iEM Image Feed: Radius and Ulna Fracture

iem image feed radius and ulna fracture
radius and ulna fracture

Her father brought a 9-year-old girl due to deformed right extremity. He was playing at home and fell from a hight on his hand. No open wounds. No past medical and surgical. Vaccination: up to date.

Examination: radial pulse is intact. He can move the fingers but with limitation due to pain. Sensation is normal. The X-ray showed both radius and ulna fracture. The patient underwent procedural sedation with IV ketamine, and the reduction was made with ortho oncall.

Cite this article as: iEM Education Project Team, "iEM Image Feed: Radius and Ulna Fracture," in International Emergency Medicine Education Project, March 31, 2021, https://iem-student.org/2021/03/31/radius-and-ulna-fracture/, date accessed: September 25, 2021

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

recognizing child maltreatment

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: September 25, 2021

Recent Blog Posts by Nadine Schottler, Great Britain

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. 
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: September 25, 2021

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The Kawasaki Disease Enigma Continues 150 years Later

kawasaki disease

Kawasaki disease (KD), or mucocutaneous lymph nodes syndrome is an immune-mediated inflammation in the walls of medium-sized arteries throughout the body. It’s complications result in the coronary arteries expanding, heart attacks, and premature death.

As the leading cause of heart disease in North American and Japanese children, KD continues to bewilder clinicians and researchers – even in the midst of a global pandemic. Possible links to SARS-CoV2 has even stirred uneasiness in patients, and physicians making diagnoses.

Beginning in Victorian-era England, a young boy presented to the doctor’s office with symptoms suggestive of scarlet fever; however, noticing heart disease in this child was just baffling. Despite being unaware of this rare disease, it was beyond physicians at the time; since then, progress has been limited as clinicians still fail to comprehend the disease’s root cause.

Dating back to 1874, KD was discovered by Samuel Gee while he was dissecting the cadaver of a seven-year-old boy.

He noticed something strange, “The pericardium was natural. The heart natural in size, and the valves healthy. The coronary arteries were dilated into aneurysms at three places, namely, at the apex of the heart a small aneurysm the size of a pea; at the base of the right ventricle, close to the tip of the right auricular appendix, and near to the mouth of one of the coronary arteries, another aneurysm of the same size; and at the back of the heart, at the base of the ventricles, and in the sulcus between the ventricles, a third aneurysm the size of a horse bean. These aneurysms contained small recent clots, quite loose. The aorta near the valves, and the aortic cusp of the mitral valve, presented specks of atheroma.

From his autopsy, evident was that Gee found aneurysms in the coronary arteries running across the surface of the boy’s heart. He then placed the specimen in a jar and provided it to the Barts Pathology Museum in London. Little did he know, that his specimen marked evidence of the earliest recorded case of KD and sparked worldwide medical curiosity. Unfortunately, when physicians 100 years later were hoping to retrieve samples from the specimen containing the boy’s heart, they were informed that it was missing.

A few years later, the disease was recognized in 1967 by the Japanese physician, Tomikasu Kawasaki. Although some researchers claimed the virus was unknown, others stated KD resulted from a bacterial or fungal toxin. The windborne theory suggested that the disease was seasonal, and as such, the direction of the swaying wind played a role in infection. Others stated that since children’s immune systems are still developing and since they have just lost the protective antibodies from their mothers, they are susceptible to infection. Therefore, in Asian American household’s diets rich in soy put Asian children at greater risk due to the isoflavones. In the 1980s, the Center for Disease Control and Prevention (CDC) suspected chemicals as the cause of KD, inferring that disease stems from agents that trigger an overreaction of the patient’s immune system. No one knew exactly what the mechanism or cause of KD was, although many scientists speculated some theories.

Over the last decade, significant progress toward understanding the pathogenesis, history, and therapeutic interventions of KD has been fruitful. Treatment aimed at the intravenous infusion of gamma globulin antibodies derived from the plasma of blood donations has helped children recover. In contrast, other therapies of corticosteroids for immunoglobulin-resistant patients and tumor inhibitors such as etanercept, infliximab, and cyclosporin A have been other medications providing relief.

The most significant clinical debate was over the possible link between the rash and the cardiac complications seen in Asian American children. Factors responsible for KD were introduced into Japan after World War II and re-emerged in a more virulent form spreading through the industrialized Western world. Advancements in medicine, improvements in healthcare, and, notably, the use of antibiotics reduced the burden of rash and fever illnesses significantly allowing KD to be recognized as a distinct clinical entity.

Nonetheless, the enigma pervades even during the COVID19 pandemic; this time, more pressing as the ever-elusive cause of KD that troubles children’s hearts affects physicians’ sleep and worries parents’ minds. Although the story of Kawasaki disease began decades ago when a young boy’s heart was locked inside a glass specimen, its ending is still being crafted. By the time the heart is found again at the museum, and placed safely for visitors treasuring ancient history, what further knowledge and progress will the scientific community have achieved? How far will humanity have come to find answers to KD and fill in the perplexing missing piece of the puzzle?

For now, there are no answers, but the enigma continues…

Cite this article as: Leah Sarah Peer, Canada, "The Kawasaki Disease Enigma Continues 150 years Later," in International Emergency Medicine Education Project, July 24, 2020, https://iem-student.org/2020/07/24/kawasaki-disease-enigma-continues/, date accessed: September 25, 2021

References and Further Reading

The Pediatric patient in the ED: Peculiar and Paramount

The Pediatric patient in the ED

Children are not young adults!

This was the opening speech of the first Pediatrics lecture in my medical school.
As Emergency Physicians, we deal with everything and everyone at the same time; in some instances, the segmentation between types of patients blurs. The pediatric patient in the middle might be a challenge if you are not working in an independent Pediatrics Emergency Department.

In some situations, you will have to make decisions by conscious contemplation rather than pattern matching, which we mostly depend on in our approach.

Having had the privilege of working in an independent Pediatrics ED, I realized how much easier decision making becomes when you have a set of mind prepared to deal with a child.

Health problems for children differ from those of adults. A child’s response to disease and stress varies with age and development; therefore, it’s fundamental to approach children in a way that identifies and tackles the differences.

child response to disease

Judge by appearance

We use heuristics frequently in our practice, perhaps the most popular among which is the (sick/not sick) paradigm. When it comes to children, appearance is of particular importance.

The look might be deceptive in adults, but it’s not the case in children; as they say, the eyes don’t lie, but it can be lied to.

For its virtual implication, appearance represents the first component of the Pediatrics assessment triangle, our quick and orderly assessment tool for children.

Power and authority

Children can’t consent or advocate for themselves, a parent or legal guardian approval is required to deliver health care. The most notable exception to this is the emergency situation, in which consent is not required, and care can be delivered if parents are not present and even against their wishes. The emergency situation gives the emergency physician the highest authority in decision making in children, which is a titanic responsibility.

pediatric patient in the ed

The Math geek

Dosing for most medications in children is weight dependent. It might be good practice for your brain but can also represent a dilemma if you are giving verbal orders and your phone is not with you. My colleague once said I was terrible at Math; that’s why I went to medical school; I think she made a good point.

Baby shark

ED is a noisy environment, but the Pediatrics ED is on another level of noise. Other than natural sounds found in the ED and crying fussy children, you will also encounter countless children’s music and disturbing games. It might sound nihilistic and resentful, but I have to be forthright, the current children’s entertaining materials lack educational value and taste, and it needs resuscitation.

pediatric ed noise

Priceless outcome

In the end, the smile on a child’s face is one of the most satisfying experiences ever and a blessing. Establishing a rapport with a child is the key to a proper exam. Children won’t trust anything that’s not genuine, and care should be delivered with love and passion. You might also need to learn some tricks and give some treats to accomplish that, in the hope that you reach the fruitful outcome of drawing a smile on God’s angelic creatures.

Cite this article as: Israa M Salih, UAE, "The Pediatric patient in the ED: Peculiar and Paramount," in International Emergency Medicine Education Project, January 13, 2020, https://iem-student.org/2020/01/13/the-pediatric-patient-in-the-ed-peculiar-and-paramount/, date accessed: September 25, 2021

Febrile Seizures

febrile seizures

A 20 Month-Old Male

It is a busy Wednesday afternoon in your pediatric emergency department. You work at a tertiary center, so you are used to receiving transfers from other hospitals for further evaluation and management. You see a new patient on the board. It is a 20 month-old male who came in as a hospital transfer for evaluation of first-time seizure. You go to bedside to start your evaluation. Parents tell you that he had three episodes of seizures in the past 6 hours. All of them lasted for less than 15 minutes, did not require medication for cessation, one of them was described as partial-focal and two were described as generalized tonic-clonic seizures, and the patient had complete return to baseline behavior a few minutes after each episode. Mom says that the patient had his axillary temperature taken by her at home and by the staff at the outside hospital and he had no fever on these measurements. However, she did notice some runny nose in the past 24 hours. As soon as the mom tells you that information, the nurse looks at you and says that the patient’s rectal temperature is 40.1 C.

Febrile Seizures

The first-step in the management of febrile seizures is to understand its definitions. Following that, we need to appropriately classify the patient’s presentation within one of the two types of febrile seizure.

Definition

  • Age greater than six-months-old and lower than five-years-old
  • Seizure in a patient with a temperature higher than 38 C
  • No inflammation or infection of the central nervous system
  • No metabolic abnormality that may cause seizures
  • No history of afebrile seizures

Two Types of Febrile Seizures

Class Age Number of seizures in 24h Duration Type of seizure Resolution Return to baseline
Simple
6 mo to 5 yo
1
< 15 min
No focal features
No meds required
Yes
Complex
6 mo to 5 yo
> 1
> 15 min
Focal features
Med required
No return to baseline in a reasonable time

You must note that you will be able to easily identify those patients who fit the criteria for simple febrile seizures and those who fit the criteria for complex febrile seizures. However, there will be a group of patients that fill one or two criteria for complex febrile seizure, but are extremely well-appearing. We will talk more about that later on during the discussion.

Workup

Simple Febrile Seizures

The evaluation of a child with a simple febrile seizure should focus on the underlying febrile illness. In the vast majority of the cases the cause for the fever will be a viral infection that does not require further evaluation and treatment other than some acetaminophen (paracetamol), ibuprofen, and oral hydration.

However, as part of your job, you need to think outside of the box and have a broad differential diagnosis for your patient’s presentation. Make sure to rule out signs of CNS infection (altered mental status, nuchal rigidity, petechial rashes, and prolonged, focal or multiple seizures); risk factors, symptoms, and signs of systemic conditions that could be causing a seizure; and, history of afebrile seizures. Special factors that increase the risk for CNS infections and that you should consider in your evaluation are age 6 -12 months with incomplete immunization status (Haemophilus influenzae type b (Hib) or Streptococcus pneumoniae) and pre-treatment with antibiotics for another disorder (which could mask meningitis).

Complex Febrile Seizure in Ill-Appearing Child

The workup in this situation is simple. The patient has meningitis until proven otherwise. You should consider starting antibiotics immediately and obtaining a full sepsis workup including complete blood cell count, urinalysis, urine culture, blood cultures, chest x-ray, and lumbar puncture for cerebrospinal fluid analysis. In addition to the infectious work-up, the differential also includes epileptic seizures, toxic ingestion, metabolic disorders, head trauma, and intracranial hypertension.

Complex Febrile Seizure in Well-Appearing Child

Now we reached the tricky part of the discussion. There are no consensus guidelines for the workup of patients with complex febrile seizures in the well-appearing child. As stated in the simple febrile seizure section, you should consider further workup if any concerns for CNS infection, systemic conditions causing seizures, or history of afebrile seizures. You should decide which workup to perform on a case by case basis. In a perfect scenario, these cases should be evaluated in conjunction with specialist consultation (e.g. with pediatric neurology) for guidance with work-up and treatment.

Case Resolution

After you finish your assessment, you make the diagnosis of complex febrile seizure because the patient had multiple seizures in less than 24 hours and had one episode with focal features. The patient is well-appearing, is fully vaccinated, has not used antibiotics recently, returns to baseline completely soon after an episode, and has no findings concerning for CNS infection on his exam. Therefore, you think that a CNS infection is less likely. Since you are facing a case of complex febrile seizure in a well-appearing child, you consult pediatric neurology for guidance with the workup and treatment. They agree with the low likelihood of CNS infection and recommend symptomatic treatment for the patient’s likely upper respiratory infection with observation during six hours in the ED. The patient has no problems during the period of observation. You re-discuss the case with pediatric neurology and they recommend discharge home with close follow-up on their clinic for further workup of other causes of seizure. A couple days later, you check the patient’s records and find that he had a spot EEG done, which was negative for epileptiform waves, and a brain MRI performed, which was unremarkable. Patient was diagnosed with complex febrile seizure and recommended to keep follow-up with his primary care physician with no need for further follow-up with pediatric neurology.

Take-Home Points

  • Always obtain a temperature from a core source, in the ED the most feasible source is a rectal temperature
  • The differential diagnosis for febrile seizures includes CNS infections, epileptic seizures, toxic ingestion, metabolic disorders, head trauma, and intracranial hypertension
  • There is no consensus about the workup and treatment of the well-appearing patient with a complex febrile seizure

References and Further Reading

  1. Festekjian A. Seizures and Status Epilepticus in Children. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e New York, NY: McGraw-Hill; . http://accessemergencymedicine.mhmedical.com/content.aspx?bookid=2158§ionid=162271372. Accessed May 12, 2019.

  2. https://www.emrap.org/episode/kiddos/febrileseizures

  3. https://www.emrap.org/episode/c3seizuresin/seizuresin 

  4. John J Millichap. Clinical features and evaluation of febrile seizures. Mar 25, 2019. https://www.uptodate.com/contents/clinical-features-and-evaluation-of-febrile-seizures?source=history_widget

Cite this article as: Henrique Puls, Brasil, "Febrile Seizures," in International Emergency Medicine Education Project, September 9, 2019, https://iem-student.org/2019/09/09/febrile-seizures/, date accessed: September 25, 2021

Toxicology Pearls – Active Charcoal – Infographic

toxicology pearls - active charcoal

Activated Charcoal Application

Emergency Indications

  • Oral intake < 60 minutes
  • the life-threatening dose of the toxic substance

Multi-Dose Activated Charcoal (MDAC) Indications

  • Life-Threatening Oral Intake of
    • Carbamazepine
    • Dapsone
    • Phenobarbital
    • Quinine
    • Theophylline

Contraindications

  • For patients with compromised airway reflexes, unless they are intubated. If the critical situation of the patient indicates intubation, then, gastric lavage may be performed. Intubation, only for decontamination, is not recommended.
  • Oral intake of caustic substances
  • Late presentation
  • Increased risk and severity of aspiration associated with AC use (e.g., hydrocarbon ingestion)
  • Need for endoscopy (e.g., significant caustic ingestion)
  • Toxins poorly adsorbed by AC (e.g., metals including iron and lithium, alkali, mineral acids, alcohols)
  • Presence of intestinal obstruction (absolute contraindication) or concern for decreased peristalsis (relative contraindication)

Equipment and Patient Preparation

There is no specific equipment for activated charcoal administration. However, drinking the charcoal can be very unpleasant for many patients, especially children. Therefore, mixing with fruit juice can be an option. In addition, if necessary nasogastric or orogastric tube placement can facilitate the active charcoal treatment.

Procedure steps

  • Recommended empirical single-dose of activated charcoal is as follows:
    • <1 year – 0.5-1 g/kg or 10-25 g
    • 1-12 years – 0.5-1 g/kg or 25-50 g
    • >12 years – 1-2 g/kg or 25-100 g
By James Heilman, MD [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)], from Wikimedia Commons
By James Heilman, MD [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)], from Wikimedia Commons
  • Multidose activated charcoal
    • Give the recurrent dose of charcoal by 0.5 g/kg (≤50 g) every 4 hours
  • How to administer:
    • If the patient is awake and cooperative, AC may be given orally. Alternatively, it may be given by gastric or nasogastric tube, if these procedures are indicated.
    • Mixing the activated charcoal with fruit juices increases tolerability.
    • If the patient is unconscious or airway is compromised, gastric lavage should be done, and activated charcoal should be given after intubation. Tracheal intubation is not recommended solely in order to give activated charcoal. Only activated charcoal is to be given, the nasogastric tube is adequate and is preferred.
    • If MDAC is indicated, the gastric tube should be withdrawn after gastric lavage and the first dose of activated charcoal. Further doses should be given via nasogastric tube.

Hints and Pitfalls

  • The substances that cannot bind to activated charcoal are as follows:
    • Lithium
    • Strong acids and bases
    • Metals and inorganic minerals
    • Alcohols
    • Hydrocarbons
  • Multi-dose activated charcoal enhances elimination of (But not necessarily indicated in all)
    • Amitriptyline
    • Aspirin
    • Caffeine
    • Carbamazepine
    • Cyclosporine
    • Dapsone
    • Digoxin
    • Disopyramide
    • Nadolol
    • Phenobarbital
    • Phenytoin
    • Piroxicam
    • Quinine
    • Sotalol
    • Sustained-release thallium
    • Theophylline
    • Valproate
    • Vancomycin
  • MDAC increase the risk of constipation and bowel obstruction in some cases. Therefore, consider adding a cathartic agent to the second or third dose of AC.

Post Procedure Care and Recommendations

  • Control possible nausea and vomiting.
  • Look for traces of aspiration or gastrointestinal complications.

Complications

Complications of AC and MDAC include:

  • Constipation, diarrhea, vomiting
  • Pulmonary aspiration

Pediatric, Geriatric, and Pregnant Patient Considerations

  • In pediatric and geriatric patients, extra caution should be exercised to avoid and monitor complications.
  • Activated charcoal is considered safe for pregnant women.

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Cite this article as: iEM Education Project Team, "Toxicology Pearls – Active Charcoal – Infographic," in International Emergency Medicine Education Project, July 29, 2019, https://iem-student.org/2019/07/29/toxicology-pearls-active-charcoal-infographic/, date accessed: September 25, 2021

Pediatric Tube Sizes – Infographic

Pediatric tube sizes

Recently, Sam Ghali reminded us how important pediatric tube sizes, and how easy to calculate them. We think every medical students, interns and PGY1s should know this now. Here is his message on Twitter:

PEDIATRIC TUBE SIZES

CALCULATE  ENDOTRACHEAL TUBE (ETT) SIZE
[Age ÷ 4] + 4
There are many formulas to calculate the endotracheal tube size for kids. The given formula is one of the most common. Let’s think a six yo patient. Your ETT size is 6/4 = 1.5, and +4 = 5.5

NASOGASTRIC/OROGASTRIC TUBE OR FOLEY CATHETER SIZE
ETT x 2
NG/OG tubes and Foley catheters are measured as FRENCH. (Fr) If your ETT size is 5.5, then your NG/OG and Foley sizes will be 5.5 x 2 = 11 Fr.

HOW DEEP YOUR ETT  SHOULD BE
ETT x 3
If your calculated tube size is 5.5, your depth should be 5.5 x 3 = 16.5 cm. So, 16.5 cm mark should be seen at the level of central incisors.

CHEST TUBE SIZE
ETT x 4
If the same six yo patient needs a chest tube, your chest tube size is 5.5 x 4 = 22 Fr. By the way, this is mainly for trauma. Moreover, do not forget, smaller size tubes can work as same as big ones.

Cite this article as: iEM Education Project Team, "Pediatric Tube Sizes – Infographic," in International Emergency Medicine Education Project, July 24, 2019, https://iem-student.org/2019/07/24/pediatric-tube-sizes-infographic/, date accessed: September 25, 2021