Edema Cerebral Infarto Pulm
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Transcript of Edema Cerebral Infarto Pulm
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CEREBRAL EDEMA
Edema of the brain is dangerous because the
rigidity of the cranium allows little room for
expansion. Increased intracranial pressure
from edema compromises cerebral blood
supply, distorts the gross structure of the brain
and interferes with central nervous system
function. Cerebral edema is divided intovasogenic, cytotoxic, and interstitial forms.
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VASOGENIC EDEMA
The most common variety of edema, is excessfluid in the extracellular space of the brain. Itresults from increased vascular permeability,
mainly in white matter. The tight endothelialjunctions of the blood brain barrier are disruptedand fluid filters into the interstitial space.Disorders associated with cerebral vasogenic
edema include trauma, neoplasms, encephalitis,abscesses, infarcts, hemorrhage, and toxic braininjury (e.g., lead poisoning).
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CYTOTOXIC EDEMA
Is equivalent to hydropic cell swelling (i.e.,accumulation of intracellular water). It is
usually a response to cell injury, such as that
produced by ischemia. Cytotoxic cerebral
edema preferentially affects the gray matter.
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INTERSTICIAL EDEMA
Is a consequence of hydrocephalus, in whichfluid accumulates in the cerebral ventricles
and periventricular white matter.
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CEREBRAL EDEMA
At autopsy, an edematous brain is soft and
heavy. Gyri are flattened and sulci narrowed.Because of alterations in brain function,
patients with cerebral edema suffer vomiting,
disorientation, and convulsions. Severe
cerebral edema leads to herniation of the
cerebral tonsils, ordinarily a lethal event.
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PULMONARY EMBOLISM
Pulmonary thromboemboli are reported in more than half of all autopsies. Furthermore, thiscomplication occurs in 1% to 2% of postoperative patients over the age of 40. The risk after surgeryincreases with advancing age, obesity, length of operative procedure, postoperative infection,cancer, and preexisting venous disease.
Most pulmonary emboli (90%) arise from deep veins of the lower extremities; most fatal ones form
in iliofemoral veins (Fig. 7-11). Only half of patients with pulmonary thromboembolism have signsof deep vein thrombosis. Some thromboemboli arise from the pelvic venous plexus and othersfrom the right side of the heart.
The clinical features of pulmonary embolism are determined by the size of the embolus, the healthof the patient, and whether embolization occurs acutely or chronically. Acute pulmonary embolismis divided into the following syndromes:
Asymptomatic small pulmonary emboli
Transient dyspnea and tachypneawithout other symptoms
Pulmonary infarction, with pleuritic chest pain, hemoptysis, and pleural effusion Cardiovascular collapse with sudden death
Chronic pulmonary embolism, with numerous (usually asymptomatic) emboli lodged in smallarteries of the lung, can lead to pulmonary hypertension.
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PULMONARY INFARTATION
Small pulmonary emboli are not ordinarily lethal. They tend tolodge in peripheral pulmonary arteries. Sometimes (15% - 20% ofall pulmonary emboli) they produce lung infarcts.
Clinically, pulmonary infarction is usually seen in the context of CHFor chronic lung disease, because the normal dual circulation of the
lung ordinarily protects against ischemic necrosis; since thebronchial artery pumps blood into the necrotic area, pulmonaryinfarcts are typically hemorrhagic. Patients experience cough,stabbing pleuritic pain, shortness of breath, and occasionalhemoptysis. Pleural effusion is common and often bloody. Withtime, the blood in the infarct is resorbed, and the center of the
infarct becomes pale. Granulation tissue forms on the edge of theinfarct, after which it is organized to form a fibrous scar.
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