Fred F. Ferri MD, FACP, in Ferri's Clinical Advisor 2022, 2022 • The history is the pivotal part of the workup for the patient with headache (Table E3). The patient should be asked to describe thepattern and onset of the pain. Patients often relate having had frequent and recurrent headaches similar to the one they have on the current visit. A marked variation in headache pattern can signal a new or serious problem. The rate of onset of pain may have significance. Pain with rapid onset of a few seconds to minutes is more likely to be vascular in origin than pain that developed over several
hours or days. However, a slow onset should not be solely relied on to rule out potential life-threatening causes for headache. Almost all studies dealing with subarachnoid bleeding report that patients moved from the pain-free state to severe pain within seconds to minutes. The “thunder clap” or “lightning strike” headache is common in acute presentations of SAH but is not highly specific. If the patient with moderate or severe
headache can indicate the precise activity in which he or she was engaging at the time of the onset of the headache (e.g., “I was just getting up out of the chair to answer the doorbell”), the suddenness of onset should warrant consideration of SAH. Careful questioning about the onset of headache may lead to the correct diagnosis of SAH, even if the pain is improving at the time of evaluation.9 The patient’sactivity at the onset of the pain may be helpful. Headaches that come on during severe exertion have a relationship to vascular bleeding, but there is enough variation to make assignment to any specific cause highly variable. The syndrome of postcoital headache is well known, but coitus is also a common time of onset for SAH. These headaches require the same evaluation on initial presentation as any other exertion-related head
pain. If there is a history of head trauma, the differential diagnosis and emergent causes are narrowed significantly. The considerations now focus on epidural and subdural hematoma, traumatic SAH, skull fracture, and closed-head injury (i.e., concussion and diffuse axonal injury). Theintensity of head pain is difficult to quantify objectively. Almost all patients
who come to the emergency department (ED) consider their headaches to be severe. Use of a pain scale may help differentiate patients initially but has more value in monitoring their response to therapy. Rapid resolution of pain in the ED, either from time or therapy, also should not be relied on to rule out serious causes of headache. Thecharacter of the pain (e.g., throbbing, steady), although sometimes helpful, may not be
adequate to differentiate one type of headache from another. Thelocation of head pain is helpful when the patient can identify a specific area. It is useful to have the patient point or try to indicate the area of pain; the emergency physician can then properly examine that area. Unilateral pain is more suggestive of migraine or a localized inflammatory process in the skull (e.g., sinus) or soft tissue. Occipital headaches are
classically associated with hypertension. Giant cell arteritis, temporomandibular joint (TMJ) disease, dental infections, and sinus infections frequently have a highly localized area of discomfort. Meningitis, encephalitis, SAH, and even severe migraine, although intense in nature, are usually more diffuse in their localization. Exacerbating oralleviating factors may be important. Patients whose headaches rapidly
improve when they are removed from their environment or recur each time they are exposed to a particular environment (e.g., basement workshop) may have carbon monoxide poisoning. Most other severe causes of head pain are not rapidly relieved or improved when patients get to the ED. Headaches on awakening are typically described with brain tumors. Intracranial infections, dental infections, and other regional causes of head pain tend not to be improved or alleviated before therapy is given. Associated symptoms and risk factors may relate to the severity of headache but rarely point to the specific causes (Box E1). Nausea and vomiting are completely nonspecific. Migraine headaches, increased intracranial pressure, temporal arteritis, and glaucoma can all manifest with severe nausea and vomiting, as can some systemic viral infections with headache. Such factors may point toward the intensity of the
discomfort but are not specific in establishing the diagnosis. Immunocompromised patients are at risk for unusual infectious causes of headache. Toxoplasmosis, cryptococcal meningitis, and abscess are very rare but may be seen in patients with ahistory of HIV or another immunocompromised state. This subset of patients may have serious central nervous system infection without typical signs or symptoms of systemic illness (e.g., fever and meningismus). Aprior history of headache, although helpful, does not rule out current serious problems. It is extremely helpful, however, to know that the patient has had a workup for severe disease. Previous visits and computed tomography, magnetic resonance imaging, and other forms of testing can provide support for or help rule out a specific diagnosis. Patients with migraine, cluster, and tension headaches tend to have a stereotypical recurrent pattern.
Adherence to these patterns is also helpful in deciding the degree to which a patient’s symptoms are pursued. Closed Head InjuryJames W. Bales, ... Richard G. Ellenbogen, in Principles of Neurological Surgery (Fourth Edition), 2018 MechanismHead injuries can be classically classified as closed or penetrating. A closed head injury is typically used to describe falls, automobile accidents, and assaults, whereas a penetrating injury describes gunshot wounds or stab injuries. The use of improvised explosive devices in military warfare has created a separate category of injury known as blast injury, which is unique in injury pattern and considerations. Although the average neurosurgical practitioner may not need to manage the acute consequences of a blast-induced head injury, the long-term consideration of this type of head injury will likely be important as more servicemen and women experience a blast injury. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323431408000251 Surgical Management of Severe Closed Head Injury in AdultsAlfredo Quiñones-Hinojosa MD, in Schmidek and Sweet: Operative Neurosurgical Techniques, 2022 Intracranial Pressure Monitoring: Indications and MethodsA mainstay in the care of patients with severe brain injuries has been the monitoring and treatment of high ICP. About two-thirds of patients with severe head injury have no significant mass lesion on the initial CT scan, but at least 80% demonstrate high ICP.74 The treatment of raised ICP is based on the concept that maintaining adequate blood supply and oxygen delivery to the brain after TBI is paramount to avoid secondary ischemia. The paradigm that ICP-guided treatment in severe TBI can reduce early mortality and improve outcome has been, however, challenged by a recent prospective clinical trial that failed to find differences in outcome between patients with invasive ICP monitoring and those with only clinical/radiologic examination.75 A recent retrospective study by the Japan Neurotrauma Data Bank Committee that included nearly 1100 patients with severe TBI showed that there was no significant difference in the rate of favorable outcome between the ICP and non-ICP monitored groups, despite the former group being aggressively managed.76 The 4th edition of the Brain Trauma Foundation Guidelines acknowledges that the question regarding which patients should undergo ICP monitoring is not clear-cut; nonetheless, they chose to re-state the 3rd edition recommendations on ICP monitoring: (1) ICP should be monitored in all savable comatose patients (GCS score 3 to 8 points) with abnormal scans (hematomas, contusions, swelling, herniation, or compressed basal cisterns); (2) ICP monitoring is also indicated in severely head-injured patients with a normal CT scan if two or more of the followings features are noted at admission: age over 40 years, unilateral or bilateral motor posturing, or systolic blood pressure (BP) less than 90 mm Hg.3,77 Two recent consensus conferences support the first indication of ICP monitoring but, on the contrary, they consider that ICP should no longer be monitored in patients with pure DAI or minimal intracranial pathology.78,79 The gold standard method for measuring ICP is an intraventricular device connected to a fluid-coupled catheter with an external strain gauge (ventriculostomy catheter), because it not only monitors ICP but also allows cerebrospinal fluid (CSF) drainage for therapeutic purposes to lower ICP (Fig. 121.4A–C). There is no class I evidence on the use of external ventricular drainage (EVD) as a first-tier or second-tier intervention in severe TBI patients, and there is clinical uncertainty regarding continuous drainage of CSF (open EVD system) versus intermittent opening as necessary to drain CSF (closed EVD system). The theoretical advantage of an open EVD system is a tighter and more stable ICP control. However, there is a risk of overdraining with potential collapse of the ventricles.80 Optical and electromagnetic neuronavigation systems can be useful to facilitate safe placement of the ventricular drain, particularly in TBI patients with diffuse brain swelling that often have small ventricles.81 Nevertheless, many centers tend to use intraparenchymal probes, especially when the ventricular size is small or it is expected that placement of a ventriculostomy will require a large number of passes. Intraparenchymal probes use fiber-optic catheters and carry a lower risk of infection and hemorrhage. Closed Head InjuryClifford M. Houseman, ... Raj K. Narayan, in Principles of Neurological Surgery (Third Edition), 2012 MechanismHead injury is classically categorized as “closed” or “penetrating” head injury. These categories are not necessarily mutually exclusive. For example, a depressed skull fracture with bone fragment extension into the brain may fit both descriptors. For practical purposes closed head injury is typically used to describe head injury after falls, automobile accidents, and assaults, and penetrating head injury is used to describe gunshot wounds and stabbings. More recently two new categories have been developed: crush and blast. Crush injury can best be described as the cranium being held between compressive forces that subject the skull and intracranial contents to increasing pressures. This force, if significant enough, can lead to failure of the calvarium as a protective shell to the intracranial contents. Blast injury has recently been added as a separate category after the experience with improvised explosive devices (IEDs) in the recent Afghanistan and Iraq conflicts. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9781437707014000208 Pediatric TraumaJean-Louis Vincent MD, PhD, in Textbook of Critical Care, 2017 Closed Head InjuriesClosed head injury or TBI is the leading cause of death in pediatric trauma, with nearly 3000 deaths annually. Childhood TBI survivors often have life-long morbidities and impairment.11 Linear and inertial forces resulting in an impact injury cause the primary injury in TBI.12 These injuries include hematomas, lacerations, and axonal shearing, and are often described as irreparable. Secondary injury refers to the injury that occurs after impact and is considered both preventable and potentially reversible. Pathologic alterations in respiratory, hemodynamic, and cellular function occur, which may lead to secondary injury and cell death. The pathways to neuron death include inadequate oxygen and nutrient supply secondary to hypoxia and decreased cerebral blood flow. Decreased cerebral blood flow can occur secondary to hypotension, decreased cardiac output, raised ICP, cerebrovascular dysregulation including vasospasm, and microthrombus formation. Elevated ICP occurs secondary to mass lesions, cerebral edema, and increases in cerebrospinal fluid and blood volumes. Other neuronal injuries occur secondary to inflammation, oxidative stress, and apoptosis. Present TBI therapies are directed primarily at supporting oxygenation, blood pressure, and cardiac output and at controlling ICP to prevent secondary injury.12 Despite insufficient evidence for definitive treatment standards in TBI, a number of guidelines have been recommended.13 These include early admission with severe TBI to a pediatric trauma center, avoidance of hypoxia, correction of hypotension, and maintenance of cerebral perfusion pressure greater than 40 mm Hg in children. There is little evidence to support the routine use of corticosteroids or the prophylactic use of antiseizure medication. Currently, a number of National Health Institute multicenter trials are under way to better elicit treatment recommendations in pediatric TBI. Initial stabilization and resuscitation follow the ATLS protocol. The underlying goal is airway protection and respiratory support to prevent hypoxemia and hypercarbia. Hyperoxia and brief, aggressive hyperventilation is indicated only if the clinical examination reveals signs of acute cerebral herniation. These maneuvers should be directed by neurosurgery and are usually initiated immediately before operative intervention. Normotension or mild hypertension and mild hypervolemia are indicated to support cardiac output and cerebral blood flow. Fluids, sedation, and vasoactive agents must be judiciously administered. Hypertonic saline may be advantageous in children with elevated ICP. All children with a suspected TBI, history of loss of consciousness, altered level of consciousness, focal neurologic signs, evidence of a depressed or basilar skull fracture, a bulging fontanelle, or persistent headache and vomiting should have a noncontrast head CT.13 Early consultation with neurosurgery is indicated in all children with significant TBI. ICP monitoring should be considered in patients with a GCS score less than 8. Even with a normal CT scan, 10% to 15% of patients with a GCS ≤8 have elevated ICP. ICP monitoring with a ventricular catheter, an external strain gauge transducer, or a catheter tip pressure transducer is considered accurate and reliable. Ventriculostomy allows cerebrospinal fluid drainage in addition to ICP monitoring. Head injuryGeraint Fuller MA MD FRCP, Mark Manford BSc MBBS MD FRCP, in Neurology (Third Edition), 2010 Pathology and pathogenesisCerebral injuryHead injury may lead to a brief loss of consciousness without associated pathological changes in the brain. The mechanism for the loss of consciousness is not clear. With more severe head injury, brain damage can occur because of the direct trauma to the brain. This arises from direct disruption of the brain, shearing of axons and intracerebral haemorrhage. These injuries occur at the site of trauma and opposite the site of injury, so-called contre-coup injury. Contre-coup injury results from acceleration/deceleration forces moving the brain within the skull. There may be secondary brain injury (Fig. 1) due to brain oedema, which causes raised intracranial pressure and can lead to cerebral herniation (p. 48). The raised intracranial pressure, usually associated with hypotension, leads to hypoperfusion of the brain and therefore cerebral ischaemia. Infratentorial lesions can obstruct CSF flow and lead to hydrocephalus. Intracranial haematomasExtradural haematomas occur when the middle meningeal artery bleeds into the extradural space (Fig. 2). This can occur some time after the head injury and should be considered in any patient with deterioration following an apparently good recovery from a head injury. Subdural haematomas occur either acutely, usually with some intracerebral bleeding, or chronically (Fig. 3). The latter occurs when damaged cortical veins ooze into the subdural space. Intracerebral haematomas (Fig. 2) are the most common, occurring both at the site of direct trauma and at the contre-coup site. The mass effect of any of these bleeds may lead to cerebral herniation. Skull fracturesThese can be divided into simple and depressed fractures and basal skull fractures. The latter are difficult to see on skull X-rays but are associated with particular physical signs such as periorbital bruising or Battle's sign (Fig. 4). These may also be associated with cranial nerve damage, especially facial and auditory nerves. Basal fractures also produce bleeding into the middle ear, seen as either blood behind the ear drum or coming from the external ear, or CSF rhinorrhoea. CSF rhinorrhoea is seen as clear fluid coming from the nose – fluid which, unlike mucus, contains glucose, which is easily tested for. (A more specific test is isotransferrin.) The presence of a skull fracture substantially increases the risk of significant intracranial haemorrhage. Basal and compound fractures can produce a dural leak, which provides a potential route of entry of infection into the CNS. Clinical featuresThe clinical features of head injury are varied and depend on the severity of the injury and the part of the brain affected. This can be complicated by delayed events such as intracranial haemorrhage. The clinical setting alters the evaluation. For example, in patients with multiple injuries, there can be trauma elsewhere, with multiple fractures and abdominal and chest trauma. In these and other patients, there may be associated cervical spine trauma. The severity of a head injury can be assessed in several ways: ▪The level of consciousness, reliably and easily measured using the Glasgow Coma Scale (p. 129), which is an important clinical measure. ▪Signs indicative of a basal skull fracture (see above). ▪The pupil reactions, an important indicator of herniation. ▪The finding of focal neurological signs. These measures can be monitored and any change is particularly important in the management of these patients. The vital signs need to be monitored. Fortunately, most patients will have less severe head injuries. The same measurements need to be made but a history may be obtainable from the patient. From the history of the episode, perhaps from witnesses, some estimate of the potential forces involved can be made. The occurrence and duration of loss of consciousness are important indicators. The duration of memory lost by the patient, before the injury (retrograde amnesia) or after the injury (anterograde amnesia), are important indicators of severity of injury. One group of patients of particular concern are those who have made an initial recovery from their head injury but then later deteriorate again after a ‘lucid interval’. This is the classical history of patients with extradural haemorrhage, though it can occur with subdural haemorrhage. It can also occur because of neck trauma resulting in carotid dissection. These complications are rare in patients who have not fractured their skull (1 in 1000). Differential diagnosesThe differential diagnosis of head injury will depend on the clinical presentation. In patients who present unconscious or confused, the differential diagnosis is wide and is discussed on page 50. In patients who have had a head injury with a period of anterograde and retrograde amnesia, there may be uncertainty as to whether the head injury was the primary event or the result of a blackout. Investigation and managementThe investigation and management depend on the severity of the head injury. Patients with mild head injuries without loss of consciousness or with loss of consciousness of less than 5 min, with a normal examination and no skull fracture, can be allowed home in the care of a responsible adult with a warning card outlining the possible types of deterioration. Patients at risk from developing complications are those with longer than 5–10 min unconsciousness, a seizure at onset, altered consciousness or focal signs on examination and evidence of a skull fracture. These patients need to be admitted and monitored. CT or MRI of the brain is needed in most of these patients. These are optimally managed in a neurosurgical centre. The aim of treatment is to prevent secondary brain damage. This focuses on avoiding hypotension, maintaining oxygenation and avoiding raised intracranial pressure. Intracranial pressure may be reduced by surgical procedures to evacuate intracranial haematomas and shunt for hydrocephalus, and medical interventions with mannitol, mechanical ventilation and forced hyperventilation; this may need monitoring with intracranial pressure monitors. Cytotoxic oedema is maximal about 3–4 days after the injury. This specific treatment needs to be combined with general medical care as for any unconscious patient. Once the patient is stable and improving, there are many aspects that will require rehabilitation. This will involve physiotherapy and occupational therapy, and may require speech therapy. There are frequently psychological and behavioural difficulties with personality change, frontal disinhibition and memory loss. These latter problems make the rehabilitation of patients following severe head injuries somewhat different from patients with other brain injuries such as stroke and are often most effectively managed at a specialist unit. Other complicationsIn addition to the consequences of brain damage there are other complications. Post-traumatic syndromesEven after a mild head injury, patients can become anxious, have difficulty concentrating and sleep poorly. This may be associated with particular recollections of the accident and a change in behaviour, for example avoiding driving. This is a post-traumatic stress disorder. There is uncertainty about whether this is affected by compensation claims relating to any accident. Patients may develop a migraine-like headache following head injury, which usually spontaneously improves over 2 years. Anosmia (loss of sense of smell) can occur as a result of damage to the fibres passing through the cribriform plate. This is permanent. Patients may still appreciate tastes and chemical irritation such as ammonia. Post-traumatic vertigo can occur and is most commonly benign positional vertigo (p. 46). The frequency of post-traumatic epilepsy depends on the severity and type of the head injury. Severe head injuries with intracranial haematomas or post-traumatic amnesia (PTA) over 24 h have a 12% risk of epilepsy in 5 years. More moderate injury with skull fracture or PTA over 30 min has a 1.6% risk at 5 years. Milder head injuries have the same rate as the background population of 0.5%. PrognosisThe outcome of head injury depends on the severity of the injury and age of the patient, with younger patients doing better. Most head injuries are mild or moderate and there is a good recovery: if PTA is less than 1 h, 90% of patients are back at work in 2 months; if PTA is longer than 24 h then 80% of patients return to work in 6 months. Patients with more severe head injuries are often left with some disability. They do, however, continue to improve for longer, over 2 years, than patients with other brain injuries such as stroke. Head injury▪Head injury is a common cause of death and neurological disability. ▪Brain injury results from a combination of direct trauma, haemorrhage, hypoxia and raised intracranial pressure. ▪Acute management of head injuries aims to control the secondary mechanisms of brain injury: haemorrhage, hypoxia and raised intracranial pressure. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780702032240000409 Head InjuryArthur M. Lam, M. Sean Kincaid, in Complications in Anesthesia (Second Edition), 2007 DefinitionHead injury is a common problem, with an annual incidence of approximately 200 per 100,000 persons in the United States. Many of these injuries are minor, with few sequelae, but some are devastating. Car and motorcycle crashes are the most common cause of traumatic brain injury (TBI), followed by injuries from firearms, falls, and sports. Severe TBI is defined as any injury that results in a Glasgow Coma Scale (GCS) score of 8 or less after adequate cardiopulmonary resuscitation. Damage to neural tissue directly related to trauma is considered the primary injury and includes cerebral contusion, diffuse axonal injury, hemorrhage into the epidural or subdural space, and intraparenchymal hemorrhage. Secondary injury is any insult to the brain occurring after the initial TBI that causes further neuronal damage. Although cerebral ischemia or hypoxia is the ultimate cause of secondary brain injury after TBI, systemic or local insults often contribute to such injury. Among these are elevated intracranial pressure (ICP), systemic hypotension, and hypoxemia. Neuronal death is likely mediated by complex biochemical processes involving the release of excitatory amino acids (e.g., glutamate) and the cellular influx of calcium. Actual cell death may be necrotic or apoptotic in nature. Preventing or reducing secondary brain injury is the focus of most medical management of TBI in both the intensive care unit (ICU) and the operating room. TBI is often associated with other injuries (as illustrated in the case synopsis). Thus, anesthesiologists may care for a patient during surgical intervention for TBI (e.g., evacuation of subdural hematoma, decompressive craniectomy) and for laparotomy or fracture fixation, as well as in the ICU. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9781416022152501873 Head InjuryAlan R. Turtz, H. Warren Goldman, in Critical Care Medicine (Third Edition), 2008 INCIDENCEThe incidence of head injury in the United States is approximately 200 per 100,000 population per year.4 Based on a U.S. population of 250 million, approximately 500,000 people are estimated to sustain a head injury every year that is severe enough to prompt them to seek medical attention. Of these, 40,000 to 50,000 die before hospital admission.4 The peak incidence of head injury occurs at 15 to 24 years of age.5 A secondary peak has been noted for infants and the elderly. Head injury remains the most common cause of death in young adults and is two to three times more common in males.4,7–8 The incidence of head injury is inversely proportional to socioeconomic status.6 Motor vehicle accidents account for more than 50% of head injuries in the United States. Approximately 13% to 15% of head injuries are the result of gunshot wounds. In the United States more than one half of all motorcycle accidents result in death (15% of all deaths are the result of vehicular accidents) or major head injury. Helmets have been proved to reduce this problem significantly.9 In other countries, different injury patterns have been found. Pedestrian head injuries are frequent in Nigeria and certain parts of England.4–6,8–10 In some regions of South Africa, penetrating knife injury to the brain is very common.11 Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323048415500698 Head injuryJoseph Grubenhoff MD, in Berman's Pediatric Decision Making (Fifth Edition), 2011 Acute head injury is common in pediatric patients. It is responsible for more than 500,000 emergency department visits annually. Of those, there are approximately 60,000 hospitalizations and 7000 deaths. However, most children suffer only mild traumatic brain injury (mTBI; concussion). There is considerable controversy in the medical literature about how best to assess and manage victims of mild, moderate, and severe head injury. This algorithm is designed for practitioners in the office, urgent care, or community hospital setting. A.Airway, breathing, and circulation should be addressed first. Immobilize the cervical spine when significant forces or altered mental status are involved. Evaluate for irregular respirations, hypertension, and bradycardia (Cushing triad) indicating the presence of increased intracranial pressure (ICP). Note any asymmetry of pupils and the Glasgow Coma Scale (GCS) score (Table 1). A score less than 9 suggests severe injury and the loss of airway protective reflexes; consider endotracheal intubation. Expose the patient to identify any other evidence of trauma. Treat increased ICP and any life-threatening conditions. B.Once stabilized, obtain a focused history and perform a complete physical examination. History should include the mechanism and time of injury; use of any protective equipment; presence, severity, and duration of symptoms associated with brain injury (Table 2); identification of underlying medical conditions such as central nervous system (CNS) abnormalities, bleeding diatheses, and the use of intoxicants. Abusive head trauma is a leading cause of death in children younger than 1 year. Examine the head for the following findings: bruises, abrasions, lacerations, hematomas, bony depressions, and full or bulging fontanelle. Note pupil size and reactivity, optic disc margins, and the presence of retinal hemorrhages. The absence of retinal hemorrhages on a nondilated examination does not exclude them. Note any periorbital bruising (raccoon sign), mastoid bruising (Battle sign), hemotympanum, otorrhea, or rhinorrhea; these findings suggest basilar skull fracture. A neurologic examination should focus on extraocular movements, motor strength, reflexes, pain sensation and proprioception, station, and gait. C.Assess severity of injury (Table 3). The GCS provides a uniform assessment of severity that can be used to facilitate communication between physicians and institutions. D.Children 2 years or older with normal mental status at the time of evaluation, a normal neurologic examination, less than 5 seconds of loss of consciousness, no vomiting, absence of severe headache, minor mechanism, no evidence of basilar skull fracture, and no concerns for multisystem trauma do not require a computed tomographic (CT) scan. Observation of symptomatic children with mTBI (GCS ≥13) in the emergency department until it is clear their symptoms are dissipating is a reasonable alternative to obtaining head CT. Children younger than 2 years with minor mechanisms, who are acting normally per caregiver, have a normal neurologic examination and mental status, less than 5 seconds of loss of consciousness, no scalp hematoma or evidence of skull fracture, no concerns for multisystem trauma or abuse, and who have a reliable caregiver at home do not require imaging. E.Most children with blunt head injury will suffer mTBI (concussion) defined as a transient alteration in mental status that may or may not involve a loss of consciousness. Loss of consciousness is an unreliable tool for identifying mTBI and is not predictive of the severity of injury. Post-traumatic amnesia is a better predictor of severity and the likelihood of development of postconcussion syndrome. The symptoms listed in Table 2 are typical of mTBI. Concussions cause somatic, cognitive, and emotional disturbances. Informal orientation questions are poor at detecting these disturbances. Consider using a standardized concussion evaluation tool that focuses on orientation, concentration, memory, and recall, such as the Standardized Assessment of Concussion. Many commonly used concussion grading scales with return-to-play guidelines exist. None is evidence based, and there is considerable variation in recommendations. Most authors agree that children should not return to sports until they are free of symptoms both at rest and with exertion. For children with postconcussive symptoms persisting past 48 hours, consider referral to a neurologist or pediatric rehabilitation specialist for more detailed assessment. F.The use of imaging should be directed by the history and physical examination. Skull radiographs are of limited value in the evaluation of children with head injury. Negative findings do not rule out intracranial injury. Positive findings often lead to obtaining more detailed studies. Noncontrast head CT is the study of choice in acute head injury. Indications for head CT include evidence of depressed or basilar skull fracture, significant alteration or sudden deterioration in mental status, focal neurologic findings, persistent or worsening symptoms, concern for foreign body, the presence of a bleeding diathesis, or if there is a concern for abuse. Some authors recommend imaging for any infant younger than 3 months because of the greater likelihood of occult intracranial injury. G.Evidence of intracranial bleeding, presence of a foreign body, depressed or basilar skull fracture, GCS score of 8 or less, anemia or a significant decline in hematocrit, the presence of a bleeding diathesis, or intracranial instrumentation (e.g., ventriculoperitoneal shunt) should prompt immediate referral for neurosurgical evaluation. Consider referral for children with moderate injury (GCS score, 9–12) or whose mental status is not improving. H.Patients with moderate-to-severe brain injury are at risk for electrolyte disturbances (syndrome of inappropriate antidiuretic hormone secretion, diabetes insipidus) and disseminated intravascular coagulation (DIC); consider obtaining a basic metabolic panel and DIC screen. Infants with an open fontanelle are at risk for anemia caused by hemorrhage. Consider obtaining a complete blood cell count (CBC). Children younger than 1 year with linear skull fractures are at risk for development of a leptomeningeal cyst. Outpatient follow-up evaluation by a neurosurgeon is recommended. I.Post-traumatic seizures occur in about 10% of all cases of blunt head trauma, with significantly greater rates in the moderately to severely injured child; 95% occur in the first 24 hours. Studies of postinjury prophylaxis irrespective of age show reduction of seizure rates by up to 66%; there is no improvement in neurologic outcomes or risk for death. Subsequent randomized, controlled trials in children do not show this dramatic reduction in seizure rates. Given the potential risks associated with antiepileptic drugs (e.g., Stevens–Johnson syndrome), seizure prophylaxis is not recommended. Children with persistent or recurrent seizure activity warrant intracranial imaging. Benzodiazepines are the first choice for acute management. Consider fosphenytoin (or phenobarbital for infants <1 year) for ongoing seizures not responsive to benzodiazepines. Obtain a head CT for recurrent or prolonged seizures. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323054058001030 How does head injury cause increased intracranial pressure?Increased ICP is well documented in moderate and severe forms of traumatic brain injury (TBI) due to gross swelling or mass effect from bleeding. Since the brain exists within a stiff skull, increased ICP can impair cerebral blood flow (CBF) and cause secondary ischemic insult.
Which clinical finding is consistent with an increase in intracranial pressure?These are the most common symptoms of increased ICP: Headache. Blurred vision. Confusion.
What happens when intracranial pressure increases?A sudden increase in the pressure inside a person's skull is a medical emergency. Left untreated, an increase in the intracranial pressure (ICP) may lead to brain injury, seizure, coma, stroke, or death.
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