PATHOPHYSIOLOGY OF EDEMA

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3rd MBBSMorning Group A1 (Roll No. 1-10)

Kay Zin Soe

K Thari Swe

Kaung Sett Lwin

Kaung Zaw Htet

Kaung Htet Kyaw

Kaung Htet Kyaw

Kaung Htet Lin

Kaung Naing Maw

Kaung Myat Kyawe

Kaung Myat Phyoe

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DEFINITION

• Oedema results from the accumulation of excess fluid in the interstitial spaces or serous cavities.

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Classification

Depending on nature of fluid

• Inflammatory edema ( due to increased vascular permeability)

• Non-inflammatory edema ( due to osmotic or hydrostatic pressure imbalance)

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• Depending on site of collection

Generalized edema due to transudation of salt and water, as in

e.g- hypoproteinemic syndrome

congestive cardiac failure

acute glomerular nephritis

nephrotic syndrome

cirrhosis

Localized edema due to • increased permeability of small blood vessels, e.g, infection, trauma, burns,

allergy• lymphatic obstruction, e.g – malignancy, filariasis, chronic infection. • venous obstruction, e.g – thrombosis, malignant infiltration

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CAUSES OF EDEMA (MNEMONICS) 

THE LEAK OF VEINS

Tumor

Heart failure

Enteropathy (protein-losing)

 

Liver failure

Endocrine (hypothyroidism, aldosterones,diabetes)

Altitude sickness

Kidney disease (renal failure, nephrotic syndrome)

 

Obstruction of lymphatics

Filariasis

 

Venous thrombosis

Eclampsia / pregnancy

Iatrogenic

Nutritional deficiency

Sepsis / capillary leakage

(from Davidson Differential Diagnosis Mnemonics)8.3.2013

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General Principles in the formation of Interstitial Fluid

About 24 litres of fluid are filtered through the capillaries per day.

85% - reabsorbed into the capillaries.

15% - returned to the circulation via lymphatics

The formation of ISF is regulated according to the Starling hypothesis,

which incorporates 5 factors –

capillary hydrostatic pressure,

interstitial tissue pressure,

plasma oncotic pressure,

endothelial permeability and

lymphatic function.

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The arterial hydrostatic pressure, in excess of tissue pressure, tends to cause transudation of salt and water out of the capillaries

The oncotic pressure of plasma proteins tends to draw fluid back in.

There is thus on overall loss of fluid from the capillary at its arterial end, reabsorption at the venous end.

About 15% of fluid accumulating in the interstitial space passes into lymphatic vessels. From here, it passes into the general circulation via the main lymphatic channels.

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• A low plasma oncotic pressure or increased hydrostatic pressure

at the venous end of capillary will tend to cause edema.

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Generalized Edema

• Na+ is the most important osmotically active constituent of the ECF.

• The control of EFC volume ( & the formation of edema) mainly control by the factors that regulate the accumulation of Na+ in the body and excretion of Na+ by the kidneys.

• About 85% of filtered Na+ is reabsorbed in proximal convoluted tubules.

• The remaining 15% is variably reabsorbed in the distal tubule, partly with Cl- ions and partly in exchange for K + and H+ ions.

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The regulation of sodium excretion is probably mainly through adjustment of this 15%.

'Aldosterone ' effects on distal renal tubule, causing Na+ reabsorption and K+ excretion.

This effect is blocked by spironolactone.

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An important stimulus to aldosterone release comes from Renin-Angiotensin-Aldosterone

System.

Any fall in ECF volume (e.g- hypotension, hemorrhage or dehydration)

Simulate Juxtaglomerular Apparatus of Kidney

Renin secretion

ACE

Angiotensinogen Angiotensin I Angiotensin II

(Liver) (Lung)

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Angiotensin II Stimulate "aldosterone" secretion from adrenal cortex

Vasoconstriction

Secretion of ADH by acting on hypothalamus

Final result is salt & water retentions.

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Generalized Edema

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Hypoproteinemic State

The major part of plasma oncotic pressure can be attributed to its albumin content.

Hypoalbuminemia may be due to - failure of synthesis protein malnutrition (Kwashiorkor) cirrhosis long lasting ill-health from many causes increased loss as in nrephrotic syndrome. When serum albumin falls below 25 g/l, there is transudation of

solutes (mainly salt and water) out of the capillaries into intercellular space.

When this comportment is expanded by about 10%, clinically evident edema appears.

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↓ Plasma protein level (esp. albumin)

↓oncotic pressure

transudation of solutes

Edema

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Heart Failure

↓Cardiac output

Accumulation of fluid in LV

Congestion of blood in LA

Congestion of blood in pulmonary veins

↑ Capillary hydrostatic pressure

Pulmonary edema

↓Effective arterial blood volume

↓Renal perfusion

RAA System activation

↑ADH

↑aldosterone

Salt & water retentions

Fluid overload

Left Heart Failure

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↓ Contraction of RV

Congestion of RA

Congestion of SVC & IVC

↑Congestion in venules & capillaries

↓Cardiac output from LV

↓Arterial Blood Volume

RAA System activation ↑ADH

Salt & Water retentions

Right Heart Failure

Generalized Edema

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Passive congestion of "Liver“

Liver function

↓ Plasma protein synthesis

↓ Plasma oncotic pressure

Generalized Edema

In Heart failure, unless the cardiac output is restored or renal sodium and water retention is reduced (e.g.- diuretics, or aldosterone antagonists),

fluid retentions occurs and edema worsens.

 

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Nephrotic Syndrome

Heavy Proteinuria

Hypoalbuminuria

Leaky glomerular

capillary wall ↓Plasma oncotic pressure

Generalized edema

Fluid retention Hypervolemia

Salt & Water RAA system Retention

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Cirrhosis

Cirrhosis

Nodule & fibrosis plasma protein synthesis

Sinusoidal hypertension ↓ oncotic pressure

Portal Hypertension Generalize Edema

Ascities

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Investigations of Generalized edema

Chest X-ray - sign of heart failure, cardiomegaly

Plasma albumin - low in nephrotic syndrome, cirrhosis, malnutrition

Blood urea and electrolytes - diminished GFR in renal disease or in severe cardiac failure

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Localized edema1. Oedema due to increased Permeability of

small Blood vessels

Increased permeability is due to local release of inflammatory mediators, e.g.-histamine, bradykinin , and cytokines ,which cause vasodilation and increase capillary permeability.

e.g. Acute inflammatory edema(e.g.-infection)

Allergic edema

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Angio-edema is a specific form of allergic edema, affecting face, lip & mouth.

Swelling may develop rapidly and may be life-threatening if upper airway is involved.

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(2)Lymphatic Obstruction

• Impaired lymphatic drainage result in edema (lymphedema).

• Lymph vessels have a large collateral circulation, so that , with any block, edema extend over a wide area.

• Secondary cancer in lymph nodes may cause edema , but usually the block is more extensive by dissection of nodes and radiography, e.g.-in the treatment of breast cancer.

• In filariasis, lymphatic obstruction occurs due to the widespread fibrosis in lymphatic channels caused by the adult filarial worms.

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(3)Venous obstruction

Major cause - deep vein thrombosis, external pressure from a tumor or pregnancy, or valvular incompitance.

SVCO is caused by a tumor in superior mediastinum, commonly lung cancer.

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Investigations of Localized edema

• Chest X-ray – SVCO• Pelvic ultrasound or CT scan – pelvic tumor or lymphatic

enlargement• Lymphangiography – abnormal lymphatic architecture,

lymph nodes replaced by tumor• Doppler ultrasound or venography – to confirm diagnosis

of venous obstruction

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Examination of EdemaApply firm pressure with your thumb for at least 15 sec on

antero-medial aspect of shin. (Macleod’s)

Finger pressure leaves temporary indentions in the skin

Pitting Edema Lymphoedema and myxoedema do not pit on pressure.

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References

• Macleod's Clinical Examination, 12th Edition• Robbins and Cotran Pathologic Basis of Disease,8th Edition• Davidson's Principles & Practice of Medicine, 21st Edition• Tutorials in Differential Diagnosis, 4th Edition• Dr. Daw Myint Myint Khin's Symptom Analysis• Internet Websites.

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Case Discussion

Presented By Ma Kay Zin Soe

Patient’s History

Particulars of the patient• A 64 year old, gentleman, U Hla Win, a bank manager,

was admitted to MU (II), MGH on 23.2.2013 with the chief complaint of -

Breathlessness for 3 monthsSwelling of the leg for 2 weeksCough for 2 weeks

History of Present Illness

Breathlessness- The patient complained of breathlessness for 3 months which worsen in cold weather and at night. He was not able to lie flat (orthopnoea) and woke up at night due to difficulty in breathing (PND). He was dyspnoeic at rest and couldn’t do light works. (Dyspnoea on exertion) NYHA- grade IV

Cough- The patient complained of dry cough sometimes with sputum (white color). He became dyspnoeic after coughing and also complained of wheezing.

Swelling of the leg- He had swelling of the leg for 2 weeks. It started from foot and progressed to the knee. There is swelling of the abdomen.

Associated symptoms- He has palpitation when hungry but no chest pain.

System Review • On reviewing respiratory system, he has cough sometimes with

sputum, dyspnoea, wheezing but no haemoptysis and chest pain.• On reviewing gastrointestinal system, he has loss of appetite,

abdominal distension but no vomiting, nausea, indigestion, heartburn, abdominal pain and change in bowel habit.

• On reviewing genito-urinary system, he has reduced urine output but no dysuria and haematuria.

• There are no cardinal symptoms of central nervous system such as headache, dizziness, faints, fits, altered sensation, weakness, visual disturbance, hearing problems.

• On reviewing endocrine system, he has palpitation but neither fine finger tremor nor eye signs.

Past Medical and Surgical History

• The patient has a history of tuberculosis in 1994 and took proper medication. He has no history of hospitalization, blood transfusion, rheumatic fever, hepatitis, heart disease, diabetes mellitus and hypertension.

Family History

• He is married and has 9 children. All are healthy. There is no sign of similar illness in his family.

Drug History

• He has no regular taking drugs and no known drug allergy.

Social History

• He had been smoking for about 30 years and betel chewing for about 20years. He has a habit of alcohol drinking.

Physical Examination

General Survey• A 64 year old gentleman with average height and weight

is lying in his bed. He is well conscious and well cooperated. He is rather dyspnoeic but not restless. (He is given oxygen). A canular is inserted in the right hand. No gynaecomastia and no spider naevi.

General Examination

• Forehead- febrile • Eye-pallor (-), jaundice (+), subconjunctival hemorrhage

(-), xanthelesma (-), corneal arcus (+), features of Horner’s syndrome

• Nose- nasal flaring (-), nasal polyp (-)• Ear and nose discharge- discharge (-)• Mouth- angular stomatitis (-)• Lips- tobacco staining (-), pursed lip breathing (-)

• Tongue- central cyanosis (-), oral thrush (-)• Teeth and gums- dental caries (+)• Tonsillar enlargement (-)• Neck- dilated veins (+), visible neck gland enlargement (-),

accessory muscles of respiration are working, supraclavicular excavatum (+)

• Upper extremities- clubbing (+), peripheral cyanosis (-), pallor (-), flapping tremor (-), features of CO2 retention (-), Osler’s node (-), Janeway’s leision (-)

• Lower extremities- peripheral cyanosis (-), clubbing (+), dependent oedema (+)

Systemic Examination

Cardiovascular SystemPulse• Rate-68 beats/min• Rhythm- regular• Volume- moderate• Character- no special character• Condition of the vessel wall- not thickened• Equality on both sides-equal on both sides• Radio-femoral delay- no radio-femoral delay• All peripheral pulses are intact

Blood pressure-100/ 70 mmHg

JVP-5.5cm above the sternal angle(raised)

Examination of the Precordium

• Inspection-shape of the chest is symmetrical on both side and there is no precordial bulging. Diffuse precordial pulsation is not seen. Apex beat not visible. There is no epigastric pulsation. There is no scar, skin lesion, dilated veins over the Precordium.

• Palpation- apex beat is palpable at left 5th ICS within the midclavicular line with normal character and no thrill. There is no left parasternal heave. There is no epigastric pulsation. There is palpable P2 but no palpable A2.

• Percussion- is omitted. (not pericardial effusion)

• Auscultation- - At the MITRAL AREA-normal first and second heart sounds. No added

sound and no murmur.

- At the TRICUSPID AREA- normal first and second heart sounds. No added sound and no murmur.

- At the PULMONARY AREA-normal first heart sound and loud second heart sound. No added sound and no murmur.

- At the AORTIC AREA- normal first and second heart sounds. No added sound and no murmur.

Signs of Congested Heart Failure

• Raised JVP(+)• Bilateral fine basal crepitation (+)• Dependent bilateral oedema (+)• Enlarge tender liver (-)

Respiratory System

Lying position• Inspection

-Shape of the chest is symmetrical on both sides. Respiratory rate is 15 times/min.

-Chest wall movement is symmetrical on both sides.

-Apex beat is not visible.

-There is no scar, skin lesion, dilated veins. There is no supraclavicular, suprasternal, intercostal, sub costal muscles indrawing.

• Palpation- trachea is slightly deviated to right. Chest wall movement is symmetrical on both sides. Vocal fremitus is reduced on left lower zone. Palpable accompaniments are absent.

• Percussion- normal resonance (+). Liver dullness starts at 5th ICS. Cardiac dullness is from 2nd to 5th ICS.

• Auscultation- vesicular breath sound with ronchi is heard all over the lungs' field. Vocal resonance is reduced on the left lower zone.

Sitting position

• Inspection-shape of the chest wall is symmetrical on both sides. Chest wall movements are equal on both sides. There is a cyst on the right upper part of the back.

• Palpation-chest wall movements are symmetrical on both sides. Vocal fremitus is reduced on the left lower zone.

• Percussion- normal resonance ispressent all over the lungs' field.

• Auscultation- vesicular breath sound with bilateral basal crepitation is heard. Vocal resonance is reduced on the left lower zone.

Abdominal Examination

• Inspection- Contour is normal, flanks are full, abdomen moves with respiration, no visible mass, no visible peristalsis, no scar, skin lesions and dilated veins.

• Palpation- There is no tenderness and no palpable mass. Liver and spleen are not palpable. Kidneys are not blottable.

• Percussion-shifting dullness (+)• Auscultation- Normal bowel sounds are present.

Differential diagnosis

Generalize oedema and ascities are present, so this may be due to

• Congested cardiac failure• Acute glomerulonephritis• Nephrotic syndrome • Cirrhosis of liver The patients has clubbed fingers and ascites which are the

characteristics of cirrhosis of liver but no palmar erythema,no spider naevi, no gynaecomastia, no splenomegaly,no haematamesis, no malena. Therefore cirrhosis of liver is excluded.

The patient has no smoky urine(no proteinuria), no haematuria. So, Nephrotic syndrome and acute glomerulonephritis are excluded.

And there is no weight loss, no diarrhea, and no steatorrhoea. Therefore nutritional disorder is excluded.

Signs of heart failure such as dyspnoea, orthopnoea, PND, cough, ascites, ankle oedema are present.

Provisional Diagnosis

• Congested cardiac failure

Investigation

• ECG, Chest X-ray, Echocardiography, • Blood for complete picture,• Ultrasound abdomen,• Urine REME,• Serum electrolytes• LFTs

Good Luck