Printable list of all neonatal and paediatric SAQs

College Answer

At birth closure of the umbilical vessels increases systemic vascular resistance and lung expansion leads to a dramatic fall in pulmonary vascular resistance. Pulmonary blood flow increases, leading to a rise in left atrial pressure and functional closure of the foramen ovale. The ductus arteriosus constricts under the effects of elevated oxygen pressures and local prostaglandins.

Persistent foetal pattern circulation is essentially due to persistent hypoxia and elevated PVR, which may be due to:

1)   low lung volume (hyaline membrane disease, perinatal asphyxia)

2)   pulmonary hypoplasia (eg diaphragmatic hernia)

3)   meconium aspiration

4)   chronic placental insufficiency

5)   perinatal hypoxia

6)   sepsis ( group B strep)

7)   hyperviscosity syndrome

Discussion

These diagrams are from van Vonderen et al (2014):

In textual long form, which defeats the point of point form:

• Foetal lungs are cleared of fluid and aerated. 
  • ​With the first breaths, the lungs are aerated, creating an FRC. The foetus is capable of generating negative pressures in excess of 30 cm H₂O, and these are triggered by light, warm temperature and handling.
  • Transpulmonary pressures generated by the first breaths probably play the dominant role. The pressure generated by the first breaths causes the interstitial space pressure to become subatmospheric, attracting the fluid into that space.
  • Adrenaline released during birth stimulated the lung endothelium to activate sodium channels which then reabsorb sodium out of lung water. This causes an osmotic shift of fluid out of the lung.
  • There is also the theory that passing through the vagina somehow squeezes water out of the foetal lung. Direct measurements have found that this squeeze equates to around 70 cm H₂O. However, the foetal chest does not get much of that pressure - most of it is squandered on deforming the foetal skull. 
• FRC is created and maintained
  • First breaths create and maintain the FRC by being expiration-limited, like a sort of intentional gas trapping. The infant ends up finishing the prolonged expiration on a closed glottis with abdominal muscles still forcefully contracting. 
  • Crying, grunting etc - all these manoeuvres serve this principle
  • The effect of this is that the alveoli are splinted
  • Surfactant also serves to reduce lung recoil, maintaining open alveoli
• Aeration of lungs leads to decreased pulmonary arterial resistance
  • ​The sudden drop in the pulmonary vascular resistance makes the lungs a path of least resistance for right ventricular blood.
  • Right ventricular output is therefore directed into the pulmonary circulation, increasing left ventricular preload.
  • Some of the pulmonary blood flow also consists of oxygenated blood rom the ductus arteriosus.
  • Aeration is not the only factor contributing to changes in pulmonary vascular resistance: Oh's Manual also mentions gradual postnanatal regression of smooth muscle in the pulmonary vessel walls.
• Foramen ovale shunt is reversed.
  • Pre-birth, much of LV preload consist of venous return through the foramen ovale.
  • There is an inverse relationship between pulmonary blood flow and flow though the foramen ovale.
  • As pulmonary blood flow contributes more and more of LV venous return, so the foramen ovale is forced closed.
• Ductus arteriosus shunt is reversed. 
  • Ductus arteriosus is a large shunt from the pulmonary arteries to the aorta, and its diameter is approximately the same as that of the descending aorta.
  • It shunts right ventricular blood into the systemic circulation, bypassing the lungs. About 10% of the RV output still goes into the pulmonary circulation.
  • With decreased pulmonary vascular resistance, this shunt is reversed. Then, about 50% of the pulmonary blood flow ends up being oxygenated blood from the aorta, shunting back into the pulmonary circulation via the ductus arterisus
• Ductus venosus will remain patent for days, but will eventually close.
  • ​Ductus venosus sends some of the left umbilical vein blood flow directly to the inferior vena cava. About 50% of the blood in the IVC passes through the liver and the rest bypasses the liver via the ductus venosus.
  • Functional closure occurs very shortly after birth, but this ductus ends up being anatomically patent for some number of days. If it fails to close, it turns into an intrahepatic portosystemic shunt. If it closes politely, it becomes the ligamenum venosum.
• Systemic vascular resistance is increased by clamping of the umbilical cord
  • The umbilical/placental circulation is a high-flow, low-resistance system. 
  • Before birth the left ventricular preload is mostly dependent on umbilical venous blood flow, i.e. blood returning from the placenta.
  • After the cord is clamped, LV preload depends mainly on venous return via pulmonary blood flow.
  • Clamping the cord ends up increasing systemic vascular resiastance and improving venous return to the heart by 30-50%.

Causes of a persistent foetal pattern of circulation

An excellent resource for this is D'cunha et al (2001). In short, a persistently foetal pattern of circulation is mainly caused by anything which keeps pulmonary vascular resistance high. That could be a whole host of causes. The linked article organises them into acute or chronic:

Chronically increased PVR in a structurally normal heart

• Primary persistent foetal circulation (due to hypermuscularisation of the pulmonary vessels from prolonged hypoxia or ischaemia in utero)
  • Placental insufficiency
  • Hyperviscosity, eg. high haematocrit due to late umbilical clamping
  • Prepartum ingestion of COX inhibitors which could prematurely close the ductus arteriosus

Acutely increased PVR due to physiological pulmonary vasoconstriction

• Hypoxia
• Hypercapnea
• Acidosis
• Hypothermia

Causes of perinatal hypoxia, acidosis and hypothermia

• Sepsis
• Diaphragmatic hernia
• Hyaline membrane disease
• Pulmonary thromboembolism

References

Fishman, Alfred P., and Dickinson W. Richards. "Physiological changes in the circulation after birth." Circulation of the Blood. Springer New York, 1982. 743-816.

van Vonderen, Jeroen J., et al. "Measuring physiological changes during the transition to life after birth." Neonatology 105.3 (2014): 230-242.

Koos, Brian J., and Arezoo Rajaee. "Fetal breathing movements and changes at birth." Advances in Fetal and Neonatal Physiology. Springer New York, 2014. 89-101.

Hooper, Stuart B., et al. "Cardiovascular transition at birth: a physiological sequence." Pediatric research (2015).

D’cunha, Chrysal, and Koravangattu Sankaran. "Persistent fetal circulation." Paediatrics & child health 6.10 (2001): 744.

College Answer

The transfer from the fetal to the neonatal state is complex.  There is a close relationship between the simultaneously occurring cardiovascular and respiratory changes.  Closure of umbilical vessels results in an increase in peripheral resistance and blood pressure. Respiratory centre activation (clamping of umbilical vessels, and cold) results in expansion of previously collapsed lungs.   The resultant dramatic decrease in pulmonary vascular resistance increases blood flow through the lungs, and increases return to the left atrium. This, plus the reduced return to the right atrium (clamped umbilical vein) and the increased resistance to left ventricular outflow reverse the pressure gradient across the atria (closing the valve over the foramen ovale.  The fall in pulmonary artery pressure (decreased PVR) and the increased aortic pressure results in flow reversal through the ductus arteriosus. Constriction and closure of the ductus arteriosus appears to be initiated by the high arterial oxygen tension which is now in the aortic blood. The neonate is still at risk of reversion to a foetal circulation early after birth, especially in the presence of physiological stresses and congenital abnormalities.

Discussion

These diagrams are from van Vonderen et al (2014):

In textual long form, which defeats the point of point form:

• Foetal lungs are cleared of fluid and aerated. 
  • ​With the first breaths, the lungs are aerated, creating an FRC. The foetus is capable of generating negative pressures in excess of 30 cm H₂O, and these are triggered by light, warm temperature and handling.
  • Transpulmonary pressures generated by the first breaths probably play the dominant role. The pressure generated by the first breaths causes the interstitial space pressure to become subatmospheric, attracting the fluid into that space.
  • Adrenaline released during birth stimulated the lung endothelium to activate sodium channels which then reabsorb sodium out of lung water. This causes an osmotic shift of fluid out of the lung.
  • There is also the theory that passing through the vagina somehow squeezes water out of the foetal lung. Direct measurements have found that this squeeze equates to around 70 cm H₂O. However, the foetal chest does not get much of that pressure - most of it is squandered on deforming the foetal skull. 
• FRC is created and maintained
  • First breaths create and maintain the FRC by being expiration-limited, like a sort of intentional gas trapping. The infant ends up finishing the prolonged expiration on a closed glottis with abdominal muscles still forcefully contracting. 
  • Crying, grunting etc - all these manoeuvres serve this principle
  • The effect of this is that the alveoli are splinted
  • Surfactant also serves to reduce lung recoil, maintaining open alveoli
• Aeration of lungs leads to decreased pulmonary arterial resistance
  • ​The sudden drop in the pulmonary vascular resistance makes the lungs a path of least resistance for right ventricular blood.
  • Right ventricular output is therefore directed into the pulmonary circulation, increasing left ventricular preload.
  • Some of the pulmonary blood flow also consists of oxygenated blood rom the ductus arteriosus.
  • Aeration is not the only factor contributing to changes in pulmonary vascular resistance: Oh's Manual also mentions gradual postnanatal regression of smooth muscle in the pulmonary vessel walls.
• Foramen ovale shunt is reversed.
  • Pre-birth, much of LV preload consist of venous return through the foramen ovale.
  • There is an inverse relationship between pulmonary blood flow and flow though the foramen ovale.
  • As pulmonary blood flow contributes more and more of LV venous return, so the foramen ovale is forced closed.
• Ductus arteriosus shunt is reversed. 
  • Ductus arteriosus is a large shunt from the pulmonary arteries to the aorta, and its diameter is approximately the same as that of the descending aorta.
  • It shunts right ventricular blood into the systemic circulation, bypassing the lungs. About 10% of the RV output still goes into the pulmonary circulation.
  • With decreased pulmonary vascular resistance, this shunt is reversed. Then, about 50% of the pulmonary blood flow ends up being oxygenated blood from the aorta, shunting back into the pulmonary circulation via the ductus arterisus
• Ductus venosus will remain patent for days, but will eventually close.
  • ​Ductus venosus sends some of the left umbilical vein blood flow directly to the inferior vena cava. About 50% of the blood in the IVC passes through the liver and the rest bypasses the liver via the ductus venosus.
  • Functional closure occurs very shortly after birth, but this ductus ends up being anatomically patent for some number of days. If it fails to close, it turns into an intrahepatic portosystemic shunt. If it closes politely, it becomes the ligamenum venosum.
• Systemic vascular resistance is increased by clamping of the umbilical cord
  • The umbilical/placental circulation is a high-flow, low-resistance system. 
  • Before birth the left ventricular preload is mostly dependent on umbilical venous blood flow, i.e. blood returning from the placenta.
  • After the cord is clamped, LV preload depends mainly on venous return via pulmonary blood flow.
  • Clamping the cord ends up increasing systemic vascular resiastance and improving venous return to the heart by 30-50%.

References

Fishman, Alfred P., and Dickinson W. Richards. "Physiological changes in the circulation after birth." Circulation of the Blood. Springer New York, 1982. 743-816.

van Vonderen, Jeroen J., et al. "Measuring physiological changes during the transition to life after birth." Neonatology 105.3 (2014): 230-242.

Koos, Brian J., and Arezoo Rajaee. "Fetal breathing movements and changes at birth." Advances in Fetal and Neonatal Physiology. Springer New York, 2014. 89-101.

Hooper, Stuart B., et al. "Cardiovascular transition at birth: a physiological sequence." Pediatric research (2015).

D’cunha, Chrysal, and Koravangattu Sankaran. "Persistent fetal circulation." Paediatrics & child health 6.10 (2001): 744.

College Answer

Anatomic paediatric airways offer significant potential challenges to the critical care practitioner. Factors to consider include:

•    Absolute size of airway (including trachea), small mandible, large tongue (use of chart, formula [age/4 + 4 mm if > 1 yr] or Braselow measurement tape to allow sizing of ETT, and depth estimates essential [age/2 + 12 cm from lower lip]; often need smaller blade [narrower, shorter]; concern about tracheostomy)

•    Large head (neck already flexed, not need pillow or as much head extension for intubation and airway management)

•    Epiglottis long and stiff and may obscure view (may need to include epiglottis under laryngoscope blade, or consider using straight blade)

•    Larynx high, anterior and the narrowest point is usually the laryngeal outlet/cricoid cartilage (often use uncuffed tubes, increased concern about laryngeal stenosis)

Other  specific management concerns related  to  the  small  size  of  the  artifical  airways include: importance of fixation (ease of dislodgement), increased likelihood of blockage, circuit/mechanics to minimise work of breathing.

Discussion

This is another question which would benefit from a tabulated answer.

Esther Weathers has made available an excellent document in which the pediatric airway caveats are explained, as well as the ways around them.

References

Heard, A. M. B., R. J. Green, and P. Eakins. "The formulation and introduction of a ‘can't intubate, can't ventilate’algorithm into clinical practice." Anaesthesia64.6 (2009): 601-608.

Stacey, Jonathan, et al. "The ‘Can't Intubate Can't Oxygenate’scenario in Pediatric Anesthesia: a comparison of different devices for needle cricothyroidotomy." Pediatric Anesthesia 22.12 (2012): 1155-1158.

Weathers E., "The Anatomy of the Pediatric Airway" 2010 -RC EDUCATIONAL CONSULTING SERVICES, INC.

Santillanes, Genevieve, and Marianne Gausche-Hill. "Pediatric airway management." Emergency medicine clinics of North America 26.4 (2008): 961-975.

HOLM‐KNUDSEN, R. J., and L. S. Rasmussen. "Paediatric airway management: basic aspects." Acta Anaesthesiologica Scandinavica 53.1 (2009): 1-9.

Cardwell, Mary, and Robert WM Walker. "Management of the difficult paediatric airway." BJA CEPD Reviews 3.6 (2003): 167-170.

College Answer

Many candidates missed multiple aspects of management, usually because they did not follow a systematic approach (eg. according to EMST guidelines). Basic principles of management

according to EMST guidelines are the same – ie primary survey (ABCDE), resuscitation, secondary survey, re-evaluation, definitive care. However, candidates need to recognise and accommodate the different characteristics of the 6 year old trauma patient:

Mechanism of injury: falls and assaults more likely

Patterns of injury: more likely blunt trauma with multiorgan injury and head injury common

Physiologic and anatomic differences:

•    Different airway anatomy

•    Large body surface area/volume ratio – implications for exposure and heat loss

•    Different normal physiologic values

•    Increased cardiovascular reserve – 30% blood volume may be lost before vital signs change; hypotension indicates >45% loss

•    Immature skeleton – Incomplete skeletal calcification, with more flexible bones– eg pulmonary contusions without rib fractures common; ligament flexibility and increased head mass makes cervical spine injuries above C4 more likely and Spinal Cord Injury Without Obvious Radiological Abnormality (SCIWORA) may occur.

Assessment:

•    History – may be difficult to obtain

•    Examination – may need to modify for age - eg modified GCS, but a 6 year old can be scored as per an adult

•    Investigations – may require modification – eg uncooperative child may require GA for CT

•    Treatment:

•    Airway: uncuffed tube, size estimated from age, cervical precautions

•    Breathing

•    Circulation: IV access may be difficult, consider intraosseous needle. Fluid boluses calculated according to weight (20ml/kg) as are maintenance requirements

•    Disability: modified GCS

•    Exposure: care to maintain body temperature

•    Drug doses calculated according to weight (average 6 year old 20kg)

•    Equipment sizes (eg chest drains, urinary catheters, nasogastric) appropriate for size – Broselow tape useful

Other specific issues:

•    Psychological issues – patient and parents

•    Consent issues

•    Potential child abuse

•    Consider transfer to a specialist paediatric centre

Discussion

The examiners complained that a systematic approach needed to be followed, but the college answer also fails to use such an approach. Typicaly, trauma management follows an "ABCDE" system. The summary below offers a brief systematic discussion of the differences between adult and paediatric trauma, following the ATLS system of 

• Airway: 
  • More difficult anatomy; cricothyroidotomy is challenging
  • Breathing:
  • Tension pneumothorax is harder to identify. 
  • Ribs rarely fracture (cartilaginous): force is transmitted to the lungs, causing more pulmonary contusions. Hypoxia is of more rapid onset.
• ​Circulation:
  • Increased reserve of compensation: more blood may be lost before manifestations of shock are seen.
• Disability:
  • Modified GCS must be used. Greater risk of raised ICP because of anatomical differences (bigger brain, smaller skull). C-spine injury is usually much higher (C1-C3) and is possible without radiological evidence (SCIWORA).
• Exposure:
  • Hypothermia is more likely (mass:BSA ratio)
• Family and social issues:
  • ​very important: family is the "F" in "ABCDEF" of paediatric trauma
  • counselling of carer
  • Guilt, blame, etc
• Abdominal issues:
  • Organs are unprotected by rib cage
  • Spleen and liver are often lacerated
  • Shallow pelvis fails to protect the bladder
  • Kidneys are more mobile and less defended
  • Laparotomy is rarely indicated
• Metabolic problems:
  • Hyperglycaemia and glycogen reserve depletion is more rapid; hypercatabolism develops early
• Injury patterns as compared with adults:
  • more multiple injuries (force is transmitted to more of the body)
  • improved survival from trauma
  • shorter ICU stay, fewer complications
  • need to consider non-accidental causes
  • Burns are of a different pattern : more head/face from falling pots, more hands from grabbing hot objects

More detail is available in the chapter on Trauma in Children. When preparing for such a low-yield topic, one has got to keep in mind the relative value of storing this information versus the revision of more frequently examined topics.

References

College Answer

- Call for help (Intensive care/Anaesthesia/ENT colleagues)
– Examine reasons for difficult laryngoscopy –
a) was she a difficult intubation in the 1st instance b) Poor positioning of head
c) Faulty suction, wrong laryngoscope blade
d) Use of wrong sized ETT through a swollen cords
- Important to recognise that people die from failed intubation because of failure to oxygenate, not failure to intubate
- Ensure ongoing bag-mask ventilation
- Use of LMA as an airway or as a conduit for fiberoptic intubation.
-If  LMA  not  successful,  try  reintubation  with  bougie  +  laryngeal  pressure  to  improve visualisation -
- If despite all of these, still cannot ventilate, consider cricothyroidotomy / tracheostomy

Additional points that may score marks
a) Attempt at intubation to be made with gaseous induction, two anaesthetists and full range of difficult intubation options, if it is safe to move to OT, but most PICUs can do this.
b) Mentioning that cricothyroidotomy is difficult in child
c) As nature of neurosurgery not known, mention of worsening ICP because of hypercarbia adds to the emergent nature of the situation

Discussion

This is a discussion of a "can't intubate, can't ventilate" algorithm.

Everybody should have one. ANZCA certainly suggests several. They dont specifically endorse any specific algortithm, but rather suggest that airway experts should have in their repertoir at least one.

For the answer to this question, I used the algorithm suggested by Heard et al.

In brief:

• Call for senior anaesthetic help. The person with the best paediatric airway management expertise should intubate the child.
• Explore alternatives to intubation. In the case of the child with an airway obstruction or stridor, this may consist of  the following options:
  • Heliox 
  • Adrenaline nebs
  • Steroids (if the aetiology calls for it)
• Optimise pre-intubation management: This consists of adequate pre-oxygenation. It may be necessary for the child to be pre-oxygenated in the parents' lap
  • Sit up 90°
  • CPAP may help by reducing the dynamic component of stridor 
  • Atropine can be given (20 µg/kg) to dry secretions
• Explore airway control options: 
  • ​Inhalational induction is usually Plan A. The whole point is to maintain spontaneous respiration throughout the process, using gas to attain a level of anaesthesia which permits intubation. Best to induce them in a sitting position. Be prepared to wait- gas induction is slow in airway obstruction. When the patient is ready, they are rapidly made supine and intubated by laryngoscopy.
  • IV induction with paralysis is usually Plan B.
  • If unable to intubate, proceed to LMA. If LMA ventilation is sucessful, one can prepare for a repeat attempt at intubation, with a variety of difficult intubation equipment avalable, senior staff on standby, and with manoeuvres to improve visibility (eg. improved head position, BURP, videolaryngoscopy)
  • If unable to ventilate with LMA, proceed to needle cricothyroidotomy. This is difficult in children. Skileld proceduralists only seem to have a 60% success rate, and puncture the posterior wall of the trachea about 47% of the time.
  • If jet oxygenation can be accomplished, one has some time to set up for a Seldinger dilation and insertion of a pediatric ETT, or for a retrgrade intubation.
  • If jet ventilation cannot be accomplished, one must assess the difficulty of anterior neck anatomy.
    • if the anatomy is easy, one can proceed to a scalpel-bougie tecnique (where one makes an incision in the cricothyroid membrane and railroads the tube in over a hollow jet ventilation bougie)
    • if the anatomy is difficult, one must perform a scalpel-needle cricothyroidotomy (where the cricothyroid membrane is identified by palpation through an incision, so that the jet cannula can be inserted)
• Optimise team communication: Ensure all team personnel are aware of the algorithm and understand the steps.
• Optimise first attempt:
  • ​Videolaryngoscopy
  • Skilled staff present and briefed about Plan A and Plan B
• Optimise subsequent attempts:
  • ​Checked equipment with backup models
  • Senior anaesthetist and ENT surgeon available
  • Ensure availability of ultra-fine (~ 2mm) intubating bronchoscope for paediatric work

References

Heard, A. M. B., R. J. Green, and P. Eakins. "The formulation and introduction of a ‘can't intubate, can't ventilate’algorithm into clinical practice." Anaesthesia64.6 (2009): 601-608.

Stacey, Jonathan, et al. "The ‘Can't Intubate Can't Oxygenate’scenario in Pediatric Anesthesia: a comparison of different devices for needle cricothyroidotomy." Pediatric Anesthesia 22.12 (2012): 1155-1158.

College Answer

Call for help
This should be in context-

a) if the child becomes hypoxic/has a respiratory arrest etc-proceed with attempt bag mask 
ventilation 100% oxygen immediately - attempt intubation. 

b) If there is time-aim to have the person with the best paediatric airway management expertise 
-intubate child

Optimise medical management 
a) High flow oxygen 
b) if child hypoxic -can discuss avoiding distressing the child by holding mask away from face and 
with child on parents lap (unless really sick) 
c) IV steroids-adequate dose 00.6mglkg dexamethasone 
d) NEB adrenaline 5mg (repeated doses) 
e) Oxygen/Helium mixture if tolerates 
Adequate discussion of preparationfor intubation 
a) range of ETTs (size 4.0, 4.5. 5.0, 5.5)

b) two laryngoscopes with range of blade sizes-straight/curved 
c) small diam "bougie" 
d) cannula for percutaneous needle cricothyroidotomy + method for oxygen delivery 
e) suction

Intubation: One of 2 approaches 
(1) Inhalational induction of anaesthesia with maintenance of spontaneous ventilation until adequate
depth of anaesthesia achieved to allow intubation (or to assess ability to ventilate-then proceed to 
paralyse child) 
Or (2) IV induction-with paralysis 
There must be some discussion regarding risks of either technique. Mere mention of IV approach will
not be enough to gain marks • There must be some discussion regarding risks of either technique 
However, if not trained in inhalational anaesthetic techniques-reasonable to proceed with IV 
induction of anaesthesia +muscle paralysis -with risk of being unable to ventilate 
Alternate strategies if unable to intubate 
Ventilate with LMA/face mask until help arrives 
Rarely need to proceed to needle cricothyroidotomy

Discussion

In brief:

• Call for senior anaesthetic help. The person with the best paediatric airway management expertise should intubate the child.
• Explore alternatives to intubation. In the case of the child with an airway obstruction or stridor, this may consist of  the following options:
  • Heliox 
  • Adrenaline nebs
  • Steroids (if the aetiology calls for it)
• Optimise pre-intubation management: This consists of adequate pre-oxygenation. It may be necessary for the child to be pre-oxygenated in the parents' lap
  • Sit up 90°
  • CPAP may help by reducing the dynamic component of stridor 
  • Atropine can be given (20 µg/kg) to dry secretions
• Explore airway control options: 
  • ​Inhalational induction is usually Plan A. The whole point is to maintain spontaneous respiration throughout the process, using gas to attain a level of anaesthesia which permits intubation. Best to induce them in a sitting position. Be prepared to wait- gas induction is slow in airway obstruction. When the patient is ready, they are rapidly made supine and intubated by laryngoscopy.
  • IV induction with paralysis is usually Plan B.
  • If unable to intubate, proceed to LMA. If LMA ventilation is successful, one can prepare for a repeat attempt at intubation, with a variety of difficult intubation equipment available, senior staff on standby, and with manoeuvres to improve visibility (eg. improved head position, BURP, videolaryngoscopy)
  • If unable to ventilate with LMA, proceed to needle cricothyroidotomy. This is difficult in children. Skilled proceduralists only seem to have a 60% success rate, and puncture the posterior wall of the trachea about 47% of the time.
  • If jet oxygenation can be accomplished, one has some time to set up for a Seldinger dilation and insertion of a pediatric ETT, or for a retrograde intubation.
  • If jet ventilation cannot be accomplished, one must assess the difficulty of anterior neck anatomy.
    • if the anatomy is easy, one can proceed to a scalpel-bougie tecnique (where one makes an incision in the cricothyroid membrane and railroads the tube in over a hollow jet ventilation bougie)
    • if the anatomy is difficult, one must perform a scalpel-needle cricothyroidotomy (where the cricothyroid membrane is identified by palpation through an incision, so that the jet cannula can be inserted)
• Optimise team communication: Ensure all team personnel are aware of the algorithm and understand the steps.
• Optimise the first attempt:
  • Videolaryngoscopy
  • Skilled staff present and briefed about Plan A and Plan B
• Optimise subsequent attempts:
  • Checked equipment with backup models
  • Senior anaesthetist and ENT surgeon available
  • Ensure availability of ultra-fine (~ 2mm) intubating bronchoscope for paediatric work

References

Heard, A. M. B., R. J. Green, and P. Eakins. "The formulation and introduction of a ‘can't intubate, can't ventilate’algorithm into clinical practice." Anaesthesia64.6 (2009): 601-608.

Stacey, Jonathan, et al. "The ‘Can't Intubate Can't Oxygenate’scenario in Pediatric Anesthesia: a comparison of different devices for needle cricothyroidotomy." Pediatric Anesthesia 22.12 (2012): 1155-1158.

Weathers E., "The Anatomy of the Pediatric Airway" 2010 -RC EDUCATIONAL CONSULTING SERVICES, INC.

Santillanes, Genevieve, and Marianne Gausche-Hill. "Pediatric airway management." Emergency medicine clinics of North America 26.4 (2008): 961-975.

HOLM‐KNUDSEN, R. J., and L. S. Rasmussen. "Paediatric airway management: basic aspects." Acta Anaesthesiologica Scandinavica 53.1 (2009): 1-9.

Cardwell, Mary, and Robert WM Walker. "Management of the difficult paediatric airway." BJA CEPD Reviews 3.6 (2003): 167-170.

College Answer

The transfer from the fetal to the neonatal state is complex.  There is a close relationship between the simultaneously occurring cardiovascular and respiratory changes. Closure of umbilical vessels results in  an  increase in  peripheral resistance and  blood pressure.

Respiratory centre activation (clamping of umbilical vessels, and cold) results in expansion of previously collapsed lungs.  The resultant dramatic decrease in pulmonary vascular resistance increases blood flow through the lungs, and increases return to the left atrium. This, plus the reduced return to the right atrium (clamped umbilical vein) and the increased resistance to left ventricular outflow reverse the pressure gradient across the atria (closing the valve over the foramen ovale.  The fall in pulmonary artery pressure (decreased PVR) and the increased aortic pressure results in flow reversal through the ductus arteriosus. Constriction and closure of the ductus arteriosus appears to be initiated by the high arterial oxygen tension which is now in the aortic blood.  The neonate is still at risk of reversion to a foetal circulation early after birth, especially in the presence of physiological stresses and congenital abnormalities.

Discussion

These diagrams are from van Vonderen et al (2014):

In textual long form, which defeats the point of point form:

• Foetal lungs are cleared of fluid and aerated. 
  • ​With the first breaths, the lungs are aerated, creating an FRC. The foetus is capable of generating negative pressures in excess of 30 cm H₂O, and these are triggered by light, warm temperature and handling.
  • Transpulmonary pressures generated by the first breaths probably play the dominant role. The pressure generated by the first breaths causes the interstitial space pressure to become subatmospheric, attracting the fluid into that space.
  • Adrenaline released during birth stimulated the lung endothelium to activate sodium channels which then reabsorb sodium out of lung water. This causes an osmotic shift of fluid out of the lung.
  • There is also the theory that passing through the vagina somehow squeezes water out of the foetal lung. Direct measurements have found that this squeeze equates to around 70 cm H₂O. However, the foetal chest does not get much of that pressure - most of it is squandered on deforming the foetal skull. 
• FRC is created and maintained
  • First breaths create and maintain the FRC by being expiration-limited, like a sort of intentional gas trapping. The infant ends up finishing the prolonged expiration on a closed glottis with abdominal muscles still forcefully contracting. 
  • Crying, grunting etc - all these manoeuvres serve this principle
  • The effect of this is that the alveoli are splinted
  • Surfactant also serves to reduce lung recoil, maintaining open alveoli
• Aeration of lungs leads to decreased pulmonary arterial resistance
  • ​The sudden drop in the pulmonary vascular resistance makes the lungs a path of least resistance for right ventricular blood.
  • Right ventricular output is therefore directed into the pulmonary circulation, increasing left ventricular preload.
  • Some of the pulmonary blood flow also consists of oxygenated blood rom the ductus arteriosus.
  • Aeration is not the only factor contributing to changes in pulmonary vascular resistance: Oh's Manual also mentions gradual postnanatal regression of smooth muscle in the pulmonary vessel walls.
• Foramen ovale shunt is reversed.
  • Pre-birth, much of LV preload consist of venous return through the foramen ovale.
  • There is an inverse relationship between pulmonary blood flow and flow though the foramen ovale.
  • As pulmonary blood flow contributes more and more of LV venous return, so the foramen ovale is forced closed.
• Ductus arteriosus shunt is reversed. 
  • Ductus arteriosus is a large shunt from the pulmonary arteries to the aorta, and its diameter is approximately the same as that of the descending aorta.
  • It shunts right ventricular blood into the systemic circulation, bypassing the lungs. About 10% of the RV output still goes into the pulmonary circulation.
  • With decreased pulmonary vascular resistance, this shunt is reversed. Then, about 50% of the pulmonary blood flow ends up being oxygenated blood from the aorta, shunting back into the pulmonary circulation via the ductus arterisus
• Ductus venosus will remain patent for days, but will eventually close.
  • ​Ductus venosus sends some of the left umbilical vein blood flow directly to the inferior vena cava. About 50% of the blood in the IVC passes through the liver and the rest bypasses the liver via the ductus venosus.
  • Functional closure occurs very shortly after birth, but this ductus ends up being anatomically patent for some number of days. If it fails to close, it turns into an intrahepatic portosystemic shunt. If it closes politely, it becomes the ligamenum venosum.
• Systemic vascular resistance is increased by clamping of the umbilical cord
  • The umbilical/placental circulation is a high-flow, low-resistance system. 
  • Before birth the left ventricular preload is mostly dependent on umbilical venous blood flow, i.e. blood returning from the placenta.
  • After the cord is clamped, LV preload depends mainly on venous return via pulmonary blood flow.
  • Clamping the cord ends up increasing systemic vascular resiastance and improving venous return to the heart by 30-50%.

References

Fishman, Alfred P., and Dickinson W. Richards. "Physiological changes in the circulation after birth." Circulation of the Blood. Springer New York, 1982. 743-816.

van Vonderen, Jeroen J., et al. "Measuring physiological changes during the transition to life after birth." Neonatology 105.3 (2014): 230-242.

Koos, Brian J., and Arezoo Rajaee. "Fetal breathing movements and changes at birth." Advances in Fetal and Neonatal Physiology. Springer New York, 2014. 89-101.

Hooper, Stuart B., et al. "Cardiovascular transition at birth: a physiological sequence." Pediatric research (2015).

D’cunha, Chrysal, and Koravangattu Sankaran. "Persistent fetal circulation." Paediatrics & child health 6.10 (2001): 744.

College Answer

(a) Assessment

Important points include:

a)  Past medical history. Premature delivery, neonatal ventilation, any previous respiratory disease, congenital heart disease or other syndromes (eg trisomy 21). All of these worsen the prognosis, and increase the likelihood of the need for respiratory support.

b)  Diagnosis: must exclude undiagnosed congenital cardiac condition;

is this RSV bronchiolitis? PCR analysis of the naso-pharyngal aspirate is the usual way of making this diagnosis. Other differentials include pertussis and influenza, both of which have the potential to be worse.

Length of history of this illness. In the normal child, RSV bronchiolitis runs a course of 7 – 10 days. So a severe presentation in the first 3 days is more serious than the fifth or sixth day, although a biphasic disease suggests possible secondary infection (Staphylococcus or Streptococcus) .

c)  Current observation. Pulse and respiratory rate, severity of respiratory distress, and history of apnoeas requiring resuscitation.

d) If the child has very significant respiratory distress, has had more than one significant apnoea, has very high pulse or respiratory rate, is desaturating despite significant oxygen therapy (such as >60% FiO2), or presence of exhaustion –then ICU/HDU admission is indicated and consideration of transfer to a paediatric facility.

(b) Management includes

1) oxygen therapy,

2) Minimal handling with grouped cares

3) consideration of IV fluids and fasting whilst under assessment.

4) If ventilatory support is required this can be with CPAP via N/P tube/ bubble

CPAP/high flow nasal prong oxygen or face mask BIPAP.

5) Antibiotics are indicated if there are grounds for suspecting a superadded bacterial infection.

6) Aminophylline or Caffeine may be useful in reducing the number of apnoeas if the child has been premature.

7) A few children, usually in the high risk groups above, will need mechanical ventilation or if there is consideration of transportation/retrieval. Comment that intubation and ventilation will prolong the PICU course by 2- 3 days.

Could also mention other advocated therapies

Eg nebulized adrenaline/salbutamol/heliox /Ribavarin– and comment that these therapies have not been proven to be effective in all cases but a few may respond.

Discussion

Assessment:

History

• Background (looking for the risk factors of severe bronchiolitis)
• Duration of illness (normal course is 7-10 days, should completely resolve within 1 month)
• History of complications
• Feeding history (i.e. adequate oral intake)
• Episodes of restlessness or lethargy
• History of unusual, severe or prolonged course (makes you think of congenital heart disease or some sort of defect in the immune system)

Examination

• Clinical features consistent with bronchiolitis
• Clinical features of severity
• Assessment for the need for intubation or NIV
• Clinically may also have mayconjunctivitis, pharyngitis, or acute otitis media

Investigations

• PCR for RSV, usually from nasal swabs
• Bloods will have a low yield
• CXR has no role to play unless you strongly suspect foreign body aspiration

Management:

• Airway: ​ 
  • Assess the need for intuibation (rarely required)
  • Nasal suctioning to clear upper airway (not deep nasopharyngeal, but rather shallow nasal suctioning)
  •  
• Ventilation:
  • Just oxygen to begin with
  • Aim for sats of over 90%
  • CPAP or HFNP may be the next step of escalation. With infants, maximum flow rate is about L/min. 
  • Invasive mechanical ventilation may be required, but HFNP frequently prevents the need for this.
  • Respiratory distress will escalate whenever the child is handled; the key to respiratory success is to minimise handling and to group all routine cares so that the child gets long breaks between distressing events.
  • Apnoeas may be helped by caffeine or aminophylline
• Advanced strategies to improve gas exchange
  • ​Nebulised hypertonic saline 
  • Nebulised surfactant
  • Heliox
  • ECMO
  • None of these are strongly based in any sociaety recommendations, and sucess is mainly known from case reports
• Circulation:
  • ​IV maintenance fluids and resuscitation of dehydration
  • Assessment for any coexisting cardiac disease with TTE
• Electrolytes
  • Watch for SIADH: apparently that is one of the possible complications
• Nutrition
  • ​Nasogastric feeding to make up for recent deficit
• Antibiotics
  • ​Routine use of IV antibiotics is not indicated
  • Ribavirin has been trialled, and is also not recommended for routine treatment of RSV
    infection but may be considered in select immunocompromised individuals
  • Palivizumab, a humanized monoclonal antibody (IgG) directed against RSV, may be used in at-risk populations for prevention (eg. premature infants during RSV season).
• Strategies which have been trialled and which clearly do not work:
  • ​Nebulised bronchodilators
  • Montelucast
  • Corticosteroids (no evidence of benefit, and may even increase the duration of viral shedding)
  • Chest physiotherapy (probably no benefit)
  • Caffeine or aminophylline (they were supposed to decrease the risk of apnoeas, but they do not seem to work)
  • However, it must be mentioned that the trials of all these interventions excluded the "severe" category of patients.

References

Plint, Amy C., et al. "Epinephrine and dexamethasone in children with bronchiolitis." New England Journal of Medicine 360.20 (2009): 2079-2089.

Lowell, Darcy I., et al. "Wheezing in infants: the response to epinephrine." Pediatrics 79.6 (1987): 939-945.

Ralston, S. L., A. S. Lieberthal, and H. C. Meissner. American Academy of Pediatrics Subcommittee on Diagnosis and Management of Bronchiolitis. "Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis". Pediatrics 134.5 (2014): e1474-e1502.

Osvald, Emma Caffrey, and Jane R. Clarke. "NICE clinical guideline: bronchiolitis in children." Archives of disease in childhood-Education & practice edition (2015): edpract-2015.

Alansari, Khalid, et al. "Caffeine for the Treatment of Apnea in Bronchiolitis: A Randomized Trial." The Journal of pediatrics (2016).

College Answer

Anatomic paediatric airways offer significant potential challenges to the critical care practitioner. Factors to consider include:

•    Absolute size of airway (including trachea), small mandible, large tongue (use of chart, formula [age/4 + 4 mm if > 1 yr] or Braselow measurement tape to allow sizing of ETT, and depth estimates essential [age/2 + 12 cm from  lower  lip]; often  need  smaller  blade [narrower,  shorter];  concern about tracheostomy)
•    Large  head  (neck  already  flexed,  not  need  pillow  or  as  much  head extension for intubation and airway management)
•    Epiglottis  long  and  stiff  and  may obscure  view  (may  need  to  include epiglottis under laryngoscope blade, or consider using straight blade)
•    Larynx  high,  anterior  and  the narrowest  point  is usually  the laryngeal outlet/cricoid cartilage (often use uncuffed tubes, increased concern about laryngeal stenosis)

Other specific management concerns related to the small size of the artificial airways  include:  importance   of  fixation  (ease  of  dislodgement),   increased likelihood of blockage, circuit/mechanics to minimise work of breathing.

Discussion

The difficult paediatric airway 

References

Heard, A. M. B., R. J. Green, and P. Eakins. "The formulation and introduction of a ‘can't intubate, can't ventilate’algorithm into clinical practice." Anaesthesia64.6 (2009): 601-608.

Stacey, Jonathan, et al. "The ‘Can't Intubate Can't Oxygenate’scenario in Pediatric Anesthesia: a comparison of different devices for needle cricothyroidotomy." Pediatric Anesthesia 22.12 (2012): 1155-1158.

Weathers E., "The Anatomy of the Pediatric Airway" 2010 -RC EDUCATIONAL CONSULTING SERVICES, INC.

Santillanes, Genevieve, and Marianne Gausche-Hill. "Pediatric airway management." Emergency medicine clinics of North America 26.4 (2008): 961-975.

HOLM‐KNUDSEN, R. J., and L. S. Rasmussen. "Paediatric airway management: basic aspects." Acta Anaesthesiologica Scandinavica 53.1 (2009): 1-9.

Cardwell, Mary, and Robert WM Walker. "Management of the difficult paediatric airway." BJA CEPD Reviews 3.6 (2003): 167-170.

College Answer

(a) Assessment

Important points include:

a)  Past medical history. Premature delivery, neonatal ventilation, any previous respiratory disease, congenital heart disease or other syndromes (eg trisomy 21). All of these worsen the prognosis, and increase the likelihood of the need for respiratory support.

b)  Diagnosis: must exclude undiagnosed congenital cardiac condition;
is this RSV bronchiolitis? PCR analysis of the naso-pharyngal aspirate is the usual way of making this diagnosis. Other differentials include pertussis and influenza, both of which have the potential to be worse.

c)  Length of history of this illness. In the normal child, RSV bronchiolitis runs a course of 7 –
10 days. So a severe presentation in the first 3 days is more serious than the fifth or sixth day, although a biphasic disease suggests possible secondary infection (Staphylococcus or Streptococcus).

d)  Current observation. Pulse and respiratory rate, severity of respiratory distress, and history of apnoeas requiring resuscitation.

e)  If the child has very significant respiratory distress, has had more than one significant apnoea, has very high pulse or respiratory rate, is desaturating despite significant oxygen therapy (such as >60% FiO2), or presence of exhaustion –then ICU/HDU admission is indicated and consideration of transfer to a paediatric facility.
(b) Management includes a)  Oxygen therapy
b)  Minimal handling with grouped cares
c)  Consideration of IV fluids and fasting whilst under assessment
d)  If ventilatory support is required this can be with CPAP via N/P tube/ bubble CPAP/high flow nasal prong oxygen or face mask BIPAP
e)  Antibiotics are indicated if there are grounds for suspecting a superadded bacterial infection f)      Aminophylline or Caffeine may be useful in reducing the number of apnoeas if the child has
been premature
g)  A few children, usually in the high risk groups above, will need mechanical ventilation or if there is consideration of transportation/retrieval. Comment that intubation and ventilation will prolong the PICU course by 2- 3 days

Could also mention other advocated therapies
Eg nebulized adrenaline/salbutamol/heliox /Ribavarin– and comment that these therapies have not been proven to be effective in all cases but a few may respond.

Discussion

Assessment:

History

• Background (looking for the risk factors of severe bronchiolitis)
• Duration of illness (normal course is 7-10 days, should completely resolve within 1 month)
• History of complications
• Feeding history (i.e. adequate oral intake)
• Episodes of restlessness or lethargy
• History of unusual, severe or prolonged course (makes you think of congenital heart disease or some sort of defect in the immune system)

Examination

• Clinical features consistent with bronchiolitis
• Clinical features of severity
• Assessment for the need for intubation or NIV
• Clinically may also have mayconjunctivitis, pharyngitis, or acute otitis media

Investigations

• PCR for RSV, usually from nasal swabs
• Bloods will have a low yield
• CXR has no role to play unless you strongly suspect foreign body aspiration

Management:

• Airway: ​ 
  • Assess the need for intuibation (rarely required)
  • Nasal suctioning to clear upper airway (not deep nasopharyngeal, but rather shallow nasal suctioning)
  •  
• Ventilation:
  • Just oxygen to begin with
  • Aim for sats of over 90%
  • CPAP or HFNP may be the next step of escalation. With infants, maximum flow rate is about L/min. 
  • Invasive mechanical ventilation may be required, but HFNP frequently prevents the need for this.
  • Respiratory distress will escalate whenever the child is handled; the key to respiratory success is to minimise handling and to group all routine cares so that the child gets long breaks between distressing events.
  • Apnoeas may be helped by caffeine or aminophylline
• Advanced strategies to improve gas exchange
  • ​Nebulised hypertonic saline 
  • Nebulised surfactant
  • Heliox
  • ECMO
  • None of these are strongly based in any sociaety recommendations, and sucess is mainly known from case reports
• Circulation:
  • ​IV maintenance fluids and resuscitation of dehydration
  • Assessment for any coexisting cardiac disease with TTE
• Electrolytes
  • Watch for SIADH: apparently that is one of the possible complications
• Nutrition
  • ​Nasogastric feeding to make up for recent deficit
• Antibiotics
  • ​Routine use of IV antibiotics is not indicated
  • Ribavirin has been trialled, and is also not recommended for routine treatment of RSV
    infection but may be considered in select immunocompromised individuals
  • Palivizumab, a humanized monoclonal antibody (IgG) directed against RSV, may be used in at-risk populations for prevention (eg. premature infants during RSV season).
• Strategies which have been trialled and which clearly do not work:
  • ​Nebulised bronchodilators
  • Montelucast
  • Corticosteroids (no evidence of benefit, and may even increase the duration of viral shedding)
  • Chest physiotherapy (probably no benefit)
  • Caffeine or aminophylline (they were supposed to decrease the risk of apnoeas, but they do not seem to work)
  • However, it must be mentioned that the trials of all these interventions excluded the "severe" category of patients.

References

Plint, Amy C., et al. "Epinephrine and dexamethasone in children with bronchiolitis." New England Journal of Medicine 360.20 (2009): 2079-2089.

Lowell, Darcy I., et al. "Wheezing in infants: the response to epinephrine." Pediatrics 79.6 (1987): 939-945.

Ralston, S. L., A. S. Lieberthal, and H. C. Meissner. American Academy of Pediatrics Subcommittee on Diagnosis and Management of Bronchiolitis. "Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis". Pediatrics 134.5 (2014): e1474-e1502.

Osvald, Emma Caffrey, and Jane R. Clarke. "NICE clinical guideline: bronchiolitis in children." Archives of disease in childhood-Education & practice edition (2015): edpract-2015.

Alansari, Khalid, et al. "Caffeine for the Treatment of Apnea in Bronchiolitis: A Randomized Trial." The Journal of pediatrics (2016).

College Answer

Call for help 
This should be in context –
a)  If the child becomes hypoxic/has a respiratory arrest etc – proceed with attempt bag mask ventilation 100% oxygen immediately – attempt intubation.
b)  If  there  is  time  –  aim  to  have  the  person  with  the  best  paediatric  airway management expertise – intubate child

Optimise medical management 
a) High flow oxygen
b) if child hypoxic – can discuss avoiding distressing the child by holding mask away from face and with child on parents lap (unless really sick)
c) IV steroids – adequate dose (` 0.6mg/kg dexamethasone d) NEB adrenaline 5mg (repeated doses)
e) Oxygen/Helium mixture if tolerates

Adequate discussion of preparation for intubation 
a) range of ETT’s (size 4.0, 4.5. 5.0, 5.5)
b) two laryngoscopes with range of blade sizes – straight/curved c) small diam “bougie”
d) cannula for percutaneous needle cricothyroidotomy + method for oxygen delivery
e) suction

Intubation: One of 2 approaches 
(1) Inhalational induction of anaesthesia with maintenance of spontaneous ventilation until adequate  depth  of  anaesthesia  achieved  to  allow  intubation  (or  to  assess  ability  to ventilate – then proceed to paralyse child)
Or (2) IV induction – with paralysis
There must be some discussion regarding risks of either technique. Mere mention of IV approach will not be enough to gain marks. There must be some discussion regarding risks of either technique
However, if not trained in inhalational anaesthetic techniques – reasonable to proceed with
IV induction of anaesthesia + muscle paralysis – with risk of being unable to ventilate

Alternate strategies if unable to intubate Ventilate with LMA/face mask until help arrives Rarely need to proceed to needle cricothyroidotomy

Discussion

Ohs Manual has a whole chapter on pediatric airway managemnt, and the child with stridor receives some attention (page 1099). I will paraphrase their suggestion regarding the management of such a problem.

In brief:

• Call for senior anaesthetic help. The person with the best paediatric airway management expertise should intubate the child.
• Explore alternatives to intubation. In the case of the child with an airway obstruction or stridor, this may consist of  the following options:
  • Heliox 
  • Adrenaline nebs
  • Steroids (if the aetiology calls for it)
• Optimise pre-intubation management: This consists of adequate pre-oxygenation. It may be necessary for the child to be pre-oxygenated in the parents' lap
  • Sit up 90°
  • CPAP may help by reducing the dynamic component of stridor 
  • Atropine can be given (20 µg/kg) to dry secretions
• Explore airway control options: 
  • ​Inhalational induction is usually Plan A. The whole point is to maintain spontaneous respiration throughout the process, using gas to attain a level of anaesthesia which permits intubation. Best to induce them in a sitting position. Be prepared to wait- gas induction is slow in airway obstruction. When the patient is ready, they are rapidly made supine and intubated by laryngoscopy.
  • IV induction with paralysis is usually Plan B.
  • If unable to intubate, proceed to LMA. If LMA ventilation is sucessful, one can prepare for a repeat attempt at intubation, with a variety of difficult intubation equipment avalable, senior staff on standby, and with manoeuvres to improve visibility (eg. improved head position, BURP, videolaryngoscopy)
  • If unable to ventilate with LMA, proceed to needle cricothyroidotomy. This is difficult in children. Skileld proceduralists only seem to have a 60% success rate, and puncture the posterior wall of the trachea about 47% of the time.
  • If jet oxygenation can be accomplished, one has some time to set up for a Seldinger dilation and insertion of a pediatric ETT, or for a retrgrade intubation.
  • If jet ventilation cannot be accomplished, one must assess the difficulty of anterior neck anatomy.
    • if the anatomy is easy, one can proceed to a scalpel-bougie tecnique (where one makes an incision in the cricothyroid membrane and railroads the tube in over a hollow jet ventilation bougie)
    • if the anatomy is difficult, one must perform a scalpel-needle cricothyroidotomy (where the cricothyroid membrane is identified by palpation through an incision, so that the jet cannula can be inserted)
• Optimise team communication: Ensure all team personnel are aware of the algorithm and understand the steps.
• Optimise first attempt:
  • ​Videolaryngoscopy
  • Skilled staff present and briefed about Plan A and Plan B
• Optimise subsequent attempts:
  • ​Checked equipment with backup models
  • Senior anaesthetist and ENT surgeon available
  • Ensure availability of ultra-fine (~ 2mm) intubating bronchoscope for paediatric work

References

Heard, A. M. B., R. J. Green, and P. Eakins. "The formulation and introduction of a ‘can't intubate, can't ventilate’algorithm into clinical practice." Anaesthesia64.6 (2009): 601-608.

Stacey, Jonathan, et al. "The ‘Can't Intubate Can't Oxygenate’scenario in Pediatric Anesthesia: a comparison of different devices for needle cricothyroidotomy." Pediatric Anesthesia 22.12 (2012): 1155-1158.

Weathers E., "The Anatomy of the Pediatric Airway" 2010 -RC EDUCATIONAL CONSULTING SERVICES, INC.

Santillanes, Genevieve, and Marianne Gausche-Hill. "Pediatric airway management." Emergency medicine clinics of North America 26.4 (2008): 961-975.

HOLM‐KNUDSEN, R. J., and L. S. Rasmussen. "Paediatric airway management: basic aspects." Acta Anaesthesiologica Scandinavica 53.1 (2009): 1-9.

Cardwell, Mary, and Robert WM Walker. "Management of the difficult paediatric airway." BJA CEPD Reviews 3.6 (2003): 167-170.

College Answer

a)  List the possible causes of stridor at rest in a previously well 3 year old child

•    viral croup
•     epiglottitis
•    inhaled foreign body
•    severe bilateral tonsillitis, meeting in the midline (eg: infectious mononucleosis)
•    tonsillar abscess
•    retropharyngeal infection/abscess
•    spasmodic (recurrent allergic) croup
•    allergic reaction/angio-oedema
•    bacterial tracheitis
•    intra-thoracic  obstruction  vascular  rings  (less  likely  in  prev.  well),  peri-tracheal tumours
•    diphtheria
•    other   congenital   causes   (laryngomalacia,   tracheomalacia,   tracheal   webs   etc)
unlikely in this setting, no marks for these responses

b)  What features elicited on history, examination and imaging would help in refining the diagnosis

1.   History:
•    past history including neonatal problems, previous intubation
•    vaccination especially HiB
•    prodrome, URTI symptoms
•    choking episodes (FB)
•    febrile symptoms
•    cough (implies epiglottitis unlikely)

2.   Examination
•    (minimise disturbance to child, examine in parent’s lap)
•    toxicity & fever
•    swallowing / drooling
•    petechial rash in HiB sepsis
•    inspect the throat (without instrumentation  and if child cooperative),  looking for tonsillar hyperplasia, uvula swelling, FB

3.   Radiology:
•    very limited utility, may be unsafe to transfer
•    possibly if radio-opaque FB suspected
•    lateral soft tissue neck of no/little value

c) What are the indications for intubation in this situation?

•    Complete or imminent airway obstruction
•    Worsening airway obstruction despite appropriate therapy (eg steroids + nebulised adrenaline in croup)
•    Dangerous reduction in conscious state
•    Uncorrectable hypoxaemia

d)  List the key management issues in securing the airway

•    Call for help
•    Choice of anaesthetic technique  - inhalational versus intravenous
•    Failed intubation drill

Discussion

a)  List the possible causes of stridor at rest in a previously well 3 year old child

b)  What features elicited on history, examination and imaging would help in refining the diagnosis

c) What are the indications for intubation in this situation?

...little can be added to the college answer...

d)  List the key management issues in securing the airway

In brief:

• Call for senior anaesthetic help. The person with the best paediatric airway management expertise should intubate the child.
• Explore alternatives to intubation. In the case of the child with an airway obstruction or stridor, this may consist of  the following options:
  • Heliox 
  • Adrenaline nebs
  • Steroids (if the aetiology calls for it)
• Optimise pre-intubation management: This consists of adequate pre-oxygenation. It may be necessary for the child to be pre-oxygenated in the parents' lap
  • Sit up 90°
  • CPAP may help by reducing the dynamic component of stridor 
  • Atropine can be given (20 µg/kg) to dry secretions
• Explore airway control options: 
  • ​Inhalational induction is usually Plan A. The whole point is to maintain spontaneous respiration throughout the process, using gas to attain a level of anaesthesia which permits intubation. Best to induce them in a sitting position. Be prepared to wait- gas induction is slow in airway obstruction. When the patient is ready, they are rapidly made supine and intubated by laryngoscopy.
  • IV induction with paralysis is usually Plan B.
  • If unable to intubate, proceed to LMA. If LMA ventilation is sucessful, one can prepare for a repeat attempt at intubation, with a variety of difficult intubation equipment avalable, senior staff on standby, and with manoeuvres to improve visibility (eg. improved head position, BURP, videolaryngoscopy)
  • If unable to ventilate with LMA, proceed to needle cricothyroidotomy. This is difficult in children. Skileld proceduralists only seem to have a 60% success rate, and puncture the posterior wall of the trachea about 47% of the time.
  • If jet oxygenation can be accomplished, one has some time to set up for a Seldinger dilation and insertion of a pediatric ETT, or for a retrgrade intubation.
  • If jet ventilation cannot be accomplished, one must assess the difficulty of anterior neck anatomy.
    • if the anatomy is easy, one can proceed to a scalpel-bougie tecnique (where one makes an incision in the cricothyroid membrane and railroads the tube in over a hollow jet ventilation bougie)
    • if the anatomy is difficult, one must perform a scalpel-needle cricothyroidotomy (where the cricothyroid membrane is identified by palpation through an incision, so that the jet cannula can be inserted)
• Optimise team communication: Ensure all team personnel are aware of the algorithm and understand the steps.
• Optimise first attempt:
  • ​Videolaryngoscopy
  • Skilled staff present and briefed about Plan A and Plan B
• Optimise subsequent attempts:
  • ​Checked equipment with backup models
  • Senior anaesthetist and ENT surgeon available
  • Ensure availability of ultra-fine (~ 2mm) intubating bronchoscope for paediatric work

References

Cavanagh, Florence. "Stridor in children." Proceedings of the Royal Society of Medicine 58.4 (1965): 272.

Pfleger, Andreas, and Ernst Eber. "Assessment and causes of stridor." Paediatric respiratory reviews 18 (2016): 64-72.

College Answer

a)

• Normal BP for neonate 75/40 mmHg range 60-80 systolic 40-50 diastolic
• Normal pulse rate for neonate 100-160,100 when asleep 160 when crying
• Normal RR for Neonate 30-60 – average 40
• Saturation >93% on room air

b)

• Distortion of the chest wall (sternal and rib retraction, recession of intercostal, subcostal and suprasternal spaces) Accept alternative terminology
• Pallor
• Apnoea
• Bradycardia
• Lethargy, listlessness, decreased level of consciousness

c)

• Upper airway obstruction
• Bronchiolitis
• Pneumonia
• Aspiration
• Cardiac failure (usually associated with high pulmonary blood flow, VSD, PDA, truncus arteriosus etc; left heart obstructive lesions; coarctation of the aorta; aortic stenosis)
• Sepsis

d)

• Increased metabolic demand – oxygen consumption twice that of the adult
• Structural immaturity of the thoracic cage – ribs short and horizontal, bucket motion is minimal - infant is dependant on diaphragmatic displacement of abdominal contents to increase volume of the thorax any increase in abdominal distension may compromise respiratory function.
• Infant airways – small and more prone to obstruction
• Immaturity of immune system increasing susceptibility to infection
• Immature development of the respiratory system – particularly in premature infants with surfactant deficiency, alveolar instability, reduced lung compliance
• Immaturity of respiratory control – immature respiratory centre results in inadequate respiratory drive and can lead to apnoea.
• Congenital abnormalities – either respiratory or cardiovascular may lead to early respiratory failure
• Perinatal injuries – pneumothorax, neuromuscular including perinatal asphyxia which can result in apnoeas.

Discussion

This question addresses the candidate's knowledge of the most recent APLS resuscitation guidelines.

Normally, the majority of these neonatal resuscitation questions are souced directly from the APLS handbook, which one receives as part of the APLS course reading material.

Certainly, for questions b) c) and d) this was the case. However, the values for normal vital signs I found in the 4th edition of the book (for the under-1 age group) were different to those quoted in the college answer. Even a quick Googly frolic through teh interweb yields a bewidering plethora of normal ranges. Exactly where did the college derive its values from?

In the "model answer" I parroted the college values.

The normal values "at birth" in Oh's Manual are as follows:

• BP = 75/40
• HR 125 (94-155)
• RR 50

b) This answer was souced directly from the APLS handbook, page 60 (4th edition)

c) This is a question about the potential causes of respiratory distress in the neonate. Again, there is a list of causes of respiratory failure in the APLS handbook, which the college answer borrows heavily from. There is no real way to improve on a list like this. I have transcribed it almost direclty, excluding causes which are irrelevant to this age group.

d) The same chapter in the APLS handbook also discusses the reasons why neonates are predisposed to respratory failure. Again, it is difficult to improve on this list. You will find it on page 74 of the 4th edition.

References

the APLS handbook, 4th edition; as well as Oh's Manual.

College Answer

a) Initial management

• •  ABCDEFG approach.
• •   Oxygen
• •   Venous access (IO if required)
• •   Secure airway if needed
• Fluid bolus (20ml/kg early boluses ; aim for reversal of immediately life-threatening shock; post FEAST more controversial but remains key management)
• Keep warm
• Check BSL as an early priority
• Early administration of empiric antibiotics

• Investigations- blood gas essential mentioned essential for full marks; others may be mentioned as delayed (arterial, venous or capillary all reasonable; venous quick and useful)

• Investigations: blood culture, FBC, ELFT, formal BSL as early keys, stool culture and viral screen, urine culture, nasopharyngeal aspirate for respiratory viruses, CXR

b) Assessment of dehydration

• Clinical assessment of dehydration can be difficult, especially in young infants, and rarely predicts the exact degree of dehydration accurately. 
• The most useful individual signs for predicting 5% dehydration in children are an abnormal capillary refill time, abnormal skin turgor and abnormal respiratory pattern. Combinations of examination signs provide a much better method than any individual signs in assessing the degree of dehydration.
• Clinical assessment therefore comprises some of the following indicators of dehydration:

Loss of body weight:

• Normal: no loss of body weight.
• Mild dehydration: 5-6% loss of body weight.

• Moderate: 7-10% loss of body weight.
• Severe: over 10% loss of body weight.

Clinical features of mild-to-moderate dehydration; 2 or more of:

• Restlessness or irritability.

• Sunken eyes (also ask the parent).

• Thirsty and drinks eagerly.

Clinical features of severe dehydration; 2 or more of:

• Abnormally sleepy or lethargic.

• Sunken eyes.

• Drinking poorly or not at all.

• Pinch test (skin turgor): the sign is unreliable in obese or severely malnourished children.

• Normal: skin fold retracts immediately.

• Mild or moderate dehydration: slow; skin fold visible for less than 2 seconds.

• Severe dehydration: very slow; skin fold visible for longer than 2 seconds.

• Other features of dehydration include dry mucous membranes, reduced tears and decreased urine output.

• Additional signs of severe dehydration include circulatory collapse (e.g. weak rapid pulse, cool or blue extremities, hypotension), rapid breathing, sunken anterior fontanelle.

Discussion

1) Initial management of the non-specifically shocked child can consist of the following generic steps, copied and pasted from the chapter on paediatric shock:

1. Assess the need for intubation.
   - At this stage, senior assistance from somebody expert in paediatric critical care is required, as the intubation may be difficult.
2. Administer 100% oxygen.
3. Establish venous access.
   - Give a 20ml/kg bolus, FEAST be damned.
   - Inotropes and vasopressors if no longer fluid-responsive
   - Parameters guiding resuscitation (eg. lactate, haemodynamic variables, urine output) differ little from adult standards
4. Sedation and analgesia to support tolerance of invasive therapies
   (also decreases demands on the cardiac output)
5. Electrolyte correction
6. Maintenance fluid:  As per college answer, "add 100 ml of 50% dextrose to 900 ml 0.9% NaCl and infuse this at 2/3 maintenance rate (16 ml/hr in this case) (accept 24 ml/hr for 1^st 48 hours)". 
   - A urinary catheter will also be required.
7. No protein in diet until metabolic screen is cleared
   - Maintain normoglycaemia with infusion of 10% dextrose of dextrose-rich maintenance fluid
8. Blood transfusion may not be warranted
9. Empiric antibiotics if sepsis is suspected, within 1 hour.
   - Cultures of blood and urine.
   - Consider antivirals if there is suspicion of viral meningitis or encephalitis

2) Assessment of dehydration offered by the college is based on Gorelick et al (1997). Here it is, interpreted as a table:

That whole "two or more" thing also comes from Gorelick (1997). "A subset of four factors—capillary refill >2 seconds, absent tears, dry mucous membranes, and ill general appearance—predicted dehydration as well as the entire set, with the presence of any two or more of these signs indicating a deficit of at least 5%".  In general, when it comes to assessing dehydration, Gorelick et al recommend using a combination of three signs (this is also mentioned in the college answer) - a combination of three signs had a sensitivity of 87% and specificity of 82% for detecting a water deficit of 5% or more.

The FEAST trial earns a mention because mortality was found to be increased in the group of severely ill febrile African children who received fluid boluses. It was published in the previous year, and caused something of a moral panic ("What? No fluids for our sick children?"). It seems cardiovascular collapse rather than fluid overload is the cause of death among these children. It has brought into question the administration of early 20-40ml/kg boluses to these kids.

However, the college still seems to support this practice, though they acknowledge it as "controversial". In fact, even the WHO has persisted with its recommendations to give fluid boluses in septic children, which has prompted some authors to question the degree of its attachment to evidence.

References

Maitland K, Kiguli S, Opoka RO, Engoru C, Olupot-Olupot P, Akech SO, Nyeko R, Mtove G, Reyburn H, Lang T, Brent B, Evans JA, Tibenderana JK, Crawley J, Russell EC, Levin M, Babiker AG, Gibb DM: Mortality after fluid bolus in African children with severe infection. N Engl J Med 2011, 364:2483-2495

Kiguli, Sarah, et al. "WHO guidelines on fluid resuscitation in children: missing the FEAST data." BMJ: British Medical Journal 348 (2014).

Steiner, Michael J., Darren A. DeWalt, and Julie S. Byerley. "Is this child dehydrated?." Jama 291.22 (2004): 2746-2754.

Levine, Adam C., et al. "Empirically Derived Dehydration Scoring and Decision Tree Models for Children With Diarrhea: Assessment and Internal Validation in a Prospective Cohort Study in Dhaka, Bangladesh." Global Health: Science and Practice 3.3 (2015): 405-418.

Freedman, Stephen B., et al. "Diagnosing clinically significant dehydration in children with acute gastroenteritis using noninvasive methods: a meta-analysis." The Journal of pediatrics 166.4 (2015): 908-916.

Friedman, Jeremy N., et al. "Development of a clinical dehydration scale for use in children between 1 and 36 months of age." The Journal of pediatrics 145.2 (2004): 201-207.

Gorelick, Marc H., Kathy N. Shaw, and Kathleen O. Murphy. "Validity and reliability of clinical signs in the diagnosis of dehydration in children." Pediatrics 99.5 (1997): e6-e6.

College Answer

a)
 A convulsion associated with an elevated temperature greater than 38°C.
 A child younger than six years of age.
 No evidence of central nervous system infection or inflammation.

 No evidence of acute systemic metabolic abnormality that may produce convulsions.
 No history of previous afebrile seizures.
 Generalised rather than focal.
 Short (< 15 min) rather than prolonged.
 Single rather than multiple.

b)
Benzodiazepines:

a) Diazepam – 0.1 to 0.3 mg/Kg IV over 2 – 5 minutes, maximum 10 mg per dose - or

b) Midazolam - 0.1 – 0.3 mg/kg bolus IV, can be given in an infusion 0.1 to 0.5 mg/Kg/hr.
o Advantage – rapid onset, terminates seizures under most circumstances, can be administered by other routes-IM, P/R, nasally.
o Disadvantage – excessive sedation, respiratory depression. May need airway control including intubation.

Phenytoin:

15 – 20 mg/kg IV bolus dose at rate of < 50 mg/min, 5 – 10 mg/kg maintenance daily 12 hours after.
o Advantage - preventing recurrence of SE for extended periods of time.
o Disadvantages – Slow onset of action up to 30 minutes, Hypotension, cardiovascular collapse, ataxia, nystagmus, blurred vision, and coma.

Barbiturates

– Phenobarbitone: 10 – 20 mg/Kg initially up to 40 mg/Kg if needed to control seizure activity.
o Advantage – more effective than phenytoin in controlling seizure activity.
o Disadvantage – severe respiratory depression, requires monitoring in HDU/ ICU, may require intubation and ventilation.

Thiopentone: 2 – 3 mg/kg bolus IV, repeat as needed.
o Advantage – most potent of any epileptic agent.
o Disadvantages – IV anaesthetic agent hence requires intubation and ventilation for administration, hypotension.

Propofol: 1 – 3 mg /Kg bolus, 1 – 3 mg/Kg/hour.
o Advantage – quick onset and offset.
o Disadvantage – very few studies to support its use in status epilepticus, propofol infusion syndrome at high doses, requires intubation and ventilation.

Sodium Valproate - Loading dose: 20 – 40 mg/kg followed by a continuous I.V. infusion of 1 – 5 mg/kg/hour.
o Advantages – studies showing effective in 78% cases refractory to diazepam, phenytoin and phenobarb, less sedating than barbiturates.
o Disadvantages – fatal hepatotoxicity can occur hence contra-indicated in significant hepatic impairment.

Levetiracetam – Newer anti-epileptic agent – 15 (5 – 30) mg/kg bolus dose, 25 – 50mg/kg maintenance in two divided doses.
o Advantage – very good safely profile.
o Disadvantage – Limited published data in paediatric age group.

Discussion

By the most recently attempted definition, febrile convulsions are "a seizure occurring in childhood after one month of age, associated with a febrile illness that is not caused by an infection of the central nervous system". There are actually two definitions, which differ slightly. In brief summary, these are seziures which occur in the presence of fever and in the absence of any other good reason for seizures, in an age range variably described as under 6 years, 1 month to five years, 3 months to five years, and six months to six years.

The Royal Children's Hospital Clinical Guidelines has a slightly different age range to both of the above, and closely resembles the college answer. Clearly, both must have the same source.

The list of criteria for the diagnosis of simple febrile convulsions:

• Fever >38.0°
• No history of neonatal seizures
• No previous unprovoked seizures
• No focal neurological features (i.e. generalised seizure)
• Tonic-clonic seizure
• Occurs after 6 months of age, and before the age of 6
• Lasts less than 15 minutes
• Occurs only once per episode of febrile illness.

The list of criteria for the diagnosis of complex febrile convulsions:

• Fever >38.0°
• No history of neonatal seizures
• No previous unprovoked seizures
• Focal seizure
• Tonic-clonic seizure
• Occurs after 6 months of age, and before the age of 6
• Lasts longer than 15 minutes
• Occurs several times within the same episode of febrile illness.
• Incomplete recovery after 1 hour.

The college then goes on to ask for five drugs – one from each class, as well as their dose, their advantages and disadvantages. Such a question lends itself well to a tabulated answer.

Much of this information can be found it its raw untreated form in Slater's chapter on neurological emergencies in children, from Oh's Manual.

References

Oh's Intensive Care manual:  Chapter 109   (pp. 1121) Neurological  emergencies  in  children  by Anthony  J  Slater.

Waruiru, C., and R. Appleton. "Febrile seizures: an update." Archives of Disease in childhood 89.8 (2004): 751-756.

Syndi Seinfeld, D. O., and J. M. Pellock. "Recent Research on Febrile Seizures: A Review." J Neurol Neurophysiol 4 (2013): 165.

Commission on Epidemiology and Prognosis, International League Against Epilepsy. "Guidelines for epidemiologic studies on epilepsy." Epilepsia 34.4 (1993).

Freeman JM. Febrile seizures: a consensus of their significance, evaluation, and treatment. Consensus development conference of febrile seizures. 1980. National Institute of Health.  Pediatrics 1980;66: 1009–12.

Ventura, Alessandro. "From the American Academy of Pediatrics: Clinical Practice Guideline: Febrile Seizures: Guideline for the Neurodiagnostic Evaluation of the Child With a Simple Febrile Seizure." Pediatrics 127.2 (2011): 389-394.

Wright, Chanin, et al. "Clinical pharmacology and pharmacokinetics of levetiracetam." Frontiers in neurology 4 (2013).

College Answer

• Prominent occiput - Causes some neck flexion in the supine position. This can interfere with attempts to visualize the glottic opening during laryngoscopy. Placing a towel roll under the shoulders can improve airway alignment.
• Large tongue - Infants and young children have large tongues relative to the size of the oral cavity. Can cause airway obstruction and interfere with laryngoscopy.
• Larger tonsils and adenoids - Can cause airway obstruction. Placement of nasal airway may cause bleeding and aspiration.
• Superior laryngeal position - located opposite the C3 to C4 vertebrae, compared with the C4 to C5 in adults. Visualization of glottis more challenging.
• Large, floppy epiglottis - the epiglottis projects into the airway and covers more of the glottis. A straight blade needed to directly lift the epiglottis for improved visualisation during direct laryngoscopy.
• Short trachea - The short trachea predisposes to right endobronchial intubation or inadvertent extubation. Use of formula (age/2 +12 cm from lower lip) to estimate tube length. Special attention to fixation.
• Narrow trachea - Small decreases in the airway size from secretions, oedema, or external compression will cause obstruction. The needle or surgical cricothyroidotomy technically challenging in infants and children. (0.5)
• Anatomic subglottic narrowing - this narrowing can create an effective anatomic seal without the need for a cuffed ETT. Foreign bodies can become lodged below the cords.

Additional Examiners’ Comments: Some candidates did not read the question thoroughly and did not include strategies in their answer

Discussion

The master list of ways in which a child's airway poses a problem:

References

Heard, A. M. B., R. J. Green, and P. Eakins. "The formulation and introduction of a ‘can't intubate, can't ventilate’algorithm into clinical practice." Anaesthesia64.6 (2009): 601-608.

Stacey, Jonathan, et al. "The ‘Can't Intubate Can't Oxygenate’scenario in Pediatric Anesthesia: a comparison of different devices for needle cricothyroidotomy." Pediatric Anesthesia 22.12 (2012): 1155-1158.

Weathers E., "The Anatomy of the Pediatric Airway" 2010 -RC EDUCATIONAL CONSULTING SERVICES, INC.

Santillanes, Genevieve, and Marianne Gausche-Hill. "Pediatric airway management." Emergency medicine clinics of North America 26.4 (2008): 961-975.

HOLM‐KNUDSEN, R. J., and L. S. Rasmussen. "Paediatric airway management: basic aspects." Acta Anaesthesiologica Scandinavica 53.1 (2009): 1-9.

Cardwell, Mary, and Robert WM Walker. "Management of the difficult paediatric airway." BJA CEPD Reviews 3.6 (2003): 167-170.

College Answer

References

Steiner, Michael J., Darren A. DeWalt, and Julie S. Byerley. "Is this child dehydrated?." Jama 291.22 (2004): 2746-2754.

Levine, Adam C., et al. "Empirically Derived Dehydration Scoring and Decision Tree Models for Children With Diarrhea: Assessment and Internal Validation in a Prospective Cohort Study in Dhaka, Bangladesh." Global Health: Science and Practice 3.3 (2015): 405-418.

Freedman, Stephen B., et al. "Diagnosing clinically significant dehydration in children with acute gastroenteritis using noninvasive methods: a meta-analysis." The Journal of pediatrics 166.4 (2015): 908-916.

Friedman, Jeremy N., et al. "Development of a clinical dehydration scale for use in children between 1 and 36 months of age." The Journal of pediatrics 145.2 (2004): 201-207.

Gorelick, Marc H., Kathy N. Shaw, and Kathleen O. Murphy. "Validity and reliability of clinical signs in the diagnosis of dehydration in children." Pediatrics 99.5 (1997): e6-e6.

Holliday, Malcolm A., and William E. Segar. "The maintenance need for water in parenteral fluid therapy." Pediatrics 19.5 (1957): 823-832.

Meyers, Rachel S. "Pediatric fluid and electrolyte therapy." The Journal of Pediatric Pharmacology and Therapeutics 14.4 (2009): 204-211.

Wang, Jingjing, Erdi Xu, and Yanfeng Xiao. "Isotonic versus hypotonic maintenance IV fluids in hospitalized children: a meta-analysis." Pediatrics (2013): peds-2013.

Neilson, Julie, et al. "Intravenous fluids in children and young people: summary of NICE guidance." BMJ: British Medical Journal (Online) 351 (2015).

College Answer

Difficult to give exact template, as style may vary, but should include:

Initial Assessment/Primary Survey

Assess for signs of life and if absent commence CPR, check underlying rhythm and treat appropriately following APLS guidelines

Airway and breathing Administer 100% oxygen

Intubation for airway protection and suction with ETT cuffed size 7 (ILCOR guidelines – cuffed ETTs acceptable in children) (age/4 +4) (half size bigger and smaller available) with C spine precautions Ventilate with appropriate settings (Vt 6-8ml/kg, RR 15-20, PEEP > 5cm H2O)

SpO₂ and ETCO₂ monitoring, ABG and CXR

May get some discussion re management of ARDS

Circulation

Assess pulse rate and volume, blood pressure and capillary return, Doppler may be helpful if hypothermic Secure IV and arterial access

If inadequate circulation fluid bolus of 20 ml/kg 0.9% Saline – avoid hypotonic intravenous fluids Consider vasopressor support early

Blood glucose, FBE, U & E

Cerebral support

Avoid any further episodes of hypoxia and hypercarbia. Avoid hyperoxia

Optimise circulation

BSL control

Temperature

Actively rewarm to core temperature of 34^oC

Passively rewarm over 34^oC

If post cardiac arrest – maintain hypothermia 32.5 – 33.5^oC for > 24 hours

Could allow a normothermia strategy, but fever must be controlled

Other

Primary and secondary survey for associated trauma

Look for precipitating cause (hypoglycaemia, epilepsy, toxin ingestion, marine envenomation) Antibiotics not indicated routinely

Collateral history – immersion time, resuscitation at scene, medical history Admit to ICU with appropriate paediatric expertise

Counsel family regarding likely outcomes.

Discussion

Generic issues in the resuscitation of drowning, from the chapter on immersion submersion and drowning:

• Drowning is the process of experiencing respiratory impairment from submersion or immersion in a liquid
• Common complications of drowning include death from hypoxic arrest, laryngospasm, aspiration of water and gastric contents, ARDS and pulmonary oedema due to loss of surfactant, hypothermia and cerebral hypoxia which is the main determinant of long-term morbidity.
• Uncommon complications of drowning include electrolyte derangement, haemolysis, renal failure due to haemoglobinuria, and infection (due to aspiration of unclean water).
• Predictors of poor neurological outcome following drowning include immersion for more than 5 minutes, a delay in CPR longer than 10 minutes, GCS of 3 and fixed dilated pupils on admission, severe acidosis (pH < 7.00) and abnormal neurology during admission (eg. GCS less than 6 and abnormal brainstem function after 48 hours).

Resuscitation of the drowned patient

Pre-hospital issues:

• Unskilled rescuers should avoid drowning themselves.
• Do not start CPR while still in the water (one should not need to say this)
• CPR should not be of the compression-only variety (you really need the breaths)
• Avoid all active attempts to "force" the water out by placing the person face-down or any sort of abdominal thrusting, as this will only lead to the aspiration of stomach contents.
• Do not stop the resuscitation of the hypothermic drowning victim (the ICU doctors might want to publish another case report of miraculous ECMO-aided survival).

Emergency management issues

1. Assessment of the airway and of the need for immediate intubation.
   Drowning is associated with a high risk of aspiration (and not just of lake water).
2. Ventilation with high FiO₂
   High PEEP, 12-15
   Investigation of possible aspiration with CXR and ABG
3. Establishment of IV access and correction of hypovolemia;
   drowning victims may become hypovolemic following prolonged immersion due to the hydrostatic effects of water (particularly salt water)
4. Investigate causes of drowning related to intracranial events, eg. ICH, or trauma resulting from a fall into submerged obstacles
5. Assessment of temperature, and rewarming (the immersed patient is invariably hypothermic, as it is rare to drown in a body of water with an ambient temperature higher than human core body temperature).

ICU management issues

1. Assessment of the airway device effectiveness (i.e. is it in the right main bronchus?)
   Bronchoscopy and suction as indicated by copious aspirated material.
2. Lung protective ventilation; open lung strategy
   No benefit in corticosteroids
3. Assess the effectiveness of volume resuscitation; give more.
4. Sedation as required: no specific recommendations can be made.
   If the patient has had a cardiac arrest, therapeutic hypothermia might be worthwhile.
5. Electrolytes are unlikely to be deranged by this stage.
6. Renal function is unlikely to be impaired
7. There is no reason to omit normal nasogastric feeds
8. Monitor Hb, and satisfy yourself that there is no haemolysis.
9. There is no need for antibiotics.

Uniquely paediatric issues in the resuscitation of drowning, from the chapter on resuscitation of the drowned child

Need to search for predisposing conditions and risk factors:

• Young age (high centre of gravity)
• Adolescence (alcohol, drugs, poor judgement)
• Epilepsy (risk increased up to 14 fold)
• Developmental delay
• Long QT (arrhythmias triggered by cold water)

Unique paediatric issues:

• C-spine immobilisation in the very young (under 5) age group is usually unnecessary
• Transfer to paediatric ICU is required
• Hypothermia is usually a poor prognostic indicator
• Asphyxia is more common than immersion phenomena, unlike in adult swimmers
• Family needs to be councelled: emotional response to the accidental drowning of a child is typically guilt and self-accusation

Non-accidental drowning needs to be considered as the cause

• Unfortunately, by itself abusive drowning leaves no pathognomonic stigmata
• Evidence of other physical abuse may be present
• Child may have been left with an unsuitable carer (eg. an alcoholic relative)
• History of mental illness or substance abuse in the carer
• Presentation may be late
• Story may be inconsistent with the findings
• Age group of the child outside of the usual range for bathtub immersion (i.e. older than 24 months).
• Care must be taken not to add stigma of culpability and accusation to an already emotionally difficult situation for the parent

Prognostication

• 30%-50% will die
• 10% survive with severe neurological sequelae
• The rest may recover unremarkably

Features which favour non-survival or severe disability:

• Apnoea on presentation to ED
• Coma (GCS < 8) on presentation to ED
• pH < 7.00 
• Need for CPR in the ED
• CPR for longer than 10 minutes
  (data from Christensen et al, 1997)

References

Fandel, Ivar, and Eduardo Bancalari. "Near-drowning in children: clinical aspects." Pediatrics 58.4 (1976): 573-579.

Pearn, John H. "Secondary drowning in children." Br Med J 281.6248 (1980): 1103-1105.

Burford, Amy E., et al. "Drowning and near-drowning in children and adolescents: a succinct review for emergency physicians and nurses." Pediatric emergency care 21.9 (2005): 610-616.

Austin, Sébastien, and Iain Macintosh. "Management of drowning in children." Paediatrics and Child Health 23.9 (2013): 397-401.

Watson, R. Scott, et al. "Cervical spine injuries among submersion victims." Journal of Trauma and Acute Care Surgery 51.4 (2001): 658-662.

Nixon, James, and John Pearn. "Non-accidental immersion in bathwater: another aspect of child abuse." British medical journal 1.6056 (1977): 271.

Nixon, James, and John Pearn. "Emotional sequelae of parents and sibs following the drowning or near-drowning of a child." Australian and New Zealand Journal of Psychiatry 11.4 (1977): 265-268.

Kemp, Alison M., A. M. Mott, and Jonathan Richard Sibert. "Accidents and child abuse in bathtub submersions." Archives of disease in childhood 70.5 (1994): 435-438.

Coryell, Jason, and Laura M. Ibsen. "Pediatric Drowning." Pediatric Critical Care Medicine. Springer London, 2014. 665-676.

Biggart, Matthew J., and Desmond J. Boh. "Effect of hypothermia and cardiac arrest on outcome of near-drowning accidents in children." The Journal of pediatrics 117.2 (1990): 179-183.

Moler, Frank W., et al. "Multicenter cohort study of out-of-hospital pediatric cardiac arrest." Critical care medicine 39.1 (2011): 141.

Christensen, David W., Paul Jansen, and Ronald M. Perkin. "Outcome and acute care hospital costs after warm water near drowning in children." Pediatrics 99.5 (1997): 715-721.

College Answer

Any five of: 

• Bacterial pneumonia
• Recurrent viral triggered wheezing in atopic children (but too young for a diagnosis of asthma)
• Chronic lung disease of ex-prematurity (broncho-pulmonary dysplasia)
• Occult congenital heart disease or cardiac failure
• Foreign body aspiration
• Congenital vascular rings
• Aspiration pneumonia due to gastro-oesophageal reflux

Any five of:                                             

• Tachypnoea
• Nasal flaring
• Grunting
• Subcostal or intercostal recession
• Tracheal tug
• Use of accessory muscles
• Apnoeic episodes
• Hypoxia on pulse oximetry

Any four of:            

• Ex prematurity
• Less than 12 weeks old
• Chronic Lung Disease
• Upper airway disease
• Congenital heart disease
• Immunodeficiency
• Neurological disease
• Smokers in the household
• Crowded households
• Attending day-care
• Older siblings

                d)                                                             

Mild disease:

• continue feeding, comfort

More severe disease:

• Nasogastric feeding and/or iv fluids
• High flow humidified fresh gas by nasal cannulae (titrated F_iO₂, FGF 1-2 L/kg/min)
• Non-invasive CPAP
• Intubation rarely required

Discussion

a) 

The whole table of differentials for respiratory failure in children is reproduced below. However, there are specific broncholitis mimics which need to be mentioned, as they also present with wheeze. 

These are:

• Asthma
• Recurrent viral-triggered wheezing
• Bacterial pneumonia
• Chronic lung disease of ex-prematurity (or some other sort of chonic lung disease)
• Foreign body aspiration
• Aspiration pneumonia
• Congenital heart disease with heart failure
• Vascular rings (eg. pulmonary artery slings)

Causes of respiratory failure in children, more broadly:

b)

Clinical signs of severity in bronchiolitis:

• Tachypnoea (over 70)
• Nasal flaring
• Grunting
• Subcostal or intercostal recession
• Tracheal tug ("suprasternal resession")
• Use of accessory muscles
• Apnoeic episodes
• Hypoxia on pulse oximetry (less than 90%)
• Head bobbing
• Decreased level of consciousness

c) Risk factors for severe bronchiolitis:

• Ex prematurity
• Low birth weight
• Less than 12 weeks old
• Bronchopulmonary dysplasia of ex-prematurity
• Anatomical defects of the upper airways
• Hemodynamically significant congenital heart disease
• Immunodeficiency
• Neurological disease
• Smokers in the household
• Crowded households
• Attending day-care
• Older siblings
• Concurrent birth siblings
• High altitude 

d) Supportive therapies in the management of bronchiolitis:

• Airway: ​ 
  • Assess the need for intuibation (rarely required)
  • Nasal suctioning to clear upper airway (not deep nasopharyngeal, but rather shallow nasal suctioning)
  •  
• Ventilation:
  • Just oxygen to begin with
  • Aim for sats of over 90%
  • CPAP or HFNP may be the next step of escalation. With infants, maximum flow rate is about L/min. 
  • Invasive mechanical ventilation may be required, but HFNP frequently prevents the need for this.
  • Respiratory distress will escalate whenever the child is handled; the key to respiratory success is to minimise handling and to group all routine cares so that the child gets long breaks between distressing events.
  • Apnoeas may be helped by caffeine or aminophylline
• Advanced strategies to improve gas exchange
  • ​Nebulised hypertonic saline 
  • Nebulised surfactant
  • Heliox
  • ECMO
  • None of these are strongly based in any sociaety recommendations, and sucess is mainly known from case reports
• Circulation:
  • ​IV maintenance fluids and resuscitation of dehydration
  • Assessment for any coexisting cardiac disease with TTE
• Electrolytes
  • Watch for SIADH: apparently that is one of the possible complications
• Nutrition
  • ​Nasogastric feeding to make up for recent deficit
• Antibiotics
  • ​Routine use of IV antibiotics is not indicated
  • Ribavirin has been trialled, and is also not recommended for routine treatment of RSV
    infection but may be considered in select immunocompromised individuals
  • Palivizumab, a humanized monoclonal antibody (IgG) directed against RSV, may be used in at-risk populations for prevention (eg. premature infants during RSV season).
• Strategies which have been trialled and which clearly do not work:
  • ​Nebulised bronchodilators
  • Montelucast
  • Corticosteroids (no evidence of benefit, and may even increase the duration of viral shedding)
  • Chest physiotherapy (probably no benefit)
  • Caffeine or aminophylline (they were supposed to decrease the risk of apnoeas, but they do not seem to work)
  • However, it must be mentioned that the trials of all these interventions excluded the "severe" category of patients.

References

Plint, Amy C., et al. "Epinephrine and dexamethasone in children with bronchiolitis." New England Journal of Medicine 360.20 (2009): 2079-2089.

Lowell, Darcy I., et al. "Wheezing in infants: the response to epinephrine." Pediatrics 79.6 (1987): 939-945.

Ralston, S. L., A. S. Lieberthal, and H. C. Meissner. American Academy of Pediatrics Subcommittee on Diagnosis and Management of Bronchiolitis. "Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis". Pediatrics 134.5 (2014): e1474-e1502.

Osvald, Emma Caffrey, and Jane R. Clarke. "NICE clinical guideline: bronchiolitis in children." Archives of disease in childhood-Education & practice edition (2015): edpract-2015.

Alansari, Khalid, et al. "Caffeine for the Treatment of Apnea in Bronchiolitis: A Randomized Trial." The Journal of pediatrics (2016).

College answer

Concurrent resuscitation, assessment and treatment of this extremely sick child, addressing the hypotension, acute kidney injury, severe shock and dehydration and profound metabolic derangement.

Stabilisation of the child prior to transfer to a tertiary paediatric institution with close liaison with paediatric team for advice on management. 

Use Broselow tape, guidelines on paediatric drug doses, dedicated paediatric resuscitation equipment etc. to ensure appropriate doses of fluids and drugs, tube sizes, ventilator settings etc. 

Steps in management

• Call for help
• Assess airway and breathing o inadequate ventilation, depressed level of consciousness, profound dehydration and shock
• 100% oxygen and support ventilation with BVM if required. This child will need intubation but need to optimise cardiac output before proceeding with this (consider waiting until transport team arrive for maximum support)
• Establish venous access, IO line or peripheral venous (central venous access only if second person available to perform or if child more stable)
• Immediate treatment of hypoglycaemia with 2 – 5 ml/kg 10% dextrose. Ongoing glucose to maintain blood sugar levels measured hourly at the very least. 
• Ongoing volume resuscitation with 10 – 20 ml/kg boluses of 0.9% sodium chloride, reassess perfusion and repeat as needed. Some children require up to 100 ml/kg fluid resuscitation (caution if cardiogenic shock present) 
• Electrolyte replacement as required
• Ongoing maintenance fluid – e.g. add 100 ml of 50% dextrose to 900 ml 0.9% NaCl and infuse this at 2/3 maintenance rate (16 ml/hr in this case) (accept 24 ml/hr for 1^st 48 hours)
• Assess % dehydration and replace over 48 hours using maintenance fluid (unless sodium increases > 150 mmol/L) Formula: Vol = % Dehydration x body weight x 10 (in mls)
• Use an inotrope: e.g. adrenaline (other inotropes acceptable)
• IV antibiotics within one hour. These can be stopped after 48 hours if cultures negative
• Treat hyperkalaemia if still present after treatment of shock (usually K⁺ levels drop as shock treated) o IV CaCl₂
  • IV boluses 8.45% NaHCO₃ (Dose in mmol or ml = desired HCO₃ – measured HCO₃ x (weight in kg x 0.6)
  •  Dextrose/insulin
• Urinary catheter to monitor hourly urine output
• Consideration of non-infectious causes 
• Organisation of transfer/retrieval team
• Keep the parents up to date

Exact doses of drugs/fluids not expected but reference to need to look up/check dosing carefully in this instance

Additional Examiners‟ Comments:

Most candidates did well in this question. Failure to immediately treat the hypoglycaemia was a fatal error.

Discussion

"Concurrent resuscitation, assessment and treatment" seems to make the redundant distinction between resuscitation and treatment. Some treatments are resuscitative, and resuscitation is a treatment. But that pedantry aside, this college answer is stereotypic for the management of the child with nonspecific shock.

An example approach is offered below:

1. Assess the need for intubation.
   - At this stage, senior assistance from somebody expert in paediatric critical care is required, as the intubation may be difficult.
2. Administer 100% oxygen.
3. Establish venous access.
   - Give a 20ml/kg bolus, FEAST be damned.
   - Inotropes and vasopressors if no longer fluid-responsive
   - Parameters guiding resuscitation (eg. lactate, haemodynamic variables, urine output) differ little from adult standards
4. Sedation and analgesia to support tolerance of invasive therapies
   (also decreases demands on the cardiac output)
5. Electrolyte correction
6. Maintenance fluid:  As per college answer, "add 100 ml of 50% dextrose to 900 ml 0.9% NaCl and infuse this at 2/3 maintenance rate (16 ml/hr in this case) (accept 24 ml/hr for 1^st 48 hours)".
   - A urinary catheter will also be required.
7. No protein in diet until metabolic screen is cleared
   - Maintain normoglycaemia with infusion of 10% dextrose of dextrose-rich maintenance fluid
8. Blood transfusion may not be warranted
9. Empiric antibiotics if sepsis is suspected, within 1 hour.
   - Cultures of blood and urine.
   - Consider antivirals if there is suspicion of viral meningitis or encephalitis

For maintenance calculation, the following formula is the gold standard, found in this 1957 paper by Holliday and Segar. A good modern revision was performed by Meyers (2009). In short, 

• First 10kg: 4ml/kg/hr
• Second 10kg: 2ml/kg/hr
• All other kgs: 1ml/kg/hr

The reduced  2/3 of the maintenance rate is usually given  to critically ill children because of their propensity to secrete ADH, thereby causing water retention. A full maintenance rate is usually given to the well child fasted for theatre.

Isotonic fluids should be used for maintenance, in contrast to the college answer.  Wang et al (2013) suggest that they are safer than hypotonic fluids. This contrasts slightly with the college answer. NICE guidelines (Neilson et al, 2015) also recommend isotonic crystalloid for maintenance, and make no mention of the dextrose cocktail which the college recommend ("add 100 ml of 50% dextrose to 900 ml 0.9% NaCl"). The RCH guidelines from Melbourne recommend the routine use of Plasmalyte 148 together with 5% dextrose, without offering any references. The 900/100 mixture describe by the college in this case is in any case nearly isotonic (though fairly hyperosmolar, 550mOsm/L or thereabout)

References

Steiner, Michael J., Darren A. DeWalt, and Julie S. Byerley. "Is this child dehydrated?." Jama 291.22 (2004): 2746-2754.

Levine, Adam C., et al. "Empirically Derived Dehydration Scoring and Decision Tree Models for Children With Diarrhea: Assessment and Internal Validation in a Prospective Cohort Study in Dhaka, Bangladesh." Global Health: Science and Practice 3.3 (2015): 405-418.

Freedman, Stephen B., et al. "Diagnosing clinically significant dehydration in children with acute gastroenteritis using noninvasive methods: a meta-analysis." The Journal of pediatrics 166.4 (2015): 908-916.

Friedman, Jeremy N., et al. "Development of a clinical dehydration scale for use in children between 1 and 36 months of age." The Journal of pediatrics 145.2 (2004): 201-207.

Gorelick, Marc H., Kathy N. Shaw, and Kathleen O. Murphy. "Validity and reliability of clinical signs in the diagnosis of dehydration in children." Pediatrics 99.5 (1997): e6-e6.

Holliday, Malcolm A., and William E. Segar. "The maintenance need for water in parenteral fluid therapy." Pediatrics 19.5 (1957): 823-832.

Meyers, Rachel S. "Pediatric fluid and electrolyte therapy." The Journal of Pediatric Pharmacology and Therapeutics 14.4 (2009): 204-211.

Wang, Jingjing, Erdi Xu, and Yanfeng Xiao. "Isotonic versus hypotonic maintenance IV fluids in hospitalized children: a meta-analysis." Pediatrics (2013): peds-2013.

Neilson, Julie, et al. "Intravenous fluids in children and young people: summary of NICE guidance." BMJ: British Medical Journal (Online) 351 (2015).

College answer

a)

Inborn error of metabolism
Sepsis (viral likely)
Cardiac disease- especially duct dependent disease  
Trauma (NAI)
Drugs / Toxins 
 

b)

History: 
Exposure to ill persons including siblings and parents.  
“Colds”, chicken pox and maternal herpes should be specifically solicited.
Maternal Group B Strep swab should be reviewed
Injury 
Cyanotic spells  Apnoeas 
Family history including infant deaths, inborn errors of metabolism (IEMs), cardiac disease, degree of consanguinity 
 
Examination: 
General exam - trauma, rash Liver edge (failure, hepatitis) Murmurs Femoral pulses 
 
Investigations: 
CXR
ECG
Ammonia
Urine amino and organic acids (if can’t be processed, take while acidotic and store) Cultures if not done
CMV, HSV PCR
Consider skeletal survey if any suggestion of injury  
Cranial ultrasound (widely available)
Echo if available 
 
c) Ongoing liaison with receiving centre.  

Restore then maintain BSL using 10% Glucose (2.5-5ml/kg 10% glucose bolus then 6mg/kg/min infusion.) 
Restore intravascular volume (even post FEAST fluid bolus reasonable)
Direct therapy if specific pathology found- e.g. alprostadil infusion if evidence of duct dependent cardiac disease

 Empiric antibiotics
Empiric antiviral given results above (acyclovir or ganciclovir)
Nil protein intake till initial metabolic results in- maintain on glucose as above

Lung protective ventilation

General ICU housekeeping. 
 
Examiners Comments: 
 
Reasonably well done. Part a) was answered better than b) and c). Some candidates did not read the question completely and described intubation of the baby. 
 

Discussion

This question, and the college answer, are weirdly identical to Question 10 from the first paper of 2015, except now they have capitalised the word "Paediatric", and in 2018 the bloods merely "show," instead of now being "shown below". What was the merit of making these changes without altering any other features of the question?  What is the significance of these changes? Surely there must be some reason behind them, because it would have required less effort to simply cut and paste the SAQ. However, this line of thinking is unproductive. Trying to get into the examiner's heads in the pursuit of some hidden eldritch meaning, there is some risk that a trainee might suddenly be confronted with the Lovecraftian cosmic horror of realising that nobody is carefully tending to the wording or syntax of these SAQs. Gibbering madness may ensue. 

In context of these matters, below one may see that the author has cut-and-pasted the entire discussion section from Question 10 from the first paper of 2015, with subtle changes which on the surface might appear random and cosmetic.

a) Differentials for this shock-like presentation:

b) Assessment of this shock state:

c) Approach to management, which is very generic:

1. Assess the need for endotracheal intubation.
   - At this stage, senior assistance from somebody expert in paediatric critical care is required, as the intubation may be difficult.
2. Administer 100% oxygen.
3. Establish venous access.
   - Give a 20ml/kg bolus, FEAST be damned.
   - Inotropes and vasopressors if no longer fluid-responsive
   - Parameters guiding resuscitation (eg. lactate, haemodynamic variables, urine output) differ little from adult standards
4. Sedation and analgesia to support tolerance of invasive therapies
   (also decreases demands on the cardiac output)
5. Electrolyte correction
6. Maintenance fluid:  As per college answer, "add 100 ml of 50% dextrose to 900 ml 0.9% NaCl and infuse this at 2/3 maintenance rate (16 ml/hr in this case) (accept 24 ml/hr for 1^st 48 hours)". On close inspection, this concoction resembles the premixed "4% and 1/5^th " bags.
   - A urinary catheter will also be required.
7. No protein in diet until metabolic screen is cleared
   - Maintain normoglycaemia with infusion of 10% dextrose of dextrose-rich maintenance fluid
8. Blood transfusion may not be warranted
9. Empiric antibiotics if sepsis is suspected, within 1 hour.
   - Cultures of blood and urine.
   - Consider antivirals if there is suspicion of viral meningitis or encephalitis

References

College answer

References

College answer

Most candidates gave good answers and used an appropriate structure. Those candidates who did not gain good marks, gave answers which lacked pertinent details, especially around control of seizures in Paediatrics patients. 

Discussion

What would have been an "appropriate structure"  here, which 82.7% of the candidates apparently knew? The stem gives no context other than"an 8-year-old child having their first generalized seizure", which makes you think that, when it asks for initial assessment and management, only the most generic responses were required. Also,  the use of the word "having" suggests "they are having it right now in front of you". Thus:

• Resuscitation
  • Administer oxygen
  • Secure the airway if it is unprotected
  • Achieve IV access, collect a routine panel of blood samples including blood cultures,  and administer IV benzodiazepines
• Assessment
  • History from parents
    • Provoking factors (medications, toxins, metabolic factors eg. diabetes and DKA, recent illness)
    • Predisposing factors (eg. brain injury)
    • Behaviour immediately prior to the event (eg. aura)
  • Examination findings
    • Seizure vs. other causes of decreased level of consciousness with rigidity or abnormal movements (eg. cardiac event such as arrhythmia, followed by syncope)
    • Focal neurological signs pointing to intracranial pathology
    • Features of sepsis (eg. febrile convulsion)
    • Meningism 
    • Features suggestive of non-convulsive status (eg. dilated pupils, rigidity, clonus)
    • Systemic features suggestive of autoimmune disease or vasculitis
    • General examination/inspection findings suggestive of congenital abnormalities
• Investigations
  • Biochemistry
    • Normal bloods (BSL/FBC/EUC/CMP/LFT/coags) as well as ammonia level, and serum 
  • Electrophysiology
    • EEG, including awake and sleeping
  • Imaging
    • CT brain (ideally also involving contrast)
    • Lumbar puncture 
    • MRI brain
• Medium-term management
  • Antiepileptic agents (from Pohlmann-Eden et al, 2006):
    • Initially, and while being worked up: benzodiazepines
    • For focal seizures—carbamazepine, clobazam (especially children), gabapentin, lamotrigine, oxcarbazepine, topiramate, valproate x
    • For generalised seizures—Levitiracetam, lamotrigine, topiramate, valproate.
  • Parents: counselling, specifically re. implications of epilepsy (if this is in fact the diagnosis) and regarding the likelihood of recurrence

References