APPROACH TO EDEMA

Dr .A. Vimala, MD, DM, FRCP(London)

Former HOD ,Vice Principal (MCK)
Senior Consultant Nephrology
Govindan’s Hospital & Cosmopolitan Hospitals Trivandrum
Objectives
• Definition
• Pathophysiology
• Classification
• Clinical approach to find etiology
• Investigations
• Treatment
• Summary
 Distribution of body water -70kg adult

ICF
Intra-cellular
TBW
Fluid vol
(Total Body Interstitial fluid
28L
Water) 10.5L
ICF
42L
Extra-cellular
Fluid vol Plasma
14L 3L
Transcellular fluid
Definition
Accumulation of fluid in interstitial compartment
• Predominantly water
• Can contain protein and cells depending on the cause
• Minimal fluid required to clinically elicit is 4 to 5L
Extracellular fluid volume expansion is often dependent.
Ambulatory patients, edema is in the feet and lower legs;
Patients requiring bed rest develop edema in the buttocks, genitals, and
posterior thighs.
• Women who lie on only one side may develop edema in the dependent
breast.
• Lymphatic obstruction causes edema distal to the site of obstruction.
Body Fluid
Compartments
Starling’s law of physical forces
• Net pressure determining fluid transport
• {Hydrostatic pressure in the capillaries -
Oncotic pressure in the capillaries } –
{Hydrostatic pressure in the interstitium -
Oncotic pressure in the interstitium}

Increased movement of fluid from the intravascular to the interstitial space or decreased
movement of water from the interstitium into the capillaries or lymphatic vessels.

• Increased capillary hydrostatic pressure

• Decreased plasma oncotic pressure

• Increased capillary permeability

• Obstruction of the lymphatic system

Pathophysiology of Edema - Increased hydrostatic
pressure in capillaries
Fluid shifts into interstitial space

Intravascular volume depletion

Activates renin-angiotensin-aldosterone –vasopressin

(ADH)

Renal sodium retention + Exogeneous sodium intake

(increases osmolality)

Water Retention by the kidneys to help maintain plasma

volume
Pathophysiology of Edema
Lack of adequate plasma oncotic pressure
Oncotic pressure mainly by Albumin

Decreased movement of fluid out of the interstitial

space into the capillaries

• Starvation. decreased intake

• Protein-losing Enteropathy,- mal absorption, chronic diarrhea
• Liver Failure, - decrease synthesis of Albumin
• Nephrotic Syndrome, - loss of protein in urine
Pathophysiology (contd)

Angioedema Focal edema Lymphatic obstruction

Toxin or • Mediators, • Failure to remove

inflammatory including mast protein and white
damage to the cell–derived blood cells (along
capillary walls mediators (eg, with some water)
causes increased histamine, from the
capillary leukotrienes, interstitium..
permeability prostaglandins)
and bradykinin
and complement-
derived mediators
Case Study 1:
30 year old lady attends OP with complaints of swelling.

• .

• Is it symmetric or asymmetric ?

• Asymmetric only of right lower limb

• Causes of asymmetric edema

• Inflammation –Cellulitis
• Venous obstruction – Deep vein thrombosis
• Lymphatic obstruction

• Is it pitting or non-pitting?

• Pitting – New Onset edema

• Non Pitting – chronic Edema
Case Study 1 (Contd)
30 year old lady attends OP with complaints of swelling.
• Pitting Edema
• Is it associated with pain, redness, fever?
• Yes
• probably cellulitis;
• investigations CBC, pus culture, treatment - antibiotics

• No

• Ask for history of recent surgery, prolonged bed ridden state, history of Covid

or other thrombogenic conditions like APLA syndrome

• If any of above:
• probably deep vein thrombosis
• investigation – doppler of femoral vein
• Treatment – anti-coagulants
• Non Pitting edema
• Lymphatic obstruction
• Any history of malignancy –
• CA Breast – Lymph edema of upper limb
• prescribe exercise.
Case Study 2
16yr old male, complaining of swelling of both eyelids

• Does the swelling also involve feet and abdomen?

• Yes

• Is there any history of hematuria?

• No

• Is there reduction in urine output?

• No
Case Study 2 (Contd)
16yr old male, complaining of swelling of both eyelids
• Any history of vomiting, difficulty in breathing or headache
• No
• On examination, BP 120/80mm Hg

• Probable cause – Nephrotic syndrome

• Investigation – Urine routine, 24hr urinary protein, Serum Creatinine, Serum

Protein/Albumin, Lipid profile, Urine culture, X-ray chest, USG Abdomen

• Treatment – predominantly steroids, additional immunosupressance if required.

• Cause of edema
• Decrease plasma oncotic pressure
• History of hematuria, hypertension, oliguria

• Probably acute nephritic syndrome

• Investigations

Urine routine, 24hr urinary protein, Serum Creatinine, Serum

Protein/Albumin, Lipid profile, Urine culture, X-ray chest, USG
Abdomen

• exclude secondary cause- IRGN,SLE etc

Edema caused by increased hydrostatic pressure due to
sodium, water retention
Case Study 3
60yr old male, complaining of swelling of feet
• History of diabetes melitus of 5yr duration,
History of hypertension for which he is taking amlodipin.
• Is he ever told to have proteinuria
• No
• Does he have history of treatment for Diabetic Retinopathy
• No
• Urine routine – normal. No microalbuminuria
• Renal profile – normal

• Probable cause – Amolodipin induced edema

• Exclude hypothyroidism
Case Study 4
40yr old alcoholic with history of jaundice presents with
distension of abdomen and edema of feet.

• Any history of fever, abdominal pain, diarrhea, reduction in

urine output
• No
• Is he jaundiced
• No

• Investigation – Urine Routine, LFT, Renal profile

• Investigation shows hypoalbuminemia

• Probable cause – decreased oncotic pressure

Case Study 5
70yr old gentleman presents with difficulty in breathing and edema

• History of chest pain - Yes

• Suggestive of coronary disease

• History of hypertension

• Hypertensive left ventricular failure

• Renal Profile investigation show increased Creatinine 5mg

• Probable cause – acute pulmonary edema due to fluid overload and acute
left ventricular failure
• Increased hydrostatic pressure leading to salt and water retention aggravated by
kidney failure
Miscellaneous cause
• Idiopathic edema
• This is usually seen in females maybe pre-menstrual or no obvious
cause
• Hypothyroidism
Red Flags
• Sudden onset
• Significant pain
• Shortness of breath
• Fever
• History of a heart disorder or an abnormal cardiac examination
• Haemoptysis, dyspnea, or pleural friction rub
• Hepatomegaly, jaundice, ascites, splenomegaly, or hematemesis
• Unilateral leg swelling with tenderness
 Evaluation of edema
Patients with generalized edema,
Urine routine, - Alb/cr ratio, microscopic hematuria
complete blood count (CBC), blood urea creatinine,
serum electrolytes,serum protein –Albumin

Special investigations,
Brain natriuretic peptide (BNP) for suspected heart failure
D-dimer for suspected pulmonary embolism.

• Patients with isolated lower-extremity swelling

Ultrasonography.,Doppler
• Treatment of Edema
Treatment
• eatment of Edema
Identify specific cause and treat
 Dietary Restriction Of Dietary Sodium.

 Advanced Cirrhosis Or Nephrotic Syndrome -Severe Sodium Restriction (≤ 1 G/Day).

 Potassium Salts Are Often Substituted For Sodium Salts To Make Sodium Restriction Tolerable;

 Caution In Patients Receiving Potassium-sparing Diuretics, Angiotensin-converting Enzyme (Ace)

Inhibitors, Or Angiotensin Ii Receptor Blockers (Arbs) And In Those With A Kidney Disorder Because

Potentially Fatal Hyperkalemia Can Result.

In patients with heart failure or nephrotic syndrome
with or without diabetes
 Sodium-glucose cotransporter 2 (SGLT2) inhibitors

(eg, canagliflozin, dapagliflozin, empagliflozin)

 lower serum glucose in patients with diabetes

 induce diuresis by increasing natriuresis and glycosuria without

significantly affecting serum electrolytes

Treatment (contd)
Loop or thiazide diuretics. ,
monitor for hypokalemia

potassium-sparing diuretics
monitor for hyperkalemia

Combine Thiazides with potassium sparing diuretics

Precautions in elderly when drugs are used
for edema
• Starting doses low and evaluating patients thoroughly when the dose is changed

• Monitoring for orthostatic hypotension if diuretics, ACE inhibitors, angiotensin

II receptor blockers, or beta-blockers are used

• Frequently testing for hypokalemia or hyperkalemia

• Not stopping calcium channel blockers because of pedal edema, which is benign

• monitoring daily weight helps in monitoring clinical improvement or deterioration

immensely.
• Key Points
Take home messge
• Generalised edema- CLD, HEART Failure, Renal disease

• Localised edema – Exclude local causes – venous obstruction, lymphatic

obstruction, infection

• Don’t treat edema for cosmetic purpose

• Acute onset edema – detailed evaluation

• Treatment depends on the cause

Summary
• In summary, we went over the definition, classification and
pathophysiology of different types of edema.
• Case studies were presented to illustrate, how to diagnose,
investigate and identify probable causes of different edema types for
patients with varied medical history or none.
•THANK YOU