Last updated on May 16, 2019 at 12:00
We don’t normally read a lot about the lymphatic system, and there’s not a lot to say about its pathophysiology either. The book doesn’t write a lot about it either. However, problems with the lymphatics usually cause oedema, so we’ll start there.
Oedema can be divided into local and general types. The peripheral type can be divided into pitting and non-pitting types. All types are caused by an imbalance in fluid homeostasis that causes abnormal fluid accumulation in the interstitium. We’ll focus on the localized types.
In any type of oedema is fluid lost from the plasma to the interstitium. The decreased plasma volume activates the RAAS-system, which causes an increase in aldosterone called secondary hyperaldosteronism. Recall that aldosterone causes potassium loss, so all types of oedema run the risk of hypokalaemia.
It’s called “pitting” because if you press on the oedema a “pit” will remain. This happens because the fluid below the pressed point is moved around in the interstitium and needs some time to come back. Pitting oedema is mostly seen in the lower extremities and in these cases:
- Cardiac failure
- Inflammation, burns, allergic reactions, trauma
- By increased capillary permeability
The role of cardiac failure in pitting oedema formation was discussed here.
Inflammation, burns, allergic reactions and trauma trigger the body to increase the capillary permeability of the nearby capillaries, to allow oedema.
In non-pitting oedema the extra fluid isn’t freely movable because the fluid contains proteins or mucopolysaccharides that don’t allow the fluid to move. Therefore, the fluid isn’t moved when the oedema is pressed, so no pit is formed. Two types of non-pitting oedema exist: lymphoedema and myxoedema.
Lymphoedema occurs due to a blockage or impairment of the lymphatic circulation, so that the circulation isn’t sufficient to remove the extra fluid. It’s often due to secondary causes like removal of lymph nodes during surgery, as is procedure in mastectomy for example.
True myxoedema occurs only in hypothyroidism. For reasons not well understood will mucopolysaccharides be deposited in the interstitium in this disorder, which binds fluids in the interstitium. These patients have a characteristic “puffy” appearence.
What was previously called “pretibial myxoedema” is nowadays called simply “dermopathy”. It’s not a true myxoedema like in hypothyroidism. It occurs in Graves disease, a type of hyperthyroidism. These patients have inflamed and swollen skin, often around the legs but also other places. Intraorbital dermopathy is what causes the characteristic exophthalmos (outbulging of the eyes) in Graves’ hyperthyroidism.
In generalized oedema the swelling is found on the whole body and not just in the legs. It’s mostly caused by decreased protein content in the blood (mainly albumin), caused by different factors.
In nephrotic syndrome there is a large protein loss via the urine because of failing kidneys. It also occurs in chronic renal insufficiency for the same reason.
Cirrhosis of the liver prevents the liver from making the normal amounts of plasma proteins, which also causes hypoalbuminemia.
Protein deficiency can lead to hypoalbuminemia.
The extreme form of generalized oedema is called anasarca. Anasarca is also called cardiogenic oedema.
9. Acute heart failure
11. Vasovagal syncope