Oedema Flashcards
Define oedema:
Abnormal accumulation of interstitial fluid in tissues due to an imbalance between movement into the tissues from the capillaries and removal from the tissue by lymphatics.
Pathophysiology of oedema
- Oedema results from increased movement of fluid from the intravascular compartment to the intersitial space OR decreased movement of water from the interstitium into the capillaries or lymphatic vessels
- Mechanism involves:
-
Increased capillary hydrostatic pressure
- increase in venous pressure –> leads to increase in capillary hydrostatic pressure – >leads to efflux ino the interstitium
- E.g. HF/Cor pulmonale, venous thrombosis
-
decreased plasma oncotic pressure / plasma proteins
- oncotic pressure in vessels > than in the interstitum, if there is a ↓serum protein levels= ↓oncotic gradient = ability to hold fluid in vascular space.
- E.g. ↓albumin production (liver cirrhosis) or increase in urinary albumin loss (nephrotic syndrome).
-
increased capillary permeability
- ↑blood vessel permeability to the action of cytokines, PG/NO –> leads to large serum proteins moving into the interstitial space –> ↓ oncotic gradient/ net outflow of fluid into the interstitium
- e.g. sepsis (circulating cytokines), hypothyroid myxodema, angioedema, anaphylaxis
-
obstruction of the lymphatic system
- E.g. malignancy, infextion, surgery or radiotherapy
-
Increased capillary hydrostatic pressure
What are the differentials for generalised oedema?
- Cardiac failure
- Renal failure
- hypoalbuminaemia (liver failure)
- idiopathic cyclic oedema
- pretibial myxoedema
What are the differentials for local oedema?
DVT
Chronic venous insufficiency (venous wall and or valves in leg veins do not work effectively)
lymphoedema
What is pitting oedema vs non pitting oedema?
causes of each?
- Pitting –> caused by fluid retention, responds to pressure
- Non pitting –> Does not respond to pressure and there are three main causes:
- Lymphoedema (blockage of lymphatic drainage)
- Pretibial Myxoedema –> altered vascular permeability + deposition of hyaluronic acid/ accumulation of excess glycosaminoglycans in the dermis and subcutaneous tissue –> attracts fluid –> associated with Graves disease
- Lipoedema –> abnormal fat deposition under the skin, retains fluid.
Identify features of Hx relevant to each of the differential diagnosis for oedema?
- Duration of oedema? (Long standing Cardiovascular, varicose veins?) Acute (DVT or think glomerulonephritis/ anaphylaxis)
- distribution:
- Unilateral or bilateral?
- Unilateral –> Venous/ lymphatic/ traumatic or infectious?
- Bilateral–> Raised venous pressure? Or low serum albumin?
- localised –> cellulitis/ lymph/venous obstruction
- Generalised –> cardiac, renal, liver/ hypoalbuminaemia/ hypothyroidism
- Periorbital –> renal cause
- Ankles/sacrum/ pulmonary –> Heart failure
- Hands/face/ lying down –> low protein
- Unilateral calf –> DVT
- Face + lips –> angioedema
- abdominal –> ascites
- Unilateral or bilateral?
- Any trauma?
- Relevant PMH? E.g. Cardiac (MI/CVD/Peripheral vascular disease) Liver, Renal? Recent surgery or prolonged travel (DVT)
- Other symptoms:
- Constipation/ cold intolerance/fatigue –> hypothyroidism
- orthopnea/ PND –> cardiac failure
- oliguria/ haematuria –> nephritis
- GI sx? Liver –> ascites
- chest pain/cough/dysponea –> mediastinal obstruction tumour
- bowel dysfunction –> protein losing enteropathy
- painful swollen calf –> DVT, cellulitis, osteomyelitis
- immobility?
- Pelvic mass or pregnancy?
- Drug history –> Steroids, NSAID’s , CCB’s?
General Examination features for oedema?
- General examination:
- Fever, O2 sats, warmth, how far up, break in skin, any break in the skin, pain in joints, change in skin colour
- nourishment –> nutritional deficiency –> hypoproteinaemia
- Pallor –> cardiac/ GI causes
- Jaundice –> cirrhosis
- cyanosis –> cardiac
- clubbing –> cardiac and liver
Investigations for oedema?
- Bedside:
- Urinalysis –> proteinuria or haematuria (nephrotic/ nephritic syndromes)
- ECG –> HF/MI
- Bloods:
- FBC –> infection or anaemia (which can aggravate HF)
- biochemistry:
- ↑creatinine- renal
LFT- ↓liver fxn, ↓albumin (In renal/liver and malnutrition)
Glucose- infecxn (DM)
TFT- hypothyroidism
- ↑creatinine- renal
- Clotting –> spontaneous haematoma
- D dimer –> VTE (DVT or chronic venous insufficiency)
- Imaging:
- Echo –> HF
- CXR –> HF or lung mets
- USS/CT –> haeamatoma, tumour, abdo or pelvic mass
- Duplex doppler USS or venography –> Provides image of moving blood within a vessel for asessement of DVT OR AV fistula
- Special tests:
- Lymphoscintigraphy –> inject radioactive material into skin which should accumulate in regional lymph nodes –> lymphoedema (Hypoplasia or obstruction)
- lymph node biopsy –> infection, tumour
- Renal biposy –> glomerulonephritides
Diagnostic approach for oedema?
- 1) Is it localised or unilateral?
- localised –> think venous or lymphatic obstruction OR cellulitis
- Peripheral/generalised –> ascites or pulmonary oedema present?
- 2) Is JVP raised?
- If elevated –> think cardiac/renal/iatrogenic fluid overload
- If not – > assess serum albumin
- If LOW –> assess for proteinuria
- YES –> nephrotic syndrome
- NO –> hepatic failure or malnutrition
- If Normal –> reassess JVP/ reconsider Lymphatic or venous obstruction, Drugs (NSAID/S CBB’s).
- If LOW –> assess for proteinuria
General management for oedema?
- Treat the cause
- Bilateral –> Loop or thiazide diuretics (careful in hypovolaemia and renal function)
- Elevate legs
- Graduated stocking support –> for chronic venous disease
- management highly dependent on the cause, empirical diuretics inappropriate in abscence of diagnosis.
Specific causes: Cardiac failure
Pathophysiology
RF
Hx
Exam
Heart failure –> pitting dependant oedema due to usually right sided HF and back pressure into the venous system ↑Hydrostatic pressure
RF: Right sided HF, constrictive pericarditis, CVD, HTN, MI, valvular disease, pericardial, arryhtmias or drugs
Hx: Dysponea, orthopneoa, PND fatigue
Exam: Bilateral pitting oedema, Tachycardia, HTN, Raised JVP, HF/Resp signs / pulmonary oedema
Specific cause: Renal failure
Pathophysiology
Hx
Exam
Investigation
- Pitting dependant oedema ↓ oncotic pressure from protein loss (albumin) + acute nephritis ↓renal perfusion and GFR –> leads to decreased Urine output, RAAS activation & Na/H2O retention –> Increase intravascular volume, HTN .
- Hx: decreased Urine output (oliguria), haematuria/ frothy urine (proteinuria)
- Exam: bilateral pitting oedema +/_ ascites, pulmonary crackles and ↑ JVP
- Investigation: ↑serum creatinine and urea, GFR & UO decrease
Specific causes: Hypoalbuminaemia
Pathophysiology
RF
HX
Exam
Investigation
Pathophysiolgy: Pitting oedema due to decreased oncotic pressure, caused by either liver failure/cirrhosis, nephrotic syndrome, malnutrtion, protein losing enteropathy
Hx: Nephrotic frothy urine, △freq/quantity
Cirrhosis RF presence, bilat oedema.
Ex: Both bilat, norm JVP
Cirrhosis spleno, ascites, jaundice, caput.
Ix: Nephrotic ↓ albumin, ↑↑urine protein
Cirrhosis LFTs (↓alb, >20sPT/bilirubin), USS
(small scarred, ↑portal pressure, spleno).
Specific causes oedema: Drugs
Pitting dependent oedema, often SE of increased Na/H2O retention –> increased fluid volume and pressure
Causes: CCB’s/NSAIDS/Prolonged steroid/ insulin
Hx and exam: Drug hx - CCB (dihydropyridines - amlodipine/nifedipine) , NSAIDS (lose renal prostaglandin synthesis - lose afferent arteriole vasodilation), steroid or insulin use
Bilateral pitting oedema with normal JVP
Specific causes: Idiopathic cyclic oedema:
Pathophysiology
RF’s
Hx/Exam
Mx:
- pitting oedema due to vessel hyperpermeability –> volume overload and fluid retention
- Occurs in premenopausal women in absence of cardiac/hepatic or renal disease (F 20-40 yrs), variable
- not menstrual related and a diagnosis of exclusion
- RF: Female, intermittent fasting, diuretic use
- Hx/Exam: Mild swelling of hands/feet/abdo/breasts/face) often worse at the end of the day, often overweight
- Mx: no prolonged standing, weight loss and decrease salt intake
Specific causes of oedema: Pretibial myxoedema
Pathophysiology
Hx
Ex
Ix
Mx
- Patho: Pitting oedema, altered vascular permeability, and the deposition of hyaluronic acid / accumulation of excess glycosaminoglycans deposied in dermis and subcut tissues –> associated with Graves disease
- Hx: FHx, Female, Smoker, often
- Exam: Early lesions –> non pitting bilateral, asymmetrical plaques, scaly thickened hardened skin.
- Diagnosis: Due to TSH receptor antibodies that mimic TSH. Suppressed serum TSH, elevated levels circulating T3/T4, detectable TSH receptor antibodies, high thyroid uptake of radioactive iodine.
- Tx: Radioactive iodine therapy, thyroid surgery, antithyroid drugs –> Carbimazole (prevents iodination of thyroglobulin – reduce production of T3 and T4).
Causes of localised oedema: DVT
Patho
Hx
Exam
Ix
Mx
- DVT –> pitting localised, increased hydrostatic pressure due to emboli blocking venous return
- Hx: Acute/subacute pain, unilateral oedema
- Exam: unilateral tender, warm, erythematous, palpable cord behind leg, normal JVP
- Ix: Wells score –> 1st D dimer, 2nd USS vein ultransonography/venography
- Mx: anticoagulant- warfarin or rivaroxaban
