and low # of neutrophils
High:
- Color: light yellow, clear
- TP>/equal to 2.5
- TNCC: <5000
- Predominant cell type: Mononuclear cells
(macrophages, small
lymphocytes)
- May also see: Mesothelial cells and variable # of neutrophils
Describe the mechanisms for exudate formation.
Due to inflammation of the pleural or peritoneal surface
- Inflammation (“serositis”) –>vascular and mesothelial permeability –> leaky vessels &
mesothelium –> exudation of
fluid, protein, & cells. - Inflammatory stimulus can be sterile or infectious
- Chemokines attract nflammatory cells
- Resulting effusion –> high cellularity, high
protein
When someone says a animal has “septic effusion” what does that mean? and can it ever be non-septic?
Yes it can be non-septic.
Septic can mean either “a patient have sepsis” OR it is used to mean “containing bacteria” (but NOT necessarily implying the clinical syndrome of sepsis)
Septic exudates refer to those with infectious, usually bacterial, causes.
EX: Gastrointestinal tract leakage
