Page 118 - Textbook of Pathology, 6th Edition

102 brain differs from elsewhere in the body since there are no of the body as also in the internal organs due to excessive
draining lymphatics in the brain but instead, the function of deposition of glycosaminoglycans in the interstitium.
fluid-electrolyte exchange is performed by the blood-brain Microscopically, it appears as basophilic mucopoly-
barrier located at the endothelial cells of the capillaries. saccharides.
Cerebral oedema can be of 3 types:
DEHYDRATION
1. VASOGENIC OEDEMA. This is the most common type
and corresponds to oedema elsewhere resulting from Dehydration is a state of pure deprivation of water leading
increased filtration pressure or increased capillary perme- to sodium retention and hence a state of hypernatraemia. In
ability. Vasogenic oedema is prominent around cerebral other words, there is only loss of water but no loss of sodium.
SECTION I
contusions, infarcts, brain abscess and some tumours.
Clinically, the patients present with intense thirst, mental
Grossly, the white matter is swollen, soft, with flattened confusion, fever, and oliguria.
gyri and narrowed sulci. Sectioned surface is soft and ETIOLOGY. Pure water deficiency is less common than salt
gelatinous. depletion but can occur in the following conditions:
Microscopically, there is separation of tissue elements by
the oedema fluid and swelling of astrocytes. The 1. GI excretion:
perivascular (Virchow-Robin) space is widened and clear i) Severe vomitings
halos are seen around the small blood vessels. ii) Diarrhoea
iii) Cholera
2. CYTOTOXIC OEDEMA. In this type, the blood-brain 2. Renal excretion:
barrier is intact and the fluid accumulation is intracellular. i) Acute renal failure in diuretic phase
The underlying mechanism is disturbance in the cellular ii) Extensive use of diuretics
osmoregulation as occurs in some metabolic derangements, iii) Endocrine diseases e.g. diabetes insipidus, Addison’s
acute hypoxia and with some toxic chemicals. disease

Microscopically, the cells are swollen and vacuolated. In 3. Loss of blood and plasma:
some situations, both vasogenic as well as cytotoxic i) Severe injuries, severe burns
cerebral oedema results e.g. in purulent meningitis. ii) During childbirth
4. Loss through skin:
3. INTERSTITIAL OEDEMA. This type of cerebral oedema i) Excessive perspiration
occurs when the excessive fluid crosses the ependymal lining ii) Hyperthermia
General Pathology and Basic Techniques
of the ventricles and accumulates in the periventricular white
matter. This mechanism is responsible for oedema in non- 5. Accumulation in third space:
communicating hydrocephalus. i) Sudden development of ascites
ii) Acute intestinal obstruction with accumulation of fluid in
Hepatic Oedema the bowel.
While this subject is discussed in detail in Chapter 21, briefly MORPHOLOGICAL FEATURES. Although there are no
the mechanisms involved in causation of oedema of the legs particular pathological changes in organs, except in
and ascites in cirrhosis of the liver is as under: advanced cases when the organs are dark and shrunken.
i) There is hypoproteinaemia due to impaired synthesis of However, there are haematological and biochemical
proteins by the diseased liver. changes. There is haemoconcentration as seen by increased
ii) Due to portal hypertension, there is increased venous PCV and raised haemoglobin. In late stage, there is rise in
pressure in the abdomen, and hence raised hydrostatic blood urea and serum sodium. Renal shutdown and a state
pressure. of shock may develop.
iii) Failure of inactivation of aldosterone in the diseased liver
and hence hyperaldosteronism. OVERHYDRATION
iv) Secondary stimulation of renin-angiotensin mechanism Overhydration is increased extracellular fluid volume due
promoting sodium and water retention.
to pure water excess or water intoxication. Clinically, the
Nutritional Oedema patients would present with disordered cerebral function e.g.
nausea, vomiting, headache, confusion and in severe cases
Oedema due to nutritional deficiency of proteins (kwashiorkor, convulsions, coma, and even death.
prolonged starvation, famine, fasting), vitamins (beri-beri due
to vitamin B deficiency) and chronic alcoholism occurs on ETIOLOGY. Overhydration is generally an induced
1
legs but sometimes may be more generalised. The main condition and is encountered in the following situations:
contributing factors are hypoproteinaemia and sodium-water 1. Excessive unmonitored intravascular infusion:
retention related to metabolic abnormalities. i) Normal saline (0.9% sodium chloride)
ii) Ringer lactate
Myxoedema
2. Renal retention of sodium and water:
Myxoedema from hypothyroidism (Chapter 27) is a form of i) Congestive heart failure
non-pitting oedema occurring on skin of face and other parts ii) Acute glomerulonephritis