A nurse is caring for a client who has a cerebral aneurysm. In the event of a ruptured cerebral aneurysm, which of the following manifestations would be present in the client? (Select All that Apply.)

A ruptured cerebral aneurysm causes acute subarachnoid hemorrhage with sudden arterial bleeding into the subarachnoid space. This results in rapid intracranial pressure elevation, meningeal irritation, and focal neurological deficits due to disrupted cerebral perfusion and cranial nerve compression.

Rationale:

A. Light sensitivity occurs due to meningeal irritation from blood in the subarachnoid space. This triggers photophobia commonly seen in subarachnoid hemorrhage. The inflammatory response around meninges increases sensory nerve irritation leading to intolerance of bright light exposure.

B. Loss of consciousness occurs due to abrupt rise in intracranial pressure and decreased cerebral perfusion. A ruptured aneurysm can cause sudden global cerebral hypoperfusion, leading to syncope or coma depending on hemorrhage severity and brainstem involvement.

C. A dilated pupil indicates cranial nerve III compression from expanding hematoma or herniation. Oculomotor nerve dysfunction disrupts parasympathetic control of pupil constriction, producing unilateral mydriasis and suggesting impending transtentorial herniation, a neurosurgical emergency.

D. Visual disturbances occur from increased intracranial pressure and optic pathway involvement. Compression or ischemia of visual cortex or optic nerves leads to blurred vision, diplopia, or transient vision loss depending on hemorrhage location and severity.

E. Nausea and vomiting result from stimulation of the medullary vomiting center due to elevated intracranial pressure. Increased pressure disrupts normal brainstem function and is a common early sign of acute intracranial pathology including aneurysmal rupture.

F. Numbness on one side of the face reflects focal cranial nerve involvement or cortical sensory pathway disruption. A ruptured aneurysm may compress trigeminal pathways or cause localized ischemia leading to unilateral facial sensory deficits and neurological asymmetry.