Pediatric Seizures (2025)

by Neema Francis, Faiz Ahmad, Thiagarajan Jaiganesh

You Have A New Patient!

A 5-year-old female was brought into the ED as her parents noticed that she was not very responsive. She was diagnosed with otitis media 3 days ago and has been taking oral amoxicillin for it. This morning, she became irritable and was less active than usual. On arrival at the ED triage, the patient was tachypneic (40 bpm), tachycardic (145 bpm), and had a temperature of 39.4°C.

The image was produced by using ideogram 2.0.

The child did not respond to vocal stimuli but was opening her eyes spontaneously. She had a sluggish pupillary response to light, and she seemed unaware of her surroundings. Suddenly, the patient began seizing, with her eyes up-rolled and her hands clenched and stretched downwards.

What Do You Need To Know?

Importance

Pediatric seizures are a significant health concern due to their high incidence, diagnostic complexity, diverse causes, and potential for severe consequences. Seizures are among the most common neurological disorders in children, with approximately 4–10% experiencing at least one seizure by age 16 [1,2]. The incidence is highest in the first year of life and remains substantial throughout childhood, particularly in children under three years old [3]. Seizures can result from various causes, including fever, infections, genetic disorders, head injuries, metabolic disturbances, and structural CNS abnormalities, which often complicates diagnosis and treatment [3,4]. Prolonged seizures, such as status epilepticus lasting five minutes or more, can lead to lactic acidosis, neuronal injury, network alterations, or even neuronal death, particularly when lasting beyond 30 minutes [3]. These severe outcomes impact development, quality of life, and increase the risk of comorbidities such as intellectual disability, depression, and anxiety. Children with epilepsy face a 5–10 times higher mortality risk compared to their peers and are prone to medical complications and long-term educational and social challenges [3,5]. The condition places a significant burden on healthcare systems and induces considerable psychological stress on children and their families [6,7]. 

Epidemiology

Seizures affect up to 10% of children, with incidence rates ranging from 33.3 to 82 cases per 100,000 annually, peaking in the first year of life and declining during adolescence [6,8]. Most (94%) of children presenting to the emergency department (ED) with a first seizure are under 6 years of age [4]. Febrile seizures, the most common type in young children, affect 3–4% of all children, primarily those under five years old [5,6]. Neonatal seizures, with distinct characteristics due to brain immaturity, are a common neurological condition in newborns [9]. Key risk factors include a family history of seizures, fever, CNS infections (e.g., meningitis, viral infections), head injuries, pre-existing neurological conditions, and maternal factors such as alcohol use, smoking, and prenatal exposures [3,7].

Seizures can be symptomatic or idiopathic. Acute symptomatic seizures arise from recent events, while remote symptomatic seizures result from chronic conditions. Generalized tonic-clonic seizures are the most frequent type [4], while status epilepticus (SE), a critical condition, is often triggered by fever or CNS infections in children [3]. Genetic factors, metabolic disorders, electrolyte imbalances, and structural brain abnormalities are recognized as key causes [6]. Mortality in pediatric epilepsy is 2–4 times higher than the general population and significantly elevated in children with neurological comorbidities, with sudden unexpected death in epilepsy (SUDEP) as a leading cause [3]. Febrile seizures are often benign, but complex febrile seizures may increase the risk of future epilepsy [2,6]. 

Pathophysiology

The pathophysiology of pediatric seizures involves complex interactions of neuronal excitation and inhibition in the brain, influenced by age, developmental stage, and underlying conditions [9]. Seizures arise from abnormal, excessive, and synchronous neuronal activity, leading to transient signs and symptoms such as involuntary muscle activity [3,9]. This activity stems from an imbalance between excitatory and inhibitory neurotransmission.

Basic Mechanisms of Seizures

The primary mechanism behind seizures involves either a deficit in neuronal inhibition or an excess of excitatory stimuli. The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) plays a crucial role. In mature brains, GABA inhibits neuronal firing, maintaining balance in the central nervous system [3]. However, in neonatal brains, the immature GABA system can paradoxically cause excitation, making neonates more susceptible to seizures [9]. Additionally, alterations in GABA function, such as receptor dysfunction, can lead to prolonged and high-intensity neuronal stimulation, further increasing excitability. Voltage-gated ion channels and excitatory neurotransmitters like glutamate also contribute to seizure generation. Glutamate receptors, such as NMDA and AMPA, are primary excitatory receptors in the CNS and are involved in seizure propagation.

Age-Related Factors and Neuronal Imbalance

The immature state of the neonatal brain predisposes it to seizures due to developmental differences. In early life, the formation of excitatory synapses occurs before the development of inhibitory synapses, contributing to an imbalance in neuronal activity [7,9]. Additionally, the GABA receptor in neonates can cause depolarization rather than hyperpolarization, further enhancing neuronal excitability. Ion channel imbalances, especially the premature maturation of channels involved in depolarization, exacerbate this vulnerability [7].

Specific Factors Contributing to Seizures

Several specific factors influence seizure pathophysiology:

  1. Genetic Factors: Mutations in genes regulating synapse development, ion transport, protein phosphorylation, and gene transcription can disrupt neuronal activity [7].
  2. Metabolic Disturbances: Conditions like hypoglycemia, hypocalcemia, hyponatremia, and other metabolic imbalances impair neuronal function, triggering seizures [2,3].
  3. Hypoxic Conditions: Perinatal asphyxia and hypoxic-ischemic encephalopathy damage brain cells, increasing seizure risk [2,6,7].
  4. Infections: CNS infections such as meningitis and encephalitis disrupt normal brain function, leading to seizures [2,4,10].
  5. Structural Abnormalities: Malformations of cortical development and acquired lesions alter neuronal networks, predisposing to seizures [2,9].
  6. Fever: Although the exact mechanism is unclear, fever lowers the seizure threshold in some children, particularly those prone to febrile seizures [2]. In febrile seizures, inflammatory mediators such as IL-1 have been shown to increase neuronal stimulation. Animal models and preliminary studies suggest that these mediators play a role in seizure pathophysiology, although the clinical significance remains under investigation.

Medical History

A detailed history is crucial for accurately diagnosing and managing seizures in children. The history should focus on the events immediately preceding the seizure, the seizure itself, and the period following the seizure. It is important to obtain information from the child (when possible) and any witnesses [2]. When taking a medical history for pediatric seizures in the emergency department, it is important to gather information about the following key features [2,3,7-9,11,12]:

1. History of Present Illness:

  • Onset and duration of seizures: This information helps determine the type and underlying cause of the seizure. Note how the event began, including any preceding aura. An aura is a subjective sensation or experience that may precede a seizure [2,9].
  • Precipitating factors: Certain triggers, such as sleep deprivation, fever, trauma, or stress, can increase the likelihood of seizures in some children [2,4,7].
  • Description of the seizure: A detailed description of the seizure (e.g., focal or generalized) is crucial, including the child’s behavior, movements, and any changes in consciousness. Any evidence of partial (focal) onset, such as twitching or jerking on one side of the body, should also be noted [2]. It is also important to note if the child experienced incontinence during the seizure. It’s important to gather information about the postictal period including the length of the period, and any focal neurologic deficits, such as weakness or confusion, that may be present after the seizure. Also important is whether the child was able to easily fall back asleep after the seizure.
  • Current symptoms and vital signs: Assess the child’s current symptoms, vital signs, and whether they have recovered from the seizure or not.

2. Past Medical History:

  • Developmental and medical history: Information about the child’s developmental milestones and any previous medical conditions or treatments is important in identifying potential causes of seizures [6].
  • Immunization status: Some seizures are related to diseases that are preventable by vaccination, so it’s important to inquire about the child’s immunization history.
  • Previous seizures: This may indicate an underlying neurological condition or epilepsy. 
  • Previous treatment for seizures: Determine whether the child has received prior treatment for seizures, including medications, and if these treatments were effective [2].

3. Medication History:

  • Assess whether the child is taking any medications that can lower the seizure threshold or exacerbate seizures.

4. Family History:

  • A family history of seizures or other neurological disorders may suggest a genetic predisposition.

It is important to note that seizures may sometimes occur without a clear cause. The emergency department’s priority is stabilizing the patient and preventing further seizures or complications.

Several risk factors for pediatric seizures should be considered during medical history-taking. There may be a higher likelihood of seizures occurring in children who have a familial history of seizures or epilepsy. Children born prematurely or with a low birth weight may be at an increased risk of seizures because they are more likely to have brain injuries or developmental problems. Children with neurological disorders, such as cerebral palsy, or brain injuries, such as traumatic brain injury, may also be at an increased risk of seizures because these conditions can cause abnormal electrical activity in the brain. Metabolic disorders, such as hypoglycemia or hyponatremia, are also known risk factors. Certain infections, such as meningitis or encephalitis, can cause inflammation in the brain and are thus predisposing factors for pediatric seizures. Developmental disorders, such as autism or intellectual disability, have also been identified as risk factors for pediatric seizures. Having one or more of these risk factors does not necessarily mean that a child will develop seizures, but it is essential to be aware of them to detect seizures early and initiate appropriate treatment.

As with all medical emergencies, it is important to look out for red flags. Concerns should be raised if the seizure was delayed or related to a head injury. Developmental delay or regression should be ruled out. Bleeding disorders or anticoagulation therapy are important considerations during history-taking in cases of pediatric seizures. It is also critical to rule out CNS infections as a possible cause of the seizure. Red flags in the history may include fever, headache, photophobia, vomiting, bulging fontanelles, neck stiffness, decreased consciousness, and focal neurologic symptoms.

Physical Examination

A thorough physical examination is essential when evaluating a child with a suspected seizure. It aids in identifying underlying causes, associated conditions, and guiding further diagnostic and treatment decisions. The examination should be performed in conjunction with a detailed history and adapted to the child’s clinical condition and developmental stage [7,12]. Children with seizures may have developmental delays or regression, which can indicate an underlying problem.

Initial Assessment

  1. Stabilization: If the child is actively seizing, focus on stabilizing the airway, breathing, and circulation (ABC) and stopping the seizure [2,10,12].
  2. Vital Signs [2,5,7]:
    • Temperature: Identify fever (above 38°C/100.4°F), the most common cause of seizures in children.
    • Heart Rate and Blood Pressure: Monitor for abnormalities that may indicate underlying conditions or complications.
    • Oxygen Saturation: Ensure adequate oxygenation.

General Appearance

  1. Level of Consciousness: Assess alertness and orientation. Note any altered mental status, which may suggest ongoing issues like status epilepticus or other underlying conditions [4,10].
  2. Activity Level and Responsiveness: Observe for irritability, excessive sleepiness, or signs of distress. Are they irritable? Are they playful? Are they well-kept? Look for signs of neglect or child abuse.
  3. Dysmorphic Features: Look for unusual physical features that may suggest a genetic or developmental syndrome [2].

Head and Neck Examination

  1. Head Circumference: Measure head size, especially in infants, as microcephaly can indicate an underlying condition [2,6].
  2. Signs of Trauma: Check for bruising or swelling that may suggest head injury.
  3. Fontanelles: In infants, examine the anterior fontanelle for bulging, which may indicate increased intracranial pressure.
  4. VP Shunt: Assess for ventriculoperitoneal (VP) shunt placement and any signs of malfunction or infection [2].
  5. Meningeal Signs: Look for nuchal rigidity or other signs of meningeal irritation, suggesting CNS infection [12].
  6. Eye and ear examination: Changes in pupils, papilledema, and retinal hemorrhages, or abnormal movements of the eyes that can indicate brain injury. Bulging tympanic membranes can indicate otitis media.

Skin Examination

  1. Bruising: Identify unexplained bruising, which may point to bleeding disorders or child abuse.
  2. Skin Rashes: Look for signs such as café au lait spots (indicative of neurofibromatosis), adenoma sebaceum or ash leaf spots (associated with tuberous sclerosis) [6], and port wine stains (typical of Sturge-Weber syndrome).
  3. Neurocutaneous Markers: Use a Woods lamp to detect signs of neurocutaneous syndromes.

Cardiovascular and Abdominal Examination

  1. Heart Sounds: Listen for abnormalities that may indicate a cardiac issue. Heart murmurs or arrhythmias that may be related to seizures.
  2. Abdomen: Palpate for masses or organomegaly, which may suggest a metabolic disorder. Children with metabolic disorders, such as liver or kidney disease, may have an enlarged liver or spleen, which can contribute to seizures.

Neurological Examination [2,4,12]

  1. Mental Status: Evaluate consciousness, orientation, and behavior.
  2. Cranial Nerves: Check pupillary responses, eye movements, and facial symmetry.
  3. Motor Function: Assess muscle strength, tone, symmetry, and any abnormal movements. Look for Todd’s paresis or focal weakness post-seizure.
  4. Reflexes: Evaluate deep tendon reflexes, noting asymmetry.
  5. Meningeal signs: Brudzinski’s or Kernig’s sign. Neck stiffness should also be assessed.
  6. Sensory Function: Test sensory responses, noting any deficits.
  7. Gait and Coordination: Observe gait, coordination, and balance in age-appropriate children.

Postictal Examination [6]

  1. Neurological Status: Note persistent confusion, weakness, or other deficits during the postictal phase, which may help localize the seizure origin.
  2. Symmetry: Pay close attention to symmetrical muscle tone, reflexes, and movements to identify potential focal brain issues.

Important Considerations

  1. Age-Appropriate Assessment: Adjust the neurological exam based on the child’s developmental stage, as young children may not fully cooperate [6].
  2. Clinical Context: Always interpret findings within the context of the child’s history and other clinical information [12].

Alternative Diagnoses

It is important to distinguish between true seizures and seizure mimics in the pediatric population, as the causes, treatment options, and outcomes can be quite different [14,15]. Examples of seizure mimics include vasovagal syncope, breath-holding spells, reflex anoxic seizures, arrhythmias, and non-epileptic paroxysmal events. It is helpful to look for clues in the history to rule out such mimics. A vagal reflex can be precipitated by a sudden fright or minor trauma. Temper tantrums should prompt consideration of breath-holding spells, which can lead to hypoxia and, in turn, a short tonic-clonic event with a quick recovery time. Visual and auditory changes paired with lightheadedness are suggestive of a vasovagal attack. A history of palpitations or strenuous exercise just before the event could indicate arrhythmias.

Certain symptoms can indicate a genuine seizure [14,15], including but not limited to:

  • Biting of the tongue on one side (high specificity).
  • Swift blinking of the eyes.
  • Fixed gaze with dilated pupils.
  • Repetitive lip movements.
  • Elevated heart rate and blood pressure during the episode.
  • A post-seizure phase.

Fevers are the most common cause of seizures in children [16]. Febrile convulsions can be further categorized into simple or complex febrile seizures:

  • Simple febrile seizures are generalized, last less than 15 minutes, and occur only once within a 24-hour timeframe. They are typically not associated with neurological deficits or other significant findings.
  • Complex febrile seizures last longer than 15 minutes, are focal (involving only one part of the body), or occur multiple times within a 24-hour period. While both types of febrile seizures are generally benign, complex febrile seizures require further investigation to rule out organic causes and carry a slightly higher risk of developing into epilepsy or other neurological disorders later in life.

In an afebrile child presenting with seizures, the differential diagnoses are extensive. Possible causes include:

  • Structural abnormalities in the brain, such as tumors, cysts, or malformations [16].
  • Metabolic disturbances, such as hypoglycemia, electrolyte imbalances, or trauma.

Status epilepticus is a medical emergency, defined as a seizure lasting longer than 5 minutes or recurrent seizures without regaining consciousness in between [16]. It can occur in both children and neonates and is associated with significant morbidity and mortality. Non-convulsive status epilepticus should be considered in any child with an altered mental status; it is ill-defined and remains a diagnosis of exclusion.

Neonatal seizures can be caused by a variety of factors, including hypoxic-ischemic encephalopathy, metabolic disturbances, infections, and intracranial hemorrhage [16]. Neonatal seizures can have serious consequences if left untreated, including brain damage and developmental delays.

Acing Diagnostic Testing

A bedside blood glucose level should be obtained as soon as possible to rule out hypoglycemia [4,15,17]. Venous blood gas, magnesium, and phosphorus levels are also valuable investigations to assess other electrolyte imbalances [12]. When there is concern for metabolic or respiratory disturbance, an arterial blood gas test may be considered [10]. Basic laboratory tests, including CBC, CRP, urine and blood cultures, are indicated when there is suspicion of underlying infections [2,4]. Beta HCG levels may be measured in pediatric seizures because a rare cause of seizures in children is a brain tumor called a germinoma, which secretes beta HCG. Beta HCG can be detected in blood or cerebrospinal fluid (CSF) to help confirm the diagnosis. Ammonia, Lactate, Pyruvate, if an inborn error of metabolism is suspected, these tests may be performed [2]. Antiepileptic drug  levels should be measured in children with known seizure disorders to ensure they are receiving an appropriate dose. Under-dosing can result in continued seizures, while overdosing can lead to side effects such as drowsiness, nausea, or confusion. A toxicology screen may be ordered if there is a concern for drug or alcohol use [12].

Imaging studies such as CT or MRI should be considered for children with focal seizures, persistent seizures despite acute management, or seizures in children under six months of age [4,6]. Signs of elevated intracranial pressure (ICP) also warrant imaging, especially in the context of a history of bleeding disorders or anticoagulant use. Although MRI provides superior anatomic detail, it often requires sedation, which can interfere with the patient’s assessment, making CT the preferred initial imaging study.

Lumbar puncture is recommended for infants aged 6 to 12 months who have not received adequate vaccination against H. influenzae or Streptococcus pneumoniae, or whose vaccination status is unknown, as these bacteria are common causes of bacterial meningitis in this age group [6]. Additionally, lumbar puncture should be considered in infants receiving active antibiotic therapy, as antibiotics can mask meningeal signs. Infants with focal or prolonged seizures, abnormal neurological examinations, or toxic appearance are high-risk groups in which lumbar puncture is strongly advised.

 

An electroencephalogram (EEG) is a non-invasive test that measures electrical activity in the brain and is crucial for identifying seizure activity and epileptiform discharges [5,6,18]. It aids in classifying seizure disorders, such as generalized or partial seizures, and can detect specific patterns associated with particular epilepsy syndromes [18]. Ideally, an EEG should be performed within 24 hours of the seizure to maximize its diagnostic utility [6].

Risk Stratification

The range of potential causes for non-febrile seizures in pediatric patients is broad, including metabolic imbalances, mass lesions, and non-accidental trauma. One specific diagnosis that is relatively common in children under 6 months of age and easily detectable to prevent extensive invasive testing is hyponatremia caused by formula over-dilution. In the emergency department, 3 ml/kg of 3% hypertonic saline is the mainstay of therapy.

A first febrile seizure is concerning and requires prompt evaluation and management [16]. It may be a sign of an underlying medical condition. Some factors increase the risk of bacterial infection, such as age less than 6 months or more than 60 months with the first febrile seizure, or age less than 12 months with incomplete or unknown immunization history. In addition, a first febrile seizure in a clinically unwell child with symptoms of infection, meningeal signs, or dehydration may indicate a more serious underlying condition and requires urgent medical attention.

Febrile status epilepticus, which is a prolonged seizure lasting more than 30 minutes or a series of seizures without full recovery between them, is another potential complication that can occur in the context of a febrile illness. It is important to recognize the signs and symptoms of febrile status epilepticus, such as a fever, stiff neck, or convulsions, and seek immediate medical attention to prevent serious neurological damage.

Management

The management of pediatric seizures in the emergency department primarily focuses on stabilizing the patient, treating the underlying cause, and preventing further seizures or complications [16,19]. The initial management of an actively seizing child includes ensuring that the child’s airway is protected and providing adequate oxygen and circulatory support. Oxygen can be supplied via a nasal cannula or simple face mask, and preparations for endotracheal intubation should be made if airway management requires escalation. The next step is to assess vital signs and check blood glucose levels to rule out hypoglycemia. Intravenous (IV) or intraosseous (IO) access should be established promptly, and the patient should be connected to a monitor by this stage. In febrile seizures, antipyretic therapy is the mainstay of treatment to relieve symptoms and is usually sufficient. Seizures lasting 15 minutes or longer should be managed in accordance with status epilepticus protocols, with the goal of rapidly stopping the seizure using antiepileptic medications to prevent permanent neuronal injury.

A seizure lasting 5 minutes is highly likely to be prolonged; thus, most protocols use a 5-minute definition. Initial management includes maintaining airway, breathing, and circulation (ABCs), administering oxygen, and preparing for intubation if required [16,19]. Hypoglycemia, defined as a capillary blood glucose (CBG) level of less than 60 mg%, should be corrected with a bolus of IV 10% dextrose at 5 mL/kg; this can be repeated to normalize serum glucose levels. IV or IO access should be secured, and blood samples should be sent for investigations. Benzodiazepines are the first-line antiepileptic agents. Options include intramuscular (IM) Midazolam (10 mg for patients >40 kg; 5 mg for patients 13–40 kg), IV Lorazepam (0.1 mg/kg/dose, maximum 4 mg/dose; can be repeated once), or IV Diazepam (0.15–0.2 mg/kg/dose, maximum 10 mg/dose; can be repeated once). If these are not feasible, IV Phenobarbital (15 mg/kg/dose as a single dose), rectal Diazepam (0.2–0.5 mg/kg, maximum 10 mg/dose; can be repeated once), or intranasal/buccal Midazolam may be used.

If first-line therapy is unsuccessful, second-line agents should be administered. Options include IV Fosphenytoin (20 mg PE/kg, maximum 1,500 mg PE/dose as a single dose), IV Valproic Acid (40 mg/kg, maximum 3,000 mg/dose as a single dose), or IV Levetiracetam (60 mg/kg, maximum 4,500 mg/dose as a single dose). IV Phenobarbital (15 mg/kg as a single dose) is another option if other agents are not appropriate. If first- and second-line therapies fail, anesthetic doses of Thiopental, Midazolam, Phenobarbital, or Propofol can be administered. This requires continuous EEG monitoring.

If the patient responds to any of these agents and returns to baseline, symptomatic medical therapy should be initiated. Management of non-convulsive status epilepticus follows a similar approach to that of convulsive status epilepticus. (Figure 1) [20]

Figure 1 - Interventions and management of SE in the ED and inpatient setting [2]. (SEHA pediatric seizure algorithm. Permission granted by Dr. Thiagarajan Jaiganesh)

In neonates, the same stabilization principles apply, including maintaining ABCs, collecting blood samples, and checking and correcting electrolytes [16]. IV Phenobarbitone (20 mg/kg) is administered as the first-line antiepileptic; this can be repeated in 5 mg/kg boluses every 15 minutes (maximum dose of 40 mg/kg) until the seizure is aborted. If the seizure persists, IV Phenytoin (15–20 mg/kg), diluted in equal parts with normal saline, should be administered at a maximum rate of 1 mg/kg/min over 35–40 minutes.

If the seizure remains unresolved, IV Lorazepam (0.05–0.1 mg/kg) or Diazepam (0.25 mg/kg bolus or 0.5 mg/kg rectal) may be used. Alternatively, IV Midazolam can be administered as a continuous infusion; this involves an initial IV bolus of 0.15 mg/kg followed by a continuous infusion starting at 1 μg/kg/min, increasing by 0.5–1 μg/kg/min every 2 minutes (maximum 18 μg/kg/min). Lastly, if all else fails, 100 mg IV or oral Pyridoxine may be administered. This is particularly useful for treating Pyridoxine-dependent neonatal seizures or seizures caused by Isoniazid (INH) toxicity. (Figure 2) [21].

Figure 2 - Neonatal seizure algorithm [21] - Open access https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8857130/figure/Fig2/

When To Admit This Patient

In most cases, hospitalization is not necessary after a first unprovoked seizure, provided that a neurological examination is normal and prompt follow-up evaluation can be arranged [13]. Consultation with a neurologist and electroencephalography (EEG) can typically be performed on an outpatient basis. However, children who have experienced a prolonged seizure or who do not return to their baseline state within a few hours should be admitted to the hospital.

Hospitalization should also be considered in cases of extreme parental anxiety or if adequate follow-up evaluation cannot be arranged. It is essential to counsel parents about the increased likelihood of recurrence, which is approximately 33% overall. The risk of recurrence is higher in children under 18 months of age, when the temperature during the first convulsion is below 40°C, when the first seizure occurs within an hour of the onset of fever, or if there is a family history of febrile seizures.

Revisiting Your Patient

The image was produced by using ideogram 2.0.

Our patient was immediately moved to the resuscitation unit, placed on a simple face mask, and connected to monitors. She was administered rectal Diazepam; however, the seizure did not resolve. By this time, intraosseous (IO) access was established, and 0.1 mg/kg of Lorazepam (same as the IV dose) was given. This successfully aborted the seizure.

At this point, her vitals were as follows: temperature (T) 40°C, heart rate (HR) 93, respiratory rate (RR) 29, and blood pressure (BP) 118/90. She was lethargic and responsive only to painful stimuli. Other notable findings on examination included a full and tense anterior fontanelle, questionable neck rigidity, red and bulging tympanic membranes, reactive but unfocused pupils, a normal heart, lungs, and abdomen, good color and perfusion, and no petechiae or rashes. The patient displayed weak movement in all limbs and hyperactive deep tendon reflexes.

Pediatrics was consulted, and a presumptive diagnosis of meningitis was made. A complete blood count (CBC), C-reactive protein (CRP), blood culture, and chemistry panel were drawn. IV access was established at this point. Since increased intracranial pressure (ICP) was suspected, a lumbar puncture (LP) was initially deferred, and she was immediately given 500 mg of IV Ceftriaxone. A stat CT scan of the brain was normal, so an LP was performed, revealing visibly turbid cerebrospinal fluid (CSF).

The CSF analysis showed a white blood cell (WBC) count greater than 1000 cells/μL, with 95% neutrophils and 5% monocytes, a total protein level of 75 mg/dL, and a glucose level of 25 mg/dL. A Gram stain of the CSF revealed numerous WBCs and a few gram-positive cocci. She was admitted to the pediatric intensive care unit (PICU) for further management.

Authors

Picture of Neema Francis

Neema Francis

Dr. Neema Francis was born and raised in Dubai, UAE. She is currently a fourth-year emergency medicine resident at Tawam Hospital. She graduated with an MBBS from Gulf Medical University in 2020 and completed her internship at Sheikh Shakbout Medical City in 2021. Dr. Francis has a passion for volunteering and has been involved in various healthcare initiatives. She is also a competent researcher with publications to her name and a keen interest in emergency medicine and pediatric emergency medicine.

Picture of Faiz Ahmad

Faiz Ahmad

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.

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  18. Tharp BR. An overview of pediatric seizure disorders and epileptic syndromes. Epilepsia. 1987;28(Suppl 1):S36-S45. doi:10.1111/j.1528-1157.1987.tb05755.x.
  19. Friedman J. Emergency management of the pediatric patient with generalized convulsive status epilepticus. Paediatr Child Health. 2011;16(2):91-104. doi:10.1093/pch/16.2.91.
  20. Al-Hashaykeh NO, et al. Pediatric Status Epilepticus Clinical Practice Guideline. SEHA Pediatric Critical Care Council; 2023.
  21. Vegda H, Krishnan V, Variane G, Bagayi V, Ivain P, Pressler RM. Neonatal seizures—perspective in low-and middle-income countries. Indian J Pediatr. 2022;89(3):245-253. doi:10.1007/s12098-021-04039-2.

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.

Abdominal Pain in Children (2024)

by Prassana Nadarajah

You have a new patient!

An 18-month-old boy is brought to the emergency department (ED) by his parents due to lethargy that has persisted for the last few hours. He is a term-born child with no significant antenatal history or pre-existing medical conditions. The child had been well until five days ago when he experienced a case of viral gastroenteritis. His feeding and urine output were adequate until about three hours ago, after which he began experiencing progressive episodes of crying, accompanied by vomiting and abdominal distension. There was no diarrhea or dark-colored stools noted.

a-photo-of-a-1-and-a-half-year-old-boy-(the image was produced by using ideogram 2.0)

During the triage assessment, the child appeared unsettled but was afebrile, with other vital signs within age-appropriate ranges. There were no rashes observed on his body, and there were no blood-stained stools in his diaper.

What do you need to know?

Importance

Abdominal pain is a common reason for children to present to the Emergency Department (ED) and represents up to 5% of all presentations in some institutions [1]. The most common causes are non-surgical, and at times it may be difficult to arrive at a specific diagnosis before discharge. However, it is crucial to identify causes of abdominal pain that require early surgical intervention, particularly when a clear diagnosis cannot be made before discharge. Pay special attention to red flags such as lethargy (in neonates and infants), severe pain or irritability, bilious emesis, abdominal distension, peritoneal signs, or signs of sepsis.

The differential diagnoses (DDx) for abdominal pain vary with age groups. In younger children who cannot express themselves, reliance on parental history and a thorough physical examination is essential. Blood investigations and radiology may not be helpful, especially in early presentations, making serial examinations and observation more valuable. Additionally, remember that pain from other sites can be referred to the abdomen, particularly testicular pain.

Epidemiology

Pediatric abdominal pain is a common reason for emergency department (ED) visits, accounting for approximately 12% of all visits [2]. The median age of children presenting with abdominal pain is around 9 years, with a higher incidence in girls [2, 3]. Non-specific abdominal pain is the most prevalent diagnosis, affecting 40% of children, followed by functional abdominal pain (FAP), constipation, and viral infections [2, 4]. Despite the high prevalence of abdominal pain, a significant portion of children (62.7%) are discharged directly from the ED, while 37.3% require admission [3]. However, follow-up studies indicate that about 50% of children report ongoing pain after discharge, highlighting the chronic nature of abdominal pain [3]. 

Pathophysiology

The sensation of abdominal pain is transmitted either by somatic or visceral afferent fibres [5]. Visceral pain from the visceral peritoneum is poorly localised and is often referred to its corresponding dermatome on the abdominal wall. If you recall the human embryological development of abdominal organs, the organs developing from the foregut (oesophagus to the second part of the duodenum) have pain referred to the T8 dermatome (i.e., the epigastric area), those developing from the midgut (from the third part of the duodenum to the proximal two-thirds of the transverse colon) have pain referred to the T10 dermatome (i.e., the umbilical area), and those from the hindgut (distal one-third of the transverse colon to the rectum) refer to the T12 dermatome [6].

Somatic pain from the parietal peritoneum is more localised. Thus, any abdominal condition that progresses to involve the parietal peritoneum will result in the patient complaining of migrating pain. In unfortunate situations where this advances to bowel rupture or peritonitis (i.e., surgical abdomen), the patient will exhibit signs of peritonism. You can observe this in the history of appendicitis, where the pain initially starts in the periumbilical region and migrates to the right lower quadrant.

Referred pain also occurs due to the convergence of visceral and somatic pathways in the spinal column. Two examples of referred pain are diaphragmatic irritation leading to pain at the shoulder tip due to the convergence of visceral and somatic pathways at C4, and somatic pain from pneumonia leading to T10–11 pain perceived in the lower abdomen [5].

Initial Assessment and Stabilization

Airway & Breathing

  • Provide supplemental oxygen and attach an SPO2 probe.

Circulation

  • Assess for signs of sepsis, shock, dehydration, or the need for IV pain relief. If any of these are present, obtain IV access.
  • If in shock, administer an IV crystalloid fluid bolus of 20 ml/kg. Reassess and repeat if necessary.
  • If sepsis is suspected, obtain blood cultures via IV and administer Ceftriaxone 50 mg/kg (up to 2 g) AND metronidazole 10 mg/kg (up to 500 mg). Follow your local antibiotic guidelines.
  • If not in shock but dehydrated, initiate IV maintenance therapy.
  • Provide adequate pain control. Consider IV morphine 0.05–0.1 mg/kg or IV fentanyl 1 μg/kg.

Disability

  • Check a point-of-care glucose level in sick children. Consider hypoglycemia or DKA as alternative diagnoses.

Exposure

  • Examine the abdomen for abdominal distension, masses, or peritonism. Involve the surgical team early. This is further discussed in the physical examination section.
  • Always examine the genitals (e.g., for testicular torsion or strangulated hernia).

Medical History

In history, focus on the following:

Age of the child – DDx varies with the child’s age and the initial presenting complaints. Remember that neonates and infants often present with lethargy, irritability, poor feeding, or vomiting.

Age

Surgical diagnoses

Medical diagnoses

Birth to 3 months

  • Necrotizing enterocolitis
  • Pyloric stenosis
  • Malrotation with Midgut volvulus
  • Incarcerated hernia
  • Duodenal atresia
  • Testicular torsion
  • Non-Accidental Injury
  • Constipation
  • Reflux
  • Colic

3 months to 3 years

  • Malrotation with midgut volvulus
  • Intussusception
  • Appendicitis
  • Testicular torsion
  • Trauma
  • Non-Accidental Injury
  • Henoch-Schönlein purpura (HSP)
  • Anaphylaxis
  • Acute gastroenteritis
  • Urinary tract infection
  • Constipation
  • Mesenteric adenitis
  • Sickle cell–related vaso-occlusive crisis

3 years and above

  • Appendicitis
  • Ectopic pregnancy
  • Cholecystitis
  • Malignancy
  • Trauma
  • Testicular or ovarian torsion
  • Henoch-Schönlein purpura
  • Diabetic ketoacidosis
  • Urinary tract infection
  • Pancreatitis
  • Anaphylaxis
  • Constipation
  • Acute gastroenteritis
  • Mesenteric adenitis
  • Strep pharyngitis
  • Pneumonia
  • Renal stones
  • Inflammatory bowel disease
  • Irritable bowel disease
  • Functional abdominal pain
  • Gastritis/gastric ulcer
  • Ovarian cyst
  • Pregnancy
  • Pelvic inflammatory disease
  • Toxic ingestion

Timing of the symptoms:
a. Intussusception may follow a bout of diarrhoeal illness.
b. Appendicitis typically presents as a gradual onset of pain migrating from the periumbilical area to the right lower quadrant.

Pain character – Episodic pain is observed in intussusception and mesenteric adenitis.

Blood in stool – Consider necrotizing enterocolitis, intussusception, and volvulus.

Bilious or non-bilious vomiting – Bilious vomiting is indicative of obstruction below the ampulla of Vater. It is a classic presentation of malrotation with midgut volvulus and may also present in incarcerated/strangulated hernia or Hirschsprung disease with enterocolitis. Non-bilious vomiting is classically associated with pyloric stenosis.

Associated symptoms – A rash may be present in Henoch-Schönlein purpura. Fever, when associated with inflammation (e.g., appendicitis) or the translocation of gut bacteria, may lead to sepsis.

Oral intake, urine output (UOP), and activity levels – These are important. Escalate to a senior opinion for admission or IV hydration if these parameters are below 50% of the child’s baseline.

Other relevant history:

  • Past medical and surgical history, including birth history such as prematurity in neonates and infants.
  • Social history, especially when suspecting non-accidental injury.
  • Menstrual and sexual history in adolescent females.
  •  

Physical Examination

A good history and physical examination are very important in managing undifferentiated paediatric abdominal pain patients. You must perform an abdominal examination, including genitourinary and inguinal exams, especially in children who cannot express themselves. Remember that you may find little or no helpful clinical signs initially; however, serial examinations may reveal the condition as it evolves. A digital rectal examination is very rarely indicated, and even then, it should ideally be limited to once and performed by the surgeon [7].

Also, remember that these are children, and they may intentionally exhibit voluntary guarding during palpation if they are distressed, regardless of the cause. Covering the art of paediatric abdominal examination is beyond the scope of this chapter, but consider providing analgesia, employing distraction techniques, and building good rapport with the child.

Please ensure that your patients receive adequate analgesia before the examination, as this will make the patient cooperative, simplify the examination, and highlight clinical signs.

General Examination

  • Assess general appearance and determine whether the child looks ill or well.
  • Record temperature and other vital signs.
  • Observe for pallor and jaundice. Obtain an accurate body weight.
  • Observe the child walking to the examination bed or within the department. Children with peritonism may refuse to walk or walk slowly with a stooped posture.
  • Observe for signs of pain when coughing or jumping.

Inspection

  • Look for asymmetry and abdominal distension. Abdominal distension is less pronounced in higher bowel obstructions (e.g., midgut volvulus) than in lower bowel obstructions.
  • Check for purpuric patches, which are diffusely seen in Henoch-Schönlein purpura (HSP).

Palpation

  • Feel for any masses, tenderness, and peritonism. Remember that classic presentations of masses (e.g., an olive-shaped mass in pyloric stenosis or a sausage-shaped mass in intussusception) may not be palpable in the emergency department, as the condition may be intermittent or in an early stage.
  • Palpable bowel loops are classically associated with necrotizing enterocolitis.
  • Pyloric stenosis typically presents with a non-tender abdomen.
  • For most surgical causes, peritoneal findings can occur late. Consider the possibility of septic shock in a drowsy child presenting with abdominal tenderness on palpation.

Other Systems to Examine for Abdominal Pain [7]

  • Respiratory: Assess for signs of basal pneumonia.
  • ENT: Consider upper respiratory tract infections (URTI), tonsillitis, or adenopathy.
  • Neurological: Rule out meningitis.
  • Endocrine: Check blood glucose levels for diabetic ketoacidosis.
  • Haematological: Look for pallor and lymphadenopathy.
  • Dermatological: Look for rashes, particularly purpura/petechiae in Henoch-Schönlein purpura or zoster.
  • Renal: Check for oliguria, haematuria, or hypertension in haemolytic uraemic syndrome.

In Our Patient

Physical Examination: Abdominal examination revealed an ill-defined mass in the right upper quadrant (RUQ). No pain was elicited on testicular palpation. No anal fissures or bleeding were noted on rectal examination. There were no signs of peritonism.

When To Ask for Senior Help

Do not hesitate to contact your seniors if you are concerned about your patient. The points below serve as a guide:

  1. An ill-looking patient.
  2. May require IV access for hydration or analgesia.
  3. Presence of peritoneal signs.
  4. Signs of sepsis.
  5. Bilious vomiting.
  6. Non-accidental injury or inconsistent history.
  7. Neonates (especially premature babies), if you lack experience in treating them.
  8. Parental anxiety.

Not-To-Miss Diagnoses

Pediatric abdominal pain is a common and complex issue in emergency departments, requiring a thorough differential diagnosis to identify serious underlying conditions [8]. The etiologies of abdominal pain vary by age, with infants (<2 years) commonly presenting with congenital anomalies, malrotation, and intussusception [8]. In children aged 2-5 years, appendicitis, gastroenteritis, and mesenteric adenitis are frequent diagnoses [9], while school-aged children (5-12 years) are more likely to experience constipation, urinary tract infections, and respiratory infections [8]. Adolescents (>12 years) are at risk for pelvic inflammatory disease, pregnancy-related issues, and ovarian torsion [8]. Common conditions such as appendicitis, constipation, and gastroenteritis are prevalent across different age groups, and non-gastrointestinal causes like pneumonia and acute asthma can also manifest as abdominal pain [10]. A comprehensive approach to diagnosis and management is essential to identify serious underlying conditions that may require urgent intervention.

Causes Requiring Early Surgical Intervention

  • Peritonitis.
  • Appendicitis.
  • Testicular torsion.
  • Incarcerated hernia.
  • Necrotizing enterocolitis.
  • Intussusception.
  • Volvulus.
  • Hirschsprung’s disease.
  • Pregnancy or ectopic pregnancy in adolescent girls.
  • Ovarian torsion in adolescent girls.

Medical Causes Not to Miss

  • UTI in very young children (<5 years).
  • Diabetic ketoacidosis.
  • Sepsis.
  • Haemolytic uraemic syndrome.
  • Non-accidental injury.

Acing Diagnostic Testing

Remember that blood investigations are useful as supportive evidence for your history and physical examination, but they can be normal in surgical conditions. Avoid unnecessary venepuncture and/or IV cannulation in children unless the patient is sick or you are concerned about a not-to-miss diagnosis.

Bedside Tests

In sick patients, useful point-of-care tests include blood sugars, urine analysis, and capillary gas analysis. Blood sugars can indicate hypoglycaemia or DKA, and capillary gas analysis is useful for assessing lactate levels and metabolic acidosis. Urine analysis is helpful in confirming UTI, but ensure a proper uncontaminated sample has been collected [11]. Point-of-care ultrasound can be used for diagnosing intussusception, pyloric stenosis, or appendicitis.

Laboratory Tests

If venipuncture is performed, a full blood count, CRP, and renal function tests should be considered for all children. These tests may reveal evidence of inflammation or infection, as well as the extent of dehydration. You may also consider adding VBG and blood cultures for sicker children and tailor other testing depending on the patient (e.g., lipase for pancreatitis or beta HCG if pregnancy is suspected).

Imaging

Consider avoiding radiation or utilizing the lowest possible radiation dose. Ultrasound is the initial imaging modality of choice. In addition to point-of-care ultrasound, arrange an urgent departmental ultrasound if needed. If x-ray facilities are available, you can obtain a supine abdomen and upright/lateral decubitus view to look for free air. Computed tomography can be considered for life-threatening conditions when other modalities have failed. Magnetic resonance imaging is used in some parts of the world. It avoids radiation but may be time- or cost-prohibitive.

In Our Patient

  • Point-of-care ultrasound (POCUS) showed a target sign over the abdominal mass.
  • A diagnosis of intussusception was made.

Risk Stratification

Effective clinical decision rules (CDRs) for risk stratification of pediatric abdominal pain in emergency departments include the Pediatric Appendicitis Score (PAS) and the Pediatric Emergency Care Applied Research Network (PECARN) Pediatric Intra-Abdominal Injury rule. The PECARN rule is for trauma patients and out of the discussion in this chapter. The PAS is a valuable tool for assessing the likelihood of acute appendicitis in children presenting with abdominal pain, with studies showing that PAS scores correlate significantly with the severity of appendicitis [12]. A score below 4 has been found to rule out appendicitis, while higher scores indicate a higher risk of appendicitis [12]. Additionally, a recent Non-Specific Abdominal Pain (NSAP) Model has been developed to differentiate non-specific abdominal pain from organic causes, identifying key clinical predictors such as pain location and associated symptoms, and achieving a sensitivity of 71.8% [13]. These CDRs assist clinicians in identifying patients at risk for serious conditions, optimizing diagnostic processes, and reducing unnecessary interventions.

Management

Empiric and Symptomatic Treatment

Correct dehydration either orally in stable children or via IV in children who may need to be kept nil-by-mouth or are too sick to tolerate oral intake.

Consider keeping possible surgical patients nil-by-mouth. For bowel obstruction, consider inserting a nasogastric tube for gastric decompression.

Treat pain and distress.

  • Consider non-pharmacological methods (e.g., examine the child on the parent’s lap).

Paracetamol

  • Dose per kg: 15 mg/kg
  • Frequency: Every 4 hours (q4h)
  • Maximum Dose: 60 mg/kg/day
  • Cautions/Comments:
    • Ask for allergies.
    • Check if/when the patient took acetaminophen at home.

Fentanyl

  • Dose per kg: Intranasal 1.5 mcg/kg (for >12 months of age)
  • Frequency: Every 15 minutes
  • Maximum Dose: 3 mcg/kg
  • Cautions/Comments:
    • Not recommended for children <12 months of age.
    • Divide the dose between nostrils.
    • Consider alternative analgesia after the second dose.

Morphine

  • Dose per kg:
    • IV/Subcutaneous: 0.05–0.1 mg/kg
  • Frequency: Every 2–4 hours
  • Maximum Dose:
    • For <1 month: 0.1 mg/kg every 4–6 hours
    • For 1–12 months: 0.1 mg/kg every 2–4 hours
    • For >12 months: 0.2 mg/kg every 2–4 hours
  • Cautions/Comments:
    • There is a chance of respiratory depression if the dose exceeds the recommended amount.

If sepsis is suspected, administer IV Cefotaxime and IV Metronidazole, or follow your local antibiotic guidelines.

Cefotaxime

  • Dose per kg: IV 50 mg/kg
  • Frequency: Every 12 hours
  • Maximum Dose: 2000 mg
  • Cautions/Comments:
    • Can be given intramuscularly (IM) if IV access is difficult.

Metronidazole

  • Dose per kg: IV 10 mg/kg
  • Frequency: Every 8 hours
  • Maximum Dose: 500 mg
  • Cautions/Comments:
    • Consider alternative analgesia after the second dose.

Piperacillin + Tazobactam

  • Indication: For pseudomonal coverage in sepsis or hospital-acquired infections.
  • Dose per kg:
    • 2 months to 9 months: IV 80 mg/kg
    • 9 months: IV 100 mg/kg
  • Frequency: Every 8 hours
  • Maximum Dose: 3000 mg
  • Cautions/Comments:
    • The dose is calculated based on the piperacillin component.

IV Fluids

  • Use isotonic crystalloids. Avoid hypotonic solutions in the ED, except in rare circumstances as advised by paediatric nephrologists or paediatricians.
  • For resuscitation, use 0.9% saline in 10–20 ml/kg boluses for all ages. You can repeat the boluses as necessary, but assess for signs of heart failure before administering each bolus.
  • For IV maintenance, use a 0.9% saline and 5% dextrose combination if available. This can be prepared by mixing 450 ml of 0.9% saline with 50 ml of 50% dextrose. Alternatively, you can use 0.9% saline, Hartmann’s solution, or follow local guidelines.

When To Admit This Patient

If you are able to arrive at a diagnosis for these patients, then the disposition is often straightforward. On the other hand, patients with severe pain despite a negative physical examination and unclear diagnosis will require admission for observation and serial physical examinations.

If parents confirm that oral intake, UOP, and activity levels are less than 50% of the child’s baseline, the child should be admitted for IV hydration and observation. A short-stay unit may be suitable for such patients.

If there is a suspicion of non-accidental injury or any social circumstances (e.g., inability to return for review due to financial constraints or travel issues in rural areas), discuss admission with your senior doctor. Consider reviewing well-appearing neonates with seniors, especially if you think they can be safely discharged home.

Otherwise, well children with likely benign causes can be discharged home. Ensure that clear and close follow-up is arranged with their general practitioner or pediatrician.

Advise parents on when to return (e.g., if the child’s oral intake, UOP, or activity level reduces to less than 50% of their usual baseline, or if symptoms of sepsis or shock develop) and provide guidance on follow-up (either with their general practitioner or the nearest hospital with surgical capacity to review the child). If any outpatient radiological investigations are planned for the coming days, educate parents about the importance of attending these procedures as well.

Revisiting Your Patient

Our 18-month-old patient was confirmed to have an intussusception by point-of-care ultrasound.

On reviewing his history, the episodic crying and preceding viral illness are supportive of this diagnosis, and the lack of fever or other associated symptoms rules out most other diagnoses. The classical triad of abdominal pain, vomiting, and red-currant jelly stool described in patients is present in less than 50% of patients with the disease [14]. However, a better clue is that it is associated with lethargy even without signs of sepsis or dehydration.

His examination revealed normal vital signs, was afebrile, and had a soft, non-tender abdomen with an ill-defined lower abdominal mass, which also supports this diagnosis.
The ABCDE or primary survey did not show any other abnormalities.

He was kept nil-by-mouth, IV maintenance fluids were started, and an urgent surgical referral was made. Antibiotics were not needed at this stage as there was no other supportive evidence of associated sepsis. He was prescribed PRN pain relief with fentanyl and morphine but did not require any during the ED stay.

The surgical team reviewed him and took him to the operating theatre for air enema reduction.

Authors

Picture of Prassana Nadarajah

Prassana Nadarajah

Listen to the chapter

References

  1. Scholer SJ, Pituch K, Orr DP, Dittus RS. Clinical outcomes of children with acute abdominal pain. Pediatrics. 1996;98(4):680-685. doi:10.1542/peds.98.4.680
  2. Magnúsdóttir MB, Róbertsson V, Þorgrímsson S, Rósmundsson Þ, Agnarsson Ú, Haraldsson Á. Abdominal pain is a common and recurring problem in paediatric emergency departments. Acta Paediatr. 2019;108(10):1905-1910. doi:10.1111/apa.14782
  3. Lee WH, O’Brien S, Skarin D, et al. Pediatric Abdominal Pain in Children Presenting to the Emergency Department. Pediatr Emerg Care. 2021;37(12):593-598. doi:10.1097/PEC.0000000000001789
  4. Pant C, Deshpande A, Sferra TJ, Olyaee M. Emergency department visits related to functional abdominal pain in the pediatric age group. J Investig Med. 2017;65(4):803-806. doi:10.1136/jim-2016-000300
  5. Simpson E, Smith A. The management of acute abdominal pain in children. Journal of Paediatrics and Child Health. 1996;32(2):110-112. doi:10.1111/j.1440-1754.1996.tb00905.x
  6. Sadler TW, Langman J, Langman J. In: Langman’s Medical Embryology. Wolters Kluwer Health; 2012:208-229.
  7. Cameron P, Brown G, Biswadev M, Dalziel S, Craig S. Textbook of Paediatric Emergency Medicine. Elsevier; 2019.
  8. Reust CE, Williams A. Acute Abdominal Pain in Children. Am Fam Physician. 2016;93(10):830-836.
  9. Yang WC, Chen CY, Wu HP. Etiology of non-traumatic acute abdomen in pediatric emergency departments. World J Clin Cases. 2013;1(9):276-284. doi:10.12998/wjcc.v1.i9.276
  10. Kandamany N, O’Neill M. The Aetiology of Acute Abdominal Pain in Children 2–12 Years of Age. Archives of Disease in Childhood 2012;97:A478.
  11. The Royal Children’s hospital melbourne. The Royal Children’s Hospital Melbourne. Accessed May 25, 2023. https://www.rch.org.au/kidsinfo/fact_sheets/Urine_samples/#:~:text=Clean%20the%20skin%20around%20the%20genital%20area%2C%20using%20gauze%20if,sample%20container%20touch%20the%20skin.
  12. Vevaud K, Dallocchio A, Dumoitier N, et al. A prospective study to evaluate the contribution of the pediatric appendicitis score in the decision process. BMC Pediatr. 2024;24(1):131. Published 2024 Feb 19. doi:10.1186/s12887-024-04619-z
  13. Bouënel M, Lefebvre V, Trouillet C, Diesnis R, Pouessel G, Karaca-Altintas Y. Determining clinical predictors to identify non-specific abdominal pain and the added value of laboratory examinations: A prospective derivation study in a paediatric emergency department. Acta Paediatr. 2023;112(10):2218-2227. doi:10.1111/apa.16911
  14. Simon R.A, Hugh T.J, Curtin A.M. Childhood intussusception in a regional hospital. Aust N Z J Surg. 1994;64:699–702.

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

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.

Fundamentals of Pediatric Advanced Life Support (2024)

by Burak Çakar & Ayça Koca

Introduction

Pediatric cardiac arrest (CA) is a rare but critical event associated with high mortality and significant risk of severe sequelae [1,2]. Unlike in adults, respiratory causes are the primary contributors to CA in children. Hypoxia and bradycardia can lead to cardiopulmonary failure, which may ultimately progress to CA.

Common causes of pediatric CA include infections (e.g., pneumonia, sepsis), trauma, asphyxia, seizures, asthma, suffocation, and sudden infant death syndrome [2]. Clinical signs of cardiopulmonary arrest include respiratory arrest, absence of a palpable pulse, muscle flaccidity, unresponsiveness, cyanosis or other discoloration, and dilated pupils. Recognizing and promptly addressing these signs is crucial for improving outcomes.

Recognition of a Critically Ill Child

Early recognition of a critically ill child is essential to implementing timely interventions that may prevent progression to CA [3]. Abnormal vital signs, relative to age-specific norms, are often the most reliable indicators of impending arrest.

Pediatric Early Warning Scores (PEWS) are recommended as a systematic tool to identify children at risk of clinical deterioration [4]. PEWS evaluates three domains: behavior, cardiovascular function, and respiratory status [5]. It incorporates vital findings such as respiratory rate, heart rate, blood pressure, oxygen saturation, temperature, level of consciousness, and capillary refill time [6]. 

Monitoring Vital Signs in Children

It is essential to recognize abnormal vital signs for early recognition of pediatric deterioration.

Blood Pressure

Systolic Hypotension is defined as a systolic blood pressure below the 5th percentile for age. The threshold for concern is when the systolic blood pressure is <70 mmHg + (2x the child’s age in years).

Respiratory Rate

Tachypnea: A respiratory rate exceeding 60 breaths per minute indicates tachypnea.
Decreased Respiratory Rate: A reduction in respiratory rate in a previously tachypneic patient could signal either improvement or fatigue. Fatigue in this context could precede respiratory failure, particularly if it occurs in conjunction with other signs of decompensation.

Temperature

Fever significantly affects physiology. For every 1°C increase in body temperature:

  • The heart rate increases by approximately 10 beats per minute.
  • The respiratory rate increases by 2 to 5 breaths per minute.

End-Tidal Carbon Dioxide (EtCO2)

Changes in EtCO2 levels are critical indicators of respiratory status. A progressive increase or decrease in EtCO2 levels can signal impending desaturation and respiratory failure.

Assessment

Given the poor outcomes associated with pediatric CA, the emphasis must be on early recognition of pre-arrest states. Identifying signs of impending respiratory failure and shock, regardless of their underlying cause, should be a primary focus [4].

Findings Preceding Cardiopulmonary Arrest

Key findings preceding cardiopulmonary arrest are categorized as follows:

  1. Airway: Signs include stridor, drooling, and retractions, which indicate significant airway obstruction or distress.

  2. Breathing: Irregular respiration, bradypnea, gasping respirations, and cyanosis are warning signs of severe respiratory compromise.

  3. Circulation: Indicators such as a capillary refill time greater than 5 seconds, bradycardia, hypotension, cool extremities, weak central pulses, and the absence of peripheral pulses suggest circulatory failure.

  4. Disability: An altered level of consciousness and decreased responsiveness point toward significant neurological impairment, often accompanying or preceding arrest.

Initial Assessment

The initial assessment begins with a first impression of the child’s general appearance, breathing pattern, and circulatory status. During the primary assessment, the ABCDE approach is followed, with immediate interventions performed at each step when abnormalities are identified. Initial management focuses on supporting airway, breathing, and circulation [7].

The clinician should rapidly assess the following:

Airway

  • Assess for patency (open, requiring maneuvers/adjuncts, partially or completely obstructed)
  • Perform cervical spine stabilization for injured children.
  • Provide 100% inspired oxygen, clear the airway (e.g., suction), apply airway maneuvers, and insert airway adjuncts if the child is unconscious.
  • Initiate chest compressions immediately if the child is unresponsive and shows no signs of life.
  •  

 Breathing

  • Evaluate respiratory rate, effort, tidal volume, lung sounds, and pulse oximetry.
  • Assist ventilation manually for patients unresponsive to basic airway maneuvers or exhibiting inadequate respiratory effort.
  • Monitor oxygenation and ventilation using pulse oximetry and ETCO₂.
  • Administer appropriate medications based on the cause of respiratory distress (e.g., albuterol for status asthmaticus, inhaled racemic epinephrine for croup).
  • Consider intubation when necessary, ensuring 100% oxygen delivery via a non-rebreather mask. Apply positive pressure ventilation with a bag-valve-mask (BVM) in cases of respiratory failure.

Circulation

  • Assess skin color and temperature, heart rate and rhythm, blood pressure, peripheral and central pulses, and capillary refill time.
  • Control hemorrhage in injured children.
  • For circulation deficiencies, monitor heart rate and rhythm, and establish vascular access for volume resuscitation or medication administration.

Disability

  • Evaluate neurological status and level of consciousness using the AVPU scale (Alert, Voice, Pain, Unresponsive) and the Glasgow Coma Scale (GCS) for trauma patients.
  • Assess pupil size and reactivity to light.
  • Check for hypoglycemia using rapid bedside glucose testing or by observing the response to empiric dextrose administration.

Exposure

  • Examine for skin findings, fever or hypothermia, and evidence of trauma.

Secondary and Tertiary Assessments

  • The secondary assessment involves a detailed head-to-toe physical examination, supplemented with a medical history.
  • The tertiary assessment focuses on identifying the underlying causes of trauma, illness, or infection through ancillary studies.

Respiratory Distress and Failure

Respiratory distress and failure are common precursors to CA in children. Early recognition of breathing difficulties is essential to improving clinical outcomes.

Respiratory distress is characterized by tachypnea, nasal flaring, retractions, and the use of accessory muscles. Additional signs include agitation, hypoxia, and abnormal breath sounds, such as stridor or wheezing. If not promptly addressed, these findings can progress to a decreased respiratory rate, respiratory fatigue, and eventual respiratory arrest.

Bradycardia

In children, bradycardia is often secondary to hypoxia. A heart rate slower than the age-appropriate normal range is indicative of bradyarrhythmia. Management focuses on optimizing oxygenation and ventilation through basic airway maneuvers.

If the heart rate remains below 60 beats per minute despite adequate oxygenation and ventilation, chest compressions should be initiated. Epinephrine (0.01 mg/kg) should be administered every 3–5 minutes. For bradycardia caused by increased vagal tone or primary atrioventricular block, atropine (0.02 mg/kg; maximum single dose 0.5 mg) is recommended [7].

Tachycardia

Tachycardia refers to a heart rate that exceeds the normal range for a child’s age, considering other factors such as physical activity or fever. The management of tachycardias depends on the child’s hemodynamic condition and rhythm [7].

Pulseless Arrest

Pediatric CAs are typically the result of cardiopulmonary distress, failure, or shock. When a child has no palpable pulse and is unresponsive, cardiopulmonary resuscitation (CPR) should be initiated.

A child with pulseless arrest will present as apneic and may exhibit gasping respirations. The rhythms associated with pulseless arrest include [2]:

Shockable rhythms: Ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT).

Ventricular Fibrillation

Ventricular Tachycardia

Unshockable rhythms: Asystole, pulseless electrical activity (PEA).

Asystole

Pulseless Electrical Activity (PEA)

During CPR, reversible causes of PEA should be actively identified and addressed. The mnemonic 6H5T is useful for recalling these potential causes [2]:

  • 6 H’s:
    • Hydrogen ion (acidosis)
    • Hypoxia
    • Hypovolemia
    • Hypo- or hyper -kalemia, -calcemia, -magnesemia
    • Hypoglycemia
    • Hypo- or hyperthermia
  • 5 T’s:
    • Tension pneumothorax
    • Tamponade
    • Thrombosis (cardiac)
    • Thrombosis (pulmonary)
    • Toxic agents

By addressing these potential causes, advanced life support providers can significantly improve the likelihood of successful resuscitation.

Resuscitation

An effective resuscitation team is critical to the successful management of pediatric advanced life support (PALS). The team must perform multiple tasks simultaneously, including airway management, ventilation, vascular access, medication preparation and administration, chest compressions, monitor/defibrillator operation, recording/timing, and overall leadership.

The team leader plays a pivotal role by assigning tasks, directing team members, and modeling exemplary teamwork. In addition to medical expertise and resuscitation skills, the team must demonstrate effective communication. Key elements of effective team dynamics include:

  • Closed-loop communication
  • Clear messages
  • Defined roles and responsibilities
  • Knowing and communicating one’s limitations
  • Knowledge sharing
  • Constructive interventions
  • Reevaluation and summarization
  • Mutual respect [8]

Initiation of CPR

Timely recognition of CA, prompt initiation of high-quality chest compressions, and ensuring adequate ventilation are crucial for improving outcomes [2].

Healthcare providers should begin chest compressions promptly in any child who is unresponsive, not breathing normally, and has no signs of circulation [7, 9]. Pulse checks may be performed but should not delay the initiation of CPR for more than 10 seconds [10, 11]. Pulse palpation alone is unreliable in determining the need for compressions or confirming CA.

Since respiratory-related CA is more common in infants and children than primary cardiac causes, ensuring adequate ventilation during resuscitation is essential [2]. The recommended sequence for CPR is compressions-airway-breathing (CAB) [12].

High-quality CPR enhances blood flow to vital organs and increases the likelihood of return of spontaneous circulation (ROSC). The five key components of high-quality CPR are [2, 13]:

  • Optimal chest compression rate
  • Sufficient chest compression depth
  • Minimal interruptions in compressions
  • Complete chest recoil between compressions [7, 14]
  • Avoidance of excessive ventilation

Components of High-Quality CPR

  • Compression Rate: 100–120 compressions per minute [15–18].
  • Compression Depth:
    • At least one-third of the anterior-posterior diameter of the chest:
      • 4 cm for infants
      • 5 cm for children
      • 5–6 cm for adolescents who have reached puberty [7, 19].
    • Allow complete chest recoil after each compression.
    • Use 100% oxygen with a bag-valve-mask (BVM) during CPR.
    • Compression-Ventilation Ratios:
      • 30:2 for single rescuers.
      • 15:2 for two rescuers [7, 20].

To prevent fatigue and ensure adequate compressions, switch the person performing compressions at least every 2 minutes or sooner if necessary [7].

CPR Technique

For Infants

Single Rescuer: Use two fingers (Figure 1) or two thumbs below the nipple line (lower half of the sternum but one-finger width above the xiphisternum) [21–24].

Figure 1. Two-finger compressions

Two Rescuers: Use the two-thumb encircling hands technique (Figure 2) [25–29].

Figure 2. Thumb-encircling hands compression

If the recommended depth cannot be achieved, use the heel of one hand (Figure 3) [2, 18, 30, 31].

Figure 3. Compression with the heel of one hand

For children older than 1 year

Use either one-handed or two-handed CPR.

Perform chest compressions on a firm surface. Use a backboard or activate the bed’s “CPR mode” if available [32–35].

The Airway

Unless a cervical spine injury is suspected, the head tilt-chin lift maneuver is recommended to open the airway [36]. In trauma patients with suspected cervical spinal injury, the jaw thrust maneuver should be used. If the jaw thrust is ineffective, the head tilt-chin lift may be performed, even in cases of suspected cervical spine injury [2].

Use 100% oxygen delivered via bag-valve-mask (BVM) during CPR.

Advanced Airway Interventions During CPR

Bag-mask ventilation (BMV) is effective for most patients but requires pauses in chest compressions and carries risks of aspiration and barotrauma [2]. Advanced airway interventions, such as supraglottic airway (SGA) placement or endotracheal intubation (ETI), improve ventilation, reduce aspiration risks, and enable uninterrupted chest compressions. However, these procedures require specialized equipment and trained providers, and may be challenging for those inexperienced in pediatric intubation [2]. BMV is more reliable than advanced airway interventions during out-of-hospital pediatric CA [37–39].

For patients with advanced airway, ventilations should be asynchronous. Exceeding recommended ventilation rates can compromise hemodynamics and lower systolic blood pressure [40].

Ventilations should be tailored to age:

  • 25 breaths/min (infants)
  • 20 breaths/min (>1 year)
  • 15 breaths/min (>8 years)
  • 10 breaths/min (>12 years) [7].

Capnography should be used to confirm endotracheal tube placement and monitor for ROSC. However, ETCO₂ should not be used as a definitive quality indicator or target during PALS [7].

Drug Administration During CPR

Establish IV access as early as possible during PALS. If IV access is challenging, promptly consider intraosseous (IO) access as an alternative [7]. Drug dosing for children is typically based on weight, which can be challenging to determine in emergencies. When the actual weight cannot be obtained, various estimation methods are available [41]

The administration of vasoactive agents during CA aims to improve coronary and cerebral perfusion and increase the likelihood of ROSC. However, optimal timing and overall impact on long-term outcomes are still under investigation [42]

  • Administer epinephrine (10 mcg/kg; max 1 mg; IV or IO ) as soon as possible for non-shockable rhythms. For shockable rhythms, administer epinephrine immediately after the third shock, along with antiarrhythmic drugs. Once given, adrenaline should be repeated every 3–5 minutes until ROSC.

Antiarrhythmic drugs can reduce the risk of recurrent VF or pVT and improve the likelihood of successful defibrillation [43, 44]. Only in shockable rhythms, administer antiarrhythmic drugs immediately after the third shock, along with epinephrine.

  • Amiodarone: 5 mg/kg (max 300 mg); a second dose (max 150 mg) may follow after the fifth shock if the rhythm remains shockable.
  • Lidocaine: 1 mg/kg, as an alternative to amiodarone.

Magnesium sulfate (25–50 mg/kg) should be considered for torsades de pointes. Routine administration of sodium bicarbonate and calcium is not recommended unless specific conditions (e.g., electrolyte imbalances, drug toxicities) are present [45–48].

Flush all IV or IO resuscitation drugs with 5–10 mL of normal saline to ensure delivery to the central circulation.

Defibrillation During PALS

Shockable rhythms in children include pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VF). When identified, defibrillation should be performed immediately, regardless of the ECG amplitude. If there is uncertainty about the rhythm, it should be treated as shockable to avoid delays in care. [7].

The preferred method for defibrillation during pediatric ALS is manual defibrillation, but an automated external defibrillator (AED) can be used if manual defibrillation is unavailable. Currently, self-adhesive defibrillation pads are the standard. When using these pads:

  • Chest compressionsshould continue while the defibrillator charges.
  • The pads should be placed in either the antero-lateral (AL)or antero-posterior (AP) positions:
    • AL position: One pad below the right clavicle and the other in the left axilla.
    • AP position: The front pad in the mid-chest just left of the sternum, and the back pad between the scapulae.

Avoid contact between the pads to prevent electrical arcing.

If self-adhesive pads are unavailable, paddles with gel or pre-shaped gel pads can be used as an alternative. In this case, charging should occur directly on the chest, pausing compressions during the process [7]. Pre-planning each step is critical to minimizing delays during the intervention.

Charge the defibrillator for an initial shock of 4J/kg. Avoid exceeding the maximum doses recommended for adults (typically 120–200J, depending on the defibrillator). Pause chest compressions briefly to deliver the shock, ensuring all rescuers are clear of the patient. Resume CPR immediately after the shock, minimizing the pause to under 5 seconds. Reassess the rhythm every 2 minutes and, if it remains shockable, deliver subsequent shocks at 4J/kg. For refractory VF/pVT (requiring more than 5 shocks), incrementally increase the dose up to 8J/kg (maximum 360J) [7].

CPR should continue until an organized, potentially perfusing rhythm is recognized during a rhythm check and is accompanied by signs of ROSC, identified either clinically (e.g., eye-opening, movement, normal breathing) or through monitoring (e.g., etCO2, SpO2, blood pressure, ultrasound) [7].

A summary of the fundamentals of pediatric ALS can be found in Figure 5.

Figure 5. Pediatric cardiac arrest algorithm [7] CPR: cardiopulmonary resuscitation, EMS: emergency medical services, ALS: advanced life support, VF: ventricular fibrillation, pVT: pulseless ventricular tachycardia, PEA: pulseless electrical activity, IV: intravenous, IO: intraosseous.

Post-cardiac Arrest Management

Achieving ROSC is only the first step in resuscitation. Comprehensive post-CA care is crucial to optimizing outcomes, particularly in pediatric patients. This phase focuses on treating the underlying cause of the event and preventing secondary injuries.

Key Components of Post-Cardiac Arrest Care

Targeted Temperature Management (TTM):

  • For unconscious children after ROSC, TTM helps prevent further brain injury.

Ventilation and Oxygenation:

  • Inspired oxygen should be titrated to maintain oxygen saturation (SpO₂) between 94% and 99%.
  • For intubated patients, confirm endotracheal tube (ETT) placement and monitor ventilation to avoid hyperoxia or hypoxia, as well as hypercapnia or hypocapnia.

Hemodynamic Support:

  • Prevent and treat hypotension using parenteral fluids and vasoactive medications, guided by physiologic endpoints and cardiac function.
  • Monitor for signs of recurrent shock and intervene promptly.

Glucose Management:

  • Maintain blood glucose levels below 180 mg/dL to avoid complications associated with hyperglycemia.

Seizure Management:

  • For unconscious children after ROSC, continuous electroencephalography monitoring is also recommended to detect subclinical seizures. Seizures should be monitored and treated aggressively, as they can exacerbate neurological injury.

Temperature Regulation:

  • Avoid hyperthermia (core temperature >37.5°C) using cooling measures as necessary to reduce metabolic demands and limit neuronal damage.

Summary

Pediatric CA remains a critical event with high mortality and significant morbidity. Unlike adult CA, pediatric cases are often precipitated by respiratory failure and hypoxia, highlighting the need for timely recognition and intervention. Early identification of abnormal vital signs, particularly through tools like PEWS, and a structured approach to initial assessment using the ABCDE framework are paramount in preventing CA. Furthermore, rapid and effective resuscitation, incorporating high-quality CPR, advanced airway management, and appropriate medication use, significantly improves the likelihood of survival and favorable outcomes.

Managing pediatric CA extends beyond achieving ROSC. Comprehensive post-cardiac arrest care, including targeted temperature management, optimized ventilation and oxygenation, hemodynamic support, glucose management, and seizure control, is critical to minimize secondary injuries and improve neurological recovery. Pediatric Advanced Life Support (PALS) algorithms and effective resuscitation team dynamics play essential roles in guiding care.

Ultimately, improving outcomes in pediatric CA requires a systematic approach to prevention, timely recognition, prompt intervention, and evidence-based post-resuscitation care. Continuous education, training, and adherence to updated guidelines are essential for healthcare providers to ensure the best possible outcomes for critically ill or arrested children.

Authors

Picture of Burak Çakar

Burak Çakar

Gaziantep Islahiye State Hospital, Department of Emergency Medicine, Gaziantep, Turkey

Picture of Ayça Koca

Ayça Koca

Ayça Koca is an emergency physician at Ankara University School of Medicine, Department of Emergency Medicine. She completed both her medical degree and residency at Ankara University, where she developed a deep connection to patient care and teaching. With a special interest in medical education and simulation, she is passionate about creating engaging learning experiences to support the growth and confidence of future healthcare providers.

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  46. Matamoros M, Rodriguez R, Callejas A, et al. In-hospital pediatric cardiac arrest in Honduras. Pediatr Emerg Care. 2015;31(1):31-35.
  47. Wolfe HA, Sutton RM, Reeder RW, et al. Functional outcomes among survivors of pediatric in-hospital cardiac arrest are associated with baseline neurologic and functional status, but not with diastolic blood pressure during CPR. Resuscitation. 2019;143:57-65.
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Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

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.

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]

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]

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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]

References and Further Reading

Salter-Harris Fractures

salter harris

Case Presentation

You are a medical student doing your first clinical shift as part of your Emergency Medicine rotation. A 9-year-old boy is brought in by his father after an injury to his left hand approximately 1 hour back. As explained by the father, the child was playing at home with his elder brother when his left index finger became caught in between a door that had quickly slammed shut. Following the injury, the child was reported to be crying due to severe pain, but had no lacerations or other associated injuries. He was rushed to the hospital and presented in the ED as an anxious, weeping boy who held out his left index finger and pointed to the tip as the region of maximal pain. Mild swelling was noted at the distal interphalangeal joint as well as at the tip of the affected finger. After appropriate analgesia was initiated, the child was sent to the Radiology department for X-ray imaging. The images obtained by the department are shown below in Figures 1.1 and 1.2.

Figure 1.1
Figure 1.1
Figure 1.2
Figure 1.2

Findings

Due to the lack of ideal positioning and suboptimal cooperation from the child and his parent, the radiology technician reports back to you stating that the best images they could obtain were the ones displayed above. Although unclear, you can confidently identify a small break in the bone at the base of the distal phalanx. You mention to the father that you see a fracture on the X-ray and report back to your Attending Physician. 

The Attending Physician decides to take a break from his morning coffee and utters the dreaded question: “What kind of fracture is this?” You try to recall a lecture you had about Salter-Harris fractures but cannot recall the classification of these fractures. As if on cue, the father of the patient finds you shuffling your weight in front of the Attending Physician and asks: “You said he has a fracture, will he have to get surgery for his finger?”

“What kind of fracture is this?”

Salter-Harris Fractures

Salter-Harris Fractures refer to fractures that involve the growth plate (physis). Therefore, these fractures are applicable specifically to the pediatric population, occurring most often during periods of rapid growth (growth spurts) when the growth plate is at its weakest, close to age ranges where children tend to participate in high-risk activities (11-12 in girls and 12-14 in boys) [1].

Originally described in 1963 by Dr Robert Salter and Dr Robert Harris [2], the now infamous Salter-Harris fractures are classified by the region of bone that is affected. Figure 2 displays the gross anatomy of a normal distal phalanx similar to the picture we examined in the X-ray, labelled to reflect the different areas of the bone relative to each other. The types of fractures that can occur are outlined below.

SALTER HARRIS ANATOMY
Figure 2
  • Type I Salter-Harris Fractures (Slipped)

    Type I fractures occur when a longitudinal force is applied across the physis, resulting in a displacement (“slip”) of the epiphysis from the metaphysis. Though relatively infrequent (5%), suspicion of this fracture is raised when the epiphysis is seen to either be displaced to the side of its original position relative to the metaphysis or when the gap between the two segments is widened.

Salter-Harris Type I
Salter-Harris Type I
  • Type II Salter-Harris Fractures (Above)

    Type II fractures are the most common (75%) of the Salter-Harris fractures. As with our patient above, this fracture only involves structures “Above” the epiphysis (Metaphysis + Physis/growth plate) with virtually no fracture or displacement of the epiphysis itself. Fortunately, type I and most type II fractures can be managed conservatively with cast immobilization and splinting.

Salter-Harris Type II
Salter-Harris Type II
  • Type III Salter-Harris Fractures (Lower)

    Type III fractures involve both the physis and the epiphysis. Although relatively uncommon (10%), the involvement of the epiphysis and consequent disruption of the growth plate makes this an intra-articular fracture that usually requires surgical fixation.

Salter-Harris Type III
Salter-Harris Type III
  • Type IV Salter-Harris Fractures (Through)

    Continuing the trend of worse outcomes with higher classification types, Type IV fractures involve all three layers (metaphysis, physis and epiphysis) and thus harbor more adverse outcomes and risks, with management primarily consisting of operative internal fixation. Similar to Type III fractures, this is an intra-articular fracture and also occurs at a similar rate of 10%.

Salter-Harris Type IV
Salter-Harris Type IV
  • Type V Salter-Harris Fractures (Rammed/Crushed)

    The rarest of all the Salter-Harris fractures, type V fractures occur due to high impact compression of the growth plate. Potential disruption of the germinal matrix and compromised vascular supply to the growth plate can lead to growth arrest.

Salter-Harris Type V
Salter-Harris Type V

A convenient method to recall the Salter-Harris classifications is outlined below using the mnemonic “SALTR”

Salter-Harris Classification
Salter-Harris Classification

Case Resolution

You ascertain the patient’s fracture to be a type II Salter-Harris fracture, justifying your answer to the Attending Physician by pointing out that the affected region in the X-ray is limited to the metaphysis and physis with no epiphyseal involvement. Recognizing the potential for parental misconceptions surrounding the diagnosis of fractures in pediatric patients [3], you approach the father and explain that, though there is a fracture present, there is likely no need for any surgical intervention. You advise that the left index finger will be immobilized using a splint and further elaborate on the unlikelihood of this injury to manifest any long-term developmental or growth arrest in the affected region.

References and Further Reading

  1. Levine RH, Foris LA, Nezwek TA, et al. Salter Harris Fractures. [Updated 2019 Aug 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan
  2. Salter, Robert B.; Harris, W. Robert: Injuries Involving the Epiphyseal Plate, The Journal of Bone and Joint Surgery (JBJS): April 1963 – Volume 45 – Issue 3 – p 587-622
  3. Sofu H, Gursu S, Kockara N, Issin A, Oner A, Camurcu Y. Pediatric fractures through the eyes of parents: an observational study. Medicine (Baltimore). 2015;94(2):e407. doi:10.1097/MD.0000000000000407
[cite]

A 20-months-old head trauma: CT or Not CT?

by Stacey Chamberlain

A 20-month-old female was going up some wooden stairs, slipped, fell down four stairs, and hit the back of her head on the wooden landing at the bottom of the stairs. She did not lose consciousness and cried immediately. She was consolable after a couple of minutes and is acting normal per her parents. She has not vomited. On exam, she is well-appearing, alert, and has a normal neurologic exam. She is noted to have a left parietal hematoma measuring approximately 4×4 cm.

Should you get CT imaging of this child to rule out clinically significant head injury?

PECARN Pediatric Head Trauma Algorithm

Age < 2

Age ≥ 2

  • GCS < 15, palpable skull fracture, or signs of altered mental status
  • Occipital, parietal or temporal scalp hematoma; History of LOC≥5 sec; Not acting normally per parent or Severe Mechanism of Injury?
  • GCS < 15, palpable skull fracture, or signs of altered mental status
  • History of LOC or history of vomiting or Severe headache or Severe Mechanism of Injury?

The PECARN (Pediatric Emergency Care Applied Research Network) Pediatric Head Trauma Algorithm was developed as a CDR to minimize unnecessary radiation exposure to young children. The estimated risk of lethal malignancy from a single head CT in a 1-year-old is 1 in 1000-1500 and decreases to 1 in 5000 in a 10-year-old. Due to these risks, in addition to costs, length of stay and potential risks of procedural sedation, this CDR is widely employed given the frequency of pediatric head trauma ED visits. This CDR has the practitioner use a prediction tree to determine risk, but unlike some other risk stratification tools, the PECARN group does make recommendations based on what they consider acceptable levels of risk. In the less than 2-year-old group, the rule was found to be 100% sensitive with sensitivities ranging from 96.8%-100% sensitive in the greater than two-year-old group.

This algorithm does have some complexity and ambiguity. It requires the practitioner to know what were considered signs of altered mental status and what were considered severe mechanisms of injury. In addition, certain paths of the decision tree lead to intermediate risk zones. In these cases, the recommendation is “observation versus CT,” allowing for the ED physician to base his/her decision to image or not based on numerous contributory factors including physician experience, multiple versus isolated findings, and parental preference, among others.

Other pediatric head trauma CDRs rules have been derived and validated; however, in comparison trials, PECARN performed better than the other CDRs. Of note, in this study, physician practice (without the use of a specific CDR) performed as well as PECARN with only slightly lower specificity.

Case Discussion

For purposes of the case study, the patient falls into an intermediate risk zone of clinically important brain injury. However, a sub-analysis of patients less than two years old with isolated scalp hematomas suggests that patients were higher risk if they were < 3 months of age, had non-frontal scalp hematomas, large scalp hematomas (> 3cm), and severe mechanism of injury. Given the large hematoma in the case study patient and a severe mechanism of injury (a fall of > 3 feet in the under two age group), one might more strongly consider imaging due to these two additional higher risk factors.

[cite]

Ortho Pearls – Salter-Harris Classification

iEM-Infographic-Pearls-Ortho - Salter Harris

Recommended Chapters

Reduction of Common Fractures and Dislocations

Splinting and Casting

A kid with wrist pain!

In case you didn’t encounter a kid with wrist pain today!

Pediatric fractures affecting growth plate are classified with Salter-Harris classification. It is from I to V. 

What is your opinion about below x-ray? I, II, III, IV or V?

Please give your answer at the comment box below.

428.3 - salter harris 2

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!

Elbow Pain

In case you didn’t encounter a child with elbow pain today!

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!