dampness - oedema

8/4/2019 Dampness - Oedema

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OEDEMA

M. O. Al-Sohaibani, MBBS, FCAP, F


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OEDEMA

Definition and types The Greek word oedema means swelling. O

be defined as abnormal and excessive accufluid in the interstitial tissue spaces and serThe presence of abnormal collection of fluidcell is sometimes called intracellular oedemamore appropriately be called hydropic deThe accumulation of fluid in the bodycorrespondingly known as ascites (in thecavity), hydrothorax or pleural effusion (incavity) and hydropericardium or pericard

(in the pericardial cavity).


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The oedema may be of 2 main types.

Localized in the organ and limb; and

Generalized (anasarca or dropsy) when itdistribution, particularly noticeable in the

tissues.

Besides, there are a few special forms of

oedema fluid lies free in the interstitial spthe cells and can be displaced from one p

In the case of oedema in the subcutaneou

momentary pressure of finger produces a

known as pitting oedema. The other varipitting or solid oedema in which no pittin

on pressure e.g. in myxoedema, elephant


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Oedema fluid may be:1] transudate which is more often t

case, such as in oedema of cardi

renal disease; or2] exudate such as in inflammatory

oedema.

The differences between transudate and

exudate are tabulated.


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Pathogenesis of oedema

Oedema is caused by mechan

that interfere with normal flui

balance of plasma, interstitial

and lymph flow. The followin

mechanisms may be operating

or in combination to produce

oedema;


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Types of oedema

Decreased plasma oncotic pressure increased capillary hydrostatic pres

lymphatic obstruction.

tissue factors (increased oncotic printerstitial fluid, and decreased tiss

tension).

increased capillary permeability.

sodium and water retention.


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These mechanisms are discussed below.

1. Decreased plasma oncotic pressure:

The plasma oncotic pressure exerted by the totplasma proteins tends to draw fluid into the venormally. A fall in the total plasma protein lev(hypoproteinaemia of less than 5 g/dl), results of plasma oncotic pressure in a way that it can counteract the effect of hydrostatic pressure of

results in increased outward movement of fluidcapillary wall and decreased inward movementfrom the interstitial space causing oedema.Hypoproteinaemia usually produced generalize(anaasarca). Out of the various plasma proteinshas four times higher plasma oncotic pressure

so that it is hypoalbuminemia (albumin below results in oedema more often.


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The examples of oedema by this

mechanisms are seen in the followconditions:

Oedema of renal disease e.g. in n

syndrome, acute glomerulonephr

Ascites of liver disease e.g. in cir

Oedema due to other causes of

hypoproteinaemia e.g. in protein-

enteropathy.


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2.Increased capillary hydrostatic pr

The hydrostatic pressure of the capilforce that normally tends to drive flu

the capillary wall into the interstitial

counter acting the force of plasma on

pressure. A rise in the hydrostatic prthe venular end of the capillary whic

normally low (average 12 mmHg) to

more than the plasma oncotic pressu

in minimal or no reabsorption of fluivenular end, consequently leading to


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The examples of oedema by this mechare seen in the following disorders:

Oedema of cardiac disease e.g. in concardiac failure, constrictive pericarditi

Ascites of liver disease e.g. in cirrhosi

Passive congestion e.g. in mechanical

obstruction due to thrombosis of veinslower legs, varicosities, pressure by pruterus, tumors et.

Postural oedema e.g. transient oedemaand ankles due to increased venous pr

seen in individuals who remain standifor longtime such as traffic constables


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The examples of lymphoedema include the f

Removal of axillary lymph nodes in radical for carcinoma of the breast produces lympho

the affected arm. Pressure from outside on the main abdomina

duct such as due to tumours, effusions in seretc may produce lymphoedema. At times, thlymphatic channel may rupture and dischargthe pleural cavity (chylothorax) or into perit

(chylous ascites). Inflammation of the lymphatics as seen in fi

(infection with Wuchereria bancrofti) resultlymphoedema of scrotum and legs known aselephantiasis.

Occlusion of lymphatic channels by maligna

result in lymphoedema. Milroy's disease or hereditary lymphoedema

abnormal development of lymphatic channein families and the oedema is mainly confin

both the lower limbs.


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4. Tissue Factors:

The forces acting in the interstitial space pressure of the interstitial space and tissuare normally quite small and insignificancounteract the effect of plasma oncotic prcapillary hydrostatic pressure respectivelin some situations, the tissue factors in co

with other mechanisms play a role in cauoedema. These are as under:

Elevation of oncotic pressure of interstitioccurs due to increased vascular permeabinadequate removal of proteins by lymph

Lowered tissue tension as seen in loose stissues of eyelids and external genitalia.


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5. Increased capillary permeability:

As described previously, an intact capillary enda semipermeable membrane which permits thewater and crystalloids but allows minimal pass

plasma proteins normally. However, when theendothelium is injured by various 'capillary poas toxins and their products, histamine, anoxiacertain drugs and chemicals, the capillary perm

plasma proteins is enhanced due to developmebetween the endothelial cells. This, in turn, caplasma oncotic pressure and elevated oncotic pinterstitial fluid which consequently produces o


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The examples of oedema by this mechseen in the following conditions:

Generalized oedema due to increased permeability may occur in systemic inpoisonings, certain drugs and chemicaanaphylactic reactions and anoxia.

Localized oedema such as:

- Inflammatory oedema as seen in infallergic reactions, insect-bite, irritant dchemicals. It is generally exudate in n

- Angioneurotic oedema is an acute atlocalized oedema occurring on the ski

and trunk and may involve lips, larynxand lungs. It is possibly neurogenic oin origin.


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Sodium and water retention:

Before describing the mechanism o

oedema by sodium and water reten

essential to recollect the normal reg

mechanism of sodium and water ba Normally, about 80% of sodium is

reabsorbed by the proximal convol

tubule under the influence of intrin

mechanism or extra-renal mechanis


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Intrinsic renal mechanism is activated

response to sudden reduction in the effe

arterial blood volume (hypovolaemia) as

severe haemorrhage. Hypovolaemia stim

the arterial baroreceptors present in the c

sinus and aortic arch which in turn, send

sympathetic outflow via the vasomotor cthe brain. As a result of this, renal isch

occurs which causes reduction in the glo

filtration rate, decreased excretion of sod

the urine and consequent retention of so


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Extra-renal mechanism involves the secretionaldosterone, a sodium retaining hormone, by th

renninangiotensin-aldosterone system. Renninenzyme secreted by the granular cells in the juxglomerular apparatus. Its release is stimulatedto low concentration of sodium in the tubules. action is stimulation of the angiotensinogen whglobulin or rennin substrate present in the plasmstimulation, angiotensis I, a decapeptide, is for

plasma which is subsequently converted into aII, an octapeptide, in the lungs and kidneys. Astimulates the adrenal cortex to secrete aldostehormone. Aldosterone increases sodium reabs

the renal tubules and sometimes causes a rise ipressure.


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AHD mechanism. Retention of sodium leads to water secondarily under the influence of anti-d

hormone (ADH) or vasopressin. This hormonby the cells of the supraoptic and paraventriculthe hypothalamus and is stored in the neurohy(posterior pituitary). The release of hormone i

by increased concentration of sodium in the plahypovolaemia. Large amounts of ADH producconcentrated urine.

* Excessive retention of sodium and water and thdecreased renal excretion occur in response tohypovolaemia and lowered concentration of sorenal tubules via stimulation of intrinsic renal a

renal mechanisms as well as via release of AD


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The examples of oedema by thesmechanisms are as under:

Oedema of cardiac disease e.g. in

congestive cardiac failure.

Ascites of liver disease e.g. in cirliver.

Oedema of renal disease e.g. in n

syndrome, glomerulonephritis.


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Pathogenesis and morphology of

important types of oedema. As observed from the pathogenesis

oedema just described, more than o

mechanism may be involved in ma

examples of localized and generalizoedema. Some of the important ex

are described below:


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Renal oedema

General oedema occurs in certain disease of re

such as in nephrotic syndrome, some types ofglomerulonephritis, and in renal failure due to tubular injury.

1. Oedema in nephrotic syndrome. Since therepersistent and heavy proteinuria (albuminuria) syndrome, there is hypoalbuminaemia causing

plasma oncotic pressure resulting in severe genoedema (nephrotic oedema). The hypoalbumincauses fall in the plasma volume activating renangiotensin-aldosterone mechanism which resuretention of sodium and water, thus setting in acycle which persists till the albuminuria contintypes of mechanisms operates in the pathogene

oedema in protein-losing enteropathy, further cthe role protein loss in the causation of oedema


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The nephrotic oedema is classically moand marked and is present in the subcuttissues as well as in the visceral organsaffected organ is enlarged and heavy wcapsule.

Microscopically, the oedema fluid sepconnective tissue fibers of subcutaneouDepending upon the protein content, thfluid may appear homogenous, pale, eo

or may be deeply eosinophilic and gran


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2. Oedema in glomerulonephritis. Oedema occconditions with diffuse glomerular disease suc

diffuse glomerulonephritis and rapidly progresglomerulonephritis (nephritic oedema). In connephrotic oedema, nephritic oedema is not duehypoproteinaemia but is due to excessive reabssodium and water in the renal tubules via reninaldosterone mechanism. The protein content ofluid in glomerulonephritis is quite low (less th

The nephritic oedema is usually mild as companephrotic oedema and begins in the loose tissuon the face around eyes, ankles and genitalia. these conditions is usually not affected by grav

cardiac oedema). The salient differences between the nephrotic a

oedema are outlined.


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3. Oedema in acute tubular injury

tubular injury following shock or

chemicals results in gross oedema

body. The damaged tubules lose

capacity for selective reabsorption

concentration of the glomerular fi

resulting in increased reabsorptio

oliguria. Besides, there is excess

retention of water and electrolyte

in blood urea.


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Cardiac Oedema

Generalized oedema develops in right-sided ancongestive cardiac failure. Pathogenesis of caroedema is explained on the basis of the followihypothesis.

Reduced cardiac output causes hypovolaemia wstimulated intrinsic-renal and extra-renal horm

(rennin-angiotensin-aldosterone) mechanisms aADH secretion resulting in sodium and water rconsequent oedema.

Due to heart failure, there is elevated central vepressure which is transmitted backward to the of the capillaries, raising the capillary hydrostaand consequent transudation; this is known as

pressure hypothesis.


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Chronic hypoxia may injure the capillary waincreased capillary permeability and result in

this is called forward pressure hypothesis. Htheory lacks support since the oedema by thimechanism is exudate whereas the cardiac otypically transudate.

In left heart failure, the changes are, howeveThere is venous congestion, particularly in th

that pulmonary oedema develops rather thanoedema.

Cardiac oedema is influenced by gravity andcharacteristically dependent oedema i.e. in aambulatory patient it is on the lower extremiin a bed-ridden patient oedema appears on thgenital areas. The accumulation of fluid mayin serous cavities.


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Pulmonary oedema

Acute pulmonary oedema is the most im

form of local oedema as it causes serioufunctional impairment but has special fediffers from oedema elsewhere in that thaccumulation is not only in the tissue spalso in the pulmonary alveoli.

Etiopathogenesis. The hydrostatic prespulmonary capillaries is much lower (avmmHg). Normally the plasma oncotic padequate to prevent the escape of fluid iinterstitial space and hence lungs are norof oedema. Pulmonary oedema can resueither the elevation of pulmonary hydro

pressure or the increased capillary perm


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Elevation in pulmonary hydrostatic press(Haemodynamic oedema). In heart failureincreased in the pressure in pulmonary veins

transmitted to pulmonary capillaries. This reimbalance between pulmonary hydrostatic pthe plasma oncotic pressure so that excessivemoves out of pulmonary capillaries into the iof the lungs. Simultaneously, the endotheliu

pulmonary capillaries develops fenestrations

passage of plasma proteins and fluid into theinterstitium. The interstitial fluid so collecteby the lymphatics present around the bronchmuscular arteries and veins. As the capacitylymphatics to drain the fluid is exceeded (abincrease in fluid) the excess fluid starts accuthe interstitium (interstitial oedema) i.e. in th

tissues around bronchioles, arteries and in thsepta.


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Next follows the thickening of the

walls because of the interstitial oedUpto this stage, no significant impa

of gaseous exchange occurs. Howe

prolonged elevation of hydrostatic

and due to high pressure of interstitoedema, the alveolar lining cells br

the alveolar air spaces are flooded w

(alveolar oedema) driving the air ou

alveolus, thus seriously hampering function.


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Examples of pulmonary oedema by

mechanism are seen in the left hear

mitral stenosis, pulmonary vein obs

thyrotoxicosis, cardiac surgery, nepsyndrome and obstruction to the ly

outflow by tumor or inflammation.


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Increased vascular permeability (Irr

oedema). The vascular endothelium the alveolar epithelial cells (alveolo-camembrane) may be damaged causing ivascular permeability so that excessiv

plasma proteins leak out, initially into

interstitium and subsequently into the This mechanism explains pulmonary o

examples such as in fulminant pulmonextrapulmonary infections, inhalation substances, aspiration, shock, radiation

hypersensitivity to drugs or antisera, uand adult respiratory distress syndrom


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Acute high altitude oedema. Individuals chigh altitude suddenly without halts and with

for acclimatization to set in, suffer from seriocirculatory and respiratory ill-effects. Commdeleterious effects begin to appear after an al2500 meters is reached. These changes incluappearance of oedema fluid in the lungs, conwidespread minute hemorrhages. These cha

cause death within a few days. The underlyimechanism appears to be anoxic damage to t

pulmonary vessels. However, if acclimatizaaltitude is allowed to take place, the individu

polycythaemia, raised pulmonary arterial preincreased pulmonary ventilation and a rise inand increased cardiac output.


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Pathologic changes. Irrespective of the

underlying mechanism in the pathogenepulmonary oedema, the fluid accumulate

the basal regions of lungs. The thickene

interlobular septa along with their dilate

lymphatics may be seen in chest X-ray a

perpendicular to the pleura and are know

Kerley' lines.

Grossly, the lungs in pulmonary oedem

heavy, moist and subcrepitant. Cut surf

frothy fluid (mixture of air and fluid).


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Microscopically, the alveolar capillariecongested. Initially the excess fluid collinterstitial lung spaces (interstitial oedemlater the fluid fills the alveolar spaces (aoedema). The interstitium as well as thespaces thus contain an eosinophilic, gran

pink proteinaceous material, often admisome RBCs and macrophages. This maas brightly eosinophilic pink lines alongalveolar margin called hyaline membranstanding pulmonary oedema is prone to

infected by bacteria producing hypostatipneumonia which may be fatal.


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In chronically elevated venous pres

known as chronic passive congestiolung or brown induration, the lungs

and heavy. The sectioned surface i

brown in colour.

Microscopically, the alveolar septa

widened and the alveolar spaces co

numerous haemosiderin laden mac

(heart failure cells) and, in late stag

show variable amount of fibrosis.


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Cerebral oedema.

Cerebral oedema or swelling of bramost threatening example of oedem

mechanism of fluid exchange in the

differs from elsewhere in the body

there are no draining lymphatics inbut instead, the function of fluid-el

exchange is performed by the blood

barrier located at the endothelial ce

capillaries.


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Cerebral oedema can be of 3 types.

Vasogenic oedema. This is the most commoncorresponds to oedema elsewhere resulting frofiltration pressure or increased capillary permeVasogenic oedema is prominent around cerebrcontusions, infarcts, brain abscess and some tu

Grossly, the white matter is swollen, soft, with

gyri and narrowed sulci. Sectioned surface is sgelatinous.

Microscopically, there is separation of tissue ethe oedema fluid and swelling of astrocytes. T

perivascular (Virchowrobin) space is widened

halos are seen around the small blood vessels.


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Cytotoxic oedema. In this type, blood-brain barrier is intact and thaccumulation is intracellular. Thunderlying mechanism is disturbathe cellular osmorgulation as occu

some metabolic derangements, achypoxia and with some toxic chem

Microscopically, the cells are swvacuolated. In some situation, bo

vasogenic as well as Cytotoxic ceoedema results e.g. in purulent m


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Interstitial oedema. This type of

oedema occurs when the excessivecrosses the ependymal lining of the

ventricles and accumulates in the

periventricular white matter. This

mechanism is responsible for oedem

non-communicating hydrocephalus


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dampness - oedema

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