OEDEMA AND SHOCK

Learning Outcomes
 1. 2.

3. 4. 5.

At the end of this lecture, student sshould be able to: Define shock & oedema. Differentiate between transudate and exudate oedema define shock Explain the etiology of shock List the symptoms of shock.
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Internal Environment


Homeostasis; the mechanism where the internal environment is MAINTAINED & ENSURED. LIVING MEMBRANES with varying permeabilities e.g. vascular endothelium & cell wall play an important role in exchange of fluids, electrolytes, nutrients & metabolites. The normal composition of internal environment are: i. Water ii. Electrolytes
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The pH 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 in arterial blood iii. Renal mechanism
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Normal fluid pressures: i. Osmotic pressure (this is the pressure exerted by the chemical constituents of the body fluids). ii. Hydrostatic pressure (this is the capillary blood pressure).

OEDEMA
Increased interstitial fluid volume
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Definition & Types of Oedema

 

Greek word oedema means SWELLING. Oedema; defined as abnormal & excessive accumulation of fluid in the interstitial tissue spaces & serous cavities. 2 main types: i. LOCALISED (in the organ or limb as in venous obstruction) ii. GENERALISED (anasarca or dropsy as in systemic inflammation)
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Oedema fluid may be: i. TRANSUDATE (more often!! e.g. in oedema of cardiac & renal disease) ii. EXUDATE (e.g. in inflammatory oedema)

FEATURE 1. Definition

TRANSUDATE Filtrate of blood plasma w/out changes in endothelial permeability Non-inflammatory edema

EXUDATE Edema of inflamed tissue associated with increased vascular permeability Inflammatory edema High, readily coagulates due to high content of fibrinogen and other coagulation factors Low
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2. Character

3. Protein content Low; mainly albumin, low fibrinogen; hence no tendency to coagulate 4. Glucose content Same as in plasma

5. Specific gravity 6. pH 7. LDH 8. Effusion LDH/ Serum LDH ratio 9. Cells

Low > 7.3 Low < 0.6 Few cells, mainly mesothelial cells & cellular debris Edema in congestive cardiac failure

High < 7.3 High > 0.6 Many cells, inflammatory as well as parenchymal Purulent exudate such as pus

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Pathogenesis Of Oedema


The following 6 mechanisms may be operating single or combination to produce oedema: ii. Increased capillary hydrostatic pressure i. Decreased plasma oncotic pressure iii. Lymphatic Obstruction

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Pathogenesis Of Oedema

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i. Decreased plasma oncotic pressure



A fall in the total plasma protein (albumin) level (hypoproteinaemia). Hypoproteinaemia usually produces generalised oedema (anasarca). This results in INCREASED outward movements of fluid from the capillary wall & DECREASED inward movement of fluid from the interstitial space causing oedema.
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The examples of edema by this mechanism are: a. Oedema of renal disease b. Ascites of liver disease c. Oedema due to other causes of hypoproteinaemia.
BACK

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ii. Increased capillary hydrostatic pressure



A rise in the hydrostatic pressure at the venular end of the capillary which is normally low to a level more than the plasma oncotic pressure results in minimal or no reabsorption of fluid at the venular end. The examples of oedema by this mechanism are: i. Oedema of cardiac disease e.g. in congestive cardiac failure ii. Ascites of liver disease e.g. cirrhosis of liver iii. Passive congestion e.g. tumors iv. Postural oedema
BACK

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iii. Lymphatic obstruction (Lymphoedema):



Normally the interstitial fluid in the tissue spaces escapes by way of lymphatics so that obstruction to outflow 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 or thoracic duct such as due to tumors.
BACK
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iv. Tissue factors:



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

BACK

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v. Increased capillary permeability:



When the capillary endothelium injured by various capillary poisons such as toxins, the capillary permeability to plasma proteins is enhanced due to development of gaps between the endothelial cells.
BACK

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vi. Sodium & water retention:



Excessive retention of sodium & water and their decreased renal excretion occur in response to hypovolaemia. The examples of oedema by these mechanism are: i. Oedema of cardiac disease e.g. in congestive cardiac failure ii. Ascites of liver disease e.g. in cirrhosis of liver iii. Oedema of renal disease e.g. nephrotic syndrome, glomerulonephritis
BACK
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Types of Oedema


4 important types of oedema: i. Renal oedema ii. Cardiac oedema iii. Pulmonary oedema iv. Cerebral oedema

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i. Renal oedema


Generalised oedema occurs in certain disease of renal origin 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 the visceral organs. The affected organ is enlarged & heavy with tense capsule.
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In contrast, nephritic oedema is not due to hypoproteinemia but is due to excessive reabsorption of sodium & water in the renal tubules vie reninangiotensin-aldosteron mechanism. The protein content of oedema fluid in glomerulonephritis is quite low.

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FEATURE

NEPHROTIC OEDEMA

NEPHRITIC OEDEMA

1. Cause 2. Proteinuria 3. Mechanism

Nephrotic syndrome Heavy Low plasma oncotic pressure, Na+ & water retention Severe, generalised

Glomerulonephritis Moderate Na+ & water retention

4. Degree of oedema 5. Distribution

Mild

Subcutaneous tissues Loose tissues mainly as well as visceral (face, eyes, ankles, organs genitalia)
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ii. Cardiac oedema



Generalised oedema develops in right-sided and congestive cardiac failure. Is influenced by gravity & is thus characteristically dependent oedema. The accumulation of fluid may also occur in serous cavities.

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iii. Pulmonary oedema



Acute pulmonary oedema is the most important form of local oedema as it causes serious functional impairment but has special features. Pulmonary oedema can result from either the elevation of pulmonary hydrostatic pressure or the increased capillary permeability. As the capacity of the lymphatics to drain the fluid is exceed (about ten fold increase in fluid), the excess fluid starts accumulating in the interstitium.
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iv. Cerebral oedema:



The mechanism of fluid exchange in the brain differs from elsewhere in the body. It s because there are no draining lymphatics in the brain but instead, the function of fluid electrolyte exchange is performed by the blood brain barrier located at the endothelial cells of the capillaries.

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3 types of cerebral oedema:

a. Vasogenic oedema (most common type) - Vasogenic oedema is prominent around cerebral contusions, infarcts, brain abscess & some tumors.

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b. Cytotoxic oedema - The blood-brain barrier is intact & the fluid accumulation is intracellular. c. Interstitial oedema - Occurs when the excessive fluid crosses the ependymal lining of the ventricles & accumulation in the periventricular white matter.
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ASSESSMENT

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SHOCK
Depressed vital functions due to decreased circulating blood volume

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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

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Shock is classified into 3 main etiologic forms: i. Hypovolaemic shock ii. Septic shock (capillary damage by infection) iii. Cardiogenic shock (heart failure)

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i. Hypovolaemic shock
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Reduction in blood volume induces hypovolaemic shock. The causes of hypovolaemia include the following: a. Severe haemorrhage e.g. in trauma, surgery. b. Fluid loss e.g. severe burns.
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ii. Septic shock

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Severe bacterial infections or septicaemia induce septic shock. The predominant causes are as under: a. Gram ve septicaemia (endotoxic shock) b. Gram +ve septicaemia (exotoxic shock)

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iii. Cardiogenic shock

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Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart w/out actual reduction of blood volume results in cardiogenic shock. The causes are: a. Deficient emptying e.g. rupture of the heart b. Deficient filling c. Obstruction to the outflow e.g. pulmonary embolism
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5.6 Pathogenesis Of Shock



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

i. Reduced effective circulating volume

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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 organs and tissues
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Morphologic Complications In Shock



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

1. Hypoxic encephalopathy cerebral ischemia in compensated shock may produce altered state of consciousness. 2. Heart in shock heart is more vulnerable to the effects of hypoxia than any other organ.
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3. Shock lung lungs due to dual blood supply are generally not affected by hypovolaemic shock. 4. Shock kidney one of the important complications of shock is irreversible renal injury. 5. Adrenals in shock the adrenals show stress response in shock. 6. Haemorrhagic gastroenteropathy
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Clinical Features


The classical features of decompensated shock are characterised 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!!!
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Shock Management
   

Airway Stimulants e.g. Ammonia inhalation Fluids, electrolytes TREAT THE CAUSE!!!

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

- George Eliot -

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THANK YOU

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