Edema Cerebral Infarto Pulm

8/3/2019 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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Edema Cerebral Infarto Pulm