Dehydration Symptoms And Causes Notes

Derangements Of Body Water

The derangements of body water include the following conditions:

• Oedema and effusions
• Dehydration
• Overhydration

These are discussed here.

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1. Oedema And Effusions Definition And Types:

The Greek word oedema means swelling. Oedema is defined as abnormal and excessive accumulation of “free fluid” in the interstitial tissue spaces and serous cavities. The presence of an abnormal collection of fluid within the cell is sometimes called intracellular oedema but should more appropriately be called hydropic change.

• Free fluid in body cavities: Commonly called as effusion, it is named according to the body cavity in which the fluid accumulates. For example, ascites (in the peritoneal cavity), hydrothorax or pleural effusion (in the pleural cavity), and hydropericardium or pericardial effusion (in the pericardial cavity).
• Free fluid in interstitial space: Commonly termed as oedema, the fluid lies free in the interstitial space between the cells and can be displaced from one place to another.

In the case of oedema in the subcutaneous tissues, momentary pressure of the finger produces a depression known as pitting oedema. The other variety is non-pitting or solid oedema in which no pitting is produced on pressure for example, In myxoedema, elephantiasis.

Oedema may be of 2 main types:

1. Localised when limited to an organ or limb e.g. lymphatic oedema, inflammatory oedema, allergic oedema, pulmonary oedema, cerebral oedema etc.
2. Generalised (anasarca or dropsy) when it is systemic in distribution, particularly noticeable in the subcutaneous tissues for example, Renal oedema, cardiac oedema, and nutritional oedema.

Depending upon fluid composition, oedema fluid may be:

• Transudate which is more often the case, such as in oedema of cardiac and renal disease .
• Exudate such as in inflammatory oedema.

The differences between transudate and exudate.

Pathogenesis Of Oedema:

Oedema is caused by mechanisms that interfere with normal fluid balance of plasma, interstitial fluid and lymph flow.

The following mechanisms may be operating singly or in combination to produce oedema:

1. Decreased plasma oncotic pressure
2. Increased capillary hydrostatic pressure
3. Lymphatic obstruction
4. Tissue factors (increased oncotic pressure of interstitial fluid, and decreased tissue tension)
5. Increased capillary permeability
6. Sodium and water retention.

These mechanisms are discussed below and illustrated:

1. Decreased Plasma Oncotic Pressure :

The plasma oncotic pressure exerted by the total amount of plasma proteins tends to draw fluid into the vessels normally. A fall in the total plasma protein level (hypoproteinaemia of less than 5 g/dl, mainly hypoalbuminaemia), results in a lowering of plasma oncotic pressure in a way that it can no longer counteract the effect of hydrostatic pressure of blood.

This results in increased outward movement of fluid from the capillary wall and decreased inward movement of fluid from the interstitial space causing oedema.

Hypoproteinaemia usually produces generalised oedema (anasarca). Out of the various plasma proteins, albumin has four times higher plasma oncotic pressure than globulin; thus it is mainly hypoalbuminaemia (albumin below 2.5 g/dl) that generally results in oedema.

The examples of oedema by this mechanism are seen in the following conditions:

• Oedema of renal disease for example in, Nephrotic and Nephritic syndrome.
• Ascites of liver disease or example in Cirrhosis of the liver.
• Oedema due to other causes of hypoproteinaemia or example in Protein-losing enteropathy.

2. Increased Capillary Hydrostatic Pressure:

The hydrostatic pressure of the capillary is the force that normally tends to drive fluid through the capillary wall into the interstitial space by counteracting the force of plasma oncotic pressure.

When there is rise in the hydrostatic pressure at the venular end of the capillary to a level more than the plasma oncotic pressure, there is excessive filtration of fluid from the capillaries into tissue spaces, leading to oedema .

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

• Oedema of cardiac disease for example, In congestive cardiac failure, constrictive pericarditis.
• Ascites of liver disease for example, In cirrhosis of the liver.
• Passive congestion for example, In mechanical obstruction due to thrombosis of veins of the lower legs, varicosities, pressure by pregnant uterus, tumours etc.
• Postural oedema for example, Transient oedema of feet and ankles due to increased venous pressure seen in individuals whose job involves standing for long hours such as traffic constables and nurses.

3. Lymphatic Obstruction Normally:

The interstitial fluid in the tissue spaces escapes by way of lymphatics. Obstruction to the outflow of these channels causes localised oedema, known as lymphoedema.

The examples of lymphoedema include the following:

• Removal of axillary lymph nodes in radical mastectomy for carcinoma of the breast causing lymphoedema of the affected arm.
• Pressure from outside on the main abdominal or thoracic duct such as due to tumours, effusions in serous cavities etc may produce lymphoedema.
• At times, the main lymphatic channel may rupture and discharge chyle into the pleural cavity (chylothorax) or into peritoneal cavity (chylous ascites).
• Inflammation of the lymphatics as seen in filariasis (infection with Wuchereria bancrofti) results in chronic lymphoedema of scrotum and legs known as elephantiasis, a form of nonpitting oedema.
• Occlusion of lymphatic channels by malignant cells may result in lymphoedema.
• Milroy’s disease or hereditary lymphoedema is due to abnormal development of lymphatic channels. It is seen in families and the oedema is mainly confined to one or both the lower limbs.

4. Tissue Factors:

The two forces acting in the interstitial space—oncotic pressure of the interstitial space and tissue tension, are normally quite small and insignificant to counteract the effects of plasma oncotic pressure and capillary hydrostatic pressure respectively.

However, in some situations, the tissue factors in combination with other mechanisms play a role in causation of oedema. These are as under:

• Elevation of oncotic pressure of interstitial fluid as occurs due to increased vascular permeability and inadequate removal of proteins by lymphatics.
• Low tissue tension as seen in loose subcutaneous tissues of eyelids and external genitalia.

5. Increased Capillary Permeability:

An intact capillary endothelium is a semipermeable membrane which permits the free flow of water and crystalloids but allows minimal passage of plasma proteins normally.

However, when the capillary endothelium is injured by various ‘capillary poisons’ such as toxins and their products (for example, Histamine, anoxia, venoms, certain drugs and chemicals), the capillary permeability to plasma proteins is enhanced due to development of gaps between the endothelial cells, causing leakage of plasma proteins into interstitial fluid.

This, in turn, causes reduced plasma oncotic pressure and elevated oncotic pressure of the interstitial fluid, consequently producing oedema.

The examples of oedema due to increased vascular permeability are seen in the following conditions:

• Generalised oedema occurring in systemic infections, poisonings, certain drugs and chemicals, anaphylactic reactions and anoxia.
• Localised oedema A few examples are as under:
  • Inflammatory oedema as seen in infections, allergic reactions, insect bite, irritant drugs and chemicals. It is generally exudate in nature.
  • Angioneurotic oedema is an acute attack of localised oedema occurring on the skin of the face and trunk and may involve lips, larynx, pharynx and lungs. It is possibly neurogenic or allergic in origin.

6. Sodium And Water Retention:

The mechanism of oedema by sodium and water retention in the extravascular compartment is best described in relation to derangement in normal regulatory mechanism of sodium and water balance.

Normally, about 80% of sodium is reabsorbed by the proximal convoluted tubule under the influence of either intrinsic renal mechanism or extra-renal mechanism while retention of water is affected by the release of antidiuretic hormone.

• Intrinsic renal mechanism: Is activated in response to sudden reduction in the effective arterial blood volume (hypovolaemia) forexample,In severe haemorrhage.
  • Hypovolaemia stimulates the arterial baroreceptors present in the carotid sinus and aortic arch which, in turn, send the sympathetic outflow via the vasomotor centre in the brain.
  • As a result of this, renal ischaemia occurs which causes a reduction in the glomerular filtration rate, decreased excretion of sodium in the urine and consequent retention of sodium.
• Extra-renal mechanism: Involves the secretion of aldosterone, a sodium-retaining hormone, by the renin-angiotensin-aldosterone system.
  • Renin is an enzyme secreted by the granular cells in the juxta-glomerular apparatus. Its release is stimulated in response to low concentrations of sodium in the tubules. Its main action is stimulation of the angiotensinogen which is α₂ -globulin or renin substrate present in the plasma.
  • On stimulation, angiotensin I, a decapeptide, is formed in the plasma which is subsequently converted into angiotensin II, an octapeptide, in the lungs and kidneys by angiotensin-converting enzyme (ACE).
  • Angiotensin II stimulates the adrenal cortex to secrete aldosterone hormone. Aldosterone increases sodium reabsorption in the renal ubules and sometimes causes a rise in the blood pressure.
• ADH mechanism: Retention of sodium leads to retention of water secondarily under the influence of anti-diuretic hormone (ADH) or vasopressin.
  • This hormone is secreted by the cells of the supraoptic and paraventricular nuclei in the hypothalamus and is stored in the neurohypophysis (posterior pituitary).
  • The release of ADH is stimulated by increased concentration of sodium in the plasma and hypovolaemia. Large amounts of ADH produce zighly concentrated urine.

Thus, in summary, the possible factors responsible for causing oedema by excessive retention of sodium and water via stimulation of intrinsic renal and extra-renal mechanisms, and via release of ADH, are as under:

• Reduced glomerular filtration rate in response to hypovolaemia.
• Enhanced tubular reabsorption of sodium and consequently its decreased renal excretion.
• Increased filtration factor i.e. increased filtration of plasma from the glomerulus.
• Decreased capillary hydrostatic pressure associated with increased renal vascular resistance.

The examples of oedema by these mechanisms are as under:

• Oedema of cardiac disease for example, In congestive cardiac failure.
• Ascites of liver disease for example, In cirrhosis of liver.
• Oedema of renal disease for example, In nephrotic and nephritic syndrome.

Important Types Of Oedema:

As observed from the pathogenesis of oedema just described, more than one mechanism may be involved in many examples of localised and generalised oedema.

Some of the important examples are described below:

1. Renal Oedema:

Generalised oedema occurs in certain diseases of renal origin such as in nephrotic syndrome, nephritic syndrome, and in renal failure due to acute tubular injury.

Oedema in nephrotic syndrome:

Since there is persistent and heavy proteinuria (albuminuria) in nephrotic syndrome, there is hypoalbuminaemia causing decreased plasma oncotic pressure resulting in severe generalised oedema (nephrotic oedema).

The hypoalbuminaemia also causes fall in the plasma volume, activating the renin-angiotensin-aldosterone mechanism which results in retention of sodium and water, thus setting in a vicious cycle which persists till the albuminuria continues.

A similar type of mechanism operates in the pathogenesis of oedema in protein-losing enteropathy, adding further support to the role of protein loss in the causation of oedema.

The nephrotic oedema is classically more severe, generalised and marked and is present in the subcutaneous tissues as well as in the visceral organs.

• Grossly: The affected organ is enlarged and heavy with tense capsule.
• Microscopically: The oedema fluid separates the connective tissue fibres of subcutaneous tissues. Depending upon the protein content, the oedema fluid may appear homogeneous, pale, eosinophilic, or may be deeply eosinophilic and granular.

Oedema in nephritic syndrome:

Oedema occurring in conditions with diffuse glomerular disease such as in acute diffuse glomerulonephritis and rapidly progressive glomerulonephritis is termed nephritic oedema.

In contrast to nephrotic oedema, nephritic oedema is primarily not due to hypoproteinaemia because of low albuminuria but is largely due to excessive reabsorption of sodium and water in the renal tubules via renin-angiotensin-aldosterone mechanism.

The protein content of oedema fluid in glomerulonephritis is quite low (less than 0.5 g/dl). Nephritic oedema is usually mild as compared to nephrotic oedema and begins in the loose tissues such as on the face around the eyes, ankles and genitalia.

Oedema in these conditions is usually not affected by gravity (unlike cardiac oedema). The salient differences between the nephrotic and nephritic oedema are outlined in Table.

Oedema in acute tubular injury:

Acute tubular injury following shock or toxic chemicals results in gross oedema of the body. The damaged tubules lose their capacity for selective reabsorption and concentration of the glomerular filtrate, resulting in excessive retention of water and electrolytes, and consequent oliguria. Besides,

Differences between nephrotic and nephritic oedema:

2. Cardiac Oedema:

Generalised oedema develops in right-sided and congestive cardiac failure.

Pathogenesis of cardiac oedema is explained on the basis of the following mechanisms :

• Reduced cardiac output causes hypovolaemia which stimulates intrinsic-renal and extra-renal hormonal (renin-angiotensin-aldosterone) mechanisms as well as ADH secretion resulting in sodium and water retention (as discussed above) and consequent oedema.
•  Due to heart failure, there is elevated central venous pressure which is transmitted backward to the venous end of the capillaries, raising the capillary hydrostatic pressure and consequent transudation; this is known as back pressure hypothesis.
•  Chronic hypoxia may injure the capillary endothelium causing increased capillary permeability and result in oedema; this is called forward pressure hypothesis.

However, this theory lacks support since the oedema by this mechanism is exudate whereas the cardiac oedema is typically transudate. In left heart failure, the changes are, however, different. There is venous congestion, particularly in the lungs, causing pulmonary oedema rather than generalised oedema.

Cardiac oedema is influenced by gravity and is thus characteristically dependent oedema i.e. in an ambulatory patient it is on the lower extremities, while in a bed-ridden patient oedema appears on the sacral and genital areas. The accumulation of fluid may also occur in serous cavities.

Features to distinguish cardiac from renal oedema 

3. Pulmonary Oedema:

Acute pulmonary oedema is the most important form of local oedema as it causes serious functional impairment. However, it has special features and differs from oedema elsewhere in that the fluid accumulation is not only in the tissue space but also in the pulmonary alveoli.

• Etiopathogenesis: The hydrostatic pressure in the pulmonary capillaries is much lower (average 10 mmHg). Normally the plasma oncotic pressure is adequate to prevent the escape of fluid into the interstitial space and hence lungs are normally free of oedema. Pulmonary oedema can result from either the elevation of pulmonary hydrostatic pressure or the increased capillary permeability.

Elevation in pulmonary hydrostatic pressure (Haemodynamic oedema):

• In heart failure, there is an increase in the pressure in pulmonary veins which is transmitted to pulmonary capillary bed.
• This results in an imbalance between pulmonary hydrostatic pressure and the plasma oncotic pressure so that excessive fluid moves out of pulmonary capillaries into the interstitium of the lungs.
• Simultaneously, the endothelium of the pulmonary capillaries develops fenestrations permitting passage of plasma proteins and fluid into the interstitium. The interstitial fluid so collected is cleared by the lymphatics present around the bronchioles, small muscular arteries and veins.
• As the capacity of the lymphatics to drain the fluid is exceeded (about ten-fold increase in fluid), the excess fluid starts accumulating in the interstitium (interstitial oedema) i.e. ‘
• In the loose tissues around bronchioles, arteries and in lobular septa. This causes a thickening of the alveolar walls. Up to this stage, no significant impairment of gaseous exchange occurs.
• However, prolonged elevation of hydrostatic pressure and due to high pressure of interstitial oedema, the alveolar lining cells break and the alveolar air spaces are flooded with fluid (alveolar oedema) driving the air out of alveoli, thus seriously hampering the lung function.

Examples of pulmonary oedema by this mechanism are seen in left heart failure, mitral stenosis, pulmonary vein obstruction, thyrotoxicosis, cardiac surgery, nephrotic syndrome and obstruction to the lymphatic outflow by tumour or inflammation.

Increased vascular permeability (Irritant oedema):

• The vascular endothelium as well as the alveolar epithelial cells (alveolo-capillary membrane) may be damaged causing increase ascular permeability so that excessive fluid and plasma proteins leak out, initially into the interstitium and subsequently into the alveoli.
• This mechanism explains pulmonary oedema in conditions such as in fulminant pulmonary and extrapulmonary infections, inhalation of toxic substances, spiration, shock, radiation injury, hypersensitivity to drugs or antisera, uraemia and adult respiratory distress syndrome (ARDS).

Acute high altitude oedema:

• Individuals climbing to high altitude suddenly without halts and without waiting for acclimatisation to set in, suffer from serious circulatory and respiratory ill-effects.
• The deleterious effects often begin to appear after an altitude of 2500 metres is reached.
• These changes include appearance of oedema fluid in the lungs, congestion and widespread minute haemorrhages. These changes can cause death within a few days.
• The underlying mechanism is due to anoxic damage to the pulmonary vessels. However, if acclimatisation to high altitude is allowed to take place, the individual develops raised pulmonary arterial pressure, increased pulmonary ventilation, a rise in heart rate and increased cardiac output, and thus the ill-effects do not appear.
• Another consequence of prolonged stay at high altitude is development of polycythaemia.
• Morphologic Features Irrespective of the underlying mechanism in the pathogenesis of pulmonary oedema, the fluid accumulates more in the basal regions of lungs.

The thickened interlobular septa along with their dilated lymphatics may be seen in chest X-ray as linear lines perpendicular to the pleura and are known as Kerley’s lines.

• Grossly: The lungs in pulmonary oedema are heavy, moist and subcrepitant. The cut surface exudes frothy fluid (mixture of air and fluid).
• Microscopically: The alveolar capillaries are congested. Initially, the excess fluid collects in the interstitial lung spaces in the septal walls (interstitial oedema). Later, the fluid fills the alveolar spaces (alveolar oedema).

Oedema fluid in the interstitium as well as the alveolar spaces appears as eosinophilic, granular and pink proteinaceous material, often admixed with some RBCs and alveolar macrophages, also called heart failure cells

Organisation of alveolar oedema may be seen as brightly eosinophilic pink lines along the alveolar margin called hyaline membrane.

Long-standing pulmonary oedema is prone to get infected by bacteria producing hypostatic pneumonia which may be fatal.

4. Cerebral Oedema:

Cerebral oedema or swelling of the brain is the most life-threatening example of oedema. The mechanism of fluid exchange in the brain differs from elsewhere in the body since 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.

Cerebral oedema can be of 3 types:

1. Vasogenic
2. Cytotoxic and
3. Interstitial.

There are:

1. Vasogenic Oedema: This is the most common type and its mechanism is similar to oedema in other body sites from increased filtration pressure or increased capillary permeability. Vasogenic oedema is prominent around cerebral contusions, infarcts, brain abscess and some tumours.
   • Grossly: The white matter is swollen, and soft, with flattened gyri and narrowed sulci. The sectioned surface is soft and gelatinous.
   • Microscopically: There is separation of tissue elements by the oedema fluid and swelling of astrocytes. The perivascular (Virchow-Robin) space is widened and clear halos are seen around the small blood vessels.
2. Cytotoxic Oedema: In this type, the blood-brain barrier is intact and the fluid accumulation is intracellular. The underlying mechanism is a disturbance in the cellular osmoregulation as occurs in some metabolic derangements, acute hypoxia and with some toxic chemicals.
   • Microscopically: The cells are swollen and vacuolated. In some situations, both vasogenic as well as cytotoxic cerebral oedema results for example, In purulent meningitis.
3. Interstitial Oedema: This type of cerebral oedema occurs when the excessive fluid crosses the ependymal lining of the ventricles and accumulates in the periventricular white matter. This mechanism is responsible for oedema in non-communicating hydrocephalus.

5. Hepatic Oedema:

While oedema in chronic liver disease is  mechanisms involved in causing oedema of the legs and ascites in cirrhosis of the liver is as under:

• Hypoproteinaemia due to impaired synthesis of proteins by the diseased liver.
• Due to portal hypertension, there is increased venous pressure in the abdomen, and hence raised hydrostatic pressure.
• Failure of inactivation of aldosterone in the diseased liver and hence hyperaldosteronism.
• Secondary stimulation of renin-angiotensin mechanism promoting sodium and water retention.

6. Nutritional Oedema:

Oedema due to nutritional deficiency of proteins (kwashiorkor, prolonged starvation, famine, fasting), vitamins (beri-beri due to vitamin B1 deficiency) and chronic alcoholism occurs on legs but sometimes may be more generalised.

The main contributing factors are hypoproteinaemia and sodium-water retention related to metabolic abnormalities. In kwashiorkor occurring in children in economically deprived communities in Africa and Asia, oedema is associated with characteristic mucocutaneous ulceration and depigmentation of the hair, all of which revert back to normal on adequate nutrition.

7. Myxoedema:

Myxoedema from hypothyroidism (page 844) is a form of non-pitting oedema occurring on skin of face and other parts of the body as also in the internal organs due to excessive deposition of glycosaminoglycans in the interstitium.

Microscopically, it appears as basophilic mucopolysaccharides.