Presenting Signs: Oedema and Ascites Flashcards

1
Q
  1. Define oedema.
  2. Oedema on radiograph.
A
  1. Accumulation of fluid in tissue.
    E.g. subcutaneous oedema.
    E.g. pulmonary oedema.
    E.g. oedema of any organ.
  2. Makes radiograph hazy and unclear with structures obscured and more difficult to see.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define effusion.

A

Abnormal accumulation of fluid in a body cavity.
E.g. peritoneal effusion = ascites.
E.g. pleural effusion.
E.g. pericardial effusion.
E.g. joint effusions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Normal fluid transportation in the body.

A

Blood enters arteriole end of capillary bed and filters out into the interstitial space. Most of this fluid is reabsorbed back into the capillary bed at the venule end but small amount of net filtration mopped up by the lymphatic system and carried back to the heart via this system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the serosa made up of?

A

Mesothelial cells and connective tissue.
Mesothelial cell layer:
- diffusion barrier, transcellular transport.
- synthesise connective tissue and enzymes.
- Respond to cytokines and hormones.
The lymphatics communicate through openings between mesothelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Factors affecting movement of fluid under normal circumstances.

A

Hydrostatic pressure.
Colloid osmotic pressure.
Endothelial permeability.
Lymphatic function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does fluid accumulate?

A

More filtration occurring than reabsorption.
Increased capillary hydrostatic pressure.
Wider oncotic pressure gradient.
Increased endothelial permeability.
Loss of effective lymphatic drainage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Oedema/effusion clinical signs.

A

Depend on location of oedema/effusion.
Abdominal distension, fluid thrill.
Dyspnoea, tachypnoea.
Lameness.
Lethargy.
Inappetence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dx tests for oedema/ascites.

A

PE.
Blood tests.
Ultrasound:
- abdomen.
- heart.
Radiographs.
Urinalysis - e.g. to look for a PLN&raquo_space; hypoalbuminaemia&raquo_space; ascites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Investigation of the fluid.

A

If effusion, take sample.
EDTA tube:
- cell counts, cytology, PCV, PCR (virology).
Serum tubes:
- albumin, bilirubin, creatinine, K, triglyceride, glucose, lactate.
Sterile tubes:
- culture (bacteria, fungi).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Classification of effusions.

A

By TP and cell count.
Transudate:
- pure.
- modified.
Exudate:
- septic.
- non septic.
– haemorrhagic, chylous, bilious, malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Normal pleural/peritoneal fluid.
- vol.
- colour.
- TP. (why?)
- nucleated cell count.
- Cell types.
- purpose.
– in thorax?

A

Low volume.
Clear, straw-coloured.
TP <2.5g/dL (due to ultrafiltration of blood).
Nucleated cell count usually <1000/microlitre.
Few cells (mesothelial cells, macrophages, lymphocytes, neutrophils).
Lubrication between organs.
– transmission of forces for normal respiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Pure transudate.
    - colour.
    - SG.
    - TS.
    - nucleated cell count.
    - Cells.
  2. Why do pure transudates form?
A
  1. Clear, colourless liquid / slightly straw-coloured.
    <1.017.
    <2.5g/dL.
    <1000/microlitre.
    Few cells.
  2. Increased hydrostatic pressure. e.g. venous hypertension.
    Decreased osmotic pressure. e.g. hypoalbuminaemia.
    No change in permeability.
    - just fluid leaking out, cells and proteins staying w/in the vasculature.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of increased hydrostatic pressure.

A

Systemic venous hypertension.
- R-sided CHF.
- Portal hypertension (liver disease).
- Occlusion (neoplasia, thrombus).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of decreased oncotic pressure.

A

Hypoproteinaemia - albumin.
– PLE/PLN.
– Liver failure –> not making enough albumin,
– Repeated drainage of effusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Modified transudate.
- colours.
- SG.
- TP.
- Nucleated cell count.
- cells.

A
  • Yellow - serosanguinous.
  • 1.017-1.025.
  • 2.5g/dL-5g/dL.
  • 1000-10000/microlitre.
  • low numbers of mesothelial cells, macrophages, neutrophils, mature lymphocytes, RBCs.
    – may see atypical cells if neoplastic process.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Why do modified transudates form?
  2. Why is modified transudate the most common kind of effusion we see?
A
  1. Increased permeability of vessel wall to cells and proteins.
  2. A chronic pure transudate&raquo_space; enough inflammation&raquo_space; increased permeability will occur&raquo_space; transudate becomes modified overtime.
17
Q

Causes of modified transudate.

A

Increased hydrostatic pressure.
R-sided CHF.
Vasculitis.
Neoplasia.
Post surgery.
Organ torsions.

18
Q

Exudate appearance.
SG.
TP.
Nucleated cell count.
Cell types.
What if exudate is septic?

A

Turbid - red, yellow, white.
>1.025.
>3g/dL.
>5000/microlitre.
Mostly neutrophils and macrophages +/- atypical cell (if neoplasia).
May see intracellular bacteria - CULTURE!

19
Q

Why does exudate form?

A

Increased permeability.
Inflammatory cells.
Lymphatic drainage reduced.

20
Q

How does exudate form?

A

Local inflammatory response to foreign material (exogenous, neoplastic, endogenous).
Cytokines, oxidants, proteases - increase mesothelial and endothelial permeability.
Influx of inflammatory cells.
Leak of protein into tissue.
Obstruction of lymphatics, decreasing drainage.

21
Q

Causes of septic exudate.

A

GI leakage, penetrating wounds.
FBs.
Urogenital tract.
Respiratory tract.
Haematogenous spread.
Intracellular bacteria on cytology (contamination on slide!)

22
Q

Causes of non septic exudates.

A

Pancreatitis: intra-abdominal inflammation.
FIP: coronavirus, protein-rich effusion, straw-gold, hazy.
Vessels: haemorrhagic effusion.
Lymphatic: chylous effusion.
Organs: urine, bile.

23
Q

Haemorrhagic effusion.
- appearance.
- SG.
- TP.
- cell count.
- PCV.
- If platelets present… if not…
- secondary to …. if not, what?
- cytology.

A

Closely resemble peripheral blood (RBCs, neutrophils, lymphocytes).
>1.025.
>3g/dL.
>1000/microlitre.
>10%.
If platelets present, may see blood clots (splenic aspiration, venepuncture, acute severe haemorrhage). Usually no platelets so no clotting as clotting factors usually used up before sampling.
Secondary to blunt trauma, or coagulopathy/neoplasia.
Buffy coat and sediment.

24
Q

Cause of chylous effusion.
Appearance.
SG.
TP.
Cell count.
Cell types.
Triglyceride.
Cholesterol.
Causes.

A

Impaired lymphatic drainage from GIT into caudal vena cava.
Opaque, milky.
>1.017.
>2.5g/dL.
Variable.
Lymphocytes (neutrophils, variable macrophages).
Triglyceride more than in serum at >100mg/dL.
Cholesterol less than in serum.
Cardiac disease, lung lobe torsion, trauma, mass lesions (compression of lymph drainage), idiopathic.

25
Q

Uroabdomen.

A

Acute uroperitoneum: pure transudate.
Inflammatory response develops.
Creatinine and urea in effusion > blood.

26
Q

Bilious effusion associated with?
Appearance.
SG.
TP.
Cell types.
Bilirubin.
Causes.

A

Gall bladder injury.
Green, orange, yellow.
>1.025.
>3g/dL.
Neutrophils, macrophages containing golden, green, black brown pigment from bile.
Bilirubin in effusion > in serum.
Trauma, cholangitis, pancreatitis, surgery, concurrent bacterial infection: poor Px.

27
Q

Effusion w/ exfoliation of cells.

A

Neoplastic or reactive mesothelial cells: highly cellular effusions.
Carcinomas, mesotheliomas, round cell neoplasms (lymphoma, MCT, malignant histiocytosis).
Can also get activation of mesothelial cells due to chronic effusions.