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| Anoxia |
| Etiology •Anoxia is due to lack of oxygen transport to the brain •It may be due to exposure to CO or CN which bind with hemoglobin to form compounds which do not allow oxygen to be transported, pulmonary disease, cardiac disease or cardiac and/or respiratory arrest. •Severe blood loss can also lead to anoxia of the brain. |
| Pathogenesis •Anoxia interferes with the function of neurons causing swelling of mitochondria due to loss of their ability to process glucose and lack of energy production for the use of other organelles and membranes in the cells. •Neurons are most susceptible to anoxia followed by oligodendroglia, astrocytes and connective tissue., |
| Epidemiology •Anoxia is comman in patients exposed to CO in fires and patients who develop a cardiopulmonary arrest, particularly out of the hospital when CPR is not begun within 4 minutes. |
| General Gross Description •The brains of patients who become anoxic are usually swollen with flattening of the gyri and narrowing of the sulci and decreased size of the ventricles. |
| General Microscopic Description •The classic sign of ischemic or anoxic neurons is shrinkage and eosinophilia of the neuronal cell body. •After a week neurons disappear and reactive astrocytes are seen in their place. |
| Clinical Correlation •Patients with COHb of 50-60% often die as due many patients with cardiopulmonary arrest. •Those who survive may have severe neurologic and cerebral dysfunction. • CPR must be started within 4-5 minutes after cardio- pulmonary arrest for a good result. •Patients with high COHb are often treated with hyperbaric oxygen. |
| References • Poirer J et.al. Manual of basic neuropathology. Philadelphia: Saunders, 1990, pp.163-166. • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1308-1309. |
| Anoxia |
| Synopsis by: M. L. Grunnet M.D. (TX2000M50000)[357] |
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