Shock and Edema

8/6/2019 Shock and Edema

1/42

1

OEDEMA AND SHOCK


2/42

2

Learning OutcomesAt the end of this lecture, student sshould beable to:

1. Define shock & oedema.

2. Differentiate between transudate andexudate oedema

3. define shock

4. Explain the etiology of shock5. List the symptoms of shock.


3/42

3

Internal EnvironmentH omeostasis; the mechanism where the internalenvironment is MAINTAINED & ENSURED.

LIVING MEMBRANES with varying permeabilities e.g.

vascular endothelium & cell wall play an important rolein exchange of fluids, electrolytes, nutrients &metabolites.

The normal composition of internal environment are:

i. Water

ii. Electrolytes


4/42

4

The p H of the blood is kept constant at 7.4 0.05 in

health by the following factors:

i. Buffer system (most important buffer)- maintaining

acid base balance

ii. Pulmonary mechanism- pressure of the CO2 inarterial blood

iii. Renal mechanism


5/42

Normal fluid pressures:

i. Osmotic pressure (this is the pressureexerted by the chemical constituents of thebody fluids).

ii.H

ydrostatic pressure (this is the capillaryblood pressure).

5


6/42

6

OEDEMAIncreased interstitial fluid volume


7/42

7

D efinition & Types of Oedema

Greek word oedema means SWELLING.Oedema; defined as abnormal & excessiveaccumulation of fluid in the interstitial tissue spaces &serous cavities.

2 main types:

i. LOCALISED (in the organ or limb as in venousobstruction)

ii. GENERALISED (anasarca or dropsy as in systemicinflammation)


8/42

Oedema fluid may be:

i. TRANSUDATE(more often!! e.g. in oedema

of cardiac & renal disease)

ii. EXUDATE(e.g. in inflammatory oedema)

8


9/42

9

FEATURE TRANSUDATE EXUDATE

1. Definition Filtrate of blood

plasma w/outchanges inendothelialpermeability

Edema of inflamed

tissue associated withincreased vascularpermeability

2. Character Non-inflammatoryedema Inflammatory edema

3. Protein content Low; mainly albumin,low fibrinogen; henceno tendency tocoagulate

High, readilycoagulates due to highcontent of fibrinogenand other coagulationfactors

4. Glucosecontent

Same as in plasma Low


10/42

5 . Specific gravity Low High

6. pH > 7.3 < 7.3

7. LDH Low High

8. Effusion LDH/Serum LDH ratio

< 0.6 > 0.6

9. Cells Few cells, mainlymesothelial cells &cellular debris

Many cells,inflammatory aswell asparenchymal

10 Examples Edema incongestive cardiacfailure

Purulent exudatesuch as pus

10


11/42

11

P athogenesis Of Oedema

The following 6 mechanisms may be operating single orcombination to produce oedema:

ii. Increased capillary hydrostatic pressure

i. Decreased plasma oncotic pressure

iii. Lymphatic Obstruction


12/42

P athogenesis Of Oedema

12


13/42

13

i. Decreased plasma oncotic pressure

A fall in the total plasma protein (albumin) level(hypoproteinaemia).H ypoproteinaemia usually produces generalised

oedema (anasarca).This results in INCREASED outward movementsof fluid from the capillary wall & DECREASED

inward movement of fluid from the interstitialspace causing oedema.


14/42

The examples of edema by this mechanismare:

a. Oedema of renal diseaseb. Ascites of liver disease

c. Oedema due to other causes of

hypoproteinaemia.

14

BACK


15/42

15

ii. Increased capillary hydrostatic pressureA rise in the hydrostatic pressure at the venular end of the capillary which is normally low to a level more thanthe plasma oncotic pressure results in minimal or noreabsorption of fluid at the venular end.

The examples of oedema by this mechanism are:i. Oedema of cardiac disease e.g. in congestive cardiacfailure

ii. Ascites of liver disease e.g. cirrhosis of liveriii. Passive congestion e.g. tumors

iv. Postural oedema BACK


16/42

16

iii. Lymphatic obstruction (Lymphoedema):

Normally the interstitial fluid in the tissue spacesescapes by way of lymphatics so that obstruction tooutflow of these channels causes localised oedema.

The examples of lymphoedema are:

i. Inflammation of the lymphatics as seen in filariasis.

ii. Occlusion of lymphatic channels by malignant cells.

iii. Milroy s disease or hereditary lymphoedema.

iv. Pressure from outside on the main abdominal orthoracic duct such as due to tumors.

BACK


17/42

17

iv. Tissue factors:The forces acting in the interstitial space(oncotic pressure of the interstitial space &tissue tension).

BACK


18/42

v. Increased capillary permeability:

When the capillary endothelium injured byvarious capillary

poisons such as toxins, the capillarypermeability to plasma proteins is enhanceddue to development of gaps between the

endothelial cells.

18

BACK


19/42

19

vi. Sodium & water retention:

Excessive retention of sodium & water and theirdecreased

renal excretion occur in response to hypovolaemia.

The examples of oedema by these mechanism are:

i. Oedema of cardiac disease e.g. in congestive cardiacfailure

ii. Ascites of liver disease e.g. in cirrhosis of liver

iii. Oedema of renal disease e.g. nephrotic syndrome,

glomerulonephritis

BACK


20/42

20

Types of Oedema

4 important types of oedema:

i. Renal oedema

ii. Cardiac oedemaiii. Pulmonary oedema

iv. Cerebral oedema


21/42

21

i. Renal oedema

Generalised oedema occurs in certain disease of renalorigin such as in

a. nephrotic syndrome

b. some types of glomerulonephritis (nephritic oedema)

c. and in renal failure due to acute tubular injury.

Nephrotic oedema is clasically more severe & marked &is present in the subcutaneous tissues as well as in thevisceral organs.

The affected organ is enlarged & heavy with tensecapsule.


22/42

22

In contrast, nephritic oedema is not due tohypoproteinemia but is due to excessive reabsorption

of sodium & water in the renal tubules vie renin-angiotensin-aldosteron mechanism.

The protein content of oedema fluid inglomerulonephritis is quite low.


23/42

23

FEATURE NEPHROTIC OEDEMA NEPHRITIC OEDEMA

1. Cause Nephrotic syndrome Glomerulonephritis

2. P roteinuria Heavy Moderate

3. Mechanism Low plasma oncotic pressure, Na + & water retention

Na + & water retention

4. Degree of oedema Severe, generalised Mild

5. D istribution Subcutaneous tissues as well as visceral organs

Loose tissues mainly (face, eyes, ankles, genitalia)


24/42


25/42

iii. Pulmonary oedemaAcute pulmonary oedema is the most importantform of local oedema as it causes serious functionalimpairment but has special features.

Pulmonary oedema can result from either theelevation of pulmonary hydrostatic pressure or theincreased capillary permeability.

As the capacity of the lymphatics to drain the fluid isexceed (about ten fold increase in fluid), the excessfluid starts accumulating in the interstitium.

25


26/42

26

iv. Cerebral oedema:

The mechanism of fluid exchange in the brain differsfrom elsewhere in the body.

It s because there are no draining lymphatics in the

brain but instead, the function of fluid electrolyteexchange is performed by the blood brain barrierlocated at the endothelial cells of the capillaries.


27/42

27

3 types of cerebral oedema:

a. Vasogenic oedema (most common type)- Vasogenic oedema is prominent around cerebralcontusions,

infarcts, brain abscess & some tumors.


28/42

b. Cytotoxic oedema

- The blood-brain barrier is intact & the fluidaccumulation is intracellular.

c. Interstitial oedema- Occurs when the excessive fluid crosses theependymal lining of the ventricles &

accumulation in the periventricular whitematter.

28


29/42

ASS E SSM ENT

29


30/42

30

SH OCK

Depressed vital functions due todecreased circulating blood

volume


31/42

31

5.5 Definition & Types of Shock

SHOCK; defined as a clinical state of cardiovascular collapse

characterised by:a. an acute reduction of effective circulating blood

volume. b. an inadequate perfusion of cells & tissues.

2 main types:

i. Primary or initial shock ii. Secondary or true shock


32/42

32

Shock is classified into 3 main etiologic forms:

i. H ypovolaemic shock

ii. Septic shock (capillary damage by infection)

iii. Cardiogenic shock (heart failure)


33/42

i. Hypovolaemic shock

o Reduction in blood volume induceshypovolaemic shock.

o The causes of hypovolaemia include thefollowing:

a. Severe haemorrhage e.g. in trauma,

surgery.b. Fluid loss e.g. severe burns.

33


34/42

34

ii. Septic shock

o Severe bacterial infections or septicaemia induceseptic shock.

o The predominant causes are as under:

a. Gram ve septicaemia (endotoxic shock)

b. Gram +ve septicaemia (exotoxic shock)


35/42

35

iii. Cardiogenic shock

o Acute circulatory failure with sudden fall in cardiacoutput from acute diseases of the heart w/out actualreduction of blood volume results in cardiogenic

shock.o The causes are:

a. Deficient emptying e.g. rupture of the heart

b. Deficient filling

c. Obstruction to the outflow e.g. pulmonaryembolism


36/42

36

5.6 Pathogenesis Of Shock

2 basic features in the pathogenesis of shock:i. Reduced effective circulating volumeii. Tissue anoxia

i. Reduced effective circulating volumeo It may result by either of the following mechanisms;

a. by actual loss of blood volume b. by decreased cardiac output w/out actual loss of blood

ii. Tissue anoxia cause reduced supply of oxygen to the organsand tissues


37/42

37

Morphologic Complications In Shock

The morphologic changes in shock are due to hypoxiaresulting in degeneration & necrosis in various organs.

1. H ypoxic encephalopathy cerebral ischemia incompensated shock may produce altered state of consciousness.

2. H eart in shock heart is more vulnerable to the effectsof hypoxia than any other organ.


38/42

3 . Shock lung lungs due to dual blood supply

are generally not affected by hypovolaemicshock.

4. Shock kidney one of the important

complications of shock is irreversible renalinjury.

5. Adrenals in shock the adrenals show stress

response in shock.6. H aemorrhagic gastroenteropathy

38


39/42

39

Clinical FeaturesThe classical features of decompensated shock arecharacterised by depression of a 4 vital processes:

i. Very low blood pressure

ii. Subnormal temperature

iii. Feeble & irregular pulse

iv. Shallow & sighing respiration

In addition, the patients in shock have pale face,

sunken eyes, weakness, cold & clammy skin.With progression, the patient may develop coma &death!!!


40/42

40

Shock Management

Airway

Stimulants e.g. Ammonia inhalation

Fluids, electrolytes

TREAT TH E CAUSE!!!


41/42

41

It is never too late to become what you want to be

- George Eli ot -


42/42

42

T H ANK YOU

Shock and Edema

Documents