Author: Nadine Schottler, Great Britain

Intercalating student (following 3rd year of medical school) at QMUL. President of Emergency Medicine Society at QMUL (BLPEMS). Contributed in creating a Pan-London Medical Schools’ EM symposium and enthusiastic in increasing the exposure our students have to the ED – through talks, events, courses, and shadowing shifts. Love getting involved in research and educational events in my free time.

A Simplified Guide into Emergency Medicine – UK

A Simplified Guide into Emergency Medicine
~ Nadine Schottler, Great Britain ~ Leave a comment

The great thing about going into emergency medicine (EM) is that it allows entry into the program at various points of your career. So whether you know right off the bat following your two foundations years or whether it takes you a couple of years to make a choice, there is a straight pathway into the speciality (give or take a bit more competition!).

Acute care common stem (ACCS)

The most common entry route into emergency medicine from your foundation years is through the Acute care common stem (ACCS). This will be a 3-year training program and so becomes your CT1-3 years. This will comprise four six-month rotations in Intensive care medicine (ICM), emergency medicine (EM), anesthesia, and acute medicine (AM). Following this, there will be a one-year focus on EM and pediatric emergency medicine (PEM). In terms of examinations, the major ones that need to be completed are the MCEM Part A before the CT3 year and the MCEM Parts B and C before progressing to higher specialty training (ST4).

Defined route of entry into EM training (DRE-EM)

If one doesn’t do the ACCS and decides they want to enter EM in their ST3 year, this can be done view the DRE-EM. For the two years before entry into the DRE-EM at ST3, you need to have a minimum of 2 years of experience in substantive EM posts (which exclude any done during your foundation years). In addition, one of these posts needs to have been in the UK in the previous four years. Examples of such posts could be a core trainee level in an ACCS specialty (anesthesia, EM, ICM, AM), which at the end of the pathway would give you a Certificate of Completion of Training (CCT), or in core surgical training, which would give you a Certificate of Eligibility for Specialist Registration by the combined program route (CESR CP). Your ST3 year following acceptance into the DRE-EM can take 18 to 24 months, depending on how quickly competencies are met to enter ST4. 
 
Before entry into their ST4 years, trainees will be required to have completed the EM specialty-specific examinations before progressing into ST4:
• MCEM Part A or MRCS (Latter for DRE-EM trainees only) 
• MCEM Parts B and C
 
At the end of this training, all trainees will be required to complete the FCEM exit example before their awarded their CCT.  

Higher Specialty training (HST) in EM

This is one of the pathways into EM that can be taken following CT3/ST3. Entry at this point is by a selection through a national recruitment process. From this point, HST trainees can also apply for subspecialty training posts, such as PEM or prehospital emergency medicine. This training post doesn’t have to be full-time (i.e., done over two years instead of one year).

This simplified pathway can be seen in the figure below.

However, your route into EM isn’t always straightforward; you might be considering taking a detour, so it’s important to remember that there are backways into EM as well, and not everything will have been covered here! So make sure to check out the ACCS 2021 curriculum guide or the RCEM website for more details.

Further Reading

Cite this article as: Nadine Schottler, Great Britain, "A Simplified Guide into Emergency Medicine – UK," in International Emergency Medicine Education Project, November 8, 2021, https://iem-student.org/2021/11/08/a-simplified-guide-into-emergency-medicine-uk/, date accessed: January 17, 2022

Infectious mononucleosis

Infectious mononucleosis
~ Nadine Schottler, Great Britain ~ Leave a comment

Case Presentation

A 16-year-old boy presents to A&E with a fever, an extremely sore throat, and a recent blotchy rash on his back that has been concerning him. He complains of feeling extremely tired and lethargic for the past two weeks. He denies having recently been in contact with anyone ill and confirms that he is up-to-date with his vaccinations. He mentions a visit with his local GP last week, where his doctor prescribed a dose of amoxicillin for a suspected throat infection. He has no other significant medical history. Upon further examination, his pharynx and tonsils appear inflamed with whitewash exudate and he has swollen neck lymph nodes in both the anterior and posterior triangles of the neck.

What is/are the most appropriate next step(s) in the patient’s management?

  • A) Reassure the patient and discharge
  • B) Perform a throat swab
  • C) Arrange a full blood count and a monospot test
  • D) Arrange a rapid antigen test for group A streptococcus

The answer is c) Arrange a full blood count and a monospot test

What is Glandular Fever?

Infectious mononucleosis, also known as glandular fever, is an infection resulting most commonly (80-90%) from an Epstein-Barr virus (EBV). About 95% of adults in the world have been infected with EBV; however, it is rare for it to progress into glandular fever. Glandular fever is most commonly seen in individuals aged 15-24, but can present in all age groups. The prevalence of glandular fever is estimated to be between 5-48 cases per 1000 persons. Glandular fever is rather rate in those under 10 or older than 30 (1/1000 persons), so it may not need to be in your top differentials in those age groups! In young adults, the likelihood of developing glandular fever from a primary EBV infection is about 50%; in older adults the chances of EBV infection progressing to glandular fever is slim.

For the most part, glandular fever is not contagious. It’s mostly spread through contact with saliva; such as by kissing, sharing food, or children putting things in their mouths. It can also be spread through sexual contact. Luckily, in most occurrences, glandular fever is self-limiting and lasts two to four weeks. The most common lasting effect is fatigue, which can continue from weeks to months.

When Should You Suspect Glandular Fever?

The classic ‘triad’ of symptoms for glandular fever are: 

  • Fever
  • Lymphadenopathy
  • Pharyngitis (‘sore throat’)

Bilateral posterior cervical lymphadenopathy is typical for glandular fever. Tonsils may also be enlarged, and exudate on the tonsils is described as ‘whitewash’. 

Additional signs and symptoms that could include:

  • Prodromal symptoms: 
    • Fatigue, chills, myalgia, headache
  • Palatal petechiae
    • 1-2mm in diameter and lasting 3-4 days
  • Abdominal pains 
  • Nausea and vomiting 
  • Non-specific rash
    • In this case, the patient had a maculopapular rash which is associated with EBV infection. It can be caused by the infection directly but more commonly presents after being treat with amoxicillin; patients should not take penicillin antibiotics when they have infectious mononucleosis. 
  • Splenomegaly 

If you see, or the patient tells you, of any of the following symptoms during their visit to the emergency department, it requires hospitalization! 

  • Difficulty swallowing 
  • Difficulty breathing 
  • Severe stomach/abdominal pain

These may suggest malignancy. Difficulty swallowing and breathing are most often due to inflamed tonsils and may require steroids. Severe stomach/abdominal pain might suggest a ruptured spleen. Refer to your local guidelines for investigation and treatment if these symptoms present. 

Differential Diagnoses

Viral pharyngitis

  • This is the most common alternative diagnoses
  • Viral pharyngitis tends to be more erythematous 
  • Exudate is not common with viral pharyngitis

Bacterial tonsillitis

  • Bacterial tonsillitis is more commonly described as having ‘speckled’ exudate on tonsils, compared to the ‘whitewash’ exudate on tonsils in glandular fever
  • Lymphadenopathy is usually limited to the upper anterior cervical chain, where in glandular fever, lymphadenopathy can be commonly seen in both anterior and posterior triangles

Other differentials could include other causes of lymphadenopathy, such as inflammation/infection, lymphoma, or leukemia. Alternative viral infections should also be considered (e.g. cytomegalovirus, acute toxoplasmosis, acute viral hepatitis, inter alia). 

Investigations If Glandular Fever Is Suspected

In children younger than 12, or a person who is immunocompromised, a blood test for EBV viral serology should be arranged (if the patient has been ill for seven days). 

In individuals older than 12, a full blood count with differential white cell count and a monospot test should be arranged in their second week of illness. Glandular fever is likely if:

  • The monospot test is positive
  • The full blood count has more than 20% atypical lymphocytes 

OR

More than 10% atypical lymphocytes and the lymphocyte count is more than 50% of the total white cell count.

Treatment

The patient only needs to be hospitalized if they have stridor, difficulty swallowing, are dehydrated, or there is a chance of potentially serious complications (such as a splenic rupture). Steroids should only be used if the patient shows to have difficulty breathing, otherwise, management should be conservative. If the patient doesn’t have any of these concerning signs, it is appropriate to advise the patient of their illness and discharge them for follow-up with their GP.

Some Recommendations To Patients

Some things you can advise the patient on for self-management of glandular fever include:

  • Symptoms usually only last 2-4 weeks 
  • Fatigue may be the last symptom to resolve
  • Relieve symptoms of pain and fever with paracetamol or ibuprofen
  • Encouraging normal daily routines and that exclusion from work or school is not necessary
  • Spreading of disease can be limited by avoiding kissing and not sharing eating utensils
  • They should return to the hospital if they suspect any serious complications (such increased difficulty to breath/swallow, or severe abdominal pain)

References and Further Reading

Cite this article as: Nadine Schottler, Great Britain, "Infectious mononucleosis," in International Emergency Medicine Education Project, August 16, 2021, https://iem-student.org/2021/08/16/infectious-mononucleosis/, date accessed: January 17, 2022

Recognising Child Maltreatment and Steps to Safeguarding Children and Young People in the Emergency Department

recognizing child maltreatment
~ Nadine Schottler, Great Britain ~ Leave a comment

Safeguarding Children and Young People

In the busy and stressful environment of the emergency department (ED), it is often easy for us to miss the inexplicit signs or calls for help from children and young people! When looking at it from a broader view, the paediatric population is sometimes a part of the category of vulnerable patients who cannot ask for help, and may at times not realise they need it. Of the millions of children that pay visits to the ED a year, some present with non-accidental or non-intentional illnesses that had been brought upon by abuse or neglect. The ED can often be the first contact these children have with healthcare professionals, making it imperative that we notice the faint signs of maltreatment that may direct us towards acting for their protection.

The term safeguarding, as described by the government document, Working Together, encompasses the act of protecting children and young people from maltreatment, ensuring children and young people are growing up in a safe and healthy environment, and ensuring the best outcomes for all children and young people.

Who’s at Risk?

Parental issues, including alcohol/substance misuse, mental health problems, and domestic abuse, can indicate an unsafe environment for children. Additionally, poverty, poor housing, poor relationships with carers/parents, and a lack of support for the child can increase the risk of child maltreatment. Babies and disabled children are at an even greater risk of physical abuse.

Whose Responsibility is it to Protect and Safeguard Children and Young People?

According to various legislations, including the Children Act 2004, all healthcare staff and organisations must respond in times of suspected child maltreatment and take effective action to safeguard and protect these children. All healthcare staff should be prepared to amend their practice into a child-focused approach if there is any recognition of the risk of abuse or neglect in a child.

All NHS Trusts will have a specifically allocated doctor or nurse for safeguarding. Make sure to know who this is; they will be your point of contact if you have any concerns on safeguarding and child protection issues! This named healthcare professional will have the expertise to advise other professionals on the appropriate action to take.

What to do if a child reveals abuse:

  • Listen attentively
  • Let them know they have done the right thing by telling you
  • Tell them it is not their fault
  • Tell them you take them seriously
  • Do not confront the alleged abuser
  • Explain what you will do next
  • Report what the child has told you as soon as possible

Recognising Maltreatment

There are many forms of maltreatment a child may suffer from, including physical, emotional and mental. Many of these signs and symptoms don’t always point towards maltreatment immediately. The background history and presentation of the child will often be key to identifying issues. However, it may be worth considering child maltreatment if you notice the following:
 
  • A child that regularly has injuries (– check their records!)
  • Previous or current involvement with Children Social Care
  • The pattern of injury doesn’t make sense or match the history/explanation
  • A delay in seeking medical help (without appropriate explanation)
  • If the parent/carer leaves with the child before they are seen at the ED
      • Although there may be credible reasons for this, the Trust was responsible for ensuring all children in their care have a safe discharge. If the child leaves without the staff having been informed, action is required to ensure their safety.
  • Child missing appointments
  • Child not being registered with a GP

Physical symptoms of abuse:

  • Bruises/Swelling
  • Burns or scalds
  • Bite marks
  • Broke or fractured bones
  • Scarring
  • Signs of poisoning (vomiting, drowsiness, seizures)
  • Difficulty breathing  (as a result of drowning, suffocation, poison)
  • Evidence of neglect (unkempt, malnourished, smelly, dirty) 

Behavioural symptoms of abuse:

  • Anti-social behaviour
  • Anxiety, depression, suicidal thoughts
  • Drug/alcohol use
  • Eating disorders
  • Aggression/Tantrums
  • Bed-wetting, insomnia
  • Problems in school (slow development)

Next Steps if Maltreatment is Suspected

When abuse is suspected, a referral to social care must be made within 24 hours (the sooner, the better). Make sure records are kept! The child will have registered with the reception staff and given their demographics, but it is important that he child’s GP and school details are in the system, as well as recording the details and relationship of the person(s) accompanying the child. Have a look through previous history/attendances for any potential indicators of reoccurring/previous child maltreatment.

To prepare for making a social care referral, first discuss the concerns with a senior staff member in the ED. Ensure some of the indicators of child maltreatment (such as those listed above) are present to support the referral decision. Consider previous information available about the child that is relevant (such as those on previous medical attendances). The child’s demographics should be known and recorded, and then contact the Local authority of the area the child normally resides to see if the child is subjected to a child protection plan or maybe previously known to children’s care services. Carry out any relevant lateral checks (GP, school nurse, etc.) Consider looking at the Trust’s local Thresholds for referral document before continuing to make the referral. If any further advice is needed, the safeguarding team can be contacted.

Children presenting with self-harm or suicidal issues
Children (ages 0-16) should be referred to a paediatrician/child psychiatrist if they present with thoughts or acts of self-harm or suicide. Trust guidelines on dealing with self-harm in children 16 years and under are available at your local Trust, as well as by NICE guidelines. All children (aged 0-18) presenting with substance misuse issues or emotional issues should be further referred to CAMHS.

Upon discharge, all children should be given the appropriate resources within the department so they know who to contact for support or further information (this could include leaflets, phone numbers, etc.)

Safeguarding Children and the Data Protection Act 1998

The law permits the disclosure of confidential information when necessary to safeguard a child. Personal information (about the child or family) is confidential. Healthcare professionals are subjected to a legal duty of confidence. However, information that is relevant, pertinent, and justified in the child’s interest may be disclosed without consent.

References and Further Reading

Cite this article as: Nadine Schottler, Great Britain, "Recognising Child Maltreatment and Steps to Safeguarding Children and Young People in the Emergency Department," in International Emergency Medicine Education Project, February 3, 2021, https://iem-student.org/2021/02/03/child-maltreatment-and-safeguarding/, date accessed: January 17, 2022

Recent Blog Posts by Nadine Schottler, Great Britain

Immediate Management of Paediatric Traumatic Brain Injury

~ Nadine Schottler, Great Britain ~ Leave a comment

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. 
Cite this article as: Nadine Schottler, Great Britain, "Immediate Management of Paediatric Traumatic Brain Injury," in International Emergency Medicine Education Project, November 16, 2020, https://iem-student.org/2020/11/16/paediatric-traumatic-brain-injury/, date accessed: January 17, 2022

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