Porth's Essentials of Pathophysiology, 4e

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Nervous System

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The course of treatment after aneurysm rupture depends on the extent of neurologic deficit. The best out- comes are achieved when the aneurysm can be secured early and prevention of complications initiated. 39 Persons with mild to no neurologic deficits may undergo cerebral arteriography and early aneurysm obliteration with surgery or endovascular coiling, usually within 24 to 72 hours. Surgery involves craniotomy and inserting a specially designed silver clip that is tightened around the neck of the aneurysm. This procedure offers pro- tection from rebleeding and may permit removal of the hematoma. The use of endovascular techniques such as balloon embolization and platinum coil electrothrom- bosis is an alternative to surgery, particularly in poste- rior circulation aneurysms or poor surgical candidates. Early outcomes and fewer complications are better with coiling, while long-term rebleeding rates are reduced with surgery. 39 Some persons with subarachnoid hemor- rhage are managed medically for 10 days or more in an attempt to improve their clinical status before surgery or coiling. The complications of aneurysmal rupture include rebleeding, vasospasm with cerebral ischemia, hydro- cephalus, hypothalamic dysfunction, and seizure activ- ity. Rebleeding and vasospasm are the most serious and most difficult to treat. Rebleeding, which usually occurs on the first day after the initial rupture, results in further and usually catastrophic neurologic deficits. Cerebral vasospasm is a dreaded complication of aneurysmal rupture. The condition is difficult to treat and is associated with a high incidence of morbidity and mortality. Usually, the condition develops within 3 to 10 days (peak, 7 days) after aneurysm rupture and involves a focal narrowing of the cerebral artery or arteries that can be visualized on arteriography or by transcranial Doppler. The neurologic status gradually deteriorates as blood supply to the brain in the region of the spasm is decreased; this usually can be differ- entiated from the rapid deterioration seen in rebleed- ing. Vasospasm is treated by attempting to maintain adequate cerebral perfusion pressure through the use of vasoactive drugs or administration of large amounts of intravenous fluids to increase intravascular volume and produce hemodilution. There is risk for rebleed- ing from this therapy. Early surgery may provide some protection from vasospasm. Endovascular techniques, including balloon dilation, have been developed to treat spasmodic arterial segments mechanically. Nimodipine, a drug that blocks calcium channels and selectively acts on cerebral blood vessels, may be used to prevent or treat vasospasm. Another complication of aneurysm rupture is the development of hydrocephalus. It is caused by plug- ging of the arachnoid villi with products from lysis of blood in the subarachnoid space. Hydrocephalus is diagnosed by serial CT scans showing increasing size of the ventricles and by the clinical signs of increased ICP. Hydrocephalus may respond to osmotic diuretics, but if neurologic deterioration is significant, surgical place- ment of a shunt is indicated.

Aneurysmal subarachnoid hemorrhage represents bleeding into the subarachnoid space caused by a rup- tured cerebral aneurysm. Bleeding into the subarach- noid space can extend well beyond the site of origin, flooding the basal cistern, ventricles, and spinal sub- arachnoid space. The incidence of rupture increases with age, occurring most commonly between 40 and 60 years of age. 43 The probability of rupture increases with the size of the aneurysm; aneurysms larger than 10 mm in diameter have a 50% chance of bleeding at some point during the course of a year. 1 Of the various factors that may predispose to aneurysmal subarach- noid hemorrhage, cigarette smoking, hypertension, and excessive alcohol intake appear to constitute the greatest threat. 38 Rupture may occur at any time, but often occurs with acute increases in ICP, such as with straining at stool. The mortality rate for subarachnoid hemorrhage is high (33% to 50%), with the major- ity of deaths occurring within the first few days of hemorrhage. 38 The signs and symptoms of cerebral aneurysms can be divided into two phases: those presenting before rupture and those presenting after rupture. Most small aneurysms are asymptomatic; intact aneurysms fre- quently are found at autopsy as an incidental finding. Large aneurysms may cause chronic headache, neuro- logic deficits, or both. 38,39 Persons with subarachnoid hemorrhage often have a history of atypical headaches occurring days to weeks before the onset of hemorrhage, suggesting the presence of a small leak. These headaches are characterized by sudden onset and often are accom- panied by nausea, vomiting, and dizziness. Persons with these symptoms may be mistakenly diagnosed as having tension or migraine headaches. The onset of subarachnoid aneurysmal rupture often is heralded by a sudden and severe headache, described as “the worst headache of my life.” 38 If the bleeding is severe, the headache may be accompanied by collapse and loss of consciousness. Vomiting may accompany the presenting symptoms. Other manifestations include signs of meningeal irritation such as nuchal rigidity (neck stiffness) and photophobia (light intolerance); cranial nerve deficits, especially CN II, and sometimes CN III and CN IV (diplopia and blurred vision); stroke syndromes (focal motor and sensory deficits); cerebral edema and increased ICP; and pituitary dysfunction (diabetes insipidus and hyponatremia). Hypertension, a frequent finding, and cardiac arrhythmias result from massive release of catecholamines triggered by the sub- arachnoid hemorrhage. The diagnosis of subarachnoid hemorrhage and intra- cranial aneurysms is made by clinical presentation, CT scan, lumbar puncture, and angiography. 38,39 Lumbar puncture may reveal the presence of blood in the CSF, whereas CT may demonstrate the location and extent of subarachnoid blood. To identify the aneurysm at the source of bleeding, conventional angiography, MRA, and helical (spiral) CTA are used. Conventional catheter angiography is the definitive diagnostic tool for detect- ing the aneurysm.