Intracranial pressure (ICP) is the pressure that exists within the cranium, including its compartments (e.g., the subarachnoid space and the ventricles). ICP varies as the position of the head changes relative to the body and is periodically influenced by normal physiological factors (e.g., cardiac contractions). Adults in the supine position typically have a physiological ICP of ≤ 15 mm Hg; an ICP of ≥ 20 mm Hg indicates pathological intracranial hypertension. ICP may be elevated in a variety of conditions (e.g., intracranial tumors) and can result in a decrease in cerebral perfusion pressure (CPP) and/or herniation of cerebral structures. Symptoms of elevated ICP are generally nonspecific (e.g., impaired consciousness, headache, vomiting); however, more specific symptoms may be present depending on the affected structures (e.g., Cushing triad if the brainstem is compressed). Findings from brain imaging (e.g., a midline shift) and physical examination (e.g., papilledema) can indicate ICP elevation but may not be able to rule it out. Therefore, ICP monitoring and quantification are vital in at-risk patients. Management usually involves expedited surgery of resectable or drainable lesions, conservative measures (e.g., positioning, sedation, analgesia, and antipyretics), and medical therapy (e.g., hyperosmolar therapy such as mannitol or hypertonic saline, or glucocorticoids). Treatment options for refractory intracranial hypertension include temporary controlled hyperventilation, CSF drainage, and decompressive craniectomy (DC), as well as other advanced medical therapies (e.g., barbiturate coma, therapeutic hypothermia).

Skull fractures most typically occur as a result of blunt force trauma from contact sports, motor vehicle collisions, or falls. They are classified by anatomical location as either cranial vault fractures or basilar skull fractures. Cranial vault fractures involve one or more of the cranial vault bones, may be either open fractures or closed fractures, and are classified as linear skull fractures or depressed skull fractures. Basilar skull fractures involve one or more of the skull base bones and are classified as anterior, middle, or posterior cranial fossa fractures. Clinical features vary depending on bone involvement but may include lacerations, contusions, and hematoma of the scalp; palpable deformities; mobile bone fragments; liquorrhea; Battle sign; raccoon eyes; and signs of traumatic brain injury. Initial management of skull fractures focuses on identifying and addressing life-threatening injuries. Complications of skull fractures include CSF leaks (which increase the risk for meningitis), cranial nerve disorders (due to compression or transection), and epidural hematomas. Expectant management may be sufficient for simple fractures but neurosurgery may be necessary for unstable fractures and fractures with associated complications. Open head injuries can occur when skull fractures are associated with rupture of the dura mater, which can increase the risk of CNS infection.

Pituitary adenomas (also known as pituitary neuroendocrine tumors) are benign tumors that arise sporadically from the anterior pituitary gland. They are classified as either microadenomas or macroadenomas according to their size, and as either secretory (functional) or nonsecretory (nonfunctioning) according to their ability to secrete hormones. Secretory adenomas produce the pituitary hormone of the cell type from which they arise, which results in a state of hyperpituitarism. Nonsecretory macroadenomas can destroy the surrounding normal pituitary tissue, which results in hypopituitarism. Additionally, large macroadenomas compress the optic chiasm; therefore, patients may present with signs of mass effect such as bitemporal hemianopsia. MRI sella with IV contrast is the gold standard imaging method for the pituitary and should reveal any intrasellar masses. Pituitary hormone assays are used to evaluate patients for endocrine abnormalities, and perimetry is used to identify visual field defects. Transsphenoidal hypophysectomy is the first-line therapy for most patients with symptomatic pituitary adenomas; patients with nonsecretory microadenomas generally only require follow-up (until they become symptomatic), and prolactin-producing pituitary adenomas (prolactinomas) should be initially treated with dopamine agonists (e.g., cabergoline, bromocriptine). Pituitary irradiation is indicated in recurrent pituitary adenomas and/or if surgical therapy is contraindicated.

Cerebral venous thrombosis (CVT) is a thrombotic obstruction of the cerebral venous system that can lead to ischemic lesions (or hemorrhages) in the brain. The condition can occur at any age and is often associated with a hypercoagulable state, a trigger (e.g., delivery, head injury, CNS instrumentation) or an infection (i.e., as in septic CVT). Women are affected more frequently than men, possibly as a result of the additional risk factors of pregnancy and oral contraceptive use. Cavernous sinus thrombosis is a rare subset of CVT that is most often due to infections in the paranasal region. Headache is the most common symptom of CVT and, depending on the size and location of the clot, may be accompanied by visual impairment, focal neurological deficits, seizures, or signs of raised intracranial pressure. Neuroimaging (MRI or CT venography) of the cerebral veins and dural sinus is used to establish the diagnosis. The mainstay of management is anticoagulation alongside the treatment of any potential underlying cause (e.g., antibiotics for septic CVT). Surgical intervention (e.g., endovascular thrombolysis or decompressive craniectomy) may be necessary in patients with significant symptoms who do not respond to anticoagulation.

Abdominal aortic aneurysm (AAA) is a focal dilatation of the abdominal aorta to more than 1.5 times its normal diameter. AAAs are classified by location as either suprarenal or infrarenal aneurysms. Men of advanced age are at increased risk for their formation; smoking and hypertension are also major risk factors. AAAs are frequently asymptomatic and therefore detected incidentally. Symptomatic AAAs can manifest with lower back pain, a pulsatile abdominal mass, and a bruit on auscultation. Abdominal ultrasound is the best initial and confirmatory test to diagnose AAAs and determine their extent. Observation, close follow-up, and reduction of cardiovascular risk factors are indicated for small aneurysms, whereas pronounced (> 5.5 cm in men; > 5 cm in women) or rapidly expanding aneurysms require surgery. Surgical treatment involves open resection of the aneurysm with graft placement or, increasingly, endovascular stent placement. The prognosis is markedly worse if dissection or aneurysm rupture occurs. AAA rupture typically manifests with sudden onset of severe tearing back or abdominal pain, a painful pulsatile mass, and hypovolemic shock, and should be managed with emergent surgery. All men between 65 and 75 years of age with a history of smoking should be screened once with an ultrasound to exclude an AAA. See also thoracic aortic aneurysm for more information.

Aneurysms are typically defined as vascular enlargements with a diameter ≥ 1.5 times that of a normal artery. True aneurysms are arterial enlargements in which all three layers of the vessel wall are weakened and form part of the aneurysmal wall. False aneurysms are extraarterial hematomas contained by surrounding tissues and/or the tunica adventitia that maintain persistent communication with the arterial lumen. Arterial dissections are vascular enlargements caused by the separation of arterial wall layers as blood enters the intima-media space through a tear in the tunica intima. Aneurysms are also differentiated according to their location. Symptoms generally depend on the location and size of the aneurysm. Management may be medical, surgical, or endovascular, depending on the type of aneurysm, symptoms, and associated complications.

An aortic dissection is a tear in the inner layer of the aorta that leads to a progressively growing hematoma in the intima-media space. Risk factors for aortic dissection include age and hypertension. Patients typically present with sudden onset severe pain radiating into the chest, back, or abdomen. A widened mediastinum on chest x-ray is characteristic of the diagnosis. The diagnosis is usually confirmed with CT angiogram in stable patients and transesophageal echocardiography (TEE) in unstable patients. Treatment options range from conservative measures (e.g., blood pressure optimization) to surgery (aortic stent graft), depending on the localization and severity of the dissection. Complete occlusion of branching vessels and aortic rupture are common complications. Even with treatment, mortality rates associated with aortic dissection are high.

Acute limb ischemia (ALI) is a vascular emergency caused by the sudden loss of arterial perfusion, most commonly due to arterial thrombosis and cardiac emboli. The typical signs and symptoms of ALI are referred to as the “6 Ps”: pain, pallor, pulselessness, paralysis, paresthesia, and poikilothermia of the limb distal to the site of vascular occlusion. Prompt diagnosis based on physical examination and bedside Doppler studies is crucial to prevent loss of the limb. Imaging studies (e.g., CTA) may be obtained but should not delay urgent restoration of perfusion. Systemic anticoagulation with heparin is recommended for most patients. Definitive treatment depends on clinical presentation and limb viability. Options include endovascular or surgical revascularization for viable or threatened limbs and amputation for nonviable limbs.