Traumatic brain injury (TBI) is defined as a structural injury to the brain or a disruption in the normal functioning of the brain as a result of a blunt or Penetrating head injury. Head injury refers to trauma to the head that may or may not be associated with TBI, soft tissue injury, or skull fractures. Primary brain injury occurs as an immediate consequence of head injury at the time of the trauma.Secondary Brain Injury is indirect and results from physiological changes triggered by the initial impact and/or acute management measures; it is preventable to a certain degree. TBI is most frequently seen in young children, teenagers, and individuals older than 65 years, with falls and Motor vehicle collisons being the leading causes. The Glasgow Coma Scale is a commonly used scoring system used to assess the severity of TBI and guide management. Clinical Features of TBI depend on the severity, type, and location of brain injury. Impaired consciousness is common in severe TBI whereas patients with mild TBI may only present with transient confusion and headache.Neuroprotective measures to prevent or minimize secondary brain injury should be the main focus of initial management of all patients with TBI. Patients with moderate TBI or severe TBI should be transferred to a neurocritical care unit at the earliest. After initial resuscitation, a head CT without contrast should be obtained to identify the type and extent of injury. Definitive management varies depending on the type and severity of injury.

Intracranial epidural hematoma (EDH) refers to bleeding between the dura mater and the calvarium. Most cases of EDH are traumatic, resulting from a head injury with an associated skull fracture that ruptures or tears the middle meningeal artery, which lies in close proximity to the skull and dura mater. EDH is more common in individuals 20–30 years of age, as the dura mater is not yet densely adherent to the calvarium at this age. The classic manifestation of EDH is an initial loss of consciousness, followed by a lucid interval in which the patient gains normal or near-normal consciousness, followed by rapid neurological decline. An ipsilateral dilated pupil (anisocoria) and contralateral hemiparesis are manifestations of transtentorial uncal herniation and signal imminent neurological decline. Neuroprotective measures to prevent secondary brain injury take precedence over diagnostic tests. Diagnosis is confirmed on a noncontrast CT head, on which EDH appears as a biconvex, hyperdense lesion, typically in the temporal or temporoparietal region. Surgical decompression with craniotomy is indicated in patients with large EDH, GCS ≤ 8, and evidence of neurological deterioration. Small, asymptomatic EDH in patients with GCS > 8 can be managed conservatively with close observation and serial CT scanning. The prognosis depends on several factors, including the GCS at presentation, size of the EDH, and, crucially, the time from the onset of brain herniation to decompressive surgery. Early intervention in patients with signs of brain herniation is associated with good neurological outcomes and lower mortality rates.

Subdural hematoma (SDH) refers to bleeding into the intracranial subdural space that is typically caused by a rupture of the bridging veins. Trauma, including minor falls, cerebral atrophy, and conditions that increase the risk of bleeding (e.g., coagulopathy, hypertension) are common etiologies of SDH. According to the onset of symptoms, SDH can be classified into acute SDH, subacute SDH, and chronic SDH. Acutely symptomatic SDH typically manifests with altered mental status, focal neurological signs, and signs of increased ICP, and it can progress to brain herniation and death if not treated. Chronic SDH manifests gradually with cognitive deficits, impaired memory, personality changes, and focal neurological signs. Subacute SDH can manifest with features of acute and/or chronic SDH. In patients with acutely symptomatic SDH, neuroprotective measures to prevent secondary brain injury take precedence over diagnostics. Diagnosis is confirmed with a noncontrast head CT, which would show a crescent-shaped (concave) lesion that may cross cranial sutures typically located in the supratentorial region. Surgery is recommended in SDH that is symptomatic, ≥ 10 mm in size, or causing ≥ 5 mm shift in the midline. Conservative management can be considered for small asymptomatic SDHs in patients with no signs of increased ICP.

Subarachnoid hemorrhage (SAH) refers to bleeding into the subarachnoid space. While SAH is often caused by trauma, 5–10% of cases are nontraumatic or spontaneous, in which case they are often due to the rupture of an aneurysm involving the circle of Willis (aneurysmal SAH). Nontraumatic SAH typically manifests with sudden and severe headache, which may be accompanied by nausea, vomiting, signs of meningism, and/or acute loss of consciousness. The best initial diagnostic test is a head CT without contrast, in which acute subarachnoid bleeding can be seen as hyperdensities in the subarachnoid space. If a head CT is negative for SAH, this diagnosis can be ruled out in many patients. However, if clinical suspicion remains high, it may be necessary to perform a lumbar puncture or CT angiography. Once SAH is confirmed, angiography is always necessary in order to identify the source of bleeding (e.g., aneurysms or other vascular abnormalities) and plan definitive treatment. The management of traumatic and nontraumatic SAH consists mostly of neuroprotective measures (e.g., control of blood pressure) to prevent secondary brain injuries. In aneurysmal SAH, microsurgical clipping or endovascular coiling of the aneurysm is indicated to prevent potentially fatal rebleeding. Aneurysmal SAH has a high mortality rate as a result of complications such as rebleeding and delayed cerebral ischemia.

Intracerebral hemorrhage (ICH) refers to bleeding within the brain parenchyma. The term should not be confused with intracranial hemorrhage, which is a broader term that encompasses bleeding within any part of the skull, i.e., extradural, subdural, subarachnoid, or intracerebral bleeding. The most significant risk factor for spontaneous ICH is arterial hypertension. Symptoms are often nonspecific (e.g., headache); however, depending on the affected vessel and cerebral region, focal neurological deficits (e.g., hemiparesis) may occur. Compared with ischemic stroke, patients with ICH are more likely to present with severe headache and have rapidly progressing symptoms. The initial imaging investigation of choice is CT head without contrast, which typically shows a hyperdense mass lesion. Treatment involves management of the underlying and associated conditions (e.g., controlling hypertension, reversing coagulopathy) in order to limit hematoma expansion and prevent secondary brain injury. In severe cases, neurosurgical intervention may be required. Approximately half of patients with spontaneous ICH die within 30 days of symptom onset. Traumatic ICH may result from traumatic brain injury (TBI) and is managed similarly to spontaneous ICH.

Secondary brain injury is an indirect injury caused by physiological changes that are triggered by an acute CNS insult (e.g., traumatic brain injury, stroke, cerebral hypoxia secondary to cardiac arrest) and/or the management of the primary insult. Unlike primary brain injury, which refers to the direct, immediate, and potentially irreversible neuronal damage from an acute CNS insult, secondary brain injury is preventable or can be minimized with the early administration of neuroprotective measures. Neuroprotective measures involve the early and aggressive control of factors that are implicated in the etiology of secondary brain injury. Such measures include optimization of oxygenation, ventilation, blood pressure, blood sugar, body temperature, intracranial pressure, and electrolyte levels. In addition, seizure prophylaxis and treatment, nutritional support, and patient positioning are important aspects of neuroprotective measures.

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.