18 Clinical edema

Question 1

Starling forces that promote movement into extravascular space

Answer 1

capillary hydrostatic pressure

tissue fluid oncotic pressure

Question 2

Promote movement of fluid into the vascular compartment

Answer 2

Tissue hydrostatic pressure

Capillary plasma oncotic pressure

Question 3

Occurrence of edema

Answer 3

1 elevation of venous pressure (obstruction of venous/lymph drainage)
2 decrease in capillary plasma oncotic pressure (hypoalbuminemia)

Question 4

Pertinent information in edema

Answer 4

Location
Timing
Setting of the swelling
Associated symptoms
Drug intake

Question 5

Pitting edema

Answer 5

soft, bilateral with pitting on pressure
no skin thickening, ulceration, or pigmentation

CHF, nephrotic syndrome, liver cirrhosis, malnutrition, drug intake, chronic venous insufficiency

Question 6

Non-pitting edema (lymphedema)

Answer 6

hard and non-pitting, tight, rubbery
thickened skin, unilateral or bilateral
no drainage in angiogram

lymphedema or lymphatic obstruction

Question 7

Facial and periorbital edema

Answer 7

heart failure, copd, glomerulonephritis, cirrhosis, hypothyroidism, grave’s disease

allergy: capillary leak syndrome (dilation of capillaries)

Question 8

Damage to capillary endothelium

Answer 8

increased permeability

causes: drugs, viral/bacterial agents, thermal/mechanical trauma, hypersensitivity reaction, inflammatory edema (allergy)

Question 9

Localized edema

Answer 9

1 Inflammation of the site (infaction, angioedema, contact allergy)
2 Metabolic causes (gout)
3 Venous insufficiency/thrombosis /compression
4 Chemical burn/physical injury

Bilateral edema:
above the diaphragm = SVC obstruction (pulmonary masses or severe tuberculosis)
below the diaphragm = CHF, portal hypertension, IVC obstruction, loss of venous tone (antihypertension or vasodilators)

Question 10

Generalized edema

Answer 10

1 hypoalbuminemia
2 Inc capillary permeability (sepsis)
3 Renal retention of salt and water

Question 11

Mechanisms to restore blood volume

Answer 11

Dec EABV -> intrarenal baroreceptors and macula densa receptors -> inc renin secretion

angiotensin II: inc peripheral resistance (vasoconstriction), inc cardiac output, inc Na and H2O retention = inc abp

Question 12

Cirrhosis

Answer 12

block in hepatic venous outflow -> inc hepatic lymph formation

Intrahepatic hypertension: stimulus for renal Na retention and reduction of eabv, can cause ascites

Hypoalbuminemia: lowers capillary oncotic pressure -> fluid moves out -> dec eabv -> activate RAAS -> edema

Question 13

Drug induced edema

Answer 13

Renal vasoconstriction (nsaids, cyclosporine, antihypertensives)
Arteriolar dilatation
Augmented renal sodium 
reabsorption (steroid hormones)
Capillary damage