injuries poisoning
Traumatic Brain Injury (TBI)
Symptoms and Signs of Traumatic Brain Injury
 the injury). Young children may simply become irritable. Some patients have seizures, often within the first hour or day. After these initial symptoms, patients may be fully awake and alert, or consciousness and function may be altered to some degree, from mild confusion to stupor to Overview of Coma and Impaired Consciousness . Duration of unconsciousness and severity of obtundation are roughly proportional to injury severity but are not specific. TheGlasgow Coma Scale(GCS—see table) is a quick, reproducible scoring system to be used during the initial examination to estimate severity of TBI. It is based on eye opening, verbal response, and the best motor response. The lowest total score (3) indicates likely fatal damage, especially if both pupils fail to respond to light and oculovestibular responses are absent. Higher initial scores tend to predict better recovery. By convention, the severity of head injury is initially defined by the GCS: 13 to 15 is mild TBI 9 to 12 is moderate TBI 3 to 8 is severe TBI ). Because hypoxia and hypotension can decrease the GCS, GCS values after resuscitation from cardiopulmonary insults are more specific for brain dysfunction than values determined before Cardiopulmonary Resuscitation (CPR) in Adults . Similarly, sedatives and paralytics can decrease GCS values and should be avoided before full neurologic examination is done. Delay use of sedative and paralytic medications until after full neurologic examination whenever possible. Symptoms of various types of TBI may overlap considerably. Epidural hematoma symptomsusually develop within minutes to several hours after the injury (the period without symptoms is the so-called lucid interval) and consist of Increasing headache Decreased level of consciousness Focal neurologic deficits (eg, hemiparesis) Pupillary dilation with loss of light reactivity in such patients usually indicates herniation. Some patients who have an epidural hematoma lose consciousness, then have a transient lucid interval, and then gradual neurologic deterioration. Acute subdural hematomasare usually associated with alterations in orientation, level of arousal, and/or cognition. They are commonly associated with increased intracranial pressure (ICP) even when small due to underlying cerebral contusions and edema. Symptoms include Headache Seizures Hemiparesis Symptoms of Symptoms of specific types of TBI None Pupillary asymmetry, abnormal brain stem reflexes, and coma from brain stem compression due to uncal herniation Intracerebral hematomas and contusionscan cause focal neurologic deficits such as hemiparesis, progressive decrease in consciousness, or both. Progressive decrease in consciousness may result from anything that increases intracranial pressure, or ICP (eg, hematoma, edema, hyperemia). Autonomic dysfunction from injury to the hypothalamus and other vital subcortical structures can cause Sympathetic hyperactivity with hypertension and tachycardia Neurogenic (Takotsubo) cardiomyopathy with ischemic changes and decreased cardiac function Acute kidney injury with deterioration of renal function Increased ICPsometimes causes vomiting, but vomiting is nonspecific. Markedly increased ICP classically manifests as a combination of the following (called the Cushing triad): Hypertension (usually with increased pulse pressure) Bradycardia Respiratory depression Respirations are usually slow and irregular. Severe diffuse brain injury or markedly increased ICP may cause decorticate or decerebrate posturing. Both are poor prognostic signs. Transtentorial herniation None Basilar skull fracturemay result in the following: Leakage of CSF from the nose or throat (CSF rhinorrhea) or into the middle ear (CSF otorrhea) Blood behind the tympanic membrane (hemotympanum) or in the external ear canal if the tympanic membrane has ruptured Ecchymosis behind the ear (Battle sign) or in the periorbital area (raccoon eyes) Loss of smell and hearing, which is usually immediate, although these losses will not be noticed until the patient regains consciousness Facial nerve function may be impaired immediately or after a delay. Other fractures of the cranial vault are sometimes palpable, particularly through a scalp laceration, as a depression or step-off deformity. However, blood under the galea aponeurotica may mimic a step-off deformity. Chronic subdural hematomamay manifest with increasing daily headache, fluctuating drowsiness or confusion (which may mimic early dementia), mild-to-moderate hemiparesis or other focal neurologic deficits, and/or seizures. Amnesia may persist and be both retrograde and anterograde (ie, for eventsfollowingthe injury). Postconcussion syndrome,which commonly follows a moderate or severe concussion, includes persistent headache, dizziness, fatigue, difficulty concentrating, variable amnesia, depression, apathy, and anxiety. Commonly smell (and thus taste), sometimes hearing, or rarely vision is altered or lost. Symptoms usually resolve spontaneously over weeks to months. A range of cognitive and neuropsychiatric deficits can persist after severe, moderate, and even mild TBI, particularly if structural damage was significant. Common problems include Amnesia Behavioral changes (eg, agitation, impulsivity, disinhibition, lack of motivation) Emotional lability Sleep disturbances Decreased intellectual function Late seizures (>7 days after the injury) develop in a small percentage of patients, often weeks, months, or even years later. Spastic motor impairment, gait and balance disturbances, ataxia, and sensory losses may occur. A persistent Vegetative State and Minimally Conscious State can result from a TBI that destroys forebrain cognitive functions but spares the brain stem. The capacity for self-awareness and other mental activity is generally absent; however, autonomic and motor reflexes are preserved, and sleep-wake cycles are normal. Few patients recover normal neurologic function when a persistent vegetative state lasts for 3 months after injury, and almost none recover after 6 months. Neurologic function may continue to improve for a few years after TBI, most rapidly during the initial 6 months. 