Page 138 - Textbook of Pathology, 6th Edition

122 marrow in circulation, concussions of bones, after ii) Systemic fat embolism. Some of the fat globules may
orthopaedic surgical procedures etc. pass through the pulmonary circulation such as via patent
Trauma to soft tissue e.g. laceration of adipose tissue and foramen ovale, arteriovenous shunts in the lungs and
in puerperium due to injury to pelvic fatty tissue. vertebral venous plexuses, and get lodged in the capillaries
ii) Non-traumatic causes: of organs like the brain, kidney, skin etc.
Extensive burns Brain. The pathologic findings in the brain are
Diabetes mellitus petechial haemorrhages on the leptomeninges and minute
Fatty liver haemorrhages in the parenchyma.
Pancreatitis Microscopically, microinfarct of brain, oedema and
SECTION I
Sickle cell anaemia haemorrhages are seen. The CNS manifestations include
Decompression sickness delirium, convulsions, stupor, coma and sudden death.
Inflammation of bones and soft tissues Kidney. Renal fat embolism present in the glomerular
Extrinsic fat or oils introduced into the body.
capillaries, may cause decreased glomerular filtration.
PATHOGENESIS. The following mechanisms are proposed Other effects include tubular damage and renal
to explain the pathogenesis of fat embolism. These may be insufficiency.
acting singly or in combination. Other organs. Besides the brain and kidneys, other
findings in systemic fat embolism are petechiae in the skin,
i) Mechanical theory. Mobilisation of fluid fat may occur
following trauma to the bone or soft tissues. The fat globules conjunctivae, serosal surfaces, fat globules in the urine
released from the injured area may enter venous circulation and sputum.
and finally most of the fat is arrested in the small vessels in
the lungs. Some of the fat globules may further pass through Gas Embolism
into the systemic circulation to lodge in other organs. Air, nitrogen and other gases can produce bubbles within
the circulation and obstruct the blood vessels causing damage
ii) Emulsion instability theory. This theory explains the to tissue. Two main forms of gas embolism—air embolism
pathogenesis of fat embolism in non-traumatic cases. and decompression sickness are described below.
According to this theory, fat emboli are formed by aggrega-
tion of plasma lipids (chylomicrons and fatty acids) due to Air Embolism
disturbance in natural emulsification of fat.
Air embolism occurs when air is introduced into venous or
iii) Intravascular coagulation theory. In stress, release of arterial circulation.
General Pathology and Basic Techniques
some factor activates disseminated intravascular coagulation VENOUS AIR EMBOLISM. Air may be sucked into
(DIC) and aggregation of fat emboli.
systemic veins under the following circumstances:
iv) Toxic injury theory. According to this theory, the small i) Operations on head and neck, and trauma. The
blood vessels of lungs are chemically injured by high plasma accidental opening of a major vein of the neck like jugular,
levels of free fatty acid, resulting in increased vascular or neck wounds involving the major neck veins, may allow
permeability and consequent pulmonary oedema. air to be drawn into venous circulation.
CONSEQUENCES OF FAT EMBOLISM. The effects of fat ii) Obstetrical operations and trauma. During childbirth by
embolism depend upon the size and quantity of fat globules, normal vaginal delivery, caesarean section, abortions and
and whether or not the emboli pass through the lungs into other procedures, fatal air embolism may result from the
the systemic circulation. entrance of air into the opened-up uterine venous sinuses
and endometrial veins.
i) Pulmonary fat embolism. In patients dying after frac-
tures of bones, presence of numerous fat emboli in the iii) Intravenous infusion of blood and fluid. Air embolism
capillaries of the lung is a frequent autopsy finding because may occur during intravenous blood or fluid infusions if only
the small fat globules are not likely to appreciably obstruct positive pressure is employed.
the vast pulmonary vascular bed. However, widespread iv) Angiography. During angiographic procedures, air may
obstruction of pulmonary circulation due to extensive be entrapped into a large vein causing air embolism.
pulmonary embolism can occur and result in sudden death. The effects of venous air embolism depend upon the
following factors:
Microscopically, the lungs show hyperaemia, oedema, i) Amount of air introduced into the circulation. The volume
petechial haemorrhages and changes of adult respiratory of air necessary to cause death is variable but usually 100-
distress syndrome (ARDS). Pulmonary infarction is 150 ml of air entry is considered fatal.
usually not a feature of fat embolism because of the small ii) Rapidity of entry of a smaller volume of air is important
size of globules. In routine stains, the fat globules in the determinant of a fatal outcome.
pulmonary arteries, capillaries and alveolar spaces appear
as vacuoles. Frozen section is essential for confirmation iii) Position of the patient during or soon after entry of air is
of globules by fat stains such as Sudan dyes (Sudan black, another factor. The air bubbles may ascend into the superior
Sudan III and IV), oil red O and osmic acid. vena cava if the position of head is higher than the trunk
(e.g. in upright position) and reach the brain.