Head Trauma (2024)

by Emranur Rahman & Mansoor Husain

You Have A New Patient!

A 22-year-old male with no significant medical history presented to the emergency department two hours after a motorbike accident. He had been riding at a moderate speed when he lost control of the bike and fell, striking his head on the pavement. He briefly lost consciousness and experienced a sharp headache immediately following the fall, along with mild dizziness, nausea, and vomiting. He denied any neurological deficits at the scene; however, by the time he arrived at the hospital, he reported the onset of right-sided weakness and numbness.

The image was produced by using ideogram 2.0.

Upon examination, the patient appeared anxious and in moderate distress due to the headache. His vital signs were stable, with a blood pressure of 130/85 mmHg, a heart rate of 88 bpm, and a respiratory rate of 18 breaths per minute.

What Do You Need To Know?

Importance

Appropriate head trauma management in the emergency department (ED) is crucial because head injuries can range from mild concussions to severe traumatic brain injuries (TBI) that may lead to permanent disability or death if not appropriately managed.

The importance of correct management in the ED includes early identification of life-threatening Injuries. Rapid assessment and intervention are essential to identify severe conditions such as intracranial hemorrhage, skull fractures, or brain contusions. It also helps in prevention of secondary brain injury. Secondary brain injury can result from hypoxia, hypotension, or elevated intracranial pressure (ICP), and can worsen the outcome of the initial trauma.

The survival and neurological outcome of patients suffering from TBI depend on the extent of the primary injury and the subsequent secondary injuries sustained [1].

Epidemiology

Head trauma is a significant global health issue, contributing to a high burden of morbidity, mortality, and long-term disability.

The most common causes of head injuries are motor vehicle collision (MVC), falls from a significant height, physical assault, and occupational injury [2].

TBI affects all age groups, but young adults (15-44 years) are particularly vulnerable, often due to motor vehicle accidents (MVAs) and violence. Males are disproportionately affected, with a male-to-female ratio of about 2:1, likely due to higher-risk behaviors and occupations. Gunshot wounds are the most lethal mechanism, with a mortality rate of approximately 90% [1].

Pathophysiology

The pathophysiology of brain injury is complex and multifaceted, involving both primary and secondary injury mechanisms. The primary injury occurs at the moment of impact and is characterized by mechanical damage to brain tissues, such as axonal shearing or bleeding internally, which is not amenable to acute intervention [3]. Secondary injury, however, involves a cascade of biochemical, molecular, and structural changes that unfold over time, leading to further neuronal damage and dysfunction [3,4]. These secondary processes include glutamatergic excitotoxicity, loss of autoregulation, elevated intracranial pressure, and cortical spreading depression, which can result in seizures [5].

Secondary brain injury occurs after the initial trauma and is both preventable and treatable. Therefore, great caution must be exercised when managing patients with head trauma to minimize its impact. Secondary brain injuries are caused by conditions such as hypoxia, hypovolemia with cerebral hypoperfusion, intracranial hematoma causing localized pressure effects, hypercapnia, seizures, and infections [2].

Medical History

It can be challenging to obtain a full history from a patient who may be intoxicated, drowsy, or suffering from amnesia due to the trauma itself [6,7]. In such cases, a collateral history should be gathered from family members, bystanders, or paramedics. Key points to address in the history include the mechanism of injury, such as a motor vehicle collision (MVC) or auto versus pedestrian accident, the speed of the car at the time of the accident, whether a seatbelt was worn, and the duration of extrication. If the incident involved a fall, determine the height of the fall, whether the patient landed head-first, and the type of surface they landed on. Timing is also critical—establish exactly when the incident occurred. Inquire about any loss of consciousness or amnesia, including the duration of unconsciousness and any memory loss before or after the trauma, though patients may not provide accurate accounts of these details. Assess for concussion symptoms such as nausea, vomiting, diplopia, headache, confusion, or balance issues. Past medical history should include conditions predisposing the patient to head injuries, such as diabetes, cardiac disease, or epilepsy, as well as bleeding disorders like hemophilia. Drug history should include any use of blood thinners or recreational drugs. Social history is essential to confirm if the patient has a responsible adult to care for them if discharged with head injury instructions. Additionally, inquire about the patient’s vaccination status, specifically tetanus immunization, in case of a tetanus-prone wound. Ask about any medication or contrast allergies. Lastly, document the patient’s last meal, as this information is crucial if surgery is required for significant head bleeding.

Physical Examination

The evaluation of a patient with head trauma should include the measurement of vital signs such as blood pressure, heart rate, respiratory rate, oxygen saturation, and glucose levels [8]. Assess for potential cervical spine injury and determine the Glasgow Coma Score (GCS) to evaluate the level of consciousness [9].

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

Perform an eye examination to check pupil size and reactivity to light. Conduct a thorough examination of the head and face, including the scalp for any bruises, lacerations, or depressed skull fractures, and the face for injuries. Inspect the nose for signs of a septal hematoma. Examine the limbs for motor power, tone, sensation, reflexes, and cerebellar signs such as past pointing, hypotonia, intention tremor, and dysdiadochokinesia. Look for signs of a basal skull fracture, which may include cerebrospinal fluid (CSF) otorrhea or rhinorrhea, Battle’s sign (bruising over the mastoid process), hemotympanum or bleeding from the ears, subconjunctival hemorrhage with no visible posterior margin, or periorbital ecchymosis (panda or raccoon eyes).

LOC after head trauma, echymosis around both eyes. Warning findins for to investigate basilar skull fracture.
LOC after head trauma, echymosis behind the ears over mastoid bone. Warning findins for to investigate basilar skull fracture.

Alternative Diagnoses

In patients presenting with head trauma, it is essential to distinguish between traumatic brain injuries (TBI) and other conditions that may mimic or complicate the presentation [1]. Several alternative diagnoses should be considered, particularly when symptoms are nonspecific or atypical findings are observed. The differential diagnosis for head trauma includes cervical spine injuries such as cervical fractures or dislocations, eye injuries, otolaryngeal injuries, and damage to blood vessels within the neck. Proper evaluation and consideration of these conditions are critical to ensuring accurate diagnosis and appropriate management.

Acing Diagnostic Testing

Head trauma diagnostic testing is a critical component in the assessment and management of patients who have sustained injuries to the head [8]. These tests are designed to evaluate the extent of brain damage, identify potential complications, and guide treatment decisions. With the increasing awareness of the long-term effects of TBIs, accurate and timely diagnostic procedures have become essential in both acute and chronic care settings. Techniques such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and neurological assessments play a vital role in detecting structural abnormalities, bleeding, and other injuries.

Bedside Tests

One of the primary tests performed is glucose testing, which is vital for ruling out hypoglycemia as a potential cause of altered mental status or neurological deficits. Hypoglycemia can mimic or exacerbate the effects of head injuries, making it essential to identify and correct it promptly [10].

Laboratory Tests

Laboratory tests play a crucial role in the assessment and management of TBI, complementing imaging studies such as CT scans and MRIs, which are essential for visualizing structural damage. Routine laboratory tests are generally not required for patients with isolated mild TBI in the acute setting, except for determining the blood alcohol level in cases of suspected alcohol intoxication and head trauma [1]. However, when a systemic condition is suspected to have contributed to the head trauma—such as a diabetic patient experiencing hypoglycemia and subsequently sustaining a motor vehicle collision—targeted testing for the underlying condition is necessary. Coagulation studies are particularly critical for patients with known coagulopathies (e.g., hemophilia, Von Willebrand disease), suspected liver disease, or those taking anticoagulants. Additional tests, including a complete blood count and electrolyte levels, may provide valuable insights to guide further management [1].

Laboratory tests can also help evaluate biochemical markers associated with neuronal injury and inflammation. Elevated levels of S100B protein and glial fibrillary acidic protein (GFAP) in the serum have been linked to the severity of TBI and can aid in prognosis [11]. Furthermore, biomarkers such as ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) and neuron-specific enolase (NSE) have shown promise in differentiating between mild and severe TBI, potentially guiding treatment decisions [12]. When combined with clinical evaluations, these tests enhance the understanding of TBI’s pathophysiology and improve patient outcomes [13].

Imaging

Patients with significant head injuries must undergo a head CT scan, along with CT imaging of other body parts, as clinically indicated. Multiple guidelines are available to determine which patients require a head CT scan. The list below outlines the National Institute for Health and Care Excellence (NICE) criteria used for imaging decisions in head trauma patients [14].

Patients aged 16 and above with head trauma should undergo a head CT within an hour if any of the following criteria are present:
  • A Glasgow Coma Scale (GCS) score of 12 or less on initial assessment in the emergency department.
  • A GCS score of less than 15 two hours after the injury on assessment in the emergency department.
  • Suspected open or depressed skull fracture.
  • Any signs of basal skull fracture (e.g., haemotympanum, ‘panda eyes,’ cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
  • Post-traumatic seizure.
  • Focal neurological deficit.
  • More than one episode of vomiting.
Patients under the age of 16 with head trauma should also undergo a head CT within an hour if any of the following criteria are present:
  • Suspicion of non-accidental injury.
  • Post-traumatic seizure with no history of epilepsy.
  • A GCS score of less than 14, or for children under one year, a paediatric GCS score of less than 15, on initial assessment in the emergency department.
  • A GCS score of less than 15 two hours after the injury.
  • Suspected open or depressed skull fracture, or a tense fontanelle.
  • Focal neurological deficit.
  • Any signs of basal skull fracture (e.g., haemotympanum, ‘panda eyes,’ cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
  • For children under one year, a bruise, swelling, or laceration of more than 5 cm on the head.

Intracranial Injuries

Epidural Hemorrhage

Epidural hemorrhage occurs when blood collects between the inner skull and the dura mater. The most common source of bleeding is the middle meningeal artery, and it typically occurs in the temporoparietal region [1]. Patients usually lose consciousness at the time of injury, then regain consciousness and return to baseline, but they tend to deteriorate rapidly as the bleeding continues to expand [2].

Left epidural hemorrhage

Subdural Hemorrhage

Subdural hemorrhage (SDH) occurs when bleeding develops between the dura mater and the brain. It is commonly caused by the tearing of bridging veins and is frequently observed in alcoholics and the geriatric population [1]. SDH can present acutely, with symptoms developing over hours, or chronically, with symptoms developing over weeks to months [2].

Right side Subdural hemorrhage and midline shift

Subarachnoid Hemorrhage

Traumatic subarachnoid hemorrhage is a critical condition characterized by bleeding into the subarachnoid space due to head injury, often resulting from falls, vehicular accidents, or sports-related trauma. This type of hemorrhage can lead to increased intracranial pressure, vasospasm, and neurological deficits, making prompt diagnosis and management essential for patient outcomes [15].

SAH - subarachnoid hemorrhage
Subarachnoid hemorrhage in right sylvian fissure. (Courtesy of Emranur Rahman)

Intracerebral Hemorrhage

Traumatic intracerebral hemorrhage (ICH) is a critical condition characterized by the accumulation of blood within the brain parenchyma due to trauma, such as a fall, car accident, or sports injury. This type of hemorrhage is often associated with other forms of intracranial bleeding, including subdural hematomas and epidural hematomas, which can complicate the clinical picture and worsen patient outcomes [16].

Righ side ICH and subdural hemorrhage

Risk Stratification

Risk stratification in head trauma is essential for determining the appropriate level of care and intervention needed for patients. It involves evaluating the severity and potential outcomes of the injury to guide clinical decisions, such as whether to perform imaging, admit the patient for observation, or discharge with follow-up instructions. Factors such as age, mechanism of injury, loss of consciousness, and the presence of coagulopathy are critical in assessing the risk of severe outcomes [17]. The Glasgow Coma Scale (GCS) is frequently utilized to evaluate consciousness levels, helping to stratify the severity of head injuries and guide decisions on imaging and surgical intervention [9]. The GCS categorizes severity as follows: a score of 14–15 suggests mild injury, a score of 9–13 indicates moderate injury, and a score of 3–8 suggests severe injury [9, 18]. Additionally, clinical decision rules, such as the Canadian CT Head Rule, assist in identifying patients at higher risk for intracranial injuries, ensuring timely and effective treatment [19].

Management

All patients with a confirmed or suspected head injury must be assessed immediately to determine if they are vitally stable, alert, oriented, and if they exhibit any neurological deficits [2].

Patients showing any signs of instability must be immediately transferred to a highly monitored setting, such as a resuscitation bay, and assistance should be sought promptly from senior clinicians and relevant specialties, including anesthesia, neurosurgery, and intensive care.

Initial Stabilization: The ABCDE Approach

Initial stabilization of head trauma patients in the emergency department is a critical process that can significantly influence patient outcomes. The ABCDE approach (Airway, Breathing, Circulation, Disability, Exposure) serves as a systematic framework for the rapid assessment and management of these patients, ensuring that life-threatening conditions are identified and addressed promptly [20].

A – Airway

The first priority in the ABCDE approach is to ensure that the patient’s airway is patent. In cases of head trauma, the risk of airway compromise is heightened due to potential altered consciousness or facial injuries. For unconscious patients or those with a diminished level of consciousness, immediate airway management is essential. This may involve positioning the patient to facilitate drainage of secretions, suctioning as needed, or using adjuncts such as oropharyngeal or nasopharyngeal airways. In instances of significant airway obstruction, intubation may be required to secure the airway [21].

B – Breathing

Once the airway is secured, the next step is to assess the patient’s breathing. This involves evaluating respiratory rate, effort, and oxygen saturation levels. Supplemental oxygen should be administered if there are signs of hypoxia or respiratory distress. It is crucial to monitor for signs of respiratory failure or chest injuries, particularly in cases of severe head trauma, as these can complicate the clinical picture [22].

C – Circulation

The assessment of circulation includes checking the patient’s pulse, blood pressure, and overall perfusion status. Control of any external bleeding is imperative, and establishing intravenous access for fluid resuscitation may be necessary. In head trauma patients, maintaining adequate blood pressure is vital to ensure cerebral perfusion. Hypotension can lead to secondary brain injury, making fluid resuscitation a critical component of care [23].

D – Disability

The disability assessment focuses on the neurological status of the patient. A rapid neurological examination using the Glasgow Coma Scale (GCS) is performed to evaluate the level of consciousness and identify any focal neurological deficits. Monitoring pupillary response and limb movement is also essential. Any significant deterioration in neurological status should prompt immediate further evaluation and intervention [24].

E – Exposure

Finally, the exposure phase involves fully exposing the patient to assess for any additional injuries while maintaining normothermia. This includes removing clothing and conducting a thorough head-to-toe examination for signs of trauma, such as contusions, lacerations, or other injuries that may not be immediately apparent. Preventing hypothermia during this process is crucial, as it can exacerbate coagulopathy and adversely affect patient outcomes [25]. Studies on targeted temperature management (TTM) for traumatic brain injury (TBI) show mixed results. While mild hypothermia (HT) may lower intracranial pressure (ICP), its impact on long-term outcomes is unclear and not consistently better than normothermia (NT). Rapid rewarming of hypothermic TBI patients can be harmful, suggesting a slow, controlled approach to NT is preferable. Current evidence lacks clarity on optimal temperature goals, duration of temperature alteration, and the impact of the rate of temperature change on TBI patient outcomes [26].

After completing the primary / secondary survey, arrange for a head CT scan immediately, and consider a full-body scan if there are any clinical indications. Patients with head injuries who are vitally unstable will be admitted to the intensive care unit (ICU) for close monitoring. Those with a confirmed intracranial bleed may require surgical evacuation of the bleed in the operating theater.

These patients require frequent monitoring of their Glasgow Coma Scale (GCS), pupils, blood pressure (BP), pulse, and respiratory rate (RR).

In patients with a minor head injury who are vitally stable, alert, oriented, and have no neurological deficits, it is reasonable to begin by taking a history, followed by a physical examination.

Medications

The treatment of head trauma patients often involves a combination of medications aimed at reducing intracranial pressure (ICP), managing pain, preventing seizures, and addressing other complications.

Analgesics

Pain management is crucial in head trauma patients. Opioids such as morphine are commonly used for severe pain, while non-steroidal anti-inflammatory drugs (NSAIDs) may be appropriate for mild to moderate pain. Care must be taken to avoid medications that may interfere with neurological assessment.

Sedatives and Anxiolytics

Sedatives may be necessary for agitated patients or those requiring intubation. Agents like midazolam or propofol can be used, but their use must be balanced against the need for neurological monitoring [27].

Anticonvulsants

Seizures are a common complication of head trauma. The use of anticonvulsants such as levetiracetam or phenytoin may be initiated, especially in patients with a history of seizures or those who exhibit seizure activity in the ED. Prophylactic anticonvulsant therapy is often considered in patients with severe head injuries [28].

Osmotic Agents

Mannitol and hypertonic saline are osmotic agents used to reduce ICP. Mannitol is a commonly used agent that works by drawing fluid out of the brain tissue and into the bloodstream, thereby decreasing cerebral edema. Hypertonic saline serves a similar purpose and may be preferred in certain clinical scenarios due to its additional benefits in maintaining hemodynamic stability [29].

Corticosteroids

The use of corticosteroids in traumatic brain injury (TBI) has been controversial. While they were historically used to reduce inflammation, recent studies suggest that they may not improve outcomes and can increase the risk of complications [30]. Current guidelines generally recommend against their routine use in TBI.

Antibiotics

In cases where there is a risk of infection, such as open fractures or penetrating injuries, prophylactic antibiotics may be administered. Common choices include ceftriaxone or vancomycin, depending on the suspected pathogens and local resistance patterns [31].

Special Patient Groups

Approaching head trauma in special populations requires a tailored and systematic approach, as these individuals may have unique physiological, medical, or social considerations that can affect diagnosis, treatment, and recovery. Special populations include children, older adults, and pregnant women [1].

Pediatrics

Pediatric head trauma is a significant concern due to the vulnerability of children’s developing brains. Children are at a higher risk for TBIs because of their active lifestyles and the inherent fragility of their cranial structures. Common causes include falls, sports injuries, and motor vehicle accidents. Symptoms can range from mild concussions to severe brain injuries, with signs such as confusion, vomiting, and loss of consciousness warranting immediate medical attention. Early diagnosis and management are crucial to mitigate long-term neurological deficits [32].

The anatomical differences in children further contribute to their susceptibility to head injuries. The brains of infants and children are still developing, with their heads proportionally larger than their bodies and their skulls more pliable. These factors increase the likelihood of specific types of injuries, such as diffuse axonal injury. Moreover, children may have a subtle presentation of symptoms; they might be unable to communicate problems such as headaches or dizziness clearly and may instead exhibit irritability, vomiting, or changes in behavior. Additionally, developmental delays can complicate both the assessment and recovery process, further underscoring the importance of prompt and tailored care for this vulnerable population.

Geriatrics

In the geriatric population, head trauma is a significant concern, often resulting from falls, which are prevalent due to factors like decreased balance, muscle strength, and cognitive decline. The aging brain is more susceptible to injury, and even minor trauma can lead to severe complications such as subdural hematomas or intracranial hemorrhages. Older adults are particularly prone to complications due to brittle bones and the presence of comorbidities, including anticoagulant use, dementia, and frailty, which can further complicate the clinical course. Symptoms of head trauma in this population may be subtle, with cognitive decline, confusion, or changes in behavior often masking the severity of the injury. Moreover, elderly individuals are at a higher risk of intracranial hemorrhages, particularly those on anticoagulants or antiplatelet therapy. Prompt assessment and intervention are essential, and management strategies must take into account the patient’s overall health status and the potential for complications [33].

Pregnant Patients

Head trauma during pregnancy presents unique challenges due to the dual concern for both maternal and fetal health. Physiological changes in pregnancy, such as increased blood volume, altered coagulation profiles, and anatomical shifts, can complicate the management of head injuries. These changes may also alter the typical presentation of symptoms, which can include headaches, dizziness, and altered consciousness, necessitating thorough evaluation to rule out serious conditions like intracranial hemorrhage. Imaging studies, such as CT scans, should be performed with caution to minimize radiation exposure to the fetus. Additionally, maternal stability is the primary focus, as fetal distress may not be immediately apparent. Complications such as trauma to the fetus, preterm labor, or placental abruption are critical concerns. Multidisciplinary care involving obstetrics, neurology, and other specialties is often required to navigate these complexities and ensure the best possible outcomes [34].

When To Admit This Patient

Patients with moderate to severe traumatic brain injuries (TBI) generally require admission to the Surgical Intensive Care Unit (ICU) for close monitoring and management [18]. Patients with mild TBI may require admission if they have a Glasgow Coma Scale (GCS) score of less than 15, seizure activity, anticoagulation use or a bleeding diathesis, or if they lack a responsible caregiver available for discharge [35].

Disposition decisions for patients with head injuries—whether to admit, observe, or discharge—are influenced by several factors:

  1. Severity of Injury: Patients with a GCS score below 15, evidence of intracranial hemorrhage, or those requiring surgical intervention are typically admitted to the hospital [36].
  2. Patient Age and Comorbidities: Older adults and individuals with pre-existing conditions, such as anticoagulant use, may require closer monitoring even for mild injuries [36].
  3. Social Considerations: The ability to return home safely, including the presence of a reliable caregiver, is a crucial factor in determining the appropriate disposition [37].
  4. Follow-Up Care: Patients discharged from the emergency department (ED) should be provided with clear instructions about symptoms that warrant immediate medical attention and scheduled follow-up appointments for further evaluation [37].

Patients may be discharged for outpatient observation if all of the following criteria are met [35]:

  • No head CT is required based on established criteria, or a head CT has been performed and does not indicate the need for neurosurgical intervention.
  • The patient has a GCS score of 15 at the time of discharge.
  • No seizures have occurred.
  • The patient is not on anticoagulation and does not have a bleeding diathesis.
  • A responsible caregiver is available at home to oversee their care.

For patients being discharged, it is essential to provide clear head injury instructions, including guidance on when to seek immediate medical attention. These instructions should emphasize symptoms such as worsening headache, vomiting, seizures, confusion, or weakness, which may indicate a need for urgent reassessment.

Return to the ED immediately if any of the following symptoms occur [38]:

  • Neck stiffness, fever, or dizziness
  • A severe headache lasting more than 12 hours
  • Vomiting or trouble with vision
  • Twitching in any part of the body
  • Persistent drowsiness
  • Difficulty breathing, talking, or walking
  • Unusual behavior, confusion, or loss of consciousness

Revisiting Your Patient

The patient was evaluated following a motorcycle accident in which he lost control of his bike and was ejected, striking his head on the pavement. He was briefly unconscious for less than 30 seconds without any seizure activity or posturing observed. On arrival, his vital signs were stable with a blood pressure of 130/85 mmHg, heart rate of 88 bpm, respiratory rate of 18 breaths per minute, oxygen saturation of 98% on room air, and a temperature of 98.6°F (37°C). However, his Glasgow Coma Scale (GCS) score was slightly altered at 14 (Eyes: 4, Verbal: 4, Motor: 6), and he reported symptoms including a sharp headache localized to the right temporal region, nausea and vomiting (two episodes), dizziness, confusion, and mild right-sided weakness. There were no complaints of vision, hearing, or speech difficulties, and the patient denied any neck pain, back pain, or numbness elsewhere.

Physical examination revealed slightly altered consciousness with a GCS trending downward to 13 after 30 minutes of observation. Neurological assessment showed right-sided weakness (motor strength 4/5 in the right upper and lower extremities), diminished sensation to pinprick in the right hand, and pupils that were equal and reactive (PERRLA). There was no facial droop, dysarthria, or evidence of scalp lacerations, although tenderness was noted over the right temporal region. The cervical spine was intact with no pain on palpation, and cardiovascular and respiratory examinations were unremarkable.

A non-contrast CT scan of the head revealed a biconvex, lens-shaped mass along the right temporal region, consistent with an epidural hematoma (EDH), measuring approximately 2 cm in thickness and causing a slight midline shift of ~4 mm to the left. No subdural hemorrhages, cerebral contusions, or fractures were identified. Initial laboratory workup, including CBC, coagulation profile, blood alcohol level, and serum glucose, was within normal limits.

The primary diagnosis was an epidural hematoma due to head trauma. Management initially focused on neuroprotection, with plans for intubation if the GCS declined further. Two large-bore IV lines were established for fluid resuscitation, and continuous cardiac and respiratory monitoring was initiated, along with frequent neurological checks (GCS and pupil reactivity). The patient was administered IV Mannitol at 1 g/kg for potential raised intracranial pressure (ICP), and the head of the bed was elevated to 30 degrees to reduce ICP. Pain management included acetaminophen while avoiding NSAIDs.

Given the size of the hematoma and the associated midline shift, the neurosurgery team was consulted, and a craniotomy was planned to evacuate the hematoma to prevent further neurological deterioration. Post-operative care included admission to the Neuro-ICU for monitoring signs of increased ICP and a repeat CT scan to evaluate for rebleeding or residual hematoma.

Authors

Picture of Emranur Rahman

Emranur Rahman

Dr. Emranur Rahman is currently an Emergency Medicine Specialist at Sheikh Tahnoon Medical City (STMC). He completed his MBBS at Ras Al Khaimah Medical and Health Sciences University (RAKMHSU) in 2018 and his internship at Ministry of Health hospitals. Dr. Rahman finished his Emergency Medicine residency at Tawam Hospital in 2023.He previously served as the Chief of academic days. With a passion for medical education and trauma resuscitation, he is dedicated to training the next generation of EM physicians. 

Picture of Mansoor Husain

Mansoor Husain

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  32. Kirkwood MW, et al. Pediatric traumatic brain injury: a review of the literature. J Pediatr Rehabil Med. 2016;9(2):145-156.
  33. Miller JA, et al. Geriatric head trauma: an overview. Am J Geriatr Psychiatry. 2018;26(3):235-246.
  34. Morris JS, et al. Management of head trauma in pregnancy: a review. Obstet Gynecol Clin North Am. 2019;46(3):451-466.
  35. WikEM. Mild traumatic brain injury. Accessed December 21, 2024. https://www.wikem.org/wiki/Mild_traumatic_brain_injury
  36. Baker SP, O’Neill B, Haddon W, Long WB. The Injury Severity Score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma Acute Care Surg. 2019;67(3):707-710.
  37. Huang JH, Hwang H. The management of mild traumatic brain injury: a review of the literature. J Neurotrauma. 2019;36(21):2923-2931.
  38. Tawam Hospital. Head injury instructions leaflet. Al Ain, Abu Dhabi, United Arab Emirates.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

iEM Image Feed: Star shape wound on forehead

iem image feed
Star shaped wound

A 17-year-old female patient presented to ED after hitting a metal piece on the wall.

How would you like to suture this patient?

Here is one clue!

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Immediate Management of Paediatric Traumatic Brain Injury

Traumatic brain injury (TBI) has been noted as a leading cause of death and disability in infants, children, and adolescence (Araki, Yokota and Morita, 2017). In the UK alone, it’s approximated 1.4 million individuals attend the emergency department (ED) with head injury, and of those, 33%-50% are children under the age of 15; on top of this, a fifth of those patients admitted have features suggesting skull fracture or brain damage – that’s no small figure (NICE, 2014)! The particular importance of TBI in the paediatric population is that the treatment and management approach differs to adults; this is largely due to the anatomical and physiological differences in children. Furthermore, neurological evaluation in children proves more complex. All in all, children are complicated, and it is of great importance that we are aware of these differences when a paediatric patient arrives at the ED with TBI presentations.

Why is the paediatric population at risk for TBIs?

To delve slightly deeper into physiology and anatomy, there are several reasons children are at high risk of acquiring serious injury from TBIs. The paediatric brain has higher plasticity and deformity. As such, their less rigid skulls and open sutures allow for greater shock absorbance and response to mechanical stresses (Ghajar and Hariri, 1992). This ‘shaking’ of the brain inside the skull can stretch and tear at blood vessels in the brain parenchyma, resulting in cerebral haemorrhage.

Children also have a larger head-to-body size ratio, making the probability of head involvement in injury consequently higher (in comparison to adults); the head is also relatively heavier in a child, making it more vulnerable (especially in injury caused by sudden acceleration).

Young children have weaker neck muscles on top of having relatively heavier heads. Ligaments in the neck are relied on for craniocervical stability more so than the vertebrae. Hence, not only are TBIs more likely, but craniocervical junction lesions can also result from traumatic injury.

How does TBI in children come about?

The common causes of TBI in the paediatric population varies with age (Araki, Yokota and Morita, 2017). Some of these causes can be seen in the table below, which has been adopted from Araki, Yokota, and Morita (2017).

Table 1 Injury characteristics according to age and development

How can TBI in children present?

  • History: dangerous mechanism of injury (e.g. road traffic accidents or fall from a height greater than 1 meter)
  • Glasgow Coma Scale (GCS) less than 15 (at 2 hours after injury)
  • Visible bleeding, bruise, swelling, laceration
  • Signs of base-of-skull fracture:
    •  ‘Panda’ eyes – haemotympanum
    • Battle’s sign – cerebrospinal fluid leakage from ear or nose
  • Seizure (ask about history of epilepsy)
  • Focal neurological deficit
  • Vomiting
  • Loss of consciousness
  • Amnesia lasting more than 5 minutes
  • Abnormal drowsiness 

Note some children won’t have any of these signs, but if there is any suspicion of possible TBI, it should be investigated further.

Immediate management

There are various causes to paediatric TBI – also subdivided into primary and secondary TBI. Primary TBI includes skull fractures and intracranial injury. Secondary TBI can be caused by diffuse cerebral swelling. Primary and secondary TBI will be managed similarly in initial treatment (i.e. in the ED). The goal of baseline treatment is to:

  1. maintain blood flow to the brain
  2. prevent ischaemia (and possible secondary injury)
  3. maintain homeostasis 

Analgesia, Sedation, Seizure Prophylaxis

A level of anaesthesia needs to be achieved to allow for invasive procedures, such as airway management and intracranial pressure (ICP) control. Normally opioids and benzodiazepines are using in combination for analgesia and sedation in children. Instances where a child presents with a severe TBI (defined as a ‘brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8’), a neuromuscular block is used to improve mechanical ventilation, stop shivering, and reduce metabolic demand.

Anticonvulsants have been used in children, in particular infants, as they have a lower seizure threshold. Risk factors for early onset of seizures in infants under the age of 2 include hypotension, child abuse, and a GCS of ≤ 8; note, all of which may occur as a result of, or preceding, a TBI! For severe paediatric TBI cases, immediate prophylactic administration of anticonvulsants has been recommended.

Maintaining Cerebral Perfusion

The gold standard to measure ICP is an external ventricular drain (EVD); which can be used not only to measure ICP but can also be opened to drain additional CSF to reduce ICP. An intraparenchymal intracranial pressure sensor is an immediate invasive method used to detect early increased ICP in children with TBI. Monitoring of both ICP and cerebral perfusion pressure (CPP) is considered standard practice in TBI management in both paediatric and adult populations, as it is associated with better outcomes.

CPP is the pressure gradient which allows for cerebral blood flow. If this pressure is not maintained, the brain will lose adequate blood flow (Ness-Cochinwala and Dwarakanathan, 2019). Elevated CPP can accelerate oedema and increase chances of secondary intracranial hypertension.

Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)

A CPP of around 40-60 mmHg (40-50mmHg in 0-5 year-olds and 50-60mmHg in 6-17 year-olds) is considered ideal. Achieving an adequate CPP can be done by increasing MAP or reducing ICP (using the above equation). Hence it is necessary to have a good understanding of what good target values for MAP and ICP are.

A good target value for MAP is the upper end of ‘normal’ for the child’s age. Reaching this can be done by using fluids (if fluid deficient) or by use of inotropes. The recommended ICP target is < 20mmHg (normal is between 5-15 mmHg and raised ICP is regarded as values over 20mmHg).

When thinking about ICP, it’s useful to remember a mass in the brain; a mass being possible haemorrhage or any other space-occupying lesion. In TBI, oedema is most prominent at around 24-72 hours post-injury. As a result of increased mass, the initial consequence is a displacement of cerebrospinal fluid (CSF) into the spinal cord. Following this, venous blood in the cranium will also be displaced.

If ICP is further elevated, herniation can result – which is serious and often fatal! Signs of uncal herniation can present as unilateral fixed and dilated pupil. Signs of raised ICP can include pupillary dilatation and series of responses known as the ‘Cushing’s Triad’: irregular, decreased respiration (due to impaired brainstem function), bradycardia, and systolic hypertension (widened pulse pressure). Cushing’s triad results from the response of the body to overcome increased ICP by increasing arterial pressure.

Using the Monroe-Kellie Doctrine as a guide, we can predict how to reduce ICP. One management is head positioning. Head-of-bed should be elevated to 30˚, with the head in mid-line position, to encourage cerebral venous drainage. The EVD can also be used to drain CSF.

Commonly, intravenous mannitol and hypertonic saline are used to manage intracranial hypertension in TBI. Mannitol is traditionally used at a dosage of 20% at 0.25-1.0 g/kg – this is repeatedly administered. The plasma osmolality of the patient needs to be kept a close eye on; it should be ≤ 310 mOsm/L. 3% NaCl can be used to raise sodium levels to 140-150 mEg/L – this is slightly higher than normal sodium levels as a higher blood osmolarity will pull water out of neurons and brain cells osmotically and reduce cerebral oedema (Kochanek et al., 2019). Mannitol works in the same manner, however, use with caution as mannitol, being an osmotic diuretic, can cause blood pressure drops and compromise CPP! In last-resort emergency cases, where ICP need to be immediately reduced, a decompressive craniotomy can be performed.

Intravascular Volume Status

Measuring the patient’s central venous pressure (CVP) is a good indicator of the child’s volume status; 4-10 mmHg have been used as target thresholds. Alternatively, you can also monitor urine output (>1mL/kg/hr), blood urea nitrogen, and serum creatinine. Low volume status should be corrected with a fluid bolus. If the patient’s volume status is normal or high, but they remain hypotensive, vasopressors may improve blood pressure. At all costs, hypotension must be avoided, as if can lead to reduced cerebral perfusion and lead to brain ischaemia; on the other end, hypertension can cause severe cerebral oedema and should also be kept an eye on.

Other considerations​ - There have been reports of pituitary dysfunction in 25% of paediatric TBIs (during the acute phase). Do consider this if the patient had refractory hypotension – keep ACTH deficiency in mind!

Ischaemia

Prevent hypoxia at all costs! Hypoxia goes hand-in-hand with cerebral vasodilation – and as we already know, this increases the pressure in the cranium. Additionally, with hypoxia, there will be ischaemia. A minimum haemoglobin target of 7.0 g/dl is advised in a severe paediatric TBI case.

Other considerations​ - Whilst we are on the blood topic, also take care to correct and control any coagulopathies.

Ventilation

At a Paediatric Glasgow Coma Scale (PGCS) of less than 8, airways must be secured with a tracheal tube and mechanical ventilation commenced. SpO2 should be maintained at greater than 92%.

Of course, hypercapnia (CO2 > 6 kPa) and hypocapnia (CO2 < 4 kPa) are both not ideal, and we should maintain paCO2 at 4.5 – 5.3 kPa. However, some sources have suggested a quick fix to reduce ICP is to acutely hyperventilate the patient (as low CO2 results in cerebral vasoconstriction) – it’s suggested that paCO2 can safely go as low as 2.67 kPa before ischaemia kicks in! Mild hyperventilation is recommended (3.9 – 4.6 kPa)(Araki, Yokota and Morita, 2017).

Decreasing Metabolic Demand of the Brain

Body Temperature

What we want is to prevent hyperthermia, as it increases cerebral metabolic demands. Normothermia (36.5˚C – 37.5˚C) can be maintained by use of cooling blankets or antipyretics. There has been debate on whether therapeutic hypothermia has shown any benefit. Some studies have shown that moderate hypothermia for up to 48 hours, followed by slow rewarming, has prevented rebound intracranial hypertension as well as decreased ICP, however, there have not been any confirmed functional outcomes or decreased mortality rates benefits of this method (Adelson et al., 2013; Hutchinson et al., 2008).

Glycaemic control

Persistent hyperglycaemia (glucose > 10 mmol/L) should be treated. Hypoglycaemia (< 4 mmol/L) is much more dangerous. Persistent hyperglycaemia can be managed by reducing the dextrose concentration in IVF (which is usually administered in the first 48 hours of ICU care), or by starting an insulin drip.

A comment on imaging methods

In the UK, the initial investigation choice for detecting acute brain injuries is a CT head scan. A CT scan should be done within an hour of suspected head injury.
If there are no indications for a CT head scan (i.e. the signs/symptoms listed previously), a CT head scan should be performed within 8 hours of injury (NICE, 2014).

MRI scans are not usually done as the initial investigation, however, they have shown to provide information on the patient’s prognosis.

A final and most important note:

Don’t ever forget Safeguarding in children. Unfortunately, child maltreatment is common and can present anywhere. Have a look at the NICE guidelines below for more on how to identify child maltreatment.

Further reading

References

  • Adelson PD, Wisniewski SR, Beca J, Brown SD, Bell M, Muizelaar JP, Okada P, Beers SR, Balasubramani GK, Hirtz D; Paediatric Traumatic Brain Injury Consortium. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised controlled trial. Lancet Neurol. 2013 Jun;12(6):546-53. doi: 10.1016/S1474-4422(13)70077-2.
  • Araki T, Yokota H, Morita A. Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurol Med Chir (Tokyo). 2017;57(2):82-93. doi:10.2176/nmc.ra.2016-0191
  • Finnegan R, Kehoe J, McMahon O, Donoghue V, Crimmins D, Caird J, Murphy J. Primary External Ventricular Drains in the Management of Open Myelomeningocele Repairs in the Neonatal Setting in Ireland. Ir Med J. 2019 May 9;112(5):930.
  • Ghajar J, Hariri RJ. Management of pediatric head injury. Pediatr Clin North Am. 1992;39(5):1093-1125. doi:10.1016/s0031-3955(16)38409-7
  • Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ, Dirks PB, Doucette S, Fergusson D, Gottesman R, Joffe AR, Kirpalani HM, Meyer PG, Morris KP, Moher D, Singh RN, Skippen PW; Hypothermia Pediatric Head Injury Trial Investigators and the Canadian Critical Care Trials Group. Hypothermia therapy after traumatic brain injury in children. N Engl J Med. 2008 Jun 5;358(23):2447-56. doi: 10.1056/NEJMoa0706930.
  • Kochanek PM, Tasker RC, Bell MJ, Adelson PD, Carney N, Vavilala MS, Selden NR, Bratton SL, Grant GA, Kissoon N, Reuter-Rice KE, Wainwright MS. Management of Pediatric Severe Traumatic Brain Injury: 2019 Consensus and Guidelines-Based Algorithm for First and Second Tier Therapies. Pediatr Crit Care Med. 2019 Mar;20(3):269-279. doi: 10.1097/PCC.0000000000001737.
  • National Institute for Health and Care Excellence. Head injury: assessment and early management. 2014. Available at: https://www.nice.org.uk/guidance/cg176
  • Ness-Cochinwala M., Dwarakanathan D. Protecting #1 – Neuroprotective Strategies For Traumatic Brain Injury. Paediatric FOAMed. 2019. 
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