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National Genomic Test Directory Guidance

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See also

Congenital torticollis

Key Points

1. Common, benign condition that affects the cosmetic appearance of an infant's head. Does not cause developmental delay

2. Imaging is not required, diagnosis is based on history and examination findings including the absence of features of craniosynostosis

3. Assessment includes identifying the presence of a co-existing tight sternocleidomastoid muscle (congenital muscular torticollis) and other risk factors

4. Most resolve without any treatment and will show improvement with counterpositioning measures and physiotherapy intervention

Background

Types of head shape deformities
Positional plagiocephaly

Skull deformation involving posterior flattening of either side of the head. This may result in ear misalignment and facial asymmetry

Other positional head shape deformities

Brachycephaly: symmetrical occipital flattening and widening of the head, which often co-exists with positional plagiocephaly

Scaphocephaly: elongated narrow skull with flattening on both sides of the head, occipital bulge and frontal bossing

Causes and natural history

External moulding forces due to the infant lying on their back or unilateral posture preference

Risk factors

low tone

delayed gross motor development

minimal tummy time

tight sternocleidomastoid (SCM) muscle (congenital muscular torticollis)

developmental dysplasia of the hip

Over one third of infants have plagiocephaly in the first few months of life which improves once the infant can move their head independently

Most resolve without intervention (self-correction) by the time the infant can sit without support

Self-correction occurs because of the rapid cranial growth in the first 4-6 months of life (for premature infants use 4-6 months corrected age), and ongoing growth until the anterior fontanelle closes

Self-correction in brachycephaly is evident when there is an occipital ridge present (bone remodelling starts at the base of the occiput and moves upwards towards the crown)

Plagiocephaly and brachycephaly are present in around 1% of teenagers

Differential diagnosis

Craniosynostosis

Craniofacial anomaly causing skull deformity which may be associated with abnormal brain development

Caused by premature fusion of one or more skull sutures resulting in ridging of sutures

Does not improve over time

May be an isolated finding with a single suture involved, or may be associated with other syndromes eg Apert, Crouzon syndrome

Craniosynostosis with similar head shape to plagiocephaly

Unilateral coronal craniosynostosis (causes forehead flattening)

Unilateral lambdoid craniosynostosis (causes occipital flattening on the opposite side to the forehead protuberance)

Conditions associated with positional plagiocephaly

Congenital muscular torticollis

Tightening/contracture of the SCM muscle due to limited intrauterine space (multiple pregnancy, oligohydramnios)

Usually noted within the first month of life

Clinical features

head tilt toward the same side as the tight SCM muscle

tendency to look to the opposite side of the tight SCM muscle

plagiocephaly on the opposite side of the tight SCM muscle

lump in the SCM muscle may be palpable

Early identification and management including referral to physiotherapist is beneficial as plagiocephaly will improve once the tight SCM is treated

Visual impairment

reduced vision and nystagmus result in head tilt to improve visual clarity

Cervical scoliosis

Assessment

Assess an infant for positional plagiocephaly if they present with one or more of the following

Head turning preference to one side

Head tilt

Posterior flattening on one side of the head (though parents may report a bump/bulge on the opposite 'normal' side)

Symmetrical occipital flattening (brachycephaly)

Ear displacement

Asymmetrical protuberance of the forehead

Facial asymmetry (one eye appears smaller)

History

Birth history (breech, multiple birth) and gestational age

Preference for looking to one side only during awake and asleep time

Assess for risk factors

Gross motor development eg head control, tone, sitting supported, tolerance of tummy time

Parent/carer preference in infant handling and positioning eg front or back sleeping, preferred feeding or carrying position

Onset and change in head shape over time (worsening or improvement)

Examination

Determine the type and severity of the head shape deformity

Assess for co-existing tight SCM (and other associated conditions)

Exclude craniosynostosis

Place infant on parent's lap with examiner standing at the infant's back

Observe head from above. Features which support a clinical diagnosis of plagiocephaly:

parallelogram shape head

frontal protuberance on same side as posterior flattening

ear pushed forward on same side as posterior flattening

posterior protuberance ('bump') on the opposite 'normal' side

Turn infant so their back is to parent's chest

Observe infant's head front on:

The eye on the affected side may look bigger or the cheek can be pushed forward in infants with plagiocephaly

Assess for features of a tight SCM muscle eg head tilt, restricted range of cervical rotation

Palpate

Size of anterior fontanelle

The anterior fontanelle can vary in size from small to large

1% have a closed fontanelle at 3 months of age, 38% at 12 months of age, 96% at 24 months of age

The size of the anterior fontanelle is useful in predicting response to physiotherapy or helmet therapy. An infant with an open fontanelle has more capacity for cranial growth and re-modelling

Features of craniosynostosis: ridging of coronal or sagittal sutures

Other: head circumference, eye movements, back and spine, and neurological examination to exclude other conditions associated with plagiocephaly

Severity

Severity assessment can be used to guide the need for referral to a specialist service and help monitor progress

Different modalities are available to assess the severity of the head shape deformity. One example of these is the 'Severity assessment for plagiocephaly, brachycephaly or scaphocephaly' scale (see Additional notes). Severity assessment is best undertaken by a clinician familiar with the severity scale, including community paediatric physiotherapists, who can provide ongoing follow-up

Management

Investigations

Imaging (eg cranial X-ray or CT scan) not required to confirm plagiocephaly or brachycephaly

If craniosynostosis is suspected, refer urgently to a craniofacial service that can decide on optimal diagnostic imaging. This reduces delay in appropriate management

Treatment

Do not use any pillow during sleep to prevent or manage flattening due to the risk of sudden infant death syndrome

Counterpositioning

Reducing the amount of time the infant spends lying on the flat side of their head will help improve the head shape. This is achieved by counterpositioning measures

Counterpositioning promotes active positioning of the head towards the opposite side of the flattening, by organising the environment so the infant is encouraged to turn towards that side

Counterpositioning examples for an infant with right sided plagiocephaly:

Sleep time

While in their cot, the infant will tend to look towards the doorway or centre of the room. Change the position of the cot so the infant looks to the left when the parent/caregiver enters the room

Awake time

Lay the infant on their left shoulder/side and place toys in front

Lay the infant on their back and place toys on their left side

Regular tummy time strengthens the muscles of the neck and helps develop head control

Carry the infant in a position which encourages head turning to the left

Physiotherapy

A physiotherapist can provide parent education, recommendations for infant handling, counterpositioning as well as specific exercises if congenital torticollis is present. Exercises for congenital muscular torticollis include passive stretching and strengthening of the opposite SCM muscle

A physiotherapist can monitor for improvement in head shape and provide guidance as to whether specialist referral is required

Use of helmets

There is some evidence for benefit of the use of a helmet in infants with severe deformity that is not improving with counterpositioning and physiotherapy

Even with helmet therapy there will be residual deformity of the skull

Optimal timing is around 6-7 months of age. Children with developmental delay or torticollis can be considered for a helmet with less deformity as these children are less likely to self-correct over time (because they spend more time on the flat spot)

Unlikely to benefit infants >10 months of age due to the slowing of skull growth and anterior fontanelle closure

Helmet therapy for plagiocephaly removes the pressure over the flat area, allowing the skull to grow into the space provided. For brachycephaly, it improves occipital growth and prevents further widening (it does not reverse it)

Custom made and fitted by an orthotist. Worn 23 hours per day for an average duration of 6 weeks to 3 months, depending on the improvement in head shape

Assessment for suitability is available in public clinics or private orthotist services

Consider consultation with local paediatric team when

Refer to specialist clinic (paediatrics or craniofacial service) when

Infant with severe positional head shape, worsening with time and not responding to general measures eg counterpositioning, physiotherapy

Infant with suspected craniosynostosis

Infant with congenital muscular torticollis not improving with community physiotherapist

Parent information

Plagiocephaly - misshapen head
Babys head shape fact sheet
TummyTime (rednose.org.au)

Additional notes

Example severity assessment scale for positional plagiocephaly

Includes a score from 0 (no asymmetry) to 3 (severe asymmetry) in each of the clinical features (posterior flattening, forehead asymmetry, ear misalignment, heat tilt and facial asymmetry) of plagiocephaly

Scoring thresholds for consideration of helmet therapy may vary, seek local specialist advice

Last updated January 2024

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Congenital torticollis Common, benign condition that affects the cosmetic appearance of an infant's head. Does not cause developmental delay Imaging is not required, diagnosis is based on history and examination findings including the absence of features of craniosynostosis Assessment includes identifying the presence of a co-existing tight sternocleidomastoid muscle (congenital muscular torticollis) and other risk factors Most resolve without any treatment and will show improvement with counterpositioning measures and physiotherapy intervention Positional plagiocephaly Skull deformation involving posterior flattening of either side of the head.

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THE BEIGHTON SCORING SYSTEM
The Beighton Scoring System measures joint hypermobility on a 9-point scale. The joints assessed are:

Knuckle of both little/fifth/pinky fingers

Base of both thumbs

Elbows

Knees

Spine

Where applicable, range of movement is measured using a goniometer, an instrument that measures the joint angle.

The movements that make up the Beighton score are:

PLEASE NOTE: When reading about this in professional textbooks the formal language used is as follows:

(A) With the palm of the hand and forearm resting on a flat surface with the elbow flexed at 90°, if the metacarpal-phalangeal joint of the fifth finger can be hyperextended more than 90° with respect to the dorsum of the hand, it is considered positive, scoring 1 point.

(B) With arms outstretched forward but hand pronated, if the thumb can be passively moved to touch the ipsilateral forearm it is considered positive scoring 1 point.

(C) With the arms outstretched to the side and hand supine, if the elbow extends more than 10°, it is considered positive scoring 1 point.

(D) While standing, with knees locked in genu recurvatum, if the knee extends more than 10°, it is considered positive scoring 1 point.

(E) With knees locked straight and feet together, if the patient can bend forward to place the total palm of both hands flat on the floor just in front of the feet, it is considered positive scoring 1 point.

1. Can you now [or could you ever] place your hands flat on the floor without bending your knees?

2. Can you now [or could you ever] bend your thumb to touch your forearm?

3. As a child, did you amuse your friends by contorting your body into strange shapes or could you do the splits?

4. As a child or teenager, did your kneecap or shoulder dislocate on more than one occasion?

5. Do you consider yourself "double-jointed"?

Answering yes to 2 or more of these questions suggests hypermobility (sense 85%, spec 90%)

The 5-part questionnaire was designed as a quick check to see if someone has or may have had hypermobility (Hakim and Grahame, 2003). It has been used in clinics and in research and has been translated for use in several languages and tested in several countries (Glans et al., 2020).

It was tested and designed as an alternative to the Beighton score. If you answer 'yes' to two or more of the questions, it strongly predicts a Beighton score of 4 or more, 4 being the cut-off point in criteria at the time the questionnaire was published.

There are two other tools that clinicians use in contemporary clinical practice and research. One assesses hypermobility in the arm (Nicholson and Chan, 2018), and the other hypermobility in the leg and foot (Ferrari et al., 2005 (children), Myer et al., 2017 (adults)).

These tools require a detailed examination of joints. In the arm this includes several ranges of motion at the shoulder, elbow, and wrist. In the leg this includes several ranges of movement at the hip, knee, ankle, heel, and toes.

Experts encourage clinicians to look more broadly than just testing the Beighton Score in a person presenting with local or widespread injuries and joint pain that they suspect may be related to hypermobility. However, while tools like the upper and lower limb assessments are important and helpful to the more expert clinician or researcher, they are complex and require skill. Most clinicians wishing to screen someone for hypermobility need quicker and more simple guidance.

Recently the hEDS/HSD Working Group of the International Consortium on Ehlers-Danlos syndromes and hypermobility spectrum disorders (IC-EDS and HSD, 2022) did an audit to determine which tests in the upper and lower limb tools most strongly suggest generalized joint hypermobility. Their findings are currently being studied in more detail. The aim is to determine whether adding specific extra tests (particularly ones that assess the shoulder, wrist, ankle, and toes) helps clinicians identify people with generalized hypermobility in ways that are better than only relying on the Beighton score.

Beighton P, Solomon L, Soskolne CL (1973) Articular mobility in an African population. Ann Rheum Dis 32(5):413-418

Ferrari J, Parslow C, Lim E, Hayward A. Joint hypermobility: the use of a new assessment tool to measure lower limb hypermobility. Clin Exp Rheumatol. 2005 May-Jun;23(3):413-20. PMID: 15971435.

https://www.clinexprheumatol.org/abstract.asp?a=2612 (Free to download)

Glans, M., Humble, M.B., Elwin, M. et al. Self-rated joint hypermobility: the five-part questionnaire evaluated in a Swedish non-clinical adult population. BMC Musculoskelet Disord 21, 174 (2020). https://doi.org/10.1186/s12891-020-3067-1

Hakim AJ, Grahame R. A simple questionnaire to detect hypermobility: an adjunct to the assessment of patients with diffuse musculoskeletal pain. Int J Clin Pract. 2003;57:163-6.

International Consortium on Ehlers-Danlos syndromes and hypermobility spectrum disorders. (Accessed May 2022).

Meyer, K.J., Chan, C., Hopper, L. et al. Identifying lower limb specific and generalised joint hypermobility in adults: validation of the Lower Limb Assessment Score. BMC Musculoskelet Disord 18, 514 (2017). (Free to download)

Nicholson LL, Chan C. The Upper Limb Hypermobility Assessment Tool: A novel validated measure of adult joint mobility. Musculoskelet Sci Pract. 2018 Jun;35:38-45. doi: 10.1016/j.msksp.2018.02.006. Epub 2018 Feb 22. PMID: 29510315. (Purchase from the Journal required)

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Assessing Joint Hypermobility - The Ehlers Danlos Society

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THE BEIGHTON SCORING SYSTEM The Beighton Scoring System measures joint hypermobility on a 9-point scale. The joints assessed are: Knuckle of both little/fifth/pinky fingers Base of both thumbs Elbows Knees Spine Where applicable, range of movement is measured using a goniometer, an instrument that measures the joint angle.

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Supported by the London School of Paediatrics

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See also

Key points

1. Metabolic disorders present at all ages with a variety of symptoms and signs that mimic common childhood illness. A high index of suspicion is needed to make a diagnosis

2. Consider a metabolic disorder in any newborn with unexplained encephalopathy or progressive illness, particularly following an uncomplicated pregnancy and birth

3. Once suspected, consult the metabolic team urgently

4. Collection of appropriate urine and blood samples during an acute illness is the key to diagnosis, but should not delay management

Background

Metabolic disorders are a large group of inherited conditions resulting from a block (partial or complete) to a pathway in the body's metabolism, or defects in the transport of substances

Though individually rare, collectively they represent an important cause of childhood morbidity and mortality

Newborn screening will diagnose many but not all metabolic disorders. A newborn may also become unwell before results are available

Diagnosis and management should always involve close liaison with a metabolic team

Assessment

Acute presentations where a metabolic disorder should be considered

Confusion or lethargy that may progress to coma, without clear evidence of injury, intoxication or other neurological event

Newborn with poor feeding, weak suck or hypotonia, often after asymptomatic period

Recurrent seizures

Presumed sepsis with poor response to treatment

Unexplained shock or cardiac failure

Rapid, deep breathing +/- progression to apnoea

Infant with Brief Resolved Unexplained Event (especially if recurrent)

Unexpected blood gas derangement (metabolic acidosis, respiratory alkalosis or hypoglycaemia)

Liver dysfunction, hepatomegaly or splenomegaly

Any acute presentation with multisystem involvement

History

Family history (a pre-existing family history is uncommon)

parental consanguinity

unexplained paediatric death (especially neonatal males)

relatives with similar presentations or unexplained neurodevelopmental disorders

Pregnancy and antenatal history

illness in pregnancy

diet including vegetarian/vegan diet and hyperemesis

HELLP syndrome (foetus may have a fatty acid oxidation disorder)

acute fatty liver of pregnancy

Neonatal period:

suspected sepsis without evidence of infection

lethargy, poor feeding/weak suck

vomiting, weight loss

respiratory compromise, apnoea

hypotonia

progressive encephalopathy

seizures

liver dysfunction

Progression of symptoms across childhood:

developmental delay or regression

recurrent unexplained vomiting

recurrent illness precipitated by catabolic episodes (infection, exercise, fasting) or certain foods or medicines

aversion to certain foods eg protein, fruit

unexplained neurological symptoms (behavioural changes, encephalopathy, seizures, ataxia)

unexplained exercise intolerance (myalgia, rhabdomyolysis)

acquired hepatomegaly and/or splenomegaly

Examination

Facial dysmorphism or coarsening of features

Lethargy

Hypotonia

Altered conscious state or encephalopathy

Dehydration

Jaundice

Hepatosplenomegaly

Tachypnoea, apnoea

Cardiac failure

Ocular changes (cataracts, retinal changes, optic atrophy, strabismus)

Unusual body odour eg maple syrup in MSUD, sweaty feet in isovaleric aciduria

Skin eg xanthomas, nodules, kinky hair, rash

Growth parameters

Interpretation of clinical findings should always be made in consultation with a metabolic team

Management

Investigations

Metabolites indicative of metabolic disorders are best detected at time of acute presentation

Careful collection and handling of blood, urine and CSF samples is important, but should not delay management of the unwell child
First line investigations (collection as per local hospital protocol)

Blood:

venous or capillary blood gas

glucose (point of care testing appropriate)

serum lactate (venous sample)

serum ammonia (transfer sample urgently)

other tests as clinically indicated eg FBC, UEC, LFT, CRP, cultures

Urine

ketones, glucose, pH

metabolic screen (including ammino acids and organic acids)

Interpretation of first-line investigations:

Interpretation must take account of the clinical context - unwell children without an underlying metabolic disorder frequently have deranged blood gas values

Consult the metabolic team urgently to discuss abnormal results

The acid-base state, glucose levels, ketones and ammonia may help to classify the type of metabolic disorder (see table in additional notes)

Hyperammonaemia is a medical emergency

Second line investigations

As advised by metabolic team

Treatment

Principles of management
These apply to the unwell child with a suspected metabolic disorder, and for subsequent presentations where a diagnosis is already known

Children with a known metabolic disorder will likely have their own emergency management plan

Resuscitation

Early consultation with metabolic team

as soon as a metabolic disorder is suspected

for children who present with a known metabolic condition, access the child's emergency management plan

Stop intake of any triggering factors

Maintain hydration
use intravenous or nasogastric fluids to correct dehydration and replace ongoing losses eg vomiting, diarrhoea

Prevent catabolism

intravenous fluids such as glucose 10% with sodium chloride 0.9% is standard first-line treatment for an unwell child with a metabolic disorder, except for mitochondrial conditions (these require glucose 5% with sodium chloride 0.9%)

special metabolic formula or additional IV lipids/nutrition may be required after discussion with the metabolic team

Enhance disposal of toxic metabolites

intravenous medications to chelate or divert toxic metabolites, or replenish deficient metabolites, depending on metabolic disorder in consultation with the metabolic team

haemofiltration in ICU may be required if there is a rapid deterioration due to accumulation of toxic metabolites

Peri-operative management of a child with a known or suspected metabolic disorder should:

always be planned early with the metabolic team

generally avoid prolonged fasting with provision of sufficient calories (using IV glucose-containing solutions) to prevent catabolism

Consider consultation with local paediatric team when

Any child with a suspected metabolic disease

Consider transfer when

A child requiring care beyond the comfort level of the hospital

For emergency advice and paediatric or neonatal ICU transfers, see Retrieval Services

Consider discharge when

Following discussion with local metabolic service

Additional notes
Interpretation of initial investigations

Serves as a guide only: consult the metabolic team with abnormal results

Table below is most relevant for neonates and small infants

Must also take account of the clinical context, including the period of fasting prior, hydration status, stage of illness and what fluids or other management have already been started

An unwell child without a metabolic disorder may have lactic acidosis, respiratory alkalosis hypoglycaemia and ketonaemia

¹ Inappropriately low
² Calculate by using (Na) - (Cl + HCO3). Normal 8 to 16 mmol/L

Additional Resources

Last updated June 2022

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Metabolic disorders present at all ages with a variety of symptoms and signs that mimic common childhood illness.

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Oxford IIC infectious disease training

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IIC 2024 will be held as three-day physical meeting, with a possibility of virtual participation. The Organising Committee strongly encourage attending the physical meeting if at all possible. Early registration for IIC 2024 to be sure of your place. The early bird reduced registration fees are available until 31st January 2024. UPDATE at 19th April: Registration for IIC 2024 has been paused - the course is full. If you wish to join the waiting list please contact iic@paediatrics.ox.ac.uk The registration fee includes The registration fee does not include dinner on Monday 24th June, accommodation and travel. Dinner on Monday 24th June and b&b accommodation at St Catherine's can be purchased during the registration process.
All fees quoted are for HCPs working in medicine / research. Those from industry wishing to register should contact iic@paediatrics.ox.ac.uk.
Registration for IIC 2024 will close at 12 noon UK time on Friday 7th June 2024. Late registration may be possible subject to availability and with a £50 late fee. Virtual registration is also be possible - please click HERE. Cancellation Policy:
Cancellations should be made by emailing iic@paediatrics.ox.ac.uk and subject to the terms and conditions outlined at the time of booking. A refund will be given for cancellations up until one month before the meeting, less a 10% administration charge. No refund can be given for cancellations made within one month of the meeting, nor are there refunds for no-shows.
Members of ESPID, BPAIIG and PIDS are eligible for a reduction in fees. We strongly recommend that you become a member of ESPID for all the benefits this brings. http://www.espid.org/content.aspx?Group=membership&Page=join Registration fees for IIC 2024:
Category
Trainees £
Consultants £

1 November - 31 January Earlybird member of ESPID / BPAIIG / PIDS
690
825

1 November - 31 January Earlybird non member
785
950

1 February - 21 June member of ESPID / BPAIIG / PIDS
790
925

1 February - 21 June non member
885
1050

Virtual registration: £350 / LMIC virtual registration: £50

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IIC 2024 will be held as three-day physical meeting, with a possibility of virtual participation. The Organising Committee strongly encourage attending the physical meeting if at all possible. Early registration for IIC 2024 to be sure of your place. The early bird reduced registration fees are available until 31st January 2024.

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Pediatric Neurologic Examination Videos & Descriptions: Home Page

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The PEDIATRIC NEUROLOGIC EXAM: A NEURODEVELOPMENTAL APPROACH uses over 145 video demonstrations and narrative descriptions in an online tutorial. It presents the neurological examination of the pediatric patient as couched within the context of neurodevelopmental milestones for Newborns, 3 month-olds, 6 month-olds, 12 month-olds, 18 month-olds, and 2-and-a-half year-olds. This Internet Accessible Tutorial for Medical Neuroscience in the Pediatric Neurologic Examination is authored by the University of Utah School of Medicine (Suzanne S. Stensaas, PhD), and the University of Nebraska Medical Center (Paul D. Larsen, MD). In assessing the child�s developmental level, the examiner must know the age when key social, motor, and language skills are normally acquired. The normal neurological findings one would expect for a newborn are certainly different than a 2, 6 or 12-month-old infant. Obtaining developmental milestones is an important reflection of the maturation of the child�s nervous system and assessing development is an essential part of the pediatric neurological examination. Delay in obtaining developmental milestones and abnormal patterns of development are important indicators of underlying neurological disease.

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Watch our short video guides about using your inhaler correctly. The right technique will ensure you’re getting the right dose, so you can better manage your symptoms.

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Get your child involved in their own action plan from the start

Let your child help fill it in with the GP and encourage them to ask questions.

Even if your child is very young you can tell them that the plan is where you and the doctor write down all the things that will help them stay well with their asthma.

If your child is old enough let them have a copy of their action plan, or keep a copy on their phone.

Keep your child's action plan where you can see it

Stick it on the fridge, or pin it to a noticeboard.

Ask your child's GP or asthma nurse for a digital copy so you can save it on your phone. That way it's always easy to find when you need it.

Share your child's action plan with others

Whether it's a paper or a digital copy, share your child's action plan with friends, family, teachers and carers.

It can give you peace of mind that anyone looking after your child has the information they need to keep your child well.

Use your child's asthma action plan alongside our other resources for children

As well as your child's asthma action plan, you can use our calendar and stickers to help you and your child track their asthma symptoms.

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Using a written asthma action plan can significantly reduce the risk of asthma symptoms and an asthma attack for children.

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How to identify breathing difficulty | Salbutamol discharge/escalation advice

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EAACI asthma webinar

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The EAACI Knowledge Hub features an exceptional panel of experts who discuss four specific areas that are driving the field of pediatric asthma forward. Asthma, the most prevalent chronic respiratory disease among children, significantly affects their health and quality of life and is deemed a significant healthcare concern.

The session is chaired by Stefania Arasi (Italy) and Ibon Eguiluz (Spain), and the talks are delivered by outstanding speakers.

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Eguiluz-Gracia, I. Arasi, S. Eguiluz-Gracia, I. Feleszko, W. Fiocchi, A. Gherasim, A.

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EAACI Knowledge Hub • Webinar • EAACI Webinar on Pediatric Asthma

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EAACI Asthma module

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Adcock, I. Adcock, I. Mukherjee, M. Pérez de Llano, L.

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Asthma Module: Part of EAACI’s Allergy College materials for undergraduate students

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EAACI Knowledge Hub • Webinar • Asthma Module: Part of EAACI’s Allergy College materials for undergraduate students

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Allergy Care Pathway Itchy Sneezy Wheezy Project - Homepage

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itchy sneezy wheezy - welcome to the itchy sneezy wheezy project.  this is the homepage.  follow our story by clicking the link.  this section contains comprehensive information on allergy providing learning and clinical resources.  this section contains comprehensive information on allergy providing learning and clinical resources.  this section contains videos to help you with the management of allergy conditions.  here you will find information to help you understand allergy

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Allergy Care Pathway Itchy Sneezy Wheezy Project - Homepage

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Itchy Sneezy Wheezy - Welcome to the Itchy Sneezy Wheezy Project. This is the homepage. Follow our story by clicking the link. This section contains comprehensive information on allergy providing learning and clinical resources. This section contains comprehensive information on allergy providing learning and clinical resources.

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The National Child Mortality Database (NCMD) is an NHS-funded programme delivered by the University of Bristol. We gather information on all children who die in England, so that we can improve and save children's lives in the future.

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NCMD | The National Child Mortality Database

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The National Child Mortality Database (NCMD) is an NHS-funded programme delivered by the University of Bristol. We gather information on all children who die in England, so that we can improve and save children's lives in the future.

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Anaphylaxis UK holds the PIF TICK - the UK's quality mark for health information. This certifies that we are a 'trusted information creator' and that the PDF downloads of our Factsheets are evidence-based, jargon-free, up-to-date and produced to the best possible standard.

The PIF TICK is run by the non-profit Patient Information Forum (PIF).

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Our factsheets are designed to provide you with reliable and up-to-date information about various aspects of anaphylaxis and allergies.

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Cows Milk Protein Allergy

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Crying Baby or Cow's Milk Protein Allergy?

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Paediatric Food Allergy

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Allergy UK Masterclass: Paediatric Food Allergy 01/12/22

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Paediatric Allergy training - PAT Course

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This online course will focus on the practical, clinical management of allergy in children and young people. It is the first in a series of three Paediatric Allergy Training (PAT) courses provided by the RCPCH.

What is the course about?

This online course will focus on the practical, clinical management of allergy in children and young people. It is the first in a series of three Paediatric Allergy Training (PAT) courses provided by the RCPCH.

During the course, our expert faculty will cover:

How to take an allergy focused history and allergy tests

First line management of cow's milk allergy and the 'Unsettled Infant'

Anaphylaxis and allergic rhinitis

Eczema care, egg allergy and complementary feeding.

Target Audience

PAT 1 is suitable for all professionals seeing children with allergic disease.

Learning Aims, Objectives and Outcomes:

Aim:

The PAT courses provide healthcare professionals with the knowledge and skills required to effectively manage children with food allergies and their comorbid allergic conditions.

Outcome:

By the end of this course you will be able to:

Take an allergy focused clinical history to interpret specific IgE results

Explain core allergy problems, specific IgE tests and basic disease mechanisms

Demonstrate good emergency management of food allergy and common allergic conditions

Describe first line diagnosis and dietary management strategies for cow's milk allergy; and list pregnancy, lactation, weaning diets for all children

Signpost patients to online resources and available multidisciplinary resources

Outline the importance of teaching and learning in a multi-disciplinary environment.

The Revd. Dr Mich LajeunesseRees

The Revd. Dr Mich Lajeunesse is a Consultant in Paediatric Allergy & Immunology at Southampton Children's Hospital, and an Honorary Senior Lecturer at the University of Southampton. He was appointed to Southampton in 2008 and is the lead NHS consultant for the Regional Children's Allergy Service. Dr Lajeunesse is actively involved in food allergy research, allergic reactions to vaccines and immunotherapy. He is a member of the teaching faculty of the Allergy MSc course at the University of Southampton and leads the RCPCH PAT course series.

Expression of interest

Submit your details to be alerted when the course next goes live or spaces become available.

Related resources

How to Manage: Paediatric Allergy Training 2 (PAT2)

This online course will focus on the practical clinical management of allergy in children and young people. It is the second in a series of three Paediatric Allergy Training (PAT) courses provided by RCPCH.

About us

Royal College of Paediatrics and Child Health was founded in 1996 and with members in the UK and internationally, we play a major role in postgraduate medical education, professional standards, research and policy.

RCPCH website

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How to Manage: Paediatric Allergy Training 1 (PAT1)

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Skip to content Close VisualV1 - Cross Created with Sketch. Search for an online learning, webinar or podcast VisualV1 - Home Created with Sketch. Menu This online course will focus on the practical, clinical management of allergy in children and young people.

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Welcome to our 2022/3 Programme!

We offer a combination of both face to face and online study days bringing all the Allergy Academy expertise, international speakers, practical tips and news about allergy developments to you and we are so thrilled to be doing so.

THE NEED: Those living with allergies are suffering from less access to healthcare and greater difficulty in finding expert advice. Our health professional community has emerged from lockdown with increased waiting lists, restricted times for patient appointments and less clinical capacity among their teams.

THE SOLUTION: Our study days are designed to support your timely recognition, fast decision-making and safe management for the wide range of allergic diseases and related disorders. Our days have been tailor made for healthcare professionals for the past 12 years, and now we are able to extend our reach further with our combination of in-person, hybrid and online events. Online the learning remains our biggest priority and in our interactive study days delegates can ask questions throughout the presentations, chat with other delegates online and vote in presenters' polls.

ACCESSING THE RECORDED CONTENT: All delegates who register for an event will be sent the recordings of the presentations and any resources shared by our speakers or discussed on the day. There is also previous webinar content available by registering in the Webinar Section of the website.

To check you will be able to see the streamed content, you can go to one of the streaming websites we will use for these study days to test the example video.

REGISTERING FOR EVENTS: All delegates will register through Eventbrite. When you have registered, we will use the Eventbrite platform to mail out the link and passcodes for the appropriate event. Please ask any questions by contacting our team on Allergy-Academy@kcl.ac.uk

THE FUTURE: With your help and support, we will continue to grow through our collaborations with a wide range of health care medical groups, Colleges, experts and Commissioners to enhance this offering and increase the scope of our #ALLERGYONLINE offering. Tell us what you think and keep in touch by signing up as a member at the bottom right of our home page. Thank you!

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Welcome to our 2022/3 Programme! We offer a combination of both face to face and online study days bringing all the Allergy Academy expertise, international speakers, practical tips and news about allergy developments to you and we are so thrilled to be doing so.

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Child Protection Companion

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RCPCH Child Protection Portal - Child protection and safeguarding in the UK: your essential resource to help inform clinical practice, child protection procedures, and professional and expert opinion in the legal system

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This Companion describes the essential context and the pathway of child protection cases, beginning with the medical assessment, a discrete chapter on each form of maltreatment, and continuing through to court and training.

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For full access to this content, log in to an existing user account or purchase a subscription.

About us

Child Protection Portal is managed by the Royal College of Paediatrics and Child Health. Founded in 1996 and with members in the UK and internationally, we play a major role in postgraduate medical education, professional standards, research and policy.

RCPCH website

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Child Protection Companion content - RCPCH Child Protection Portal

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This Companion describes the essential context and the pathway of child protection cases, beginning with the medical assessment, a discrete chapter on each form of maltreatment, and continuing through to court and training.

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Authored By:Elaine Kiriakopoulos MD, MScReviewed By:Robert Fisher MD, PhD

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There are many different types of seizures. New terms to describe and classify seizures have been developed by the International League Against Epilepsy. This was done to make the names of seizures more accurate, less confusing, and more descriptive of what is happening. Listen to Drs. Joe Sirven and Bob Fisher discuss the changes in this episode of our “Hallway Conversations” podcast series:

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RSM Paediatric Events

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RSM Infectious disease study day

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Dermatology Essential skills and Paediatric Dermatology learning

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all courses (guest) | british  college of dermatology

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Discover the future of dermatology with AI technology. Learn how AI can analyse skin images like a dermatologist and its potential benefits and ethical concerns. See results from a survey of patients' opinions on AI in skin diagnosis, highlighting optimism but also concerns about accuracy and privacy.

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DermNet provides Google Translate, a free machine translation service. Note that this may not provide an exact translation in all languages

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Paediatric prescribing

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Paediatric Prescribing Principles – RCPCH Learning

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Bacterial Meningitis and meningococcal septicaemia

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How to use this page

You will find the course content below. This Bacterial Meningitis & Meningococcal Septicaemia eLearning has two steps:

1) The elearning package

2) The post-course evaluation form

Once you have completed the eLearning package, a ' Mark complete ' button will be available. Click this button to complete the section.

Next, complete and submit the post-course evaluation form, and click the ' Mark complete ' button

Once all steps have been completed, a downloadable certificate of completion will be issued on the page.

If you have any questions, please contact the RCPCH Learning team

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Bacterial Meningitis & Meningococcal Septicaemia

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You will find the course content below. This Bacterial Meningitis & Meningococcal Septicaemia eLearning has two steps: 1) The elearning package 2) The post-course evaluation form Once you have completed the eLearning package, a ' Mark complete ' button will be available. Click this button to complete the section.

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Pain management

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Eczema Masterclass

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Allergy UK Eczema Masterclass September 2023

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National criteria for prompt intravenous-to-oral switch (IVOS) of antimicrobials in children and young people (including newborns)

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The national criteria for prompt intravenous-to-oral switch ( IVOS) of antimicrobials in children and young people, including newborns, contains 29 IVOS criteria categorised into 5 sections. These criteria were co-produced through a UK-wide consensus process involving 170 multidisciplinary participants.

Timing of intravenous antimicrobial review​

IVOS should be considered within 48 hours of the first dose of intravenous ( IV) antimicrobial being administered.

If no IVOS within first 48 hours, review daily thereafter.​

Clinical signs and symptoms​

Clinical signs and symptoms of infection are improving.​

Temperature has been between 36 and 38°C for the past 24 hours.​

Paediatric Early Warning Score is decreasing.

Infection markers ​

White cell count is trending towards normal range.

C-reactive protein is decreasing.

Enteral route​

Gastrointestinal tract must be functioning with no evidence of malabsorption.​

Safe swallow or enteral tube administration.​

Suitable alternative switch option available, considering spectrum of microbiological activity, oral bioavailability, palatability, any clinically significant drug interactions, or patient allergies.

No significant concerns over patient adherence to oral treatment.​

No vomiting within the last 24 hours.​

Special considerations

The following criteria may require special consideration in the context of a switch within 48 hours. However, on specialist advice, an IVOS within 48 hours may still be indicated for some patients with these infections.

Special considerations are:

deep-seated infection

infection requiring high tissue concentration that is not achievable via oral antibiotics

infection requiring prolonged intravenous antimicrobial therapy

critical infection with high risk of mortality (for example, sepsis requiring inotropes or ventilation)

patient aged 28 days and under (neonate)

patient is considered severely immunocompromised

patient is admitted on paediatric intensive care unit

Specific infections for special consideration are:

bloodstream infection

empyema

endocarditis

meningitis

osteomyelitis

severe or necrotising soft tissue infections

septic arthritis

undrained abscess

exacerbation of cystic fibrosis or bronchiectasis

central venous catheter-associated infection

Antimicrobial IVOS criteria and tool - project information

These IVOS criteria have been developed through:​

completion of a rapid systematic literature review to validate selection of IVOS criteria​

web-based survey for consensus-gathering involving 170 multidisciplinary participants from all UK nations to agree evidence-based, UK-wide IVOS criteria for hospitalised paediatric and neonate patients​

The criteria for children and young people, including newborns differ from the IVOS criteria for adults, with the addition of palatability of the alternative switch option, and the following special considerations:

patient aged 28 days and under (neonate)

patient is considered severely immunocompromised

patient is admitted on paediatric intensive care unit

exacerbation of cystic fibrosis or bronchiectasis

exacerbation of central venous catheter-associated infection

This project has been led by the UK Health Security Agency (UKHSA)'s Healthcare-Associated Infection, Fungal, Antimicrobial Resistance, Antimicrobial Use and Sepsis Division, in collaboration with NHS England AMR Programme.

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National criteria for prompt intravenous-to-oral switch (IVOS) of antimicrobials in children and young people (including newborns)

# data[].attributes.attachment_link.description
The national criteria for prompt intravenous-to-oral switch ( IVOS) of antimicrobials in children and young people, including newborns, contains 29 IVOS criteria categorised into 5 sections. These criteria were co-produced through a UK-wide consensus process involving 170 multidisciplinary participants. IVOS should be considered within 48 hours of the first dose of intravenous ( IV) antimicrobial being administered.

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British Association of Perinatal Medicine

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This document sets out standards for safely managing the neonatal airway in neonatal services in the UK. The document focuses on unit capability and aims to ensure that a safe service is always available.
The purpose of this document is to

Set out standards for ensuring safe airway management for babies in Maternity and Neonatal Services in the UK.

Outline the minimum expected departmental capabilities for airway management in different settings, recognising the current challenges in maintaining universal intubation competency in all units.

Provide guidance on optimising airway management.

Provide supporting training and assessment materials as well as signposting other suitable training resources.

Suggest areas for research and innovation to improve safe neonatal airway management.

This framework complements the existing BAPM Framework for Practise on Managing the Difficult Airway in the Neonate.

Resources

BAPM Airway Safety Standard main document

Supporting Materials for this Capability Framework
Training Materials

BAPM Airway Skills Training and Assessment Tools (Appendix A)

Tips for videolaryngoscopy (Appendix B)

A short guide to use of waveform capnography (Appendix C)

Practical Support Materials

Poster: Airway Equipment and Initial Respiratory Support Settings (Appendix D)

Intubation Checklist (Appendix E)

LISA Checklist (Appendix F)

Assessment Materials
Appendix G, H and I are Excel files.

*Please download and save these files in order to view and use the drop-down function within them.*

Intubation/ LISA Log (Appendix G)

Individual Airway Competency Assessment form (Appendix H)

Neonatal Unit Staff Airway Assessment Log (Appendix I)

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Joost van Schuppen, Laura Kox, Wes Onland, Robin Smithuis and Rick van Rijn

Radiology, Nuclear medicine and Neonatology department of the Amsterdam University Medical Centre

In this review we will discuss a systematic approach to the neonatal chest radiograph.
Close collaboration between neonatologists and radiologists is the key in achieving the correct diagnosis, since the radiographic features of many lung disorders overlap and the findings on the chest film can be rather subtle.
Clinical information like age of the neonate, gestational age and therapy with ventilation or surfactant is vital for the interpretation of the radiological findings.

We will first discuss a diagnostic approach based on radiographic and clinical findings and subsequently we will discuss the specific pulmonary diseases and complications.

Interpretations of tube positions, lines and catheter positions are discussed in Tubes and lines in neonates.

Invasive mechanical ventilation and surfactant therapy will have a huge impact on the radiographic findings and are essential clinical information for the radiologist.

Here is a list of common pulmonary disorders in neonates based on acute and chronic disease, complications of ventilation and congenital anomalies (Table).

* CPAM was previously referred to as congenital cystic adenomatoid malformation (CCAM) and presents as a mass of abnormal non-functional lung tissue

* TAPVR is total anomalous pulmonary venous return. The pulmonary veins do not connect to the left atrium, but enter the systemic venous circulation.

The approach to the neonatal chest film starts by looking at the technique of the radiograph.
Then the position of lines and tubes is analyzed.
See Lines and tubes in Neonates.
After these steps, the chest film can be interpreted for pathology.

This is done in a stepwise manner:

Consider gestational age, postnatal age, and other clinical information, including respiratory support.

Lung volume should interpreted, being either normal, hypo-inflated or hyper-inflated.

In ventilated neonates positive end expiratory pressure (PEEP) should be noted on the request. (Normal PEEP 5-8 cm H2O)

Interpretation of lung parenchyma, being either normal, lucent, or opacified.

Pathology unilateral or bilateral.

The postnatal age of the neonate in days or hours is important as some disorders are acute conditions and some disorders at a present later stage. In addition, the course of illness and therapy so far should be taken into account.

Chest abnormalities can be divided into:

Radiopaque
Other terms that are used to describe these abnormalities are high attenuation, or opacities. They can be fine or course linear, granular or reticulo-granular. They can be diffuse or focal.

Radiolucent
These are lucent abnormalities, being the result of hyperinflation of lung parenchyma, or abnormal collections of air. Depending on the location, these lucencies can follow pleura or mediastinal structures and are often sharply delineated.
Intraparenchymal abnormalities can be less circumscribed.

In some cases there is a combination of radiopaque and radiolucent abnormalities,

which makes the interpretation of the radiographic findings challenging.
For example, pulmonary interstitial emphysema (PIE) can be regarded as lucencies, but can also be interpreted as radiating linear radiopaque abnormalities.
Notice that a diaphragmatic hernia can be a focal radiopaque or radiolucent

Radiopaque - High Attenuation
RDS

Respiratory distress syndrome in preterm neonates presents with low lungvolume, air bronchograms and symmetric fine granular opacities, ranging from mild disease to complete white out of the lungs.

TTN
Transient tachypnea of the newborn is seen in full term neonates with mild respiratory distress and presents with subtle increased lung volume, parahilar linear densities and pleural effusions.
Atelectasis

MAS
Meconium aspiration is seen in full term and late term neonates and presents with coarse bilateral densities, that can be asymmetrical. There can be areas of atelectasis and air-trapping.

Atelectasis can be seen in tube malpositioning and as complication, e.g. in RDS and meconium aspiration.

Radiolucent - Low attenuation

Air Leak
Most radiolucent lung abnormalities are the result of air leakage usually as a complication of positive pressure ventilatory support and present as:

Pneumothorax

Pneumomediastinum and pericardium

Pulmonary Interstitial Emphysema (PIE)

Pneumatocele

CPAM
CPAM is the most common congenital lung malformation, but is still a rare disease. There is a microcystic and a macrocystic form. The latter presents as a radiolucent abnormality. Often in the first hours the lesion is not containing air yet and can present as radiopaque.

The ductus arteriosus is the connection between the pulmonary artery and the aorta.
Normally the ductus is open before birth and closes in term infants within the first day after birth as arterioles feeding the wall of the ductus contract in reaction to oxygen.

Preterm infants have fewer of these arterioles and sometimes an increase in oxygen does not lead to closure of the duct, which might result in a high pulmonary blood flow.
The diagnosis usually is suspected 5 - 7 days after birth, when there is pulmonary overflow or systemic steal.

Prostaglandin inhibitors
Prostaglandin inhibitorscan be used to close the open duct.
In some cases, surgical closure can be achieved either via a lateral thoracotomy with a clip, or later in life via an intra-arterial approach using a coil.

Prostaglandins
In neonates with a ductal-dependent cardiac disorder Prostaglandins can be used to keep the ductus arteriosus patent, which can be life-saving.

Premature with previously normal chest radiographs.
Image

Moderate enlargement of the heart in combination with ground glass changes of the lungs, in keeping with pulmonary edema.

Deep position of the CVC in the right atrium, normal position of gastric tube.

Ultrasound confirmed a persistent ductus arteriosus.

Premature of 25 weeks and 5 days, now 2 month old. Treatement for RDS

1. The first chest radiograph shows hyperinflation, and a markedly enlarged heart with increased vascular markings and interstitial markings.
NG tube and duodenal tube in situ.

2. After 5 days of treatment there is less hyperinflation and normalization of the heart size and vascular markings.
There still remain some interstitial markings, in keeping with BPD.

Complete atelectasis of the left lung

Treatment depends on the cause of the atelectasis, such as change of tracheal tube position, change in ventilatory support (pressure), alternating position from side to side, or in case of surfactant deficiency, intratracheal administration of surfactant.

Image
Complete atelectasis of the left lung due to selective intubation on the right. PICC line in situ with tip in superior vena cava. NG tube in situ.

Atelectasis of the right middle lobe

This preterm neonate was treated for respiratory distress, probably due to pneumonia.

Notice the position of the nasogastric catheter indicating mediastinal shift to the right.

This is a neonate of 41 weeks gestational age, who was treated for asphyxia, including hypothermia treatment. Sudden respiratory distress.

Pneumonia can be difficult to distinguish from other entities such as RDS or bronchopulmonary dysplasia.
In the majority of cases the clinical course, together with intratracheal sputum cultures and biochemical parameters are leading in the diagnosis of pneumonia.
Without signs of infection, a consolidation on a chest radiograph is unlikely to be caused by pneumonia.

Risk factors for neonatal pneumonia are:

Neonate, GA 37+6 weeks, respiratory distress, treated with CPAP after delivery. History of maternal infection.

First study the image.
What are the findings.

This child developed signs of infection, both clinically and in the laboratory findings.
The radiographic findings were attributed to neonatal pneumonia.

A full term neonate, with respiratory distress after 24 hours.

Image
Hyperinflation of both lungs and cardiac enlargement with increased interstitial markings and vascular markings. No pleural fluid.

The differential diagnosis includes TTN and neonatal pneumonia. After 48 hours there was no improvement of the respiratory distress, and the neonate developed signs of infection.

One might argue that there could be a combination of TTN and pneumonia.

Air leakage as a result of barotrauma in newborns present as:

Pneumothorax

Pneumomediastinum and pericardium

Pulmonary Interstitial Emphysema (PIE)

Tracheal rupture

Pneumatocele

Pneumothorax can occur spontaneously or as a complication of positive pressure ventilatory support.
The introduction of surfactant treatment and improved ventilatory support has significantly decreased the incidence.

When additional pneumomediastinum is present, a 'lifted thymus' can be seen, also known as the 'Spinnaker Sign'.

Pneumothorax

Neonate 3 days old with RDS. Gestational age: 34 weeks.
First study the image.
What are the findings?
Image

Pitfall
In newborns an important pitfall is the presence of a skin fold, which can be mistaken for a pneumothorax.

Skinfolds do no follow anatomical borders and can be traced outside the chest cavity or cross-over pulmonary vessels.

Left arm projecting over hemi-thorax, resulting in sharp radiopaque line (arrowhead).

Images of a neonate with respiratory distress.
37 weeks gestational age
After primary caesarean section.

Right image
On the follow up chest x-ray, the pneumothorax has spontaneously resolved.

A pneumothorax can be very subtle, since in many neonatal pulmonary disorders the lungs are not compliant and will not collapse.
Often in a supine neonate, the pneumothorax only manifests ventrally.
Sometimes only sharpening of the mediastinal structures with unilateral lucency is noted.

Image
Full term infant shortly after birth with mild pulmonary distress.

Mild diffuse linear opacification of both lungs in keeping with TTN.

Bilateral pneumothorax (arrowheads).

Sharpening of the mediastinal structures on both sides as a result of interface between mediastinum and pneumothorax.

Due to fluid in the lung parenchyma these lungs were stiff and did not collapse.

Neonate 32 weeks gestational age. Treated for RDS via CPAP, with sudden respiratory distress.

First study the image.
What are the findings?

Pneumomediastinum

Pneumomediastinum is recognized as air inside the mediastinum.
The classical sign is the so-called spinnaker sign (arrowhead).
This is caused by the thymus being 'lifted up' from the lower mediastinum by the mediastinal air.

First study the image.
What are the findings?
Image

A residual ventral pneumothorax can be recognized by the sharp paracardial and mediastinal contour on the left side.

On the right side there is a drain in situ, with no apparent residual pneumothorax, but subcutaneous emphysema, due to air leak with drain.

Pneumomediastinum is recognized as air inside the mediastinum, where there is air between the thymus and heart figure (arrowhead).

Skinfold over right hemi-thorax.

A cross table lateral view can help to confirm the presence of a pneumothorax or a pneumomediastinum.

A full term neonate after meconium aspiration.

Pneumomediastium, in combination with subcutaneous emphysema. NG tube in situ.

Pulmonary Interstitial Emphysema (PIE)

First study the image.
What are the findings?

Findings:

Bubbly air configurations bilateral indicating PIE.

Note the small mediastinal silhouette, caused by shrinking of the thymus as a result of stress.

Deep position umbilical vein line, tip likely in left atrium or pulmonary vein.

Good position ETT. NG tube in situ.

Neonate, gestational age 30 weeks, day 1, sudden deterioration after MIST.

First study the image.
What are the findings?

Neonate, gestational age 27 weeks, treated for RDS.
At age of 2 days sudden deterioration.

First study the images.
What are the findings?

Image 1
Bilateral reticulonodulair opacities in keeping with IRDS, treated via CPAP.

Image 2
At the age of 2 days the X-ray shows radiating lucencies in the left lung as a result of PIE.

These images are of a neonate gestational age 32 weeks, who was treated for RDS.

Several complications developed, including a pneumothorax on the left side, which was drained.
After drainage there was a deterioration.

Image 2
In follow up the child also developed a pneumothorax on the right side.

The most common congenital anomalies in neonates are:

Congenital pulmonary airway malformation

Congenital pulmonary airway malformation (CPAM) was until recently know as congenital cystic adenomatoid malformation (CCAM).
It is a spectrum of bronchopulmonary foregut malformations.

There are three histological types:

Type I (75% of cases) is composed of variable sized cysts, with at least one dominant cyst larger than 2 cm in diameter.

Type 2 (10-15% of cases) is composed of smaller multiple cysts of the same size, less than 1 cm in diameter.

Type 3 presents as a solid mass composed of micro cysts.

Radiographic findings in CPAM

In type I and II, multiple thin walled cysts containing air and varying in size are seen.

In type III a solid lesion is seen.

Infection of the cysts can cause air fluid levels.

Large lesions cause mass effect with mediastinal shift and atelectasis of adjacent lung parenchyma.

CPAM usually involves one lobe.

Contrast enhanced CT scan is essential in the analysis of CPAM and sequesters.
Given that CPAM and sequester often are hybrid lesions, feeding arterial vessels need to be visualized or ruled out before surgical intervention.

Images of a neonate, 40 weeks gestational age.
Antenatal suspicion of large CPAM on the left side.
At birth respiratory distress

Pulmonary sequestration

Most sequestrations are detected on antenatal ultrasound and present as a mass in the basal lobes, usually paramedian on the left.

Imaging

On radiographs a sequestration is often not detected.

Prenatal ultrasound often raises the suspicion of a sequestration, which is seen as a hyperechoic mass.

Management is controversial. Some advocate surgical resection because of the risk of infection and cardiac failure due to the left to right shunting.
Others advocate a wait and see approach, as these sequestrations can resolve spontaneously.
Before surgical management MR or CT is needed to analyze the blood supply and the type of the sequestration.

Congenital Lobar Emphysema

Congenital lobar emphysema, now known as congenital lobar overinflation, is a condition in which there is hyperexpansion of a lobe of the lungs.
Narrowing or weakness of a lobar bronchus causing a check-valve mechanism is the most likely cause.

Symptoms depend on the degree of lobar hyperexpansion.
A mildly hyperexpanded lobe may be asymptomatic and decrease in size with time and close follow-up is warranted in these cases. Progressive hyperexpansion of a lobe can occur and cause significant, sometimes life-threatening, symptoms. Those cases are treated with lobectomy.

Usually congenital lobar emphysema is detected on prenatal ultrasound.

Images of a term neonate with mild respiratory distress.
Antenatal there was suspicion of a CPAM.
The chest radiograph and CT show hyperinflation of the right upper lobe with architectural distortion.
The right lower lobe is compressed, but probably has a normal architecture.
Displacement of mediastinum and heart and atelectasis of the left lung.

Images of a 6 months old neonate with mild respiratory symptoms.

Radiograph reveals hyperinflation of left upper lobe with displacement of midline structures and some atelectasis of the lower lobe.

The CT confirms overinflation of the right upper lobe.

Diaphragmatic hernia

There are two types of hernia, the Bochdalek and the Morgagni type.
The diagnosis is often made prenatally.

The Bochdalek hernia is seen in about 95% of cases and located on the posterior side of the chest. Most often it is left sided (90%).
The Morgagni hernia, also known as retrosternal or parasternal hernia, is located parasternally, where the foramina of Morgagni are situated.

The severity of the disease is based on the degree of hypoplasia of the lung.

Imaging findings

Total or partial opacification of one side of the thorax, with no or little aeration of the ipsilateral lung.

Shift of the mediastinum to contralateral side.

The finding of part of the digestive tract in the chest cavity is pathognomic for the diagnosis.

Direct postpartum the digestive tract does not contain air, so it may go unnoticed or simulate an abnormality within the lungs.

Ultrasound demonstrated peristalsis in air and fluid containing structures confirming a large diafragmatic hernia .

These images are of a full-term neonate with shortness of breath.

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1. Lung Disease in Premature Neonates: Radiologic-Pathologic Correlation
by Agrons GA, Courtney SE, Stocker JT, Markowitz RI.
From the archives of the AFIP.
Radiographics 2005; 25:1047-1073

2. An approach to the asymmetric neonatal chest radiograph.
Alford BA, McIlhenny J.
Radiol Clin North Am 1999; 37:1079-1092.

3. Thorax, Mediastinum, Heart, and Great Vessels.
In: Van Rijn RR, Blickman JG eds.
Differential Diagnosos in Pediatric Imaging. 1th ed: Thieme, 2011; 1-138.

4. Radiological imaging of the Neonatal Chest.
Donoghue V, Baert AL, Knauth M, Sartor K,.
2nd revised Edition, Springer-Verlag, 2008, 261-273.

5. The neonatal chest X-ray.
Arthur R.
Paediatr Respir Rev 2001; 2:311-323.

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Radiology, Nuclear medicine and Neonatology department of the Amsterdam University Medical Centre In this review we will discuss a systematic approach to the neonatal chest radiograph.

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Insertion of Umbilical Catheters in Neonates

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Peripherally inserted central catheters (PICC Lines) - Neonatology guideline

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What's new / Latest updates 12/07/201 Advice for parents section: reference to April 2021 NICE guidance stating that use of antimicrobial impregnated central catheters are not recommended. This guideline is applicable to all neonatal staff caring for babies requiring Peripherally Inserted Central Catheters (PICC Lines).

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Central Line Imaging in Neonates Radiographic Views and Acceptable Line Positions

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10.1055/b-0035-122519

3 Neonatal Cranial Ultrasonography

Gerda Meijler, Linda de Vries, and Handan Güleryüz

The neonatal skull is easily accessible by ultrasound because of its small size and multiple acoustic windows. In sick or preterm neonates, serial brain imaging is indicated to follow brain development and injuries. As minimal handling is recommended, ultrasonography, which can be performed at the bedside, is the preferred tool to visualize the brain of both preterm and high-risk full-term neonates. For a successful neonatal cranial ultrasound (cUS), the examination experience of the sonographer and the use of a modern, portable ultrasound machine with appropriate transducers and presets are required. In addition, the examiner should take the necessary precautions to prevent hypothermia, infection, and disturbance of the infant.

Besides bedside imaging, there are other major advantages of cUS compared with other imaging modalities, including that it is safe, does not involve ionizing radiation, and is relatively cheap. cUS can reliably diagnose most congenital anomalies, hemorrhagic lesions, calcifications, and many forms of hypoxic-ischemic injury. It is, however, less reliable than magnetic resonance (MR) imaging for subtle lesions and does not depict myelination.

In this chapter, we will discuss ultrasound anatomy of the neonatal brain, how to differentiate normal findings from (subtle) abnormalities, the optimal timing of ultrasound examinations, and the most frequently occurring brain lesions of the preterm infant.

3.1 Ultrasound Anatomy of the Neonatal Brain

For a routine ultrasound examination of the neonatal brain, the anterior fontanel is used as the acoustic window. Appropriate presets and well-fitting, appropriate transducers are used. The scan frequency for a standard examination is set at 7.5 to 8 MHz.

The examination includes assessing anatomy, maturation, and the presence of abnormalities by:

Examples of the standard coronal planes, showing the anatomical structures in both the very preterm and the full term infant's brain, are presented in Fig. 3.1 , Fig. 3.2 , Fig. 3.3 , Fig. 3.4 , Fig. 3.5 , Fig. 3.6 , Fig. 3.7 , Fig. 3.8 , Fig. 3.9 . For details on the anatomical structures seen in these planes, we refer to recent literature.

Scanning through the anterior fontanel generally allows an accurate assessment of most supratentorial structures. The posterior parts of the brain, the infratentorial structures, and the brainstem are farther away from the transducer, especially in larger preterm and full-term neonates. These structures can therefore be reliably assessed only if the supplemental acoustic windows (posterior fontanel, mastoid fontanels, and temporal windows) are additionally used. For detailed descriptions on how to use the supplemental windows for cUS and on the anatomical structures visualized while scanning through these windows, we refer to recent literature.

3.2 Maturational Changes and Distinction between Physiologic and Pathologic Echogenic Areas in the Neonatal Brain

Areas of echogenicity are often seen in the neonatal brain. Some of these are normal and related to maturational changes, whereas others may reflect (serious) injury. The distinction is not always easy.

3.2.1 White Matter

The immature white matter is characterized by its very high water content, almost complete absence of myelin, and, in cases of very preterm birth, additionally by migrating glial cells.

So-called frontal echodensities (subtle, homogeneous, symmetric echogenic zones in the frontal white matter and bilateral echogenic lines around/below the lateral ventricles on anterior coronal cUS scans) are related to this glial cell migration and seen in preterm neonates before term equivalent age (TEA; Fig. 3.10 and Fig. 3.11 ). Frontal echodensities should be distinguished from nonphysiologic periventricular echodensities (PVE) that may indicate white matter injury. These are more echogenic, less homogeneous, and less symmetric ( Fig. 3.12 ). "Flag-shaped" echogenicities in the parietal white matter on parasagittal scans, subtle echogenic blushes superolaterally from the lateral ventricles, and linear echogenicities running parallel to the trigone of the lateral ventricles on coronal scans are all considered physiologic phenomena in both preterm and full-term neonates ( Fig. 3.13 , Fig. 3.14 , Fig. 3.15 ). These echogenicities are symmetric, and homogeneous, and they tend to fade with age. The latter are thought to represent the optic radiation. These normal echogenicities should be distinguished from pathologic PVE in the parietal white matter, which are likely to represent white matter injury ( Fig. 3.16 ).

Fig. 3.11 Physiologic echogenic lines (arrow) around the frontal horns of the lateral ventricle in very preterm neonate, gestational age 26 weeks.

Fig. 3.12 a,b Nonphysiologic periventricular echodensities (PVE) in a preterm neonate, gestational age 30 weeks. a Coronal plane showing the frontal, inhomogeneous, asymmetric PVE (arrow). b Right parasagittal plane showing patchy, inhomogeneous PVE in the frontal, parietal, and temporal white matter (arrows).

Fig. 3.13 Physiologic "flag-shaped" echogenicity in the parietal white matter (arrow). Full-term neonate, gestational age 38 weeks.

Fig. 3.14 a,b Physiologic echogenic blush in the parietal white matter (arrows). Preterm neonate, gestational age 27 weeks. a Coronal plane. b Parasagittal plane. Also note frontal echodensity (arrowhead), a physiologic finding at this age.

Fig. 3.16 Coronal a and parasagittal b cranial ultrasound images: nonphysiologic echodensities in the parietal white matter (arrows). c T1-weighted transverse MR image showing multiple punctate white matter lesions in the frontal white matter (arrowheads), also showing small right-sided germinal matrix hemorrhage. d Diffusion-weighted MR image showing extensive diffusion restriction throughout the parietal and occipital white matter (arrows). Preterm neonate, gestational age 34 weeks. MR imaging performed 3 days after birth. e (coronal) and f (parasagittal) cUS images: 2 weeks later cystic lesions have developed in the parietal white matter, still surrounded by abnormal PVE. g T1-weighted transverse MR image at high ventricular level, showing irregular dilatation of the ventricular system and deep sulci due to severe white matter loss, nearly abutting the ventricular wall, indicating white matter loss (arrows). h T2-weighted transverse MR image at mid-ventricular level, showing the abnormally shaped lateral ventricles and abnormal signal intensity in the frontal white matter (arrow heads). Also note the small right-sided IVH. MRI performed around TEA.

3.2.2 Deep Gray Matter

The immature deep gray matter has a higher cell and tissue density than the immature white matter and therefore appears relatively echogenic compared with the surrounding white matter on ultrasound scans performed in preterm infants before TEA. Especially the caudate nucleus and globus pallidus may look strikingly echogenic. The echogenicity is symmetric and homogeneous and tends to fade with age ( Fig. 3.17 ).

Echogenicity in the deep gray matter should, however, never be considered a normal phenomenon in (near)-term neonates or in preterm neonates beyond TEA. In this age group, it most likely represents hypoxic-ischemic injury, which is associated with serious consequences for outcome. The echogenicity may also be subtle and symmetric and often includes the thalami. A zone of low echogenicity can sometimes be seen between the basal ganglia and thalami, representing the internal capsule. This may cause a so-called onion peel appearance, whereby the echogenic basal ganglia and thalami are seen as separate echogenic structures and are interspersed by the low echogenicity of the internal capsule ( Fig. 3.18 ).

Fig. 3.18 a-d Abnormal echogenicity in the basal ganglia (arrow) and thalami (open arrow) in two full-term neonates with hypoxic-ischemic deep gray matter injury following acute perinatal asphyxia. (a, c) Coronal planes. (b, d) Parasagittal planes, also showing a zone of low echogenicity representing the internal capsule (arrowheads).

Other echodensities in the deep gray matter, resulting from infarction or hemorrhage, are more echogenic, asymmetric, focal, and easily distinguished from physiologic echodensities ( Fig. 3.19 ).

Lenticulostriate vasculopathy is characterized by linear or punctate hyperechoic areas in the basal ganglia and thalami. It is probably caused by a benign vasculitis of the lenticulostriate vessels and suggestive of mineralization of the arterial wall. It is seen in healthy preterm neonates, but also in association with various abnormal conditions such as central nervous system infections, metabolic disorders, and chromosomal abnormalities. It can easily be distinguished from the aforementioned physiologic deep gray matter echogenicity in preterm infants as it is linear or punctate and follows a typical vascular pattern ( Fig. 3.20 ).

Tips from the Pro

In summary, white matter echogenicities are likely to be physiologic if they have the following characteristics:

The echogenicity does not exceed that of the choroid plexus;

The echogenicity is homogeneous and symmetric;

The echogenicity fades with age.

Echogenicity in the deep gray matter is likely physiologic if it is seen in the preterm period, fades with age, and does not persist beyond TEA. It is subtle, homogeneous, and symmetric. The internal capsule should not be visible as a separate entity.

3.3 Timing of Examinations

The optimal timing and frequency of examinations is of great importance. In the preterm infant, cUS performed on the first day of life will first of all diagnose an antenatally or perinatally acquired lesion (see Fig. 3.16 ; Fig. 3.21 and Fig. 3.22 ) or congenital anomaly ( Fig. 3.23 ). Secondly, it enables the detection of (new) lesions within hours or days after the onset. Most of these lesions are clinically silent. Once the diagnosis is made, the evolution of the lesion over time should be assessed. In infants with germinal matrix-intraventricular hemorrhage (GMH-IVH), this enables timely recognition of post-hemorrhagic ventricular dilatation (PHVD), a potentially serious condition that may need intervention. Another serious complication of GMH-IVH is periventricular hemorrhagic infarction (PVHI). This lesion and its evolution can be diagnosed and followed if serial cUS scans are performed on a regular basis. In preterm infants with nonphysiologic PVE, sequential imaging will show whether the echogenicity will resolve without cystic evolution or whether cystic changes occur. Small cystic lesions develop only 3 to 6 weeks after the abnormal echogenicity is first seen and tend to resolve within several weeks. They may thus not be visible around TEA. In most infants, some degree of ventriculomegaly, resulting from white matter loss, will then be recognized. Not only cystic periventricular leukomalacia (PVL) but also nonphysiologic PVE of longer duration without cystic evolution (noncystic PVL) is associated with suboptimal neurodevelopmental outcome. Therefore, it is important to know the total duration of abnormal echogenicity.

Fig. 3.21 a-d Preterm neonate, gestational age 30 weeks, 5 days. Large left-sided subdural hemorrhage. a, b Coronal, resp. parasagittal cranial ultrasound images showing the large extra-axial hemorrhage in the temporal region. Also showing increased echogenicity in the temporal lobe (arrows) and compression of the left lateral ventricle. c, d Coronal, resp. transverse T2-weighted MR images showing, besides the extra-axial hemorrhage, abnormal signal intensity in the left temporal lobe adjacent to the extra-axial hemorrhage (open arrows) due to multiple small hemorrhages and tissue compression. The remainder of the brain parenchyma has a normal aspect for this age. MR imaging performed 6 days after birth.

Fig. 3.22 a-d Full-term neonate, traumatic delivery. a, b Coronal, resp. parasagittal cranial ultrasound (cUS) images showing increased echogenicity in the frontoparietal white matter (arrows) consistent with swelling or ischemia. Also showing increased echogenicity in the basal ganglia and thalami (open arrows), again related to edema or ischemia. Furthermore, there is a small hemorrhage in the thalamocaudate notch (arrowhead). c, d Coronal, resp. transverse (supraventricular level) T2-weighted MR images showing a left parietal epidural hematoma with some mass effect upon the adjacent frontal and parietal lobe. Areas of abnormal signal intensity in the white matter (open arrowheads). MR imaging performed 1 month after birth. The epidural hemorrhage was missed with cUS because of its high and peripheral location, being beyond the scope of cUS.

Fig. 3.23 a,b Preterm neonate, gestational age 30 weeks. a Midsagittal cranial ultrasound showing retrocerebellar fluid collection (arrow). The cerebellar vermis and other midline structures have a normal appearance. b Midsagittal T2-weighted MRI confirming a retrocerebellar cerebrospinal fluid collection without mass and with a normally developed cerebellar vermis, probably representing a small arachnoid cyst.

Although GMH-IVH generally develops within the first few days after birth and is thus diagnosed on cUS scans performed during the first week of life, white matter injury may develop at any time during the neonatal period. Late-onset cystic PVL may occur following sepsis, viral infections, necrotizing enterocolitis, surgery, or recurrent apneic spells ( Fig. 3.24 ). It is therefore important to perform serial cUS scans from the day of birth until TEA and to increase the number and intensity of cUS examinations following any acute deterioration ( Table 3.1 ).

Fig. 3.24 a-d Preterm neonate, GA 34 weeks. a, b Coronal, resp. parasagittal cUS images on the first day of life showing PVE in the frontal and parietal white matter, physiologic at this age. c, d Coronal, resp. parasagittal cUS images performed 1 month later, after the child had developed necrotizing enterocolitis. Now showing cystic lesions in the parietal white matter. In addition, there is mild dilatation of the lateral ventricle and echogenic ventricular lining (arrow), the first related to white matter loss, the latter to a small IVH.

Postnatal age

Days 1, 2, 3, a 7 a

Days 1, 3, a 7 a

Day 3 a

Abbreviations: GA, gestational age; PMA, postmenstrual age; TEA, term equivalent age.

Note: a Include scanning through posterior fontanel and mastoid fontanel.

A cUS examination around TEA is recommended in every very preterm neonate (GA < 32 weeks). It enables the detection/evaluation of the following:

1. In the preterm neonate, serial cUS scans from birth until TEA are needed to detect and follow brain injury.

In the preterm neonate, serial cUS scans from birth until TEA are needed to detect and follow brain injury. Table 3.1 shows an example of a scan protocol used in our hospitals. The frequency of cUS examinations should be increased when injury is seen and following any clinical deterioration or recurrent apneic spells.

For other useful scan protocols, we refer to recent literature.

3.4 Measurements

3.4.1 Ventricular Measurements

In preterm neonates with progressive ventricular dilatation, mostly due to PHVD, it is recommended to perform serial measurements of the ventricular system. The decision to treat ventricular dilatation depends largely on these measurements. In order to prevent any further increase in ventricular size and raised intracranial pressure and thereby white matter injury, the treatment of PHVD should be considered when ventricular dilatation is rapidly progressive. In this paragraph, we will demonstrate how ventricular measurements are performed and will refer to reference values. The most frequently used measurement of the lateral ventricles is the so- called ventricular index (VI), introduced by Levene in 1981. It is defined as the distance between the falx and the lateral wall of the anterior horns in the coronal plane. The VI is measured in the third coronal plane (at the level of the interventricular foramina of Monro) at the largest width of both lateral ventricles ( Fig. 3.25 ). The VI increases with age. Values above the 97th percentile indicate ventricular dilatation. The first sign of an increase in intracranial pressure is, however, not dilatation of the lateral ventricles, but a change in ventricular shape with rounding of the frontal horns, so-called ballooning. This phenomenon results in an increase of the width of the anterior horns. The anterior horn width (AHW) is defined as the diagonal width of the anterior horn of the lateral ventricle, measured at its widest point in the coronal plane ( Fig. 3.26 ). The AHW remains constant with age. In the majority of neonates, the AHW is less than 3 mm. Values above 6 mm are associated with ballooning, and intervention should be considered. In extremely preterm infants, dilatation of the occipital horns often occurs before an increase in frontal horn size. The occipital horns are usually more dilated than the frontal horns and may even be the only site of ventricular dilatation. The thalamo-occipital distance (TOD) is defined as the distance between the outermost point of the thalamus at its junction with the choroid plexus and the outermost part of the occipital horn. It is measured in the parasagittal plane ( Fig. 3.27 ). The TOD remains rather constant with age.

The VI graph of Levene has an age range between 27 and 40 weeks. New reference values for the VI, AHW, and TOD were recently published by Brouwer et al, with an age range between 24 and 42 weeks. A summary is presented in Table 3.2 .

3.4.2 Measurements of Cerebral Structures

Preterm infants have lower volumes of supratentorial white and gray matter on MRI performed at TEA compared with full-term infants. The corpus callosum (CC) is thinner and the cerebellar volume reduced.

The CC is the main white matter commissure connecting the cerebral hemispheres. It is essential for cognitive development and function. In a normal fetus, the CC grows rapidly, with an almost linear increase in length between 20 and 40 weeks of gestation, while the height remains rather constant during the same period. The cerebellum has important connections with supratentorial brain structures and the spinal cord. It plays an important role not only in motor control but also in language processing, auditory and visual memory, cognition, and social development and behavior. During the fetal period, growth and development of the cerebellum are rapid and critical.

In the human fetus, the CC and cerebellum are markers for brain development. This is related to the rapid growth of both structures and the fact that they are easily visualized by ultrasonography. There can be partial or complete agenesis of the CC. This may be an isolated finding but is also seen in association with other (more serious) central nervous system abnormalities and syndromes.

The cerebellar vermis is abnormal in the fetus with a Dandy-Walker malformation or variant and, again, in association with other central nervous system malformations and syndromes. The transverse cerebellar diameter (TCD) serves as a predictor of gestational age in the fetus. It is also used to assess cerebellar growth and to diagnose cerebellar hypoplasia when the gestational age is known.

In preterm infants, abnormal growth of the CC is associated with delayed cognitive and motor development. Injury to the cerebellum, a frequent complication in very preterm neonates, may severely disrupt its normal growth and development and is associated with abnormal motor and cognitive outcome and behavioral problems. Measurement of cerebral structures in the brain of the preterm neonate can be of clinical importance to diagnose and quantify brain abnormalities and altered development.

The length and height of the CC and the width (maximum anterior-posterior diameter) and height of the vermis are measured in the midsagittal plane during scanning through the anterior fontanel ( Fig. 3.28 ). The TCD (widest diameter of the cerebellum) is measured in the coronal plane through the fourth ventricle, with the mastoid fontanel used as an acoustic window ( Fig. 3.29 ).

3.5 Preterm Infants: Pathology

3.5.1 Germinal Matrix-Intraventricular Hemorrhage

GMH-IVH remains a common neurologic complication of preterm birth, occurring in about 10 to 20% of preterm infants with a GA below 30 weeks. A large IVH and especially a hemorrhage with PVHI are often associated with an adverse neurologic outcome. The risk to develop PHVD increases when GMH-IVH is more severe. About 30 to 50% of infants with a large GMH-IVH will develop PHVD, and around 20 to 40% of infants with a severe GMH-IVH will consequently need a permanent ventriculoperitoneal shunt. The presence of associated white matter injury due to a unilateral PVHI or the presence of more diffuse, bilateral white matter damage as well as the development of PHVD further increases the risk for an adverse neurodevelopmental outcome.

The classification system suggested by Volpe is suitable to describe early and late ultrasound appearances ( Table 3.3 ). It is better to avoid the use of grade 4 and instead provide a separate description of the size, site, and appearance of a parenchymal lesion. Making a distinction between a small hemorrhage restricted to the germinal matrix or a GMH with some blood ruptured through the ependyma into the ventricular lumen is not always possible. The use of the posterior fontanel as an alternative acoustic window has been advocated, showing improvement in the diagnosis of a small GMH-IVH ( Fig. 3.30 ). Using the posterior fontanel is also helpful for looking at the degree of dilatation/ballooning of the occipital horn in infants with PHVD ( Fig. 3.31 ). A GMH at a site other than the head of the caudate nucleus, like the roof of the temporal horn, often remains undiagnosed and will be diagnosed only when MR imaging is also performed.

Fig. 3.30 a,b a Preterm infant, GA 26 weeks. The coronal view, angling backwards, shows a small clot in the left ventricle (arrowhead). b The image taken through the posterior fontanel confirms the presence of an IVH (arrowhead).

Fig. 3.31 Parasagittal views of another infant, taken through the posterior fontanel, showing dilatation of the right occipital horn, posterior to the calcarine fissure (arrowhead, a). A large clot is seen in the left occipital horn (b). Enlargement of the occipital horns is present bilaterally.

A large GMH-IVH, grade 3, is diagnosed based on presence of a large clot in the ventricle, filling the ventricle more than 50%, as well as acute dilatation of the ventricle involved. A grade 3 IVH may lead to PHVD over a period of 1 to 3 weeks. The diagnosis of a grade 3 IVH cannot be made on a single examination performed during the second or third week, when ventricular dilatation is not acute but has occurred because of PHVD ( Fig. 3.32 ). The maximal extent of the hemorrhage may take a few days. Many centers therefore perform a first scan at the end of the first week. The evolution of a small GMH-IVH to a large hemorrhage would then be missed ( Fig. 3.33 ).

Fig. 3.32 a,b Preterm infant, GA 26 weeks. A large GMH-IVH is present on the left. While there is a clot filling more than 50% of the ventricle, there is also PHVD. The TOD is measured in the parasagittal view. The white matter does not appear to be involved.

Fig. 3.33 a,b Preterm infant, gestational age 26 weeks. A bilateral GMH-IVH is seen on the day of birth. On day 3, a large GMH-IVH is now present on the left, with acute dilatation of the left ventricle. Also note the pressure effect on the cavum septum pellucidum (arrow).

Blood can sometimes be seen in the cavum septum pellucidum. This is not an isolated finding but tends to occur in combination with a GMH-IVH ( Fig. 3.34 ). Blood can also extend into the corpus callosum as a consequence of involvement of the septal vein (Dudink et al; Fig. 3.35 ).

Fig. 3.34 a-c Preterm infant, GA 33 weeks. A GMH-IVH is seen on the left, associated with blood in the cavum septum pellucidum, seen in (a) coronal and (b) parasagittal views. Following punctures from a reservoir, the PHVD stabilized and the ventricular size normalized (c).

Fig. 3.35 a-c Two preterm infants (a, c) with blood within the corpus callosum (arrows), the first one with an early MRI correlate (b). This is most likely due to involvement of the septal vein.

A PVHI is usually unilateral, either globular in shape and communicating with the ventricle containing a moderate to large ipsilateral GMH-IVH, or triangular in shape, with the apex at the outer border of the lateral ventricle and not or partly communicating with the ipsilateral ventricle ( Fig. 3.36 ). In the past, PVHI was considered to be due to direct extension of the hemorrhage into the periventricular white matter, but this is no longer considered to be the most likely explanation for this type of parenchymal lesion. Most would now agree that this type of lesion is due to the presence of a GMH-IVH, which can lead to impaired venous drainage and subsequent venous infarction of the medullary veins of the white matter. This sequence of events can sometimes be followed with sequential ultrasound examinations, with change from a normal image to a stage of simple GMH-IVH and PVHI on the following day ( Fig. 3.37 ). Whereas the globular type of PVHI tends to evolve into a porencephalic cyst ( Fig. 3.38 , Fig. 3.39 , Fig. 3.40 ), the triangular type of lesion is more likely to evolve into multiple cysts, which are partly or even not at all communicating with the lateral ventricle and are therefore sometimes wrongly diagnosed as cystic PVL ( Fig. 3.41 ). This is especially likely to happen when sequential scans are not available and the initial GMH-IVH has been missed. A PVHI may also resolve with cystic evolution, with eventual ex vacuo dilatation on the affected side ( Fig. 3.42 ).

Fig. 3.36 a,b Two preterm infants with a PVHI. a A globular lesion, where there appears to be continuity between the ventricle and PVHI. A porencephalic cyst would be expected to evolve. b A GMH-IVH on the left, with a triangular PVHI. There appears to be no continuity between the ventricle and PVHI, and cystic lesions are expected to develop in the white matter.

Fig. 3.37 a-d Preterm infant, GA 27 weeks. Perinatal asphyxia and pneumothorax between days 4 and 5. Normal scan on day 1 (a), small bilateral IVH on day 4 (b), evolving into a large grade 3 IVH on the right on day 5 with a right-sided PVHI (c). Porencephalic cyst on the affected side at TEA (d).

Fig. 3.38 a-d Preterm infant, GA 30 weeks, showing a large PVHI communicating with the ventricle. There is a large resolving clot in the ventricle seen on the coronal (a) and parasagittal (b) views. At TEA, a porencephalic cyst is present (c, d). Also note the atrophy of the affected hemisphere, best seen on the coronal view.

Fig. 3.39 a,b Same patient as in Fig. 3.38 . MRI, performed at 2 weeks of age (a, T2SE) and at TEA (b, T1). There is good agreement with the ultrasound scans, but more detail is seen on the early T2SE, and asymmetry of myelination of the internal capsule (arrow) is seen at TEA b.

Fig. 3.40 a-d Preterm infant, GA 25 weeks. a Coronal image obtained on day 3 shows a PVHI. b Ten days later, the hemorrhage is resolving, and this is associated with mild PVHD. At TEA, a small porencephalic cyst is seen (c, d), which is smaller than expected based on the initial images.

Fig. 3.41 a,b Girl, GA 30 weeks. A large, triangular PVHI is seen on the right with a large ipsilateral IVH (a). At TEA, a single large cyst is seen (b), which has remained separate from the lateral ventricle.

Fig. 3.42 a-c Preterm infant, GA 34 weeks. A discrete triangular lesion (arrow) is seen lateral to the IVH (a), virtually unchanged after 1 week (arrow, b). No cystic evolution was seen, just ex vacuo dilatation, seen at TEA (c).

The PVHI is most often seen in the parietal lobe but can also develop in the frontal or temporal lobe, depending on the veins involved (see Fig. 3.42 ; Fig. 3.43 ). The site of the lesion in relation to the area of the trigone of the lateral ventricle is important for outcome prediction. If the lesion is anterior to the trigone (frontal or temporal lobe), the development of a unilateral spastic cerebral palsy is unlikely (see Fig. 3.42 and Fig. 3.43 ). The location is more important than the size of the lesion for outcome prediction. The scoring system of Bassan et al uses size, midline shift, and the presence of bilateral involvement as predictors of outcome. It is sometimes possible to see wallerian degeneration when a scan is performed through the temporal bone in a child at term or near-term age ( Fig. 3.44 ). MR imaging at TEA is highly recommended to look for asymmetry of myelination of the posterior limb of the internal capsule (PLIC), as well as atrophy of the affected cerebral peduncle ( Fig. 3.45 ). Both abnormalities (abnormal myelination of the internal capsule and wallerian degeneration) are highly predictive of abnormal motor outcome.

Fig. 3.43 a-d Two preterm infants. Coronal (a) and parasagittal (b) views of a PVHI in the frontal lobe of the first infant. Acute (c) and late (d) parasagittal views of a PVHI in the temporal lobe of the second infant.

Fig. 3.44 a-c Preterm infant, gestational age 25 weeks. Cranial ultrasound performed at 10 weeks. Large, left-sided periventricular hemorrhagic infarction with resolving clot and formation of a porencephalic cyst on coronal (a) and parasagittal (b) views. The scan taken through the right temporal bone shows atrophy of the left cerebral peduncle (arrow, c).

GMH-IVH can be associated with a cerebellar hemorrhage (CBH). This is probably explained by the comparable etiology of the two lesions; GMH-IVH originates from the germinal matrix in the supratentorial ventricular wall, whereas CBH originates from the germinal matrix in the fourth ventricle and/or the extensive granular layer covering the cerebellar surface. CBH can also occur following extension of supratentorial IVH into the fourth ventricle and cerebellum. CBH affects the smallest and sickest preterm neonates, and large CBHs are associated with adverse neurodevelopmental outcome. This is probably related to the fact that a large CBH may permanently disrupt further development of the cerebellum, which undergoes critical and rapid growth and development during the late fetal period and, in case of preterm birth, the preterm period. Recent studies have shown that when the mastoid fontanel is used as an additional acoustic window, most large (> 4mm) CBHs and clots in the fourth ventricle will be visualized ( Fig. 3.46 , Fig. 3.47 , Fig. 3.48 , Fig. 3.49 , Fig. 3.50 ). The small and punctate CBHs ( Fig. 3.51 ) will still be missed, but these are not related to an abnormal outcome, at least during the preschool period. Many centers have now included the mastoid fontanel approach to their routine cUS examinations (see Fig. 3.4 ). CBHs generally develop within the first few days after birth, around the onset of GMH-IVH. We recommend the addition of mastoid fontanel imaging to the routine anterior fontanel cUS procedure at least once in the first week of life and at least twice (with an interval of 4 to 7 days) in preterm neonates with a GMH-IVH.

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Use imaging through the mastoid fontanel at least once in the first week of life and at least twice in preterm neonates with a GMH-IVH.

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10.1055/b-0035-122519

3 Neonatal Cranial Ultrasonography

Gerda Meijler, Linda de Vries, and Handan Güleryüz

The neonatal skull is easily accessible by ultrasound because of its small size and multiple acoustic windows. In sick or preterm neonates, serial brain imaging is indicated to follow brain development and injuries. As minimal handling is recommended, ultrasonography, which can be performed at the bedside, is the preferred tool to visualize the brain of both preterm and high-risk full-term neonates. For a successful neonatal cranial ultrasound (cUS), the examination experience of the sonographer and the use of a modern, portable ultrasound machine with appropriate transducers and presets are required. In addition, the examiner should take the necessary precautions to prevent hypothermia, infection, and disturbance of the infant.

Besides bedside imaging, there are other major advantages of cUS compared with other imaging modalities, including that it is safe, does not involve ionizing radiation, and is relatively cheap. cUS can reliably diagnose most congenital anomalies, hemorrhagic lesions, calcifications, and many forms of hypoxic-ischemic injury. It is, however, less reliable than magnetic resonance (MR) imaging for subtle lesions and does not depict myelination.

In this chapter, we will discuss ultrasound anatomy of the neonatal brain, how to differentiate normal findings from (subtle) abnormalities, the optimal timing of ultrasound examinations, and the most frequently occurring brain lesions of the preterm infant.

3.1 Ultrasound Anatomy of the Neonatal Brain

For a routine ultrasound examination of the neonatal brain, the anterior fontanel is used as the acoustic window. Appropriate presets and well-fitting, appropriate transducers are used. The scan frequency for a standard examination is set at 7.5 to 8 MHz.

The examination includes assessing anatomy, maturation, and the presence of abnormalities by:

Examples of the standard coronal planes, showing the anatomical structures in both the very preterm and the full term infant's brain, are presented in Fig. 3.1 , Fig. 3.2 , Fig. 3.3 , Fig. 3.4 , Fig. 3.5 , Fig. 3.6 , Fig. 3.7 , Fig. 3.8 , Fig. 3.9 . For details on the anatomical structures seen in these planes, we refer to recent literature.

Scanning through the anterior fontanel generally allows an accurate assessment of most supratentorial structures. The posterior parts of the brain, the infratentorial structures, and the brainstem are farther away from the transducer, especially in larger preterm and full-term neonates. These structures can therefore be reliably assessed only if the supplemental acoustic windows (posterior fontanel, mastoid fontanels, and temporal windows) are additionally used. For detailed descriptions on how to use the supplemental windows for cUS and on the anatomical structures visualized while scanning through these windows, we refer to recent literature.

3.2 Maturational Changes and Distinction between Physiologic and Pathologic Echogenic Areas in the Neonatal Brain

Areas of echogenicity are often seen in the neonatal brain. Some of these are normal and related to maturational changes, whereas others may reflect (serious) injury. The distinction is not always easy.

3.2.1 White Matter

The immature white matter is characterized by its very high water content, almost complete absence of myelin, and, in cases of very preterm birth, additionally by migrating glial cells.

So-called frontal echodensities (subtle, homogeneous, symmetric echogenic zones in the frontal white matter and bilateral echogenic lines around/below the lateral ventricles on anterior coronal cUS scans) are related to this glial cell migration and seen in preterm neonates before term equivalent age (TEA; Fig. 3.10 and Fig. 3.11 ). Frontal echodensities should be distinguished from nonphysiologic periventricular echodensities (PVE) that may indicate white matter injury. These are more echogenic, less homogeneous, and less symmetric ( Fig. 3.12 ). "Flag-shaped" echogenicities in the parietal white matter on parasagittal scans, subtle echogenic blushes superolaterally from the lateral ventricles, and linear echogenicities running parallel to the trigone of the lateral ventricles on coronal scans are all considered physiologic phenomena in both preterm and full-term neonates ( Fig. 3.13 , Fig. 3.14 , Fig. 3.15 ). These echogenicities are symmetric, and homogeneous, and they tend to fade with age. The latter are thought to represent the optic radiation. These normal echogenicities should be distinguished from pathologic PVE in the parietal white matter, which are likely to represent white matter injury ( Fig. 3.16 ).

Fig. 3.11 Physiologic echogenic lines (arrow) around the frontal horns of the lateral ventricle in very preterm neonate, gestational age 26 weeks.

Fig. 3.12 a,b Nonphysiologic periventricular echodensities (PVE) in a preterm neonate, gestational age 30 weeks. a Coronal plane showing the frontal, inhomogeneous, asymmetric PVE (arrow). b Right parasagittal plane showing patchy, inhomogeneous PVE in the frontal, parietal, and temporal white matter (arrows).

Fig. 3.13 Physiologic "flag-shaped" echogenicity in the parietal white matter (arrow). Full-term neonate, gestational age 38 weeks.

Fig. 3.14 a,b Physiologic echogenic blush in the parietal white matter (arrows). Preterm neonate, gestational age 27 weeks. a Coronal plane. b Parasagittal plane. Also note frontal echodensity (arrowhead), a physiologic finding at this age.

Fig. 3.16 Coronal a and parasagittal b cranial ultrasound images: nonphysiologic echodensities in the parietal white matter (arrows). c T1-weighted transverse MR image showing multiple punctate white matter lesions in the frontal white matter (arrowheads), also showing small right-sided germinal matrix hemorrhage. d Diffusion-weighted MR image showing extensive diffusion restriction throughout the parietal and occipital white matter (arrows). Preterm neonate, gestational age 34 weeks. MR imaging performed 3 days after birth. e (coronal) and f (parasagittal) cUS images: 2 weeks later cystic lesions have developed in the parietal white matter, still surrounded by abnormal PVE. g T1-weighted transverse MR image at high ventricular level, showing irregular dilatation of the ventricular system and deep sulci due to severe white matter loss, nearly abutting the ventricular wall, indicating white matter loss (arrows). h T2-weighted transverse MR image at mid-ventricular level, showing the abnormally shaped lateral ventricles and abnormal signal intensity in the frontal white matter (arrow heads). Also note the small right-sided IVH. MRI performed around TEA.

3.2.2 Deep Gray Matter

The immature deep gray matter has a higher cell and tissue density than the immature white matter and therefore appears relatively echogenic compared with the surrounding white matter on ultrasound scans performed in preterm infants before TEA. Especially the caudate nucleus and globus pallidus may look strikingly echogenic. The echogenicity is symmetric and homogeneous and tends to fade with age ( Fig. 3.17 ).

Echogenicity in the deep gray matter should, however, never be considered a normal phenomenon in (near)-term neonates or in preterm neonates beyond TEA. In this age group, it most likely represents hypoxic-ischemic injury, which is associated with serious consequences for outcome. The echogenicity may also be subtle and symmetric and often includes the thalami. A zone of low echogenicity can sometimes be seen between the basal ganglia and thalami, representing the internal capsule. This may cause a so-called onion peel appearance, whereby the echogenic basal ganglia and thalami are seen as separate echogenic structures and are interspersed by the low echogenicity of the internal capsule ( Fig. 3.18 ).

Fig. 3.18 a-d Abnormal echogenicity in the basal ganglia (arrow) and thalami (open arrow) in two full-term neonates with hypoxic-ischemic deep gray matter injury following acute perinatal asphyxia. (a, c) Coronal planes. (b, d) Parasagittal planes, also showing a zone of low echogenicity representing the internal capsule (arrowheads).

Other echodensities in the deep gray matter, resulting from infarction or hemorrhage, are more echogenic, asymmetric, focal, and easily distinguished from physiologic echodensities ( Fig. 3.19 ).

Lenticulostriate vasculopathy is characterized by linear or punctate hyperechoic areas in the basal ganglia and thalami. It is probably caused by a benign vasculitis of the lenticulostriate vessels and suggestive of mineralization of the arterial wall. It is seen in healthy preterm neonates, but also in association with various abnormal conditions such as central nervous system infections, metabolic disorders, and chromosomal abnormalities. It can easily be distinguished from the aforementioned physiologic deep gray matter echogenicity in preterm infants as it is linear or punctate and follows a typical vascular pattern ( Fig. 3.20 ).

Tips from the Pro

In summary, white matter echogenicities are likely to be physiologic if they have the following characteristics:

Echogenicity in the deep gray matter is likely physiologic if it is seen in the preterm period, fades with age, and does not persist beyond TEA. It is subtle, homogeneous, and symmetric. The internal capsule should not be visible as a separate entity.

3.3 Timing of Examinations

The optimal timing and frequency of examinations is of great importance. In the preterm infant, cUS performed on the first day of life will first of all diagnose an antenatally or perinatally acquired lesion (see Fig. 3.16 ; Fig. 3.21 and Fig. 3.22 ) or congenital anomaly ( Fig. 3.23 ). Secondly, it enables the detection of (new) lesions within hours or days after the onset. Most of these lesions are clinically silent. Once the diagnosis is made, the evolution of the lesion over time should be assessed. In infants with germinal matrix-intraventricular hemorrhage (GMH-IVH), this enables timely recognition of post-hemorrhagic ventricular dilatation (PHVD), a potentially serious condition that may need intervention. Another serious complication of GMH-IVH is periventricular hemorrhagic infarction (PVHI). This lesion and its evolution can be diagnosed and followed if serial cUS scans are performed on a regular basis. In preterm infants with nonphysiologic PVE, sequential imaging will show whether the echogenicity will resolve without cystic evolution or whether cystic changes occur. Small cystic lesions develop only 3 to 6 weeks after the abnormal echogenicity is first seen and tend to resolve within several weeks. They may thus not be visible around TEA. In most infants, some degree of ventriculomegaly, resulting from white matter loss, will then be recognized. Not only cystic periventricular leukomalacia (PVL) but also nonphysiologic PVE of longer duration without cystic evolution (noncystic PVL) is associated with suboptimal neurodevelopmental outcome. Therefore, it is important to know the total duration of abnormal echogenicity.

Fig. 3.21 a-d Preterm neonate, gestational age 30 weeks, 5 days. Large left-sided subdural hemorrhage. a, b Coronal, resp. parasagittal cranial ultrasound images showing the large extra-axial hemorrhage in the temporal region. Also showing increased echogenicity in the temporal lobe (arrows) and compression of the left lateral ventricle. c, d Coronal, resp. transverse T2-weighted MR images showing, besides the extra-axial hemorrhage, abnormal signal intensity in the left temporal lobe adjacent to the extra-axial hemorrhage (open arrows) due to multiple small hemorrhages and tissue compression. The remainder of the brain parenchyma has a normal aspect for this age. MR imaging performed 6 days after birth.

Fig. 3.22 a-d Full-term neonate, traumatic delivery. a, b Coronal, resp. parasagittal cranial ultrasound (cUS) images showing increased echogenicity in the frontoparietal white matter (arrows) consistent with swelling or ischemia. Also showing increased echogenicity in the basal ganglia and thalami (open arrows), again related to edema or ischemia. Furthermore, there is a small hemorrhage in the thalamocaudate notch (arrowhead). c, d Coronal, resp. transverse (supraventricular level) T2-weighted MR images showing a left parietal epidural hematoma with some mass effect upon the adjacent frontal and parietal lobe. Areas of abnormal signal intensity in the white matter (open arrowheads). MR imaging performed 1 month after birth. The epidural hemorrhage was missed with cUS because of its high and peripheral location, being beyond the scope of cUS.

Fig. 3.23 a,b Preterm neonate, gestational age 30 weeks. a Midsagittal cranial ultrasound showing retrocerebellar fluid collection (arrow). The cerebellar vermis and other midline structures have a normal appearance. b Midsagittal T2-weighted MRI confirming a retrocerebellar cerebrospinal fluid collection without mass and with a normally developed cerebellar vermis, probably representing a small arachnoid cyst.

Although GMH-IVH generally develops within the first few days after birth and is thus diagnosed on cUS scans performed during the first week of life, white matter injury may develop at any time during the neonatal period. Late-onset cystic PVL may occur following sepsis, viral infections, necrotizing enterocolitis, surgery, or recurrent apneic spells ( Fig. 3.24 ). It is therefore important to perform serial cUS scans from the day of birth until TEA and to increase the number and intensity of cUS examinations following any acute deterioration ( Table 3.1 ).

Fig. 3.24 a-d Preterm neonate, GA 34 weeks. a, b Coronal, resp. parasagittal cUS images on the first day of life showing PVE in the frontal and parietal white matter, physiologic at this age. c, d Coronal, resp. parasagittal cUS images performed 1 month later, after the child had developed necrotizing enterocolitis. Now showing cystic lesions in the parietal white matter. In addition, there is mild dilatation of the lateral ventricle and echogenic ventricular lining (arrow), the first related to white matter loss, the latter to a small IVH.

Postnatal age

Days 1, 2, 3, a 7 a

Days 1, 3, a 7 a

Day 3 a

Abbreviations: GA, gestational age; PMA, postmenstrual age; TEA, term equivalent age.

Note: a Include scanning through posterior fontanel and mastoid fontanel.

A cUS examination around TEA is recommended in every very preterm neonate (GA < 32 weeks). It enables the detection/evaluation of the following:

1. In the preterm neonate, serial cUS scans from birth until TEA are needed to detect and follow brain injury.

In the preterm neonate, serial cUS scans from birth until TEA are needed to detect and follow brain injury. Table 3.1 shows an example of a scan protocol used in our hospitals. The frequency of cUS examinations should be increased when injury is seen and following any clinical deterioration or recurrent apneic spells.

For other useful scan protocols, we refer to recent literature.

3.4 Measurements

3.4.1 Ventricular Measurements

In preterm neonates with progressive ventricular dilatation, mostly due to PHVD, it is recommended to perform serial measurements of the ventricular system. The decision to treat ventricular dilatation depends largely on these measurements. In order to prevent any further increase in ventricular size and raised intracranial pressure and thereby white matter injury, the treatment of PHVD should be considered when ventricular dilatation is rapidly progressive. In this paragraph, we will demonstrate how ventricular measurements are performed and will refer to reference values. The most frequently used measurement of the lateral ventricles is the so- called ventricular index (VI), introduced by Levene in 1981. It is defined as the distance between the falx and the lateral wall of the anterior horns in the coronal plane. The VI is measured in the third coronal plane (at the level of the interventricular foramina of Monro) at the largest width of both lateral ventricles ( Fig. 3.25 ). The VI increases with age. Values above the 97th percentile indicate ventricular dilatation. The first sign of an increase in intracranial pressure is, however, not dilatation of the lateral ventricles, but a change in ventricular shape with rounding of the frontal horns, so-called ballooning. This phenomenon results in an increase of the width of the anterior horns. The anterior horn width (AHW) is defined as the diagonal width of the anterior horn of the lateral ventricle, measured at its widest point in the coronal plane ( Fig. 3.26 ). The AHW remains constant with age. In the majority of neonates, the AHW is less than 3 mm. Values above 6 mm are associated with ballooning, and intervention should be considered. In extremely preterm infants, dilatation of the occipital horns often occurs before an increase in frontal horn size. The occipital horns are usually more dilated than the frontal horns and may even be the only site of ventricular dilatation. The thalamo-occipital distance (TOD) is defined as the distance between the outermost point of the thalamus at its junction with the choroid plexus and the outermost part of the occipital horn. It is measured in the parasagittal plane ( Fig. 3.27 ). The TOD remains rather constant with age.

The VI graph of Levene has an age range between 27 and 40 weeks. New reference values for the VI, AHW, and TOD were recently published by Brouwer et al, with an age range between 24 and 42 weeks. A summary is presented in Table 3.2 .

3.4.2 Measurements of Cerebral Structures

Preterm infants have lower volumes of supratentorial white and gray matter on MRI performed at TEA compared with full-term infants. The corpus callosum (CC) is thinner and the cerebellar volume reduced.

The CC is the main white matter commissure connecting the cerebral hemispheres. It is essential for cognitive development and function. In a normal fetus, the CC grows rapidly, with an almost linear increase in length between 20 and 40 weeks of gestation, while the height remains rather constant during the same period. The cerebellum has important connections with supratentorial brain structures and the spinal cord. It plays an important role not only in motor control but also in language processing, auditory and visual memory, cognition, and social development and behavior. During the fetal period, growth and development of the cerebellum are rapid and critical.

In the human fetus, the CC and cerebellum are markers for brain development. This is related to the rapid growth of both structures and the fact that they are easily visualized by ultrasonography. There can be partial or complete agenesis of the CC. This may be an isolated finding but is also seen in association with other (more serious) central nervous system abnormalities and syndromes.

The cerebellar vermis is abnormal in the fetus with a Dandy-Walker malformation or variant and, again, in association with other central nervous system malformations and syndromes. The transverse cerebellar diameter (TCD) serves as a predictor of gestational age in the fetus. It is also used to assess cerebellar growth and to diagnose cerebellar hypoplasia when the gestational age is known.

In preterm infants, abnormal growth of the CC is associated with delayed cognitive and motor development. Injury to the cerebellum, a frequent complication in very preterm neonates, may severely disrupt its normal growth and development and is associated with abnormal motor and cognitive outcome and behavioral problems. Measurement of cerebral structures in the brain of the preterm neonate can be of clinical importance to diagnose and quantify brain abnormalities and altered development.

The length and height of the CC and the width (maximum anterior-posterior diameter) and height of the vermis are measured in the midsagittal plane during scanning through the anterior fontanel ( Fig. 3.28 ). The TCD (widest diameter of the cerebellum) is measured in the coronal plane through the fourth ventricle, with the mastoid fontanel used as an acoustic window ( Fig. 3.29 ).

3.5 Preterm Infants: Pathology

3.5.1 Germinal Matrix-Intraventricular Hemorrhage

GMH-IVH remains a common neurologic complication of preterm birth, occurring in about 10 to 20% of preterm infants with a GA below 30 weeks. A large IVH and especially a hemorrhage with PVHI are often associated with an adverse neurologic outcome. The risk to develop PHVD increases when GMH-IVH is more severe. About 30 to 50% of infants with a large GMH-IVH will develop PHVD, and around 20 to 40% of infants with a severe GMH-IVH will consequently need a permanent ventriculoperitoneal shunt. The presence of associated white matter injury due to a unilateral PVHI or the presence of more diffuse, bilateral white matter damage as well as the development of PHVD further increases the risk for an adverse neurodevelopmental outcome.

The classification system suggested by Volpe is suitable to describe early and late ultrasound appearances ( Table 3.3 ). It is better to avoid the use of grade 4 and instead provide a separate description of the size, site, and appearance of a parenchymal lesion. Making a distinction between a small hemorrhage restricted to the germinal matrix or a GMH with some blood ruptured through the ependyma into the ventricular lumen is not always possible. The use of the posterior fontanel as an alternative acoustic window has been advocated, showing improvement in the diagnosis of a small GMH-IVH ( Fig. 3.30 ). Using the posterior fontanel is also helpful for looking at the degree of dilatation/ballooning of the occipital horn in infants with PHVD ( Fig. 3.31 ). A GMH at a site other than the head of the caudate nucleus, like the roof of the temporal horn, often remains undiagnosed and will be diagnosed only when MR imaging is also performed.

Fig. 3.30 a,b a Preterm infant, GA 26 weeks. The coronal view, angling backwards, shows a small clot in the left ventricle (arrowhead). b The image taken through the posterior fontanel confirms the presence of an IVH (arrowhead).

Fig. 3.31 Parasagittal views of another infant, taken through the posterior fontanel, showing dilatation of the right occipital horn, posterior to the calcarine fissure (arrowhead, a). A large clot is seen in the left occipital horn (b). Enlargement of the occipital horns is present bilaterally.

A large GMH-IVH, grade 3, is diagnosed based on presence of a large clot in the ventricle, filling the ventricle more than 50%, as well as acute dilatation of the ventricle involved. A grade 3 IVH may lead to PHVD over a period of 1 to 3 weeks. The diagnosis of a grade 3 IVH cannot be made on a single examination performed during the second or third week, when ventricular dilatation is not acute but has occurred because of PHVD ( Fig. 3.32 ). The maximal extent of the hemorrhage may take a few days. Many centers therefore perform a first scan at the end of the first week. The evolution of a small GMH-IVH to a large hemorrhage would then be missed ( Fig. 3.33 ).

Fig. 3.32 a,b Preterm infant, GA 26 weeks. A large GMH-IVH is present on the left. While there is a clot filling more than 50% of the ventricle, there is also PHVD. The TOD is measured in the parasagittal view. The white matter does not appear to be involved.

Fig. 3.33 a,b Preterm infant, gestational age 26 weeks. A bilateral GMH-IVH is seen on the day of birth. On day 3, a large GMH-IVH is now present on the left, with acute dilatation of the left ventricle. Also note the pressure effect on the cavum septum pellucidum (arrow).

Blood can sometimes be seen in the cavum septum pellucidum. This is not an isolated finding but tends to occur in combination with a GMH-IVH ( Fig. 3.34 ). Blood can also extend into the corpus callosum as a consequence of involvement of the septal vein (Dudink et al; Fig. 3.35 ).

Fig. 3.34 a-c Preterm infant, GA 33 weeks. A GMH-IVH is seen on the left, associated with blood in the cavum septum pellucidum, seen in (a) coronal and (b) parasagittal views. Following punctures from a reservoir, the PHVD stabilized and the ventricular size normalized (c).

Fig. 3.35 a-c Two preterm infants (a, c) with blood within the corpus callosum (arrows), the first one with an early MRI correlate (b). This is most likely due to involvement of the septal vein.

A PVHI is usually unilateral, either globular in shape and communicating with the ventricle containing a moderate to large ipsilateral GMH-IVH, or triangular in shape, with the apex at the outer border of the lateral ventricle and not or partly communicating with the ipsilateral ventricle ( Fig. 3.36 ). In the past, PVHI was considered to be due to direct extension of the hemorrhage into the periventricular white matter, but this is no longer considered to be the most likely explanation for this type of parenchymal lesion. Most would now agree that this type of lesion is due to the presence of a GMH-IVH, which can lead to impaired venous drainage and subsequent venous infarction of the medullary veins of the white matter. This sequence of events can sometimes be followed with sequential ultrasound examinations, with change from a normal image to a stage of simple GMH-IVH and PVHI on the following day ( Fig. 3.37 ). Whereas the globular type of PVHI tends to evolve into a porencephalic cyst ( Fig. 3.38 , Fig. 3.39 , Fig. 3.40 ), the triangular type of lesion is more likely to evolve into multiple cysts, which are partly or even not at all communicating with the lateral ventricle and are therefore sometimes wrongly diagnosed as cystic PVL ( Fig. 3.41 ). This is especially likely to happen when sequential scans are not available and the initial GMH-IVH has been missed. A PVHI may also resolve with cystic evolution, with eventual ex vacuo dilatation on the affected side ( Fig. 3.42 ).

Fig. 3.36 a,b Two preterm infants with a PVHI. a A globular lesion, where there appears to be continuity between the ventricle and PVHI. A porencephalic cyst would be expected to evolve. b A GMH-IVH on the left, with a triangular PVHI. There appears to be no continuity between the ventricle and PVHI, and cystic lesions are expected to develop in the white matter.

Fig. 3.37 a-d Preterm infant, GA 27 weeks. Perinatal asphyxia and pneumothorax between days 4 and 5. Normal scan on day 1 (a), small bilateral IVH on day 4 (b), evolving into a large grade 3 IVH on the right on day 5 with a right-sided PVHI (c). Porencephalic cyst on the affected side at TEA (d).

Fig. 3.38 a-d Preterm infant, GA 30 weeks, showing a large PVHI communicating with the ventricle. There is a large resolving clot in the ventricle seen on the coronal (a) and parasagittal (b) views. At TEA, a porencephalic cyst is present (c, d). Also note the atrophy of the affected hemisphere, best seen on the coronal view.

Fig. 3.39 a,b Same patient as in Fig. 3.38 . MRI, performed at 2 weeks of age (a, T2SE) and at TEA (b, T1). There is good agreement with the ultrasound scans, but more detail is seen on the early T2SE, and asymmetry of myelination of the internal capsule (arrow) is seen at TEA b.

Fig. 3.40 a-d Preterm infant, GA 25 weeks. a Coronal image obtained on day 3 shows a PVHI. b Ten days later, the hemorrhage is resolving, and this is associated with mild PVHD. At TEA, a small porencephalic cyst is seen (c, d), which is smaller than expected based on the initial images.

Fig. 3.41 a,b Girl, GA 30 weeks. A large, triangular PVHI is seen on the right with a large ipsilateral IVH (a). At TEA, a single large cyst is seen (b), which has remained separate from the lateral ventricle.

Fig. 3.42 a-c Preterm infant, GA 34 weeks. A discrete triangular lesion (arrow) is seen lateral to the IVH (a), virtually unchanged after 1 week (arrow, b). No cystic evolution was seen, just ex vacuo dilatation, seen at TEA (c).

The PVHI is most often seen in the parietal lobe but can also develop in the frontal or temporal lobe, depending on the veins involved (see Fig. 3.42 ; Fig. 3.43 ). The site of the lesion in relation to the area of the trigone of the lateral ventricle is important for outcome prediction. If the lesion is anterior to the trigone (frontal or temporal lobe), the development of a unilateral spastic cerebral palsy is unlikely (see Fig. 3.42 and Fig. 3.43 ). The location is more important than the size of the lesion for outcome prediction. The scoring system of Bassan et al uses size, midline shift, and the presence of bilateral involvement as predictors of outcome. It is sometimes possible to see wallerian degeneration when a scan is performed through the temporal bone in a child at term or near-term age ( Fig. 3.44 ). MR imaging at TEA is highly recommended to look for asymmetry of myelination of the posterior limb of the internal capsule (PLIC), as well as atrophy of the affected cerebral peduncle ( Fig. 3.45 ). Both abnormalities (abnormal myelination of the internal capsule and wallerian degeneration) are highly predictive of abnormal motor outcome.

Fig. 3.43 a-d Two preterm infants. Coronal (a) and parasagittal (b) views of a PVHI in the frontal lobe of the first infant. Acute (c) and late (d) parasagittal views of a PVHI in the temporal lobe of the second infant.

Fig. 3.44 a-c Preterm infant, gestational age 25 weeks. Cranial ultrasound performed at 10 weeks. Large, left-sided periventricular hemorrhagic infarction with resolving clot and formation of a porencephalic cyst on coronal (a) and parasagittal (b) views. The scan taken through the right temporal bone shows atrophy of the left cerebral peduncle (arrow, c).

GMH-IVH can be associated with a cerebellar hemorrhage (CBH). This is probably explained by the comparable etiology of the two lesions; GMH-IVH originates from the germinal matrix in the supratentorial ventricular wall, whereas CBH originates from the germinal matrix in the fourth ventricle and/or the extensive granular layer covering the cerebellar surface. CBH can also occur following extension of supratentorial IVH into the fourth ventricle and cerebellum. CBH affects the smallest and sickest preterm neonates, and large CBHs are associated with adverse neurodevelopmental outcome. This is probably related to the fact that a large CBH may permanently disrupt further development of the cerebellum, which undergoes critical and rapid growth and development during the late fetal period and, in case of preterm birth, the preterm period. Recent studies have shown that when the mastoid fontanel is used as an additional acoustic window, most large (> 4mm) CBHs and clots in the fourth ventricle will be visualized ( Fig. 3.46 , Fig. 3.47 , Fig. 3.48 , Fig. 3.49 , Fig. 3.50 ). The small and punctate CBHs ( Fig. 3.51 ) will still be missed, but these are not related to an abnormal outcome, at least during the preschool period. Many centers have now included the mastoid fontanel approach to their routine cUS examinations (see Fig. 3.4 ). CBHs generally develop within the first few days after birth, around the onset of GMH-IVH. We recommend the addition of mastoid fontanel imaging to the routine anterior fontanel cUS procedure at least once in the first week of life and at least twice (with an interval of 4 to 7 days) in preterm neonates with a GMH-IVH.

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Use imaging through the mastoid fontanel at least once in the first week of life and at least twice in preterm neonates with a GMH-IVH.

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10.1055/b-0035-122519

3 Neonatal Cranial Ultrasonography

Gerda Meijler, Linda de Vries, and Handan Güleryüz

The neonatal skull is easily accessible by ultrasound because of its small size and multiple acoustic windows. In sick or preterm neonates, serial brain imaging is indicated to follow brain development and injuries. As minimal handling is recommended, ultrasonography, which can be performed at the bedside, is the preferred tool to visualize the brain of both preterm and high-risk full-term neonates. For a successful neonatal cranial ultrasound (cUS), the examination experience of the sonographer and the use of a modern, portable ultrasound machine with appropriate transducers and presets are required. In addition, the examiner should take the necessary precautions to prevent hypothermia, infection, and disturbance of the infant.

Besides bedside imaging, there are other major advantages of cUS compared with other imaging modalities, including that it is safe, does not involve ionizing radiation, and is relatively cheap. cUS can reliably diagnose most congenital anomalies, hemorrhagic lesions, calcifications, and many forms of hypoxic-ischemic injury. It is, however, less reliable than magnetic resonance (MR) imaging for subtle lesions and does not depict myelination.

In this chapter, we will discuss ultrasound anatomy of the neonatal brain, how to differentiate normal findings from (subtle) abnormalities, the optimal timing of ultrasound examinations, and the most frequently occurring brain lesions of the preterm infant.

3.1 Ultrasound Anatomy of the Neonatal Brain

For a routine ultrasound examination of the neonatal brain, the anterior fontanel is used as the acoustic window. Appropriate presets and well-fitting, appropriate transducers are used. The scan frequency for a standard examination is set at 7.5 to 8 MHz.

The examination includes assessing anatomy, maturation, and the presence of abnormalities by:

Examples of the standard coronal planes, showing the anatomical structures in both the very preterm and the full term infant's brain, are presented in Fig. 3.1 , Fig. 3.2 , Fig. 3.3 , Fig. 3.4 , Fig. 3.5 , Fig. 3.6 , Fig. 3.7 , Fig. 3.8 , Fig. 3.9 . For details on the anatomical structures seen in these planes, we refer to recent literature.

Scanning through the anterior fontanel generally allows an accurate assessment of most supratentorial structures. The posterior parts of the brain, the infratentorial structures, and the brainstem are farther away from the transducer, especially in larger preterm and full-term neonates. These structures can therefore be reliably assessed only if the supplemental acoustic windows (posterior fontanel, mastoid fontanels, and temporal windows) are additionally used. For detailed descriptions on how to use the supplemental windows for cUS and on the anatomical structures visualized while scanning through these windows, we refer to recent literature.

3.2 Maturational Changes and Distinction between Physiologic and Pathologic Echogenic Areas in the Neonatal Brain

Areas of echogenicity are often seen in the neonatal brain. Some of these are normal and related to maturational changes, whereas others may reflect (serious) injury. The distinction is not always easy.

3.2.1 White Matter

The immature white matter is characterized by its very high water content, almost complete absence of myelin, and, in cases of very preterm birth, additionally by migrating glial cells.

So-called frontal echodensities (subtle, homogeneous, symmetric echogenic zones in the frontal white matter and bilateral echogenic lines around/below the lateral ventricles on anterior coronal cUS scans) are related to this glial cell migration and seen in preterm neonates before term equivalent age (TEA; Fig. 3.10 and Fig. 3.11 ). Frontal echodensities should be distinguished from nonphysiologic periventricular echodensities (PVE) that may indicate white matter injury. These are more echogenic, less homogeneous, and less symmetric ( Fig. 3.12 ). "Flag-shaped" echogenicities in the parietal white matter on parasagittal scans, subtle echogenic blushes superolaterally from the lateral ventricles, and linear echogenicities running parallel to the trigone of the lateral ventricles on coronal scans are all considered physiologic phenomena in both preterm and full-term neonates ( Fig. 3.13 , Fig. 3.14 , Fig. 3.15 ). These echogenicities are symmetric, and homogeneous, and they tend to fade with age. The latter are thought to represent the optic radiation. These normal echogenicities should be distinguished from pathologic PVE in the parietal white matter, which are likely to represent white matter injury ( Fig. 3.16 ).

Fig. 3.11 Physiologic echogenic lines (arrow) around the frontal horns of the lateral ventricle in very preterm neonate, gestational age 26 weeks.

Fig. 3.12 a,b Nonphysiologic periventricular echodensities (PVE) in a preterm neonate, gestational age 30 weeks. a Coronal plane showing the frontal, inhomogeneous, asymmetric PVE (arrow). b Right parasagittal plane showing patchy, inhomogeneous PVE in the frontal, parietal, and temporal white matter (arrows).

Fig. 3.13 Physiologic "flag-shaped" echogenicity in the parietal white matter (arrow). Full-term neonate, gestational age 38 weeks.

Fig. 3.14 a,b Physiologic echogenic blush in the parietal white matter (arrows). Preterm neonate, gestational age 27 weeks. a Coronal plane. b Parasagittal plane. Also note frontal echodensity (arrowhead), a physiologic finding at this age.

Fig. 3.16 Coronal a and parasagittal b cranial ultrasound images: nonphysiologic echodensities in the parietal white matter (arrows). c T1-weighted transverse MR image showing multiple punctate white matter lesions in the frontal white matter (arrowheads), also showing small right-sided germinal matrix hemorrhage. d Diffusion-weighted MR image showing extensive diffusion restriction throughout the parietal and occipital white matter (arrows). Preterm neonate, gestational age 34 weeks. MR imaging performed 3 days after birth. e (coronal) and f (parasagittal) cUS images: 2 weeks later cystic lesions have developed in the parietal white matter, still surrounded by abnormal PVE. g T1-weighted transverse MR image at high ventricular level, showing irregular dilatation of the ventricular system and deep sulci due to severe white matter loss, nearly abutting the ventricular wall, indicating white matter loss (arrows). h T2-weighted transverse MR image at mid-ventricular level, showing the abnormally shaped lateral ventricles and abnormal signal intensity in the frontal white matter (arrow heads). Also note the small right-sided IVH. MRI performed around TEA.

3.2.2 Deep Gray Matter

The immature deep gray matter has a higher cell and tissue density than the immature white matter and therefore appears relatively echogenic compared with the surrounding white matter on ultrasound scans performed in preterm infants before TEA. Especially the caudate nucleus and globus pallidus may look strikingly echogenic. The echogenicity is symmetric and homogeneous and tends to fade with age ( Fig. 3.17 ).

Echogenicity in the deep gray matter should, however, never be considered a normal phenomenon in (near)-term neonates or in preterm neonates beyond TEA. In this age group, it most likely represents hypoxic-ischemic injury, which is associated with serious consequences for outcome. The echogenicity may also be subtle and symmetric and often includes the thalami. A zone of low echogenicity can sometimes be seen between the basal ganglia and thalami, representing the internal capsule. This may cause a so-called onion peel appearance, whereby the echogenic basal ganglia and thalami are seen as separate echogenic structures and are interspersed by the low echogenicity of the internal capsule ( Fig. 3.18 ).

Fig. 3.18 a-d Abnormal echogenicity in the basal ganglia (arrow) and thalami (open arrow) in two full-term neonates with hypoxic-ischemic deep gray matter injury following acute perinatal asphyxia. (a, c) Coronal planes. (b, d) Parasagittal planes, also showing a zone of low echogenicity representing the internal capsule (arrowheads).

Other echodensities in the deep gray matter, resulting from infarction or hemorrhage, are more echogenic, asymmetric, focal, and easily distinguished from physiologic echodensities ( Fig. 3.19 ).

Lenticulostriate vasculopathy is characterized by linear or punctate hyperechoic areas in the basal ganglia and thalami. It is probably caused by a benign vasculitis of the lenticulostriate vessels and suggestive of mineralization of the arterial wall. It is seen in healthy preterm neonates, but also in association with various abnormal conditions such as central nervous system infections, metabolic disorders, and chromosomal abnormalities. It can easily be distinguished from the aforementioned physiologic deep gray matter echogenicity in preterm infants as it is linear or punctate and follows a typical vascular pattern ( Fig. 3.20 ).

Tips from the Pro

In summary, white matter echogenicities are likely to be physiologic if they have the following characteristics:

Echogenicity in the deep gray matter is likely physiologic if it is seen in the preterm period, fades with age, and does not persist beyond TEA. It is subtle, homogeneous, and symmetric. The internal capsule should not be visible as a separate entity.

3.3 Timing of Examinations

The optimal timing and frequency of examinations is of great importance. In the preterm infant, cUS performed on the first day of life will first of all diagnose an antenatally or perinatally acquired lesion (see Fig. 3.16 ; Fig. 3.21 and Fig. 3.22 ) or congenital anomaly ( Fig. 3.23 ). Secondly, it enables the detection of (new) lesions within hours or days after the onset. Most of these lesions are clinically silent. Once the diagnosis is made, the evolution of the lesion over time should be assessed. In infants with germinal matrix-intraventricular hemorrhage (GMH-IVH), this enables timely recognition of post-hemorrhagic ventricular dilatation (PHVD), a potentially serious condition that may need intervention. Another serious complication of GMH-IVH is periventricular hemorrhagic infarction (PVHI). This lesion and its evolution can be diagnosed and followed if serial cUS scans are performed on a regular basis. In preterm infants with nonphysiologic PVE, sequential imaging will show whether the echogenicity will resolve without cystic evolution or whether cystic changes occur. Small cystic lesions develop only 3 to 6 weeks after the abnormal echogenicity is first seen and tend to resolve within several weeks. They may thus not be visible around TEA. In most infants, some degree of ventriculomegaly, resulting from white matter loss, will then be recognized. Not only cystic periventricular leukomalacia (PVL) but also nonphysiologic PVE of longer duration without cystic evolution (noncystic PVL) is associated with suboptimal neurodevelopmental outcome. Therefore, it is important to know the total duration of abnormal echogenicity.

Fig. 3.21 a-d Preterm neonate, gestational age 30 weeks, 5 days. Large left-sided subdural hemorrhage. a, b Coronal, resp. parasagittal cranial ultrasound images showing the large extra-axial hemorrhage in the temporal region. Also showing increased echogenicity in the temporal lobe (arrows) and compression of the left lateral ventricle. c, d Coronal, resp. transverse T2-weighted MR images showing, besides the extra-axial hemorrhage, abnormal signal intensity in the left temporal lobe adjacent to the extra-axial hemorrhage (open arrows) due to multiple small hemorrhages and tissue compression. The remainder of the brain parenchyma has a normal aspect for this age. MR imaging performed 6 days after birth.

Fig. 3.22 a-d Full-term neonate, traumatic delivery. a, b Coronal, resp. parasagittal cranial ultrasound (cUS) images showing increased echogenicity in the frontoparietal white matter (arrows) consistent with swelling or ischemia. Also showing increased echogenicity in the basal ganglia and thalami (open arrows), again related to edema or ischemia. Furthermore, there is a small hemorrhage in the thalamocaudate notch (arrowhead). c, d Coronal, resp. transverse (supraventricular level) T2-weighted MR images showing a left parietal epidural hematoma with some mass effect upon the adjacent frontal and parietal lobe. Areas of abnormal signal intensity in the white matter (open arrowheads). MR imaging performed 1 month after birth. The epidural hemorrhage was missed with cUS because of its high and peripheral location, being beyond the scope of cUS.

Fig. 3.23 a,b Preterm neonate, gestational age 30 weeks. a Midsagittal cranial ultrasound showing retrocerebellar fluid collection (arrow). The cerebellar vermis and other midline structures have a normal appearance. b Midsagittal T2-weighted MRI confirming a retrocerebellar cerebrospinal fluid collection without mass and with a normally developed cerebellar vermis, probably representing a small arachnoid cyst.

Although GMH-IVH generally develops within the first few days after birth and is thus diagnosed on cUS scans performed during the first week of life, white matter injury may develop at any time during the neonatal period. Late-onset cystic PVL may occur following sepsis, viral infections, necrotizing enterocolitis, surgery, or recurrent apneic spells ( Fig. 3.24 ). It is therefore important to perform serial cUS scans from the day of birth until TEA and to increase the number and intensity of cUS examinations following any acute deterioration ( Table 3.1 ).

Fig. 3.24 a-d Preterm neonate, GA 34 weeks. a, b Coronal, resp. parasagittal cUS images on the first day of life showing PVE in the frontal and parietal white matter, physiologic at this age. c, d Coronal, resp. parasagittal cUS images performed 1 month later, after the child had developed necrotizing enterocolitis. Now showing cystic lesions in the parietal white matter. In addition, there is mild dilatation of the lateral ventricle and echogenic ventricular lining (arrow), the first related to white matter loss, the latter to a small IVH.

Postnatal age

Days 1, 2, 3, a 7 a

Days 1, 3, a 7 a

Day 3 a

Abbreviations: GA, gestational age; PMA, postmenstrual age; TEA, term equivalent age.

Note: a Include scanning through posterior fontanel and mastoid fontanel.

A cUS examination around TEA is recommended in every very preterm neonate (GA < 32 weeks). It enables the detection/evaluation of the following:

1. In the preterm neonate, serial cUS scans from birth until TEA are needed to detect and follow brain injury.

In the preterm neonate, serial cUS scans from birth until TEA are needed to detect and follow brain injury. Table 3.1 shows an example of a scan protocol used in our hospitals. The frequency of cUS examinations should be increased when injury is seen and following any clinical deterioration or recurrent apneic spells.

For other useful scan protocols, we refer to recent literature.

3.4 Measurements

3.4.1 Ventricular Measurements

In preterm neonates with progressive ventricular dilatation, mostly due to PHVD, it is recommended to perform serial measurements of the ventricular system. The decision to treat ventricular dilatation depends largely on these measurements. In order to prevent any further increase in ventricular size and raised intracranial pressure and thereby white matter injury, the treatment of PHVD should be considered when ventricular dilatation is rapidly progressive. In this paragraph, we will demonstrate how ventricular measurements are performed and will refer to reference values. The most frequently used measurement of the lateral ventricles is the so- called ventricular index (VI), introduced by Levene in 1981. It is defined as the distance between the falx and the lateral wall of the anterior horns in the coronal plane. The VI is measured in the third coronal plane (at the level of the interventricular foramina of Monro) at the largest width of both lateral ventricles ( Fig. 3.25 ). The VI increases with age. Values above the 97th percentile indicate ventricular dilatation. The first sign of an increase in intracranial pressure is, however, not dilatation of the lateral ventricles, but a change in ventricular shape with rounding of the frontal horns, so-called ballooning. This phenomenon results in an increase of the width of the anterior horns. The anterior horn width (AHW) is defined as the diagonal width of the anterior horn of the lateral ventricle, measured at its widest point in the coronal plane ( Fig. 3.26 ). The AHW remains constant with age. In the majority of neonates, the AHW is less than 3 mm. Values above 6 mm are associated with ballooning, and intervention should be considered. In extremely preterm infants, dilatation of the occipital horns often occurs before an increase in frontal horn size. The occipital horns are usually more dilated than the frontal horns and may even be the only site of ventricular dilatation. The thalamo-occipital distance (TOD) is defined as the distance between the outermost point of the thalamus at its junction with the choroid plexus and the outermost part of the occipital horn. It is measured in the parasagittal plane ( Fig. 3.27 ). The TOD remains rather constant with age.

The VI graph of Levene has an age range between 27 and 40 weeks. New reference values for the VI, AHW, and TOD were recently published by Brouwer et al, with an age range between 24 and 42 weeks. A summary is presented in Table 3.2 .

3.4.2 Measurements of Cerebral Structures

Preterm infants have lower volumes of supratentorial white and gray matter on MRI performed at TEA compared with full-term infants. The corpus callosum (CC) is thinner and the cerebellar volume reduced.

The CC is the main white matter commissure connecting the cerebral hemispheres. It is essential for cognitive development and function. In a normal fetus, the CC grows rapidly, with an almost linear increase in length between 20 and 40 weeks of gestation, while the height remains rather constant during the same period. The cerebellum has important connections with supratentorial brain structures and the spinal cord. It plays an important role not only in motor control but also in language processing, auditory and visual memory, cognition, and social development and behavior. During the fetal period, growth and development of the cerebellum are rapid and critical.

In the human fetus, the CC and cerebellum are markers for brain development. This is related to the rapid growth of both structures and the fact that they are easily visualized by ultrasonography. There can be partial or complete agenesis of the CC. This may be an isolated finding but is also seen in association with other (more serious) central nervous system abnormalities and syndromes.

The cerebellar vermis is abnormal in the fetus with a Dandy-Walker malformation or variant and, again, in association with other central nervous system malformations and syndromes. The transverse cerebellar diameter (TCD) serves as a predictor of gestational age in the fetus. It is also used to assess cerebellar growth and to diagnose cerebellar hypoplasia when the gestational age is known.

In preterm infants, abnormal growth of the CC is associated with delayed cognitive and motor development. Injury to the cerebellum, a frequent complication in very preterm neonates, may severely disrupt its normal growth and development and is associated with abnormal motor and cognitive outcome and behavioral problems. Measurement of cerebral structures in the brain of the preterm neonate can be of clinical importance to diagnose and quantify brain abnormalities and altered development.

The length and height of the CC and the width (maximum anterior-posterior diameter) and height of the vermis are measured in the midsagittal plane during scanning through the anterior fontanel ( Fig. 3.28 ). The TCD (widest diameter of the cerebellum) is measured in the coronal plane through the fourth ventricle, with the mastoid fontanel used as an acoustic window ( Fig. 3.29 ).

3.5 Preterm Infants: Pathology

3.5.1 Germinal Matrix-Intraventricular Hemorrhage

GMH-IVH remains a common neurologic complication of preterm birth, occurring in about 10 to 20% of preterm infants with a GA below 30 weeks. A large IVH and especially a hemorrhage with PVHI are often associated with an adverse neurologic outcome. The risk to develop PHVD increases when GMH-IVH is more severe. About 30 to 50% of infants with a large GMH-IVH will develop PHVD, and around 20 to 40% of infants with a severe GMH-IVH will consequently need a permanent ventriculoperitoneal shunt. The presence of associated white matter injury due to a unilateral PVHI or the presence of more diffuse, bilateral white matter damage as well as the development of PHVD further increases the risk for an adverse neurodevelopmental outcome.

The classification system suggested by Volpe is suitable to describe early and late ultrasound appearances ( Table 3.3 ). It is better to avoid the use of grade 4 and instead provide a separate description of the size, site, and appearance of a parenchymal lesion. Making a distinction between a small hemorrhage restricted to the germinal matrix or a GMH with some blood ruptured through the ependyma into the ventricular lumen is not always possible. The use of the posterior fontanel as an alternative acoustic window has been advocated, showing improvement in the diagnosis of a small GMH-IVH ( Fig. 3.30 ). Using the posterior fontanel is also helpful for looking at the degree of dilatation/ballooning of the occipital horn in infants with PHVD ( Fig. 3.31 ). A GMH at a site other than the head of the caudate nucleus, like the roof of the temporal horn, often remains undiagnosed and will be diagnosed only when MR imaging is also performed.

Fig. 3.30 a,b a Preterm infant, GA 26 weeks. The coronal view, angling backwards, shows a small clot in the left ventricle (arrowhead). b The image taken through the posterior fontanel confirms the presence of an IVH (arrowhead).

Fig. 3.31 Parasagittal views of another infant, taken through the posterior fontanel, showing dilatation of the right occipital horn, posterior to the calcarine fissure (arrowhead, a). A large clot is seen in the left occipital horn (b). Enlargement of the occipital horns is present bilaterally.

A large GMH-IVH, grade 3, is diagnosed based on presence of a large clot in the ventricle, filling the ventricle more than 50%, as well as acute dilatation of the ventricle involved. A grade 3 IVH may lead to PHVD over a period of 1 to 3 weeks. The diagnosis of a grade 3 IVH cannot be made on a single examination performed during the second or third week, when ventricular dilatation is not acute but has occurred because of PHVD ( Fig. 3.32 ). The maximal extent of the hemorrhage may take a few days. Many centers therefore perform a first scan at the end of the first week. The evolution of a small GMH-IVH to a large hemorrhage would then be missed ( Fig. 3.33 ).

Fig. 3.32 a,b Preterm infant, GA 26 weeks. A large GMH-IVH is present on the left. While there is a clot filling more than 50% of the ventricle, there is also PHVD. The TOD is measured in the parasagittal view. The white matter does not appear to be involved.

Fig. 3.33 a,b Preterm infant, gestational age 26 weeks. A bilateral GMH-IVH is seen on the day of birth. On day 3, a large GMH-IVH is now present on the left, with acute dilatation of the left ventricle. Also note the pressure effect on the cavum septum pellucidum (arrow).

Blood can sometimes be seen in the cavum septum pellucidum. This is not an isolated finding but tends to occur in combination with a GMH-IVH ( Fig. 3.34 ). Blood can also extend into the corpus callosum as a consequence of involvement of the septal vein (Dudink et al; Fig. 3.35 ).

Fig. 3.34 a-c Preterm infant, GA 33 weeks. A GMH-IVH is seen on the left, associated with blood in the cavum septum pellucidum, seen in (a) coronal and (b) parasagittal views. Following punctures from a reservoir, the PHVD stabilized and the ventricular size normalized (c).

Fig. 3.35 a-c Two preterm infants (a, c) with blood within the corpus callosum (arrows), the first one with an early MRI correlate (b). This is most likely due to involvement of the septal vein.

A PVHI is usually unilateral, either globular in shape and communicating with the ventricle containing a moderate to large ipsilateral GMH-IVH, or triangular in shape, with the apex at the outer border of the lateral ventricle and not or partly communicating with the ipsilateral ventricle ( Fig. 3.36 ). In the past, PVHI was considered to be due to direct extension of the hemorrhage into the periventricular white matter, but this is no longer considered to be the most likely explanation for this type of parenchymal lesion. Most would now agree that this type of lesion is due to the presence of a GMH-IVH, which can lead to impaired venous drainage and subsequent venous infarction of the medullary veins of the white matter. This sequence of events can sometimes be followed with sequential ultrasound examinations, with change from a normal image to a stage of simple GMH-IVH and PVHI on the following day ( Fig. 3.37 ). Whereas the globular type of PVHI tends to evolve into a porencephalic cyst ( Fig. 3.38 , Fig. 3.39 , Fig. 3.40 ), the triangular type of lesion is more likely to evolve into multiple cysts, which are partly or even not at all communicating with the lateral ventricle and are therefore sometimes wrongly diagnosed as cystic PVL ( Fig. 3.41 ). This is especially likely to happen when sequential scans are not available and the initial GMH-IVH has been missed. A PVHI may also resolve with cystic evolution, with eventual ex vacuo dilatation on the affected side ( Fig. 3.42 ).

Fig. 3.36 a,b Two preterm infants with a PVHI. a A globular lesion, where there appears to be continuity between the ventricle and PVHI. A porencephalic cyst would be expected to evolve. b A GMH-IVH on the left, with a triangular PVHI. There appears to be no continuity between the ventricle and PVHI, and cystic lesions are expected to develop in the white matter.

Fig. 3.37 a-d Preterm infant, GA 27 weeks. Perinatal asphyxia and pneumothorax between days 4 and 5. Normal scan on day 1 (a), small bilateral IVH on day 4 (b), evolving into a large grade 3 IVH on the right on day 5 with a right-sided PVHI (c). Porencephalic cyst on the affected side at TEA (d).

Fig. 3.38 a-d Preterm infant, GA 30 weeks, showing a large PVHI communicating with the ventricle. There is a large resolving clot in the ventricle seen on the coronal (a) and parasagittal (b) views. At TEA, a porencephalic cyst is present (c, d). Also note the atrophy of the affected hemisphere, best seen on the coronal view.

Fig. 3.39 a,b Same patient as in Fig. 3.38 . MRI, performed at 2 weeks of age (a, T2SE) and at TEA (b, T1). There is good agreement with the ultrasound scans, but more detail is seen on the early T2SE, and asymmetry of myelination of the internal capsule (arrow) is seen at TEA b.

Fig. 3.40 a-d Preterm infant, GA 25 weeks. a Coronal image obtained on day 3 shows a PVHI. b Ten days later, the hemorrhage is resolving, and this is associated with mild PVHD. At TEA, a small porencephalic cyst is seen (c, d), which is smaller than expected based on the initial images.

Fig. 3.41 a,b Girl, GA 30 weeks. A large, triangular PVHI is seen on the right with a large ipsilateral IVH (a). At TEA, a single large cyst is seen (b), which has remained separate from the lateral ventricle.

Fig. 3.42 a-c Preterm infant, GA 34 weeks. A discrete triangular lesion (arrow) is seen lateral to the IVH (a), virtually unchanged after 1 week (arrow, b). No cystic evolution was seen, just ex vacuo dilatation, seen at TEA (c).

The PVHI is most often seen in the parietal lobe but can also develop in the frontal or temporal lobe, depending on the veins involved (see Fig. 3.42 ; Fig. 3.43 ). The site of the lesion in relation to the area of the trigone of the lateral ventricle is important for outcome prediction. If the lesion is anterior to the trigone (frontal or temporal lobe), the development of a unilateral spastic cerebral palsy is unlikely (see Fig. 3.42 and Fig. 3.43 ). The location is more important than the size of the lesion for outcome prediction. The scoring system of Bassan et al uses size, midline shift, and the presence of bilateral involvement as predictors of outcome. It is sometimes possible to see wallerian degeneration when a scan is performed through the temporal bone in a child at term or near-term age ( Fig. 3.44 ). MR imaging at TEA is highly recommended to look for asymmetry of myelination of the posterior limb of the internal capsule (PLIC), as well as atrophy of the affected cerebral peduncle ( Fig. 3.45 ). Both abnormalities (abnormal myelination of the internal capsule and wallerian degeneration) are highly predictive of abnormal motor outcome.

Fig. 3.43 a-d Two preterm infants. Coronal (a) and parasagittal (b) views of a PVHI in the frontal lobe of the first infant. Acute (c) and late (d) parasagittal views of a PVHI in the temporal lobe of the second infant.

Fig. 3.44 a-c Preterm infant, gestational age 25 weeks. Cranial ultrasound performed at 10 weeks. Large, left-sided periventricular hemorrhagic infarction with resolving clot and formation of a porencephalic cyst on coronal (a) and parasagittal (b) views. The scan taken through the right temporal bone shows atrophy of the left cerebral peduncle (arrow, c).

GMH-IVH can be associated with a cerebellar hemorrhage (CBH). This is probably explained by the comparable etiology of the two lesions; GMH-IVH originates from the germinal matrix in the supratentorial ventricular wall, whereas CBH originates from the germinal matrix in the fourth ventricle and/or the extensive granular layer covering the cerebellar surface. CBH can also occur following extension of supratentorial IVH into the fourth ventricle and cerebellum. CBH affects the smallest and sickest preterm neonates, and large CBHs are associated with adverse neurodevelopmental outcome. This is probably related to the fact that a large CBH may permanently disrupt further development of the cerebellum, which undergoes critical and rapid growth and development during the late fetal period and, in case of preterm birth, the preterm period. Recent studies have shown that when the mastoid fontanel is used as an additional acoustic window, most large (> 4mm) CBHs and clots in the fourth ventricle will be visualized ( Fig. 3.46 , Fig. 3.47 , Fig. 3.48 , Fig. 3.49 , Fig. 3.50 ). The small and punctate CBHs ( Fig. 3.51 ) will still be missed, but these are not related to an abnormal outcome, at least during the preschool period. Many centers have now included the mastoid fontanel approach to their routine cUS examinations (see Fig. 3.4 ). CBHs generally develop within the first few days after birth, around the onset of GMH-IVH. We recommend the addition of mastoid fontanel imaging to the routine anterior fontanel cUS procedure at least once in the first week of life and at least twice (with an interval of 4 to 7 days) in preterm neonates with a GMH-IVH.

Tip from the Pro

Use imaging through the mastoid fontanel at least once in the first week of life and at least twice in preterm neonates with a GMH-IVH.

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10.1055/b-0035-122519 3 Neonatal Cranial UltrasonographyGerda Meijler, Linda de Vries, and Handan Güleryüz The neonatal skull is easily accessible by ultrasound because of its small size and multip...

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Spotlight on Respiratory Allergies

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Allergy UK Masterclass: Spotlight on Respiratory

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Overview Symptoms & Diagnosis Treatment & Management

Asthma is a chronic disease involving the airways in the lungs. These airways, or bronchial tubes, allow air to come in and out of the lungs.

If you have asthma your airways are always inflamed. They become even more swollen and the muscles around the airways can tighten when something triggers your symptoms. This makes it difficult for air to move in and out of the lungs, causing symptoms such as coughing, wheezing, shortness of breath and/or chest tightness.

For many asthma sufferers, timing of these symptoms is closely related to physical activity. And, some otherwise healthy people can develop asthma symptoms only when exercising. This is called exercise-induced bronchoconstriction (EIB), or exercise-induced asthma (EIA). Staying active is an important way to stay healthy, so asthma shouldn't keep you on the sidelines. Your physician can develop a management plan to keep your symptoms under control before, during and after physical activity.

People with a family history of allergies or asthma are more prone to developing asthma. Many people with asthma also have allergies. This is called allergic asthma.

Occupational asthma is caused by inhaling fumes, gases, dust or other potentially harmful substances while on the job.

Childhood asthma impacts millions of children and their families. In fact, the majority of children who develop asthma do so before the age of five.

There is no cure for asthma, but once it is properly diagnosed and a treatment plan is in place you will be able to manage your condition, and your quality of life will improve.

An allergist / immunologist is the best qualified physician in diagnosing and treating asthma. With the help of your allergist, you can take control of your condition and participate in normal activities.

Keep pace with the latest information and connect with others. Join us on Facebook and Twitter.
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Asthma Action Plan "

Asthma Action Plan - Fillable PDF "
AAAAI does not assume responsibility for how these documents are utilized. Consult with your practice's IT resources for recommendations on document storage, transmission and HIPAA compliance. Picture-Based Asthma Action Plan "
Asthma Symptoms
According to the leading experts in asthma, the symptoms of asthma and best treatment for you or your child may be quite different than for someone else with asthma.

The most common symptom is wheezing. This is a scratchy or whistling sound when you breathe. Other symptoms include:
* Shortness of breath
* Chest tightness or pain
* Chronic coughing
* Trouble sleeping due to coughing or wheezing

Asthma symptoms, also called asthma flare-ups or asthma attacks, are often caused by allergies and exposure to allergens such as pet dander, dust mites, pollen or mold. Non-allergic triggers include smoke, pollution or cold air or changes in weather.

Asthma symptoms may be worse during exercise, when you have a cold or during times of high stress.

Children with asthma may show the same symptoms as adults with asthma: coughing, wheezing and shortness of breath. In some children chronic cough may be the only symptom.

If your child has one or more of these common symptoms, make an appointment with an allergist / immunologist:
* Coughing that is constant or that is made worse by viral infections, happens while your child is asleep, or is triggered by exercise and cold air
* Wheezing or whistling sound when your child exhales
* Shortness of breath or rapid breathing, which may be associated with exercise
* Chest tightness (a young child may say that his chest "hurts" or "feels funny")
* Fatigue (your child may slow down or stop playing)
* Problems feeding or grunting during feeding (infants)
* Avoiding sports or social activities
* Problems sleeping due to coughing or difficulty breathing

Patterns in asthma symptoms are important and can help your doctor make a diagnosis. Pay attention to when symptoms occur:
* At night or early morning
* During or after exercise
* During certain seasons
* After laughing or crying
* When exposed to common asthma triggers

Asthma Diagnosis
An allergist diagnoses asthma by taking a thorough medical history and performing breathing tests to measure how well your lungs work.

One of these tests is called spirometry. You will take a deep breath and blow into a sensor to measure the amount of air your lungs can hold and the speed of the air you inhale or exhale. This test diagnoses asthma severity and measures how well treatment is working.

A FeNO test or exhaled nitric oxide test, in patients with allergic or eosinophilic asthma, is a way to determine how much lung inflammation is present and how well inhaled steroids are suppressing this inflammation. With allergic or eosinophilic asthma, sometimes you may feel your breathing is fine, but when you measure your exhaled nitric oxide, it may still be significantly elevated, and you might do better in the long-term using slightly more of your inhaled steroid to suppress this inflammation.

Many people with asthma also have allergies, so your doctor may perform allergy testing. Treating the underlying allergic triggers for your asthma will help you avoid asthma symptoms.

There is no cure for asthma, but symptoms can be controlled with effective asthma treatment and management. This involves taking your medications as directed and learning to avoid triggers that cause your asthma symptoms. Your allergist will prescribe the best medications for your condition and provide you with specific instructions for using them.

Controller medications are taken daily and include inhaled corticosteroids (fluticasone (Flovent Diskus, Flovent HFA, Arnuity Ellipta), budesonide (Pulmicort Flexhaler), mometasone (Asmanex), ciclesonide (Alvesco), flunisolide (Aerobid), beclomethasone (Qvar) and others).

Combination inhalers contain an inhaled corticosteroid plus a long-acting beta-agonist (LABA). LABAs are symptom-controllers that are helpful in opening your airways. However, in certain people they may carry some risks.

LABAs should never be prescribed as the sole therapy for asthma. Current recommendations are for them to be used only along with inhaled corticosteroids. Combination medications include fluticasone and salmeterol (Advair Diskus, Advair HFA), fluticasone and vilanterol (Breo Ellipta), budesonide and formoterol (Symbicort), and mometasone and formoterol (Dulera).

Anticholinergics are inhaled medications that also help in opening the airways. The medication tiotropium (Spiriva Respimat) is used as maintenance therapy in asthma.

Leukotriene modifiers are oral medications that include montelukast (Singulair), zafirlukast (Accolate) and zileuton (Zyflo, Zyflo CR).

Quick-relief or rescue medications are used to quickly relax and open the airways and relieve symptoms during an asthma flare-up, or are taken before exercising if prescribed. These include: short-acting beta-agonists. These inhaled bronchodilator (brong-koh-DIE-lay-tur) medications include albuterol (ProAir HFA, Ventolin HFA, others), levalbuterol (Xopenex HFA) and pirbuterol (Maxair Autohaler). Quick-relief medications do not take the place of controller medications. If you rely on rescue relief more than twice a week, it is time to see your allergist.

Oral and intravenous corticosteroids may be required for acute asthma flare-ups or for severe symptoms. Examples include prednisone and methylprednisolone. They can cause serious side effects if used on a long term basis.

Several newer medications are also used to treat severe or difficult-to-treat asthma on a regular basis. These are injections or infusions, are called biologics, and sometimes blood tests are necessary to determine if these treatments are suitable for your particular kind of asthma. These include omalizumab (Xolair) for allergic asthma, and the medications benralizumab (Fasenra), mepolizumab (Nucala), and reslizumab (Cinqair) if your asthma occurs in association with the presence of cells called eosinophils on a blood test. Dupilumab (Dupixent) has been approved to treat eosinophilic asthma as well as asthma that is dependent on regular oral corticosteroids for treatment.

Visit the AAAAI Drug Guide for a complete list of medications commonly used to treat asthma.

If you are pregnant, you may be hesitant about taking medications, including those for asthma. This can be a mistake for your health and that of your baby-to-be. Continue taking your prescribed asthma medications and make an appointment with your allergist to discuss treatments that will help you have a healthy pregnancy. Additionally, you may want to enroll in a study designed to monitor medications and pregnancy.

People with asthma are at risk of developing complications from respiratory infections such as influenza and pneumonia. That is why it is important for asthma sufferers, especially adults, to get vaccinated annually.

With proper treatment and an asthma management plan, you can minimize your symptoms and enjoy a better quality of life.

Asthma Action Plan "

Asthma Action Plan - Fillable PDF "
AAAAI does not assume responsibility for how these documents are utilized. Consult with your practice's IT resources for recommendations on document storage, transmission and HIPAA compliance.
Picture-Based Asthma Action Plan "

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Asthma Symptoms, Diagnosis, Management & Treatment

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Overview of asthma symptoms, asthma diagnosis, asthma treatment and asthma management written by the AAAAI's leading experts in allergy, asthma and immunology.

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Meningitis: NICE guidance

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FOP exam preparation resource

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Overview

This online resource page has been designed specifically to help international candidates tackle the areas those who have previously taken the FOP exam have found most difficult.

Under each section below, you will find a range of resources linked to key learning objectives in the syllabus that will help improve your knowledge and understanding of the topics assessed in the FOP exam.

If you are a UK candidate, you are more than welcome to utilise the resources on this page. However it has been specifically developed for overseas candidates who may not have direct experience of working in the NHS and may need additional support to identify key resources.

Below is the introduction video to this resource page, filmed by Dr Priya Kumar, and our "What to expect from the FOP exam" presentation, presented by Dr Mithilesh Lal. Dr Kumar will explain how to get the best out of this resource page and Dr Lal will take you through the exam and how to approach it.

Please view the below presentation slides in "slideshow" mode to hear Dr Lal presenting.
What to expect from the FOP exam and how to approach your exam - recorded presentation by Dr Mithilesh Lal
The RCPCH gives special thanks to our FOP leads -

Dr Priya Kumar - Consultant Paediatrician and Paediatric Clinical Director at London North West University Healthcare Trust. RCPCH FOP theory and clinical examiner.

Dr Mithilesh Lal - Consultant Neonatologist and Clinical Director for Neonatal services at South Tees Foundation NHS Trust. RCPCH senior clinical examiner & Chair of Foundation Of Practice exam boards

RCPCH Exams Preparation Education Team

If at any stage you have issues accessing any of the content, please email: examprepcourses@rcpch.ac.uk. Also let us know what you think of this resource page and if there are any resources we should also include.

As of 1st September 2016 the Revalidation and CPD team of the Royal College of Paediatrics and Child Health no longer allocates a number CPD credits to courses or events. The removal of credits associated with events allows delegates to record the educational benefit of the activity through written reflection, in contrast to quantifying the significance based on the time duration of the course. This is in accordance with changes made to the CPD Scheme guidelines published in April 2016.

Detailed information and scheme guidance can be found on the RCPCH website

When recording the activity, delegates should focus on the reflection and detail the following:

What did you learn?

What effect has/will the learning had/have on your current practice?

What further learning or action, if any, is needed as a result of the original learning activity?

Should you have any questions regarding the removal of credits, please feel free to contact the CPD team

If you use the RCPCH CPD Diary, you can click here to visit the diary and record your learning: Log your learning on the RCPCH CPD Diary

About us

Royal College of Paediatrics and Child Health was founded in 1996 and with members in the UK and internationally, we play a major role in postgraduate medical education, professional standards, research and policy.

RCPCH website

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MRCPCH/DCH Foundation of Practice (FOP) Exam Preparation: resources for overseas candidates

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Skip to content Close VisualV1 - Cross Created with Sketch. Search for an online learning, webinar or podcast VisualV1 - Home Created with Sketch. Menu Overview This online resource page has been designed specifically to help international candidates tackle the areas those who have previously taken the FOP exam have found most difficult.

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Professional witness report writing

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This professional witness report writing eLearning module is aimed towards Paediatric Trainees ST6-8, SAS doctors and Consultant Paediatricians. There is one module, which should take you about 30 minutes to complete.
Learning objectives:

The ability and confidence to write effective reports for professional witness purposes

Better understand the role of the report when you are acting as a professional witness

An awareness of how to structure your report, and important elements to include and pitfalls to avoid

A firmer understanding of the necessary language required when writing a professional witness report

Further knowledge concerning the RCPCH's policies and publications in regards to report writing

Dr. Richard Reading

Subject matter expert

Creation/review

Date

Launch date

January 2017

Review date

January 2020

Next review

October 2023

As of 1st September 2016 the Revalidation and CPD team of the Royal College of Paediatrics and Child Health no longer allocates a number CPD credits to courses or events. The removal of credits associated with events allows delegates to record the educational benefit of the activity through written reflection, in contrast to quantifying the significance based on the time duration of the course. This is in accordance with changes made to the CPD Scheme guidelines published in April 2016.

Detailed information and scheme guidance can be found on the RCPCH website

When recording the activity, delegates should focus on the reflection and detail the following:

What did you learn?

What effect has/will the learning had/have on your current practice?

What further learning or action, if any, is needed as a result of the original learning activity?

Should you have any questions regarding the removal of credits, please feel free to contact the CPD team

If you use the RCPCH CPD Diary, you can click here to visit the diary and record your learning: Log your learning on the RCPCH CPD Diary

About us

Royal College of Paediatrics and Child Health was founded in 1996 and with members in the UK and internationally, we play a major role in postgraduate medical education, professional standards, research and policy.

RCPCH website

# data[].attributes.attachment_link.description
Skip to content Close VisualV1 - Cross Created with Sketch. Search for an online learning, webinar or podcast VisualV1 - Home Created with Sketch. Menu This professional witness report writing eLearning module is aimed towards Paediatric Trainees ST6-8, SAS doctors and Consultant Paediatricians. There is one module, which should take you about 30 minutes to complete.

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Vasovagal syncope
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SVT
Long QT syndrome
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Exposure to ionising radiation from medical imaging: safety advice

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When properly justified and optimised, the risks from medical x-ray and nuclear medicine imaging examinations are much less than the risks associated with the medical conditions under investigation. The risks from imaging examinations using ionising radiation relate to a very small increase in the probability of cancer occurring many years or decades after the radiation exposure, This should be considered in context - unfortunately, we all have a 1 in 4 lifetime risk of dying from cancer.