injuries poisoning
Traumatic Brain Injury (TBI)
Treatment of Traumatic Brain Injury
For mild injuries, discharge and home observation For moderate and severe injuries, optimization of ventilation, oxygenation, and brain perfusion; treatment of complications (eg, increased intracranial pressure [ICP], seizures, hematomas); and rehabilitation Multiple noncranial injuries, which are likely with motor vehicle crashes and falls, often require simultaneous treatment. Initial resuscitation of trauma patients is discussed elsewhere (see Approach to the Trauma Patient ). At the injury scene, a clear airway is secured and external bleeding is controlled before the patient is moved. Particular care is taken to avoid displacement of the spine or other bones to protect the spinal cord and blood vessels. Proper immobilization should be maintained with a cervical collar and long spine board until stability of the entire spine has been established by appropriate examination and imaging (see Diagnosis ). After the initial rapid neurologic assessment, pain should be relieved with a short-acting opioid (eg, In the hospital, after quick initial evaluation, neurologic findings (Glasgow Coma Scale [GCS] and pupillary reaction), blood pressure (BP), pulse, and temperature should be recorded frequently for several hours because any deterioration demands prompt attention. Serial GCS and CT results stratify injury severity, which helps guide treatment (see table). The cornerstone of management for all patients with traumatic brain injury (TBI) is Maintenance of adequate ventilation, oxygenation, and brain perfusion to avoid secondary brain insult Aggressive early management of hypoxia, hypercapnia, hypotension, and increased ICP helps avoid secondary complications. Bleeding from injuries (external and internal) is rapidly controlled, and intravascular volume is promptly replaced with crystalloid (eg, 0.9% saline) or preferably Technique of Transfusion to maintain cerebral perfusion. Hypotonic fluids (especially 5% D/W) are contraindicated because they contain excess free water, which can increase brain edema and ICP. Other complications to check for and to prevent include hyperthermia, hyponatremia, hyperglycemia, and fluid imbalance. If patients with mild injury did not lose consciousness or lost it only briefly and have stable vital signs, a normal head CT scan, and normal mental and neurologic function (including resolution of any intoxication), they may be discharged home provided family members or friends can observe them closely for an additional 24 hours. These observers are instructed to return patients to the hospital if any of the following develop: Decreased level of consciousness Focal neurologic deficits Worsening headache Vomiting Deterioration of mental function (eg, seems confused, cannot recognize people, behaves abnormally) Seizures Patients who had lost consciousness or have any abnormalities in mental or neurologic function and cannot be observed closely after discharge are generally observed in the emergency department or overnight in the hospital, and follow-up CT may be done in 8 to 12 hours if symptoms persist. Patients who have no neurologic changes but have minor abnormalities on head CT (eg, small contusions, small subdural hematomas with no mass effect, punctate or small traumatic subarachnoid hemorrhage) may need only a follow-up CT within 24 hours. If CT is stable and neurologic examination results are normal, these patients may be discharged home. (See also the 2016 practice guideline of the Brain Trauma Foundation of the American Association of Neurological SurgeonsGuidelines for the management of severe traumatic brain injury, 4th edition.) Patients with moderate injury often do not require intubation and mechanical ventilation (unless other injuries are present) or ICP monitoring. However, because deterioration is possible, these patients should be admitted and observed even if head CT is normal. Patients with severe injury are admitted to a critical care unit. Because airway protective reflexes are usually impaired and ICP may be increased, patients are Overview of Mechanical Ventilation while measures are taken to avoid increasing ICP. Basing management of patients with severe TBI on information from ICP monitoring is recommended to reduce in-hospital and 2-week postinjury mortality ( Treatment references ); however, some evidence suggests that management using a combination of clinical and radiographic evaluations alone results in equivalent outcomes ( Treatment principles for patients with increased ICP include Rapid-sequence orotracheal intubation Overview of Mechanical Ventilation None Monitoring of ICP and CPP Sedation as needed Maintaining euvolemia and serum osmolality of 295 to 320 mOsm/kg (295 to 320 mmol/kg) For intractable increased ICP, possibly cerebrospinal fluid (CSF) drainage, temporary hyperventilation, decompressive craniotomy, orpentobarbitalcoma Tracheal Intubation (using paralysis) is used rather than awake nasotracheal intubation if patients with TBI require airway support or Adequacy of oxygenation and ventilationshould be assessed using pulse oximetry and arterial blood gases (if possible, end-tidal CO2). The goal is a normal PaCO2 level (38 to 42 mm Hg). Prophylactic hyperventilation (PaCO2 25 to 35 mm Hg) is no longer recommended. The lower PaCO2 reduces ICP by causing cerebral vasoconstriction, but this vasoconstriction also decreases cerebral perfusion, thus potentiating ischemia. Therefore, hyperventilation (target PaCO2 of 30 to 35 mm Hg) is used only during the first several hours and for ICP that is unresponsive to other measures. Intracranial Pressure (ICP) Monitoring and CPP monitoring and control Sedationcan be used to prevent agitation, excessive muscular activity (eg, due to delirium), and help mitigate response to pain and thus help prevent increases in ICP. For sedation,propofolis often used in adults (contraindicated in children) because it has quick onset and very brief duration of action; dose is 0.3 mg/kg/h continuous IV infusion, titrated gradually upward as needed (up to 3 mg/kg/h). An initial bolus is not used. The most common adverse effect is hypotension. Prolonged use at high doses can cause pancreatitis. Benzodiazepines (eg,midazolam,lorazepam) can also be used for sedation, but they are not as rapidly acting aspropofoland individual dose-response can be hard to predict. Antipsychotics can delay recovery and should be avoided if possible. Rarely, paralytics may be needed; if so, adequate sedation must be ensured. Adequate pain controloften requires opioids. Maintaining euvolemia and normal serum osmolality(iso-osmolar or slightly hyperosmolar; target serum osmolality 295 to 320 mOsm/kg [295 to 320 mmol/kg]) is important. To control ICP, hypertonic saline solution (3% or 23.4%) is a more effective osmotic agent thanmannitol. It is given as a bolus of 2 to 3 mL/kg IV as needed or as a continuous infusion of 1 mL/kg/h. Serum sodium level is monitored and kept ≤ 155 mEq/L (155 mmol/L). Osmotic diuretics (eg,mannitol) given IV are an alternative to lower ICP and maintain serum osmolality. However, they should be reserved for patients whose condition is deteriorating or used preoperatively for patients with hematomas.Mannitol20% solution is given 0.5 to 1 g/kg IV (2.5 to 5 mL/kg) over 15 to 30 minutes and repeated in a dose ranging from 0.25 to 0.5 g/kg (1.25 to 2.5 mL/kg) given as often as needed (usually every 6 to 8 hours); it lowers ICP for a few hours.Mannitolmust be used cautiously in patients with severe coronary artery disease, heart failure, renal insufficiency, or pulmonary vascular congestion becausemannitolrapidly expands intravascular volume. Because osmotic diuretics increase renal excretion of water relative to sodium, prolonged use ofmannitolmay also result in water depletion and hypernatremia.Furosemide1 mg/kg IV is also helpful to decrease total body water, particularly when the transient hypervolemia associated withmannitolis to be avoided. Fluid and electrolyte balance should be monitored closely while osmotic diuretics are used. can be considered when increased ICP is refractory to other interventions and sometimes as a primary measure (eg, at the time of surgery to drain a significant hematoma). For craniectomy, a significant portion of the skull is removed en bloc (to be replaced later), and duraplasty is done to allow outward brain swelling. The amount and location of bone removal depends on the injury, but the opening must be sufficient to keep the swelling from compressing brain tissue against the margins of the defect. In a randomized trial comparing craniectomy and medical management, overall mortality at 6 months was reduced after craniectomy, but rates of severe disability and vegetative state were higher, and rate of good functional recovery was similar ( Treatment references ). Pentobarbitalcomais a more involved and currently less popular option for intractable increased ICP. Coma is induced by givingpentobarbital10 mg/kg IV over 30 minutes, 5 mg/kg/h for 3 hours, then 1 to 2 mg/kg/h maintenance infusion. The dose may be adjusted to suppress bursts of electroencephalogram (EEG) activity, which is continuously monitored. Hypotension is common and managed by giving fluids and, if necessary, vasopressors. Therapeutic systemic hypothermia has not proved helpful. High-dose corticosteroids had previously been advocated to decrease cerebral edema and ICP. However, corticosteroids are not useful to control ICP and are not recommended. In a large randomized, placebo-controlled study, corticosteroids given within 8 hours of TBI increased mortality and severe disability in survivors ( Treatment references ). A variety of neuroprotective agents have been and are being studied, but thus far, none has demonstrated efficacy in clinical trials. Seizure Disorders can worsen brain damage and increase ICP and therefore should be treated promptly. In patients with significant structural injury (eg, larger contusions or hematomas, brain laceration, depressed skull fracture) or a GCS score Ifphenytoinis used, a loading dose of 20 mg/kg IV is given (at a maximum rate of 50 mg/min to prevent cardiovascular adverse effects such as hypotension and bradycardia). The starting maintenance IV dose for adults is 2 to 2.7 mg/kg three times a day; children require higher doses (up to 5 mg/kg twice a day for children<4 years). Serum levels should be measured to adjust the dose. Duration of treatment depends on the type of injury and EEG results. If no seizures develop within 1 week, anticonvulsants should be stopped because their value in preventing future seizures is not established. Newer anticonvulsants are under study.Fosphenytoin, a form ofphenytointhat has better water solubility, is being used in some patients without central venous access because it decreases the risk of thrombophlebitis when given through a peripheral IV. Dosing is the same as forphenytoin.Levetiracetamis used increasingly, particularly in patients with liver disorders. Aligned closed fractures require no specific treatment. Depressed fractures sometimes require surgery to elevate fragments, manage lacerated cortical vessels, repair dura mater, and debride injured brain. Open fractures may require surgical debridement unless there is no CSF leak and the fracture is not depressed by greater than the thickness of the skull. Frontal bone fractures are repaired, especially if there is significant anterior and posterior table displacement (for cosmetic reasons) or CSF leakage into the nose from an underlying dural laceration. Use of antibiotic prophylaxis is controversial because of limited data on its efficacy and the concern that it promotes drug-resistant strains. Intracranial hematomas may require urgent surgical evacuation to prevent or treat brain shift, compression, and herniation; hence, early neurosurgical consultation is mandatory. However, not all hematomas require surgical removal. Small intracerebral hematomas rarely require surgery. Patients with small subdural hematomas can often be treated without surgery. Factors that suggest a need for emergent surgeryinclude Midline brain shift of>5 mm Compression of the basal cisterns Worsening neurologic examination findings Chronic subdural hematomas may require surgical drainage but much less urgently than acute subdural hematomas. Large or arterial epidural hematomas are treated surgically, but small epidural hematomas that are thought to be venous in origin can be followed with serial CT. Etiology of Anemia and Hyperglycemia predicts increased risk of increased ICP, impaired cerebral metabolism, urinary tract infection, and bacteremia; thus, careful glycemic control has been attempted in patients with a TBI. However, in a randomized controlled trial comparing intensive regimens (to maintain glucose < 80 to 120 mg/dL [4.4 to 6.7 mmol/L]) with traditional regimens (to maintain glucose < 220 mg/dL [12.2 mmol/L]), GCS scores were the same at 6 months, but incidence of hypoglycemic episodes was higher with the intensive regimen ( Treatment references ). Various degrees of hypothermia have been advocated to improve neurologic recovery by improving neuroprotection and decreasing ICP in the acute period after TBI. However, multiple randomized controlled trials have shown that early (within 2.5 hours), short-term (48 hours postinjury) prophylactic hypothermia does not improve outcomes in patients with severe TBI compared with standard medical treatment, and it increases the risk of coagulopathy and cardiovascular instability ( Treatment references ). Calcium channel blockers have been used in an attempt to prevent cerebral vasospasm after TBI, to maintain blood flow to the brain, and thereby to prevent further damage. However, a review of randomized controlled trials of calcium channel blockers in patients with acute TBI and traumatic subarachnoid hemorrhage concluded that their effectiveness remains uncertain ( Treatment references ). When neurologic deficits persist, rehabilitation is needed. Brain injury is best provided through a team approach that combines physical, occupational, and speech therapy, skill-building activities, and counseling to meet the patient’s social and emotional needs. Brain injury support groups may provide assistance to the families of brain-injured patients. For patients whose coma exceeds 24 hours, 50% of whom have severe persistent neurologic sequelae, a prolonged period of rehabilitation, particularly in cognitive and emotional areas, is often required. 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