injuries poisoning
Traumatic Brain Injury (TBI)
Pathology of Traumatic Brain Injury
Structural changes from head injury may be gross or microscopic, depending on the mechanism and forces involved. Patients with less severe injuries may have no gross structural damage. Clinical manifestations vary markedly in severity and consequences. Injuries are commonly categorized as open or closed. Open head injuriesinvolve penetration of the scalp and skull (and usually the meninges and underlying brain tissue). They typically involve bullets or sharp objects, but a skull fracture with overlying laceration due to severe blunt force is also considered an open injury. typically occur when the head is struck, strikes an object, or is shaken violently, causing rapid brain acceleration and deceleration. Acceleration or deceleration can injure tissue at the point of impact (coup), at its opposite pole (contrecoup), or diffusely; the frontal and temporal lobes are particularly vulnerable to this type of injury. Axons, blood vessels, or both can be sheared or torn, resulting in Diffuse axonal injury . Disrupted blood vessels leak, causing contusions, intracerebral or subarachnoid hemorrhage, and epidural or subdural hematomas (see table Concussion (see also Sports-Related Concussion ) is defined as a transient and reversible posttraumatic alteration in mental status (eg, loss of consciousness or memory, confusion) lasting from seconds to minutes and, by arbitrary definition, Gross structural brain lesions and serious neurologic residua are not part of concussion, although temporary disability can result from symptoms (such as nausea, headache, dizziness, memory disturbance, and difficulty concentrating [postconcussion syndrome]), which usually resolve within weeks. However, it is thought that multiple concussions may lead to Chronic Traumatic Encephalopathy (CTE) , which results in severe brain dysfunction. Contusions (bruises of the brain) can occur with open or closed injuries and can impair a wide range of brain functions, depending on contusion size and location. Larger contusions may cause brain edema and increased intracranial pressure (ICP). Contusions may enlarge in the hours and days following the initial injury and cause neurologic deterioration; surgery may be required. Diffuse axonal injury (DAI) occurs when rotational deceleration causes shear-type forces that result in generalized, widespread disruption of axonal fibers and myelin sheaths. A few DAI lesions may also result from minor head injury. Gross structural lesions are not part of DAI, but small petechial hemorrhages in the white matter are often observed on CT (although MRI may be more sensitive) and on histopathologic examination. DAI is sometimes defined clinically as a loss of consciousness lasting>6 hours in the absence of a specific focal lesion. Edema from the injury often increases ICP, leading to various Pathophysiology . DAI is typically the underlying injury in shaken baby syndrome. Hematomas (collections of blood in or around the brain) can occur with open or closed injuries and may be Epidural Intracerebral (intraparenchymal) Subdural Subarachnoid Hemorrhage (SAH) (SAH—bleeding into the subarachnoid space) is common in traumatic brain injury (TBI), although the appearance on CT is not usually the same as aneurysmal SAH. Blood from SAH secondary to TBI does not collect in a discrete hematoma. Subdural hematomasare collections of blood between the dura mater and the arachnoid mater. Acute subdural hematomas arise from laceration of cortical veins or avulsion of bridging veins between the cortex and dural sinuses. Acute subdural hematomas often occur in patients with Head trauma caused by falls or motor vehicle crashes Underlying cerebral contusions A contralateral epidural hematoma Compression of the brain by the hematoma and swelling of the brain due to edema or hyperemia (increased blood flow due to engorged blood vessels) can increase ICP. When both compression and swelling occur, mortality and morbidity can be high. A chronic subdural hematoma may appear and cause symptoms gradually over several weeks after trauma. Chronic subdural hematomas occur more often in patients with alcohol use disorder and older patients (especially in those taking antiplatelet or anticoagulant medications or in those with brain atrophy). Older patients may consider the head injury relatively trivial or may have even forgotten it. In contrast to acute subdural hematomas, edema and increased ICP are unusual. Epidural hematomasare collections of blood between the skull and dura mater and are less common than subdural hematomas. Epidural hematomas that are large or rapidly expanding are usually caused by arterial bleeding, classically due to damage to the middle meningeal artery by a temporal bone fracture. Without intervention, patients with arterial epidural hematomas may rapidly deteriorate and die. Small, venous epidural hematomas are rarely lethal. are collections of blood within the brain itself. In the traumatic setting, they result from coalescence of contusions. Exactly when one or more contusions become a hematoma is not well-defined. Increased ICP, Brain Herniation , and brain stem failure can subsequently develop, particularly with lesions in the temporal lobes. Penetrating injuries by definition involve fractures. Closed injuries may also cause skull fractures, which may be linear, depressed, or comminuted. The presence of a fracture suggests that significant force was involved in the injury. Most patients with simple linear fractures and no neurologic impairment are not at high risk of brain injuries, but patients with any fracture associated with neurologic impairment are at increased risk of intracranial hematomas. Skull fractures that involve special risksinclude Depressed fractures: These fractures have the highest risk of tearing the dura, damaging the underlying brain, or both. Frontal bone fractures: These fractures have a risk of frontal sinus violation, which may lead to higher risks of long-term mucocele and meningitis development due to an unrecognized cerebrospinal fluid (CSF) fistula. Temporal bone fractures that cross the area of the middle meningeal artery: In these fractures, an epidural hematoma is a risk. Fractures that cross one of the major dural sinuses: These fractures may cause significant hemorrhage and venous epidural or venous subdural hematoma. Injured venous sinuses can later thrombose and cause cerebral infarction. Fractures of the occipital bone and base of the skull (basilar bones): These bones are thick and strong, so fractures in these areas indicate a high-intensity impact and meaningfully increase risk of brain injury (eg, cerebral contusions and hematomas). Basilar skull fractures that extend into the petrous part of the temporal bone often damage middle and inner ear structures and can impair facial, acoustic, and vestibular nerve function. Basilar skull fractures may also lacerate the dura and cause CSF leakage into the ear, nose, or throat. Fractures that involve the carotid canal: These fractures can result in carotid artery dissection. Fractures in infants: The meninges may become trapped in a linear skull fracture of the parietal bone with subsequent development of a leptomeningeal cyst and expansion of the original fracture (growing fracture). 