Shoulder examination

Cite this article as:
Mark Webb. Shoulder examination, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31287

Johnny is five. He fell onto his outstretched arm and now is sat in your ED, crying and holding his shoulder adducted. Triage has been ace and given him analgesia so he is adequately comfortable before you examine him.

Joint examinations can be easily remembered by “look, feel, move” and special tests. It’s important that in addition to the joint you’re interested in that you also examine the joint above and below.

Look

  • Deformity
  • Swelling
  • Atrophy: Asymmetry  
  • Wounds
  • Bruising
  • Skin tenting (typically clavicular fractures, whereby the bony fragment is causing pressure on the skin and thought to cause skin necrosis, although this is controversial) 

A chaperone may be needed to expose the joint adequately in older children.

Feel

Feel for warmth, which could indicate septic arthritis.

From the front:

Start medially at sternoclavicular joint

Anatomy of the acromio-clavicular joint

From the back:

  • Scapula: spine, supraspinatus, infraspinatus muscle

Neurovascular assessment:

  • Check for distal pulses: brachial/ radial.
  • Always check the regimental patch for axillary nerve injury and document it.

Move

Assess for range of motion, both active and passive.

Girl flexing and extending at shoulder showing range of movement

Flexion: 180 degrees. Raise arm forward up until they point to the ceiling.

Extension: 45-60 degrees. Stretch the arm out behind them.

Girl showing range of adduction and abduction at the shoulder

ABduction: 150-160 degrees. Put arms out to the side like an aeroplane’s wings and then bring them above their head to point to the ceiling.

ADduction: 30-40 degrees. Put arms out to the side like an aeroplane’s wings and move them in front of their body so they cross over.

Girl showing range of internal and external rotation

External rotation: 90 degrees. Tuck their elbows to their side and swing the hands out.

Internal rotation: 70-90 degrees. Tuck elbows to the side and bring their hands across their tummy.

Scapula winging: Ask the child to push against the wall or your hand. If the scapula wings out this suggests long thoracic nerve pathology.

Some special tests

It is easy to get lost in the number of special tests when examining the shoulder and the trick is to perform those most relevant to the patient in front of you. Many are to test the integrity of the rotator cuff tendons, i.e. Supraspinatus, Infraspinatus, Teres minor and Subscapularis. (SITS)

Girl performing Apley scratch test

“Appley Scratch” test: (1) Ask the child to reach behind their back to touch the inferior border of the opposite scapula (internal rotation and aDDuction) and then (2) reach behind their head to touch the superior angle of the opposite scapula (external rotation an Abduction). A positive test of pain indicates tendinitis of the rotator cuff, usually supraspinatus.

Girl performing empty can test

Empty can test: Ask the child to hold their arm raised parallel to the ground and then point their thumbs towards the ground as if they were holding an empty can (this rotates the shoulder in full internal rotation while in abduction). Then push down on the child’s wrist while asking them to resist. A positive test is pain or weakness, suggestive of supraspinatus tear or suprascapular nerve neuropathy.

Girl performing lift off test

Lift off test: The child stands and places the back of their hand against their back. Put your hand against theirs, palm to palm, and ask them to push against you. A positive test is pain or weakness, indicating subscapularis muscle pathology.

Girl and boy performing scarf test

Scarf test: Ask the child to wrap their arm over the front of their neck reach down over their opposite shoulder towards the scapula (like a scarf). Pain over ACJ when doing this indicates ACJ pathology.

Although the standard approach to limb examination involves a LOOK, FEEL and MOVE (and special tests) structured assessment, in reality, if a young patient has a significant injury, a more pragmatic approach is needed. An X-ray may be warranted before a more thorough exam. This doesn’t mean that you can get away without a documented range of motion exam (even if you explain it is limited by pain) and neurovascular assessment.

Back to Johnny. You noticed a deformity over the middle third of the clavicle, but no skin tenting. He was neurovascularly intact and range of movement only marginally reduced by pain, so you discharged him with a broad arm sling and follow-up (or not) according to your local guidelines.

Selected references

Carson, S., Woolridge, D.P., Colletti, J. and Kilgore, K. (2006) Pediatric upper extremity injuries. Pediatric Clinical North American: 53(1) pp. 41-67

Chambers, P.N., Van Thiel, G.S. and Ferry, S.T. (2015) Clavicle Fracture more than a theoretical risk? A report of 2 Adolescent cases. The American Journal of Orthopedics. 44(10) 

https://fpnotebook.com/Ortho/Exam/ShldrExm.htm [Accessed April 2019]

McFarland, E.G., Garzon-Muvdi, J., Jia, X., Desai, P. and Petersen, S.A. (2010) Clinical and diagnostic tests for shoulder disorders: a critical review. British Journal of Sports Medicine. 44(5) pp. 328-32.

NationwideChildrens.org/Sports-Medicine

https://shouldercomplexgocatsnmu.weebly.com/range-of-motion.html [Accessed April 2019]

Proximal humeral fractures

Cite this article as:
PJ Whooley. Proximal humeral fractures, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31855

“Slow down!” Joel’s mom shouts at him as he whizzes past on his scooter. Joel turns to answer and doesn’t see the curb which he hits, goes flying and puts out his hand to stop himself. Mom is already running to find him holding his arm.

Proximal humeral fractures are uncommon, accounting for less than 5% of all paediatric fractures. The anatomic characteristics of the proximal humerus can explain the various fracture presentations, complications and outcomes.

Anatomy

Ossification centres

The proximal humeral physis has three ossification centres. Head, lesser tuberosity and greater tuberosity. The capital centres appear at 3 months whereas the two others appear at 1 year of age and fuse between 3 & 5 years to produce tuberosity ossification. By the time the child’s 6, the capital and tuberosity centres fuse into a single proximal epiphyseal centre. At this point it acquires a characteristic ‘tent’ or inverted V shape. This results also in a double contour that can complicate the interpretation of the images. The proximal physis accounts for approximately 80% of the longitudinal growth of the entire bone.

Periosteum

This thick sleeve of periosteum is present along the shaft and limits fracture displacement and promotes healing.

Nerves

The axillary nerve, which supplies the sensory innervation to the regimental badge area, is at potential risk in displaced proximal humeral fractures. However, axillary nerve damage is rare, the majority being only a temporary neuropraxias.

Epidemiology

Proximal humeral fractures show an early modest peak at 10-14 years of age, account for up to 3.5% of all fractures, followed by return to low levels in young adults and then a second increase in later adulthood.

These fractures account for a third of all humeral fractures in neonates and are the second most common birth injury after clavicular fractures.  However, they are still rare, occurring in only 0.03 per 1000 births.

The pattern of injury varies with age. Metaphyseal proximal humeral fractures are proportionately higher in pre-pubertal children, compared to a higher proportion of epiphyseal separation in adolescents.

As with any fracture, be aware of the potential of a non-accidental cause. These fractures, can be associated with physical abuse.

Mechanism of Injury

Indirect

Proximal humeral fractures in non-newborns commonly result from a fall backwards onto an outstretched hand with elbow extended and wrist dorsiflexed or a direct blow to the lateral aspect of the shoulder. Pathological fractures  can occur as the humerus is a common location of bone cysts and other benign lesions. This might occur with minimal trauma.

Birth injuries

The upper arm can be hyperextended or rotated during delivery, occurring more commonly in infants of diabetic mothers and with shoulder dystocia.

Clinical Evaluation

Newborns

Typically, a newborn with a proximal humeral fracture will hold their arm in extension. Consider these fractures if a history of birth trauma is given. If noted, then infection, clavicle fracture, shoulder dislocation and brachial plexus injuries need to be ruled out. These little ones may be irritable, particularly when the upper limb is moved.

Children and adolescents

As with other upper arm fractures, the typical presentation is with pain, dysfunction, bruising and swelling with a painful range of movement. Displaced fractures result in significant anterior swelling and altered shoulder appearance relative to the contralateral side.

A detailed distal neurovascular examination is needed including evaluation of the radial, ulnar, median, axillary and musculoskeletal nerves. Be particularly vigilant for any axillary nerve deficit with decreased sensation over the regimental badge area and loss of the deltoid muscle function (shoulder ABDuction).

Radiology

Proximal humeral fractures are identified on routine AP and axillary views of the humerus. If there is clinical concern of a dislocation then dedicated shoulder views should also be taken. If there is tenderness over the physis and no obvious fracture, a suspicion of a Salter Harris (SH) I fracture can be made. Imaging the contralateral humerus may be helpful to determine if there is any widening of the physis.

Patterns of fracture

There are two variations of proximal humeral fractures: metaphyseal and epiphyseal separation.

  • Metaphyseal fractures (70%) usually occur at the surgical neck, although can also occur at the metaphyseal-diaphyseal junction, typically a transverse or short oblique fracture. These fractures typically occur in 5-12 year olds.
  • Epiphyseal fractures (30%) occur in the under 5s and over 12s. The type of epiphyseal fracture depends on skeletal maturity.

SH I fractures are less common and can be seen at all ages before growth-plate closure, most commonly in <5 year olds.

SH II fractures are the most common type, chiefly in adolescents over the age of 12.

SH III & IV fractures are exceedingly rare.

A metaphyseal fracture at the surgical neck of the humerus
Epiphyseal Salter Harris II fracture of the proximal humerus in a 6 year old

Pathological fractures

40% of pathological fractures involve the proximal humerus. The leading cause is a unicameral bone cyst, as this lesion develops in the proximal humerus in 51% of cases. Other causes are aneurysmal bone cysts, non-ossifying fibromas, fibrous dysplasia and bone malignancies.

Displacement

If a proximal humeral fracture displaces, it usually does so in a varus direction, with the humeral head moving medially and posterior to the shaft. This occurs due to pectoralis major traction pulling the distal segment medially, while the rotator cuff and deltoid pull the proximal component superiorly in a tendency towards flexion and external rotation. Displacement is often absent or minimal in 40% of metaphyseal fractures, but is more common in epiphyseal injuries, occurring in up to 85%.

Proximal humerus fracture in an 11 year old with varus deformity

Classification

The Neer-Horowitz classification is the most frequently used classification system for this type of fracture. It divides the proximal humerus into 4 parts, classifying fracture by the degree of displacement as well as the fracture line, consisting of:

  1. Humeral head
  2. Greater tuberosity
  3. Lesser tuberosity
  4. Humeral shaft

One-part fractures involve 1 – 4 undisplaced parts (<1cm AND <45 degrees)

Two-part fractures account for 20% of proximal humeral fractures, involving 2 – 4 parts, 1 of which is displaced (i.e. >1cm OR >45 degrees)

  1. Surgical neck – most common
  2. Greater tuberosity – often seen with anterior shoulder dislocation. A lower threshold for displacement (>5 mm) has been proposed.
  3. Anatomical neck
  4. Lesser tuberosity

Three-part fractures account for 5% of proximal humeral fractures and involve 3 – 4 parts, 2 of which are displaced (i.e. > 1cm OR > 45 degrees)

  1. Greater tuberosity and shaft displaced with respect to lesser tuberosity and articular surface which remain together.
  2. Lesser tuberosity and shaft are displaced with respect to the greater tuberosity and articular surface which remain together.

Four-part fractures are uncommon, occurring in less than 1% of proximal humeral fractures. They involve more than 4 parts, 3 of which are displaced (i.e. >1 cm OR > 45 degrees with respect to the 4th). Four-part fractures require operative reduction.

Management

Initial treatment

Displaced fractures can be very painful so ensure pain is addressed with adequate analgesia.

The aim of immobilisation is to keep the elbow by the side, flexed to 90 degrees with the forearm against the torso. A simple sling is sufficient plus / minus a swathe for younger ages. Straps and adhesive tape can be used as described by Durrajer. Other options include a shoulder immobiliser or a U-shaped coaptation splint.

Neurovascular status must be checked before and after immobilisation.

Orthopaedic consultation should be obtained if there is:

  • associated shoulder dislocation
  • intra-articular (SH IV) fracture
  • completely displaced fracture in a child over 12 years.
  • associated neurovascular compromise
  • open fracture (rare)
  • evidence of compartment syndrome

Definitive Treatment

Newborns usually have SH I fractures, which have an excellent prognosis. A sling and a swathe is sufficient for up to 4 weeks. The primary role of follow up is to ensure there is no brachial plexus injury.

Children and adolescents with minimally displaced fractures are usually managed with a sling or shoulder immobiliser. Gentle pendulum exercise is started between weeks 2 to 4 post injury and active range of movement at 4 to 6 weeks. We would expect near to normal function by 2 months.

Significantly displaced fractures in children 12 and under should be treated with a U-slab, sling and swathe.

Acceptable angulation

  • < 5 years – any degree is allowed as proximal humeral fractures in young children have excellent remodelling potential.         
  • 5 to 12 years – 40 to 70 degrees of angulation is acceptable
  • >12 years – up to 40 degrees of angulation or 2/3 displacement.

Operative

Fractures in which immobilisation would result in unacceptable alignment are managed with closed reduction +/- fixation. Open reduction and internal fixation (ORIF) is indicated if acceptable reduction is not possible due to soft tissue interposition. Most commonly this is caused by the long head of biceps tendon, but can also be caused by the joint capsule, infolded periosteum and deltoid muscle. ORIF is also indicated in open fractures, compound fractures and intra-articular displacement of the fracture.

Complications

Complicated are rare in children, but when do occur are more common in older children, with shortening of the humerus due to physeal damage. This usually has no functional affect. Radiographic malunion can occur but rarely has any functional affect.

Non accidental injury

And finally, as with any fracture, it is imperative that a mechanism inconsistent with an injury or fracture in an otherwise healthy child should prompt escalation and involve the child protection team.

Joel’s x-ray shows a proximal humeral fracture through the surgical neck, with 20 degrees of angulation. He’s placed in a shoulder immobiliser and followed-up in fracture clinic, where he’s advised to start gentle pendulum exercises after a couple of weeks. Two months later he’s back on his scooter, helmet on, flying down the pavement without a care in the world.

References

LA. Landin. Epidemiology of the children’s fractures. J Pediatric Orthop B. 1997;6(2):79

E.J. Ortiz, M.H. Isler, J.E. Navia, R. Canosa, Pathologic fractures in children. Clin Orthop Relat Res, 432 (2005), pp. 116-126

MW Shrader et al, Proximal humerus and humeral shaft fractures in children. Hand Clin 2007;23(4);431

Pectoral girdle, shoulder region and axilla | Clinical Gate

Femoral shaft fractures

Cite this article as:
Joanna Wawrzuta. Femoral shaft fractures, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32484

An 18-month-old boy presents to the emergency department at 1am in the morning, brought in by ambulance with leg pain and inability to mobilise, with crying when being moved or attempting to move. His father tells you that he fell downstairs when they forgot to close the stairgate. On examination, his right thigh is swollen, possibly shortened and he is clearly guarding it. Given your high clinical suspicion of a femur fracture, you prescribe simple and opiate analgesia and organise an x-ray.

Incidence

Femoral shaft fractures account for 1.5 – 2% of paediatric fracture presentations. The average number of annual cases is 20 per 100,000. Despite accounting for a small proportion of all fractures, they are the most common cause for hospitalisation for a fracture.

Femoral shaft fractures can happen at any age depending on mechanism however, there is a clear bimodal age distribution with increased rates in toddlers (between 2-4 years of age) and adolescents (approximately greater than 10 years of age).  Any femur fracture before ambulatory age is uncommon and should be treated as suspicious for non accidental injury (NAI). This is especially true for femoral fractures in children less than 12 months of age (more on this later).

History

Toddlers commonly present as a result of a fall of some kind – sometimes from a height, but it can be from as little as 60cm or less. They are often running, or falling after tripping on an object.

Adolescents, on the other hand, tend to fracture their femur as a result of high mechanism trauma, such as motor vehicle accident or a fall or jump from a significant height.

Regardless of age, patients typically report thigh pain, swelling and an inability to weight bear.

Ask about the mechanism of injury, if it was witnessed, and the time of the injury particularly in the younger age group (<5 years). An unclear history, an unwitnessed fall and delay to presentation are risks factors for NAI.

Examination

The limb deformity may be gross or subtle. Significant swelling results in a tense, or firm-feeling, thigh on palpation and/or a shortened limb. Sometimes the swelling can be very mild, particularly in a toddler, but a clue to injury is a child who is not moving the leg. Always check for neurovascular compromise and for other injuries. One study by Rewers et al. (2005), suggested that 28.6% of children with a femur fracture had another associated injury.

Investigations

Plain radiograph with AP and lateral views of the femur. Imaging the ipsilateral knee and hip is recommended to rule out associated injuries.

Classification

There is no universal classification system for femur fractures so \ use description characteristics, location, stability of the fracture and whether it is open or closed.

Descriptive examples include: transverse, spiral, oblique, comminuted, greenstick, displaced/nondisplaced.

Location: proximal, middle, distal third

Stability:  stable or unstable. Stable fractures are typically transverse or short oblique; while unstable fractures are long spiral and comminuted.

Note: long spiral fractures occur when the fracture length is more than twice the diameter of the bone at that level.

Management

General principles should be adhered to as for any ED presentation. Start with a primary and secondary survey. These injuries occur as a result of trauma and other significant and life-threatening injuries need to be excluded. Next is analgesia, fracture reduction then immobilisation.

Adequate analgesia can be achieved with intranasal, oral and intravenous medications. Start with simple analgesia first (paracetamol, NSAIDS) as they are easy and quick to administer. Then move on to opioids via the oral, IV or intranasal route. Consider benzodiazepines, particularly diazepam, if muscle spasm is an issue (which it often is). While analgesia is taking its effect, start setting up for a regional nerve block. This can be a femoral nerve block (usually under ultrasound guidance), fascia iliaca block (landmark or ultrasound-guided) or a haematoma block.

Once adequate analgesia has been given, it is time to reduce the fracture using skin traction. Generally, femoral fractures are not put in a backslab in ED unless a traction splint is not available and transfer of the patient is required.

Skin traction

Skin traction requires 10% of the patient’s weight to be applied through an appropriate traction mechanism. This may occur in the ED if there are adequately trained personnel and equipment available. There are also traction splints available that can be used pre-hospital or if a traction bed is not available. Sedation may be required to apply skin traction or a traction splint.

There is a variety of traction splint available. The most common in use are the Thomas splint, CT-6 splint and Kendrick splint. Others include the Slishman Traction Splint, Mustang traction splint, Sager splint, Hare Splint and Donway splint.  The Thomas splint is recommended for transfer and is available in a paediatric size.

Taken from https://www.embeds.co.uk/

In Queensland, the ambulance service uses the CT-6 splint. It can also be used in the paediatric population. Have a look at this video by Queensland Ambulance Service on its application. The Slishman traction splint and Mustang traction splint are not specifically designed for children but the linked videos demonstrate brilliantly on child volunteers how you can adapt them for kids.

Definitive management

Spica cast application is typically done under general anaesthetic by the orthopaedic surgeons depending on the age of the child. Older children will require other definitive management.

The table summarises the guidance from The American Academy of Orthopaedic Surgeons (AAOS) of management of femoral fractures by age.

Complications

The most common complication is leg length discrepancy. This occurs due to overgrowth in younger patients. Conversely, shortening can also be an issue but is acceptable up to 2-3cm. Other complications include: osteonecrosis of the femoral head, non union, malunion and re-fracture. In terms of osteonecrosis of the femoral head, this can depend on the surgical procedure performed.

A note about other femoral injuries

Other types of fractures of the femur include proximal fractures (including neck of femur), distal femoral physeal fractures and slipped capital femoral epiphysis (SCFE, also known as SUFE)

Proximal femur fractures are rare in paediatric populations accounting for <1% of fractures. They most commonly occur due to high energy trauma such as motor vehicle accident [1,4,8]. They can occur with a low impact mechanism, but if this occurs a pathological fracture should be considered. Proximal fractures tend to need operative management with an ORIF. The most common complication for a proximal femur fracture is avascular necrosis.

The do not miss bits

Non accidental injury

The incidence of NAI in children with femoral fractures has been reported between 12-60%. In one study by Rewers et al. (2005), it was found that in children less than 3 years of age, NAI was the second most common cause of femoral fractures. This is supported by Schwend et al. (2000), who suggested that a femur fracture in children who are not yet of walking age was the strongest predictor of abuse.

Vigilance is the key to detecting NAI. The best predictors for NAI include: An unclear history, particularly with respect to the mechanism, a suspicious history, an unwitnessed fall (particularly in the younger age group), young age, a delayed presentation (typically >24hours), and associated injuries particularly of chest, abdomen and pelvis if not associated with a high speed mechanism. They also include physical and/or radiographic evidence of prior injury (multiple different aged bruises, old healing fractures on XR). In one study, 53% of children who had been abused and had a femoral fracture had evidence of polytrauma. 62% had physical and/or radiographic evidence of prior trauma and 33% had history suspicious for abuse. In terms of the risk factors listed above, children who had no risks factors had a 4% chance of NAI being the cause of their fracture compared to 24% with one risk factor, and 87% if they had 2 risk factors.

Is the type of femoral fracture a predictor of NAI? There is no current evidence that supports it being a strong predictor. Some evidence suggests that fractures associated with NAI are more likely to found in the distal femur, compared to diaphyseal fracture alone. In contrast to popular belief, there is no current evidence to strongly support that spiral fractures are more likely to be associated with NAI.

In essence, never forget to consider NAI. It is easy to miss if it isn’t thought about as a differential.

Associated injuries

Remember secondary and tertiary survey. Subtle injuries can be missed in patients with high velocity mechanisms or significant life-threatening injuries.

Pathological fractures

These should be considered if a femoral fracture occurs as a result of a low mechanism trauma. Children with metabolic disorders or malignancy are also at higher risk.

Traction

If considering applying a traction splint, don’t forget to assess for ankle/foot fractures as these are a contraindication to application. This is because the ankle and foot are generally support sites for the traction splint.

A femoral nerve block was completed with good effect after some intranasal opioid analgesia. The case was discussed with the orthopaedic team and concerns raised around NAI given the child’s age. The case was also discussed with the hospital child protection team. Traction was applied in the ED under ketamine sedation before he was admitted under orthopaedics and a spica cast was applied in theatre under general anaesthesia.

  1. https://www.orthobullets.com/pediatrics/4019/femoral-shaft-fractures–pediatric?expandLeftMenu=true
  2. Wright JG, Wang EL, Owen JL, Stephens D, Graham HK, Hanlon M, Nattrass, GR, Reynolds RK, Coyte P. Treatments for paediatric femoral fractures: a randomised trial. Lancet 2005;365:1153-58.
  3. Capra L, Levin AV, Howard A, Shouldice M. Characteristics of femur fractures in ambulatory young children. Emerg Med J 2013;30:749-753.
  4. https://radiopaedia.org/cases/paediatric-neck-of-femur-fracture
  5. Baldwin K, Pandya NK, Wolfgruber H, Drummond DS, Hosalkar HS. Femur Fractures in the Pediatric Population. Abuse or Accidental Trauma? Clin Ortop Relat Res 2011; 469:798-804.
  6. Clarke NP, Shelton FM, Taylor CC, Khan T, Needhirajan S. The incidence of fractures in children under the age of 24months in relation to non-accidental injury. Injury 2012;43(6):762-5
  7. Wood JN, Fakeye O, Mondestin V, Rubin DM, Localio R, Feudtner C. Prevalence of abuse among young children with femur fractures: a systemic review. BMC Pediatrics 2014; 14:169
  8. Rewers A, Hedegaard H, Lezotte D, Meng K, Battan FK, Emery K, Hamman, RF. Childhood Femur Fractures, Associated Injuries, and Sociodemographic Risk Factors: A Population-Based Study. Pediatrics 2005; 115; e543.
  9. Davis DD, Ginglen JG, Kwon YH, et al. EMS Traction Splint. [Updated 2020 Jul 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan
  10. https://www.rch.org.au/clinicalguide/guideline_index/fractures/femoral_shaft_emergency/
  11. https://www.embeds.co.uk/2019/02/03/thomas-spint-how-to-apply/
  12. http://www.orthoguidelines.org/topic?id=1015
  13. Cooperman DR, Merten DF. Skeletal manifestations of child abuse. In: Reece RM, Christian CW, Eds. Child abuse: medical diagnosis and management, 3rd Ed. American Academy of Pediatrics, 2009;315.
  14. Hui C, Joughin E, Goldstein S, et al. Femoral fractures in children younger than three years: the role of nonaccidental injury. J Pediatr Orthop 2008;28:297-302.
  15. Shrader MW, Bernat nM and Segal. Suspected nonaccidental trauma and femoral shaft fractures in children. Orthopedics 2011; 34(5):360
  16. Schwend RM, Werth C, Johnston A. Femur shaft fractures in toddlers and young children: rarely from child abuse. J Pediatr Orthop 2000;20:475-81.
  17. Coffe C, Haley K, Hayes J, Groner JI. The risk of child abuse in infants and toddlers with lower extremity injuries. J Pediatr Surg. 2005; 40:120-123
  18. Son-Hing JP and Olgun DZ. The frequency of nonaccidental trauma in children under the age of 3 years with femur fractures: is there a better cutoff point for universal workups? J Pediatr Orthop B 2018; 27(4): 366-388
  19. Thompson NB, Kelly DM, Warner Jr WC, Rush JK, Moisan A, Hanna Jr WR, Beaty JH, Spence DD, Sawyer JR. Intraobserver and interobserve reliability and the rold of fracture morphology in classifying femoral shaft fractures in young children. J Pediatr Orthop 2014; 34(3):352-8
  20. Leaman LA, Henrikus WL and Bresnahan JJ. Identifying non-accidental fractures in children aged <2 years. J Child Orthop 2016; 10:335-341
  21. https://coreem.net/core/pediatric-femur-fractures/

Period Problems: Menorrhagia

Cite this article as:
Tara George. Period Problems: Menorrhagia, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32371

Period problems in teens are common. They can cause significant disruption and distress to adolescents and their parents but rarely have a significant or medically worrying underlying cause. In this first of a series of articles I’ll try to provide a logical and systematic approach to assessing and managing period problems in teenagers (recognizing that this may often be able to be extrapolated to adults too for those of you who do not only see children).

Eloise is 14. She attends with her father complaining she is tired all the time.  When she saw her GP last, they arranged some blood tests – a FBC, haematinics, TFTs and coeliac screen.  The notes from the previous consultation are very sparse. It appears that mood (normal) and bowel habit (also normal) were discussed. Eloise’s dad had mentioned she eats a broad range of foods and is not vegetarian or vegan and she eats red meat 2-3 times a week. Her periods were not brought up by the last doctor. One of her aunts has coeliac disease is noted and that is why the GP had organised bloods. Eloise has come in today for her results.

Blood results showing iron deficiency anaemia

Iron deficiency anaemia (IDA) is common in young women. Paediatricians may be much more comfortable assessing dietary intake and encouraging iron supplementation or increasing iron in the diet than they are in talking about periods. 20-30% of all cases of IDA are caused by menorrhagia. Both NICE and the British Society of Gastroenterology advocate a trial of iron for menstruating females with iron deficiency, as long as coeliac disease has been ruled out and there are no red flags for cancer. Prescribing iron and advising Eloise to “eat more steak” isn’t going to address WHY she might have IDA. This could mean that she ends up on long term iron supplements unnecessarily. If she has menorrhagia significant enough to cause anaemia, it is likely to be having an impact on her education and her social life.

Approaching the subject is probably easier than you think, remembering if you are embarrassed the patient may well think there’s something to be embarrassed about”.

So let’s talk about periods….

First a little bit of nomenclature revision.

Menorrhagia – heavy periods

Dysmenorrhoea – painful periods

Oligomenorrhoea – scanty/sparse/irregular periods

Amenorrhoea – absence of periods (primary: failure to attain menarche by the age of 15 with the development of normal secondary sexual characteristics or failure to attain menarche by 13 with no development of secondary sexual characteristics. Secondary: cessation of menstruation for 3-6 months in someone who has previously had regular periods)

Intermenstrual bleeding (sometimes called metrorrhagia) – irregular and unscheduled bleeding including unexpected bleeding between periods

Menarche – the onset of menstruation (the last stage of female puberty)

The symptoms of problematic periods are not always found in isolation. Menorrhagia and dysmenorrhoea are very common and frequently coexist. It is not uncommon for periods to be irregular, painful and heavy especially in the first few months after menarche. In the UK, the average age of menarche is 12.9 years. The average girl will be in Year 8 at secondary school when she starts her periods. Most women will menstruate every 28 days, though irregular and prolonged cycles are common in early menstrual life.

The average period lasts for 2-7 days and on average 80ml of blood will be lost during the period. In developed countries a number of sanitary products are available. The majority of girls are likely to start off with disposable sanitary towels, though environmental concerns mean period pants and washable pads are gaining popularity. Tampons are often the easiest option for girls who do a lot of sport, especially swimming, and can be used from the onset of menstruation. Menstrual cups have a much greater capacity but can be tricky to get the hang of especially for young teenagers.

Absorbency of different products

What to ask in a history of menorrhagia

Start with an open question (recognising that lots of teenagers are much more comfortable with closed questions and giving specific answers): 

Tell me about your periods…

If you need to be more specific:

  • On average, how long do your periods last for?
  • How often do your periods happen?
  • Do you think they are heavy?
  • Does the bleeding change over the course of the period?
  • How often do you have to change your sanitary protection?
  • What sort of sanitary products do you use? (Pads or towels? Tampons? Period pants? Other?)
  • When did you start your periods?
  • Do you leak though your tampons/pads? If so, how often?
  • Do you pass clots? If so, how big are they?
  • How often do you need to change your pads/tampon at night?
  • Do you have to change your sheets/pyjamas?
  • Can you manage your period at school? How often do you need to leave lessons to change your sanitary product? Do you ever stay home from school because the bleeding is too heavy?
  • Are there activities you enjoy that you’ve had to stop doing because of your periods?

Eloise looks embarrassed and keeps looking at her dad. He is staring firmly at the floor looking as if he wishes it would open up and swallow him. You ask her if she would prefer to talk to you without her dad there and she nods. He takes his newspaper to the waiting area and you reassure him you’ll come and find him in a few minutes. 

Eloise tells you she started her periods at 11. They last 5-6 days on average and she has one around every 30-32 days. She uses tampons backed up with period pants as she often leaks. She uses SuperPlus tampons and on the first couple of days needs to change them every 45 minutes or so. This can be very difficult at school. She passes clots the size of grapes for a day or so each month. She has to set an alarm at night to wake her to change her protection every 2 hours but can end up with bloodstained sheets. She has stopped gymnastics and now only swims socially but not competitively. She was dropped from the squad because she wasn’t comfortable training when she had her period – the other girls had laughed when she had leaked during training. Worse still, when at a gala with lots of other teams, blood poured down her leg and she had been jeered by the crowd. She thinks her periods are heavy (heavier than all her friends) but her mum has told her this is normal and to stop making a fuss.

Whilst there is no truly objective “test” for menorrhagia, with this history and the marked iron deficiency anaemia, it is pretty straightforward to assume Eloise has menorrhagia. This is likely to be the cause for her IDA as well as affecting her sport participation, her sleep and her schooling. She had normal thyroid function tests (TFTs) as part of her tiredness workup (though it is worth noting that NICE do not recommend checking TFTs routinely in cases of simple menorrhagia). You might want to ask about other bleeding history like epistaxis, bleeding after dental extraction, family history and to consider testing for von Willebrand’s disease. NICE recommend this is for patients who have had menorrhagia from the start of their menstrual life. Most cases of menorrhagia at this age are, however, idiopathic.

Other factors to consider in your assessment

It is so important that Eloise feels listened to and heard. Her perspective is vital for compliance with any plan you make. You’ve already asked her if she thinks her periods are heavy. Now is a good time to continue to explore her ICE (“ideas, concerns and expectations”) by finding out how worried she is about her periods, whether she thinks they are a problem and if she has any ideas for what might be available to fix the problem.

Family history and past medical history are relevant here too in terms of management options as you might well want to consider the combined pill or tranexamic acid both of which are contraindicated if there is a first degree relative family history of venous thromboembolism or a known prothombotic mutation and the COCP is contraindicated if she has focal migraine. It is important to take into account the thoughts and feelings of Eloise’s parent as well during this assessment but remembering that at aged 14 she is likely to have capacity to make decisions some about her own care and be fully involved in the process.

Management of menorrhagia

The NICE guidelines on heavy menstrual bleeding contain a useful interactive flowchart for managing menorrhagia. The first line according to NICE is a levnorgestrel IUS (e.g. Mirena) but this is not always going to be the best tolerated or most suitable in a young teenager. Pragmatically in teenagers we are much more likely to opt for the second line options of tranexamic acid +/- NSAID or the combined pill.

Tranexamic acid (TXA) may be familiar to people who work in haematology or with major trauma patients as an antifibrinolytic. It is licensed for menorrhagia management to be taken as 1g three times daily for up to four days starting on the first day of the period. There are few contraindications but it cannot be taken if there is a history of VTE and should be used with caution if the patient is on the COCP because both increase thrombotic effect. TXA will reduce menstrual blood loss by up to 50%.

NSAIDs for managing menorrhagia often causes confusion as surely they make people bleed don’t they? It’s worth going back to basic pharmacophysiology and revising how NSAIDs act on prostaglandins.  NSAIDs are cyclo-oxygenase inhibitors and cyclo-oxygenase is the enzyme involved in production of prostaglandins. In menorrhagia most women will have increased levels of prostaglandins which, as you might remember, are powerful vasodilators. The local effect of prostaglandin on endometrial blood vessels causes increased bleeding. By reducing the level of prostaglandins using oral NSAIDs the blood loss volume will be reduced by up to 40%. NSAIDs will also have a significant effect on dysmenorrhoea which will frequently coexist with menorrhagia.

The COCP is frequently prescribed for menorrhagia. It is important to be familiar with the UKMEC guidelines when prescribing the COCP. Whilst the licensed regimen for COCP is to take for 21 days with a seven day break, the RCOG FSRH and most menorrhagia guidelines recommend using extended or tailored regimens. This allows for shorter pill free intervals and reduced numbers of bleeding days. Tailored regimens are associated with less frequent bleeds, and in many cases a reduced number of bleeding days.  Satisfaction with tailored regimens is high. 

Eloise seems delighted that you think her periods might not be something she simply has to “put up with”. As she isn’t sure about her family history you call dad back in and he confirms that he knows of no family history of clotting or bleeding disorders. Eloise has had several dental extractions for orthodontic work and has never bled much after these and has never had epistaxis. Eloise has never had a migraine. Her blood pressure and BMI are normal and after discussions of options you prescribe her the levest COCP using an extended tricyling regimen with a five day break after 63 pills to minimise the number of bleeds she experiences and the volume. You also prescribe oral iron and arrange a repeat haemoglobin and ferritin in 3 months, with follow up consultation in four months time.

Selected references

Heavy menstrual bleeding: assessment and management (2018, updated 2020) NICE guideline NG88

Goddard, A.F., James, M.W., McIntyre, A.S. and Scott, B.B., 2011. Guidelines for the management of iron deficiency anaemia. Gut60(10), pp.1309-1316.

Lethaby A, Augood C, Duckitt K. Nonsteroidal anti-inflammatory drugs for heavy menstrual bleeding. Cochrane Database Syst Rev. 2000;(2):CD000400. 

Nash, Z., Thwaites, A. and Davies, M., 2020. Tailored regimens for combined hormonal contraceptives. BMJ368.

UTI whizzdom – the next steps

Cite this article as:
Felicity Beal. UTI whizzdom – the next steps, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32306

A 4-month-old baby presents with a temperature and urine microscopy suggestive of a urinary tract infection. He appears well and your plan is to discharge home on an oral antibiotic, whilst awaiting culture results. His mother asks you, “Does he need any other tests?”

Why does it matter?

Urinary tract infections (UTIs) are very common in children. Studies suggest that 6-8% of febrile, unwell children presenting to their GP have a UTI. Therefore it is important to carefully select which of these children need further investigations in order to identify those with underlying renal tract problems. It is estimated that up to 15% of children with a first UTI have evidence of scarring on follow up scans. If they are missed, these children may go on to develop hypertension and possible chronic kidney disease later in life.

Which children are more likely to get a UTI?

Before the age of 6 months, UTIs are more prevalent in boys. This is partly due to the increased chance of structural abnormalities within the urinary tract. Uncircumcised boys are particularly at risk, as bacteria on the foreskin are a reservoir for infection.

However, after 6 months of age, girls are at increased risk due to their shorter urethra and its proximity to the anus. This risk is increased again in females when they become sexually active.

Risk factors for UTIs

There are several other risk factors that increase the risk of developing a urinary tract infection. The main risk factor is something we see and manage on a daily basis, another really common presentation…constipation! If you haven’t yet read Chris Dadnam’s Conversations about Constipation post, now would be a great time to have a refresher as these two conditions go hand in hand.

As the colon and rectum fill with stool, the mass effect results in incomplete bladder emptying. This results in stasis of urine. Always ask about, and treat, constipation… If this is left unmanaged UTIs will continue to be a problem. 

After taking a good constipation history and examining the abdomen, it’s important you assess the spine looking for dimples, swellings, birthmarks or hairy patch lesions that can be associated with a neuropathic bladder. This should be followed by a lower limb neurological assessment. I think of this as running a bath after a hard day at work. You are unable to fully empty the tub afterwards but continue to add more bathwater to the tub every time… this will encourage infection to harbour. Recurrent UTIs may be the main presenting complaint in young children and should always prompt a review of the spine.

Foreign bodies such as intermittent or indwelling catheters also pose a risk. But it is essential to remember the last risk factor, not visible to the eye … namely urinary reflux.

Is this the same as vesico-ureteric reflux?

Yes. This is simply a term describing where, anatomically, the reflux occurs – from the bladder (vesico) to the ureters (ureteric). Urine flows back up from the bladder to the ureters causing a bidirectional flow of urine.

VUR can be primary, i.e. within a normal renal tract, or secondary, due to an abnormal renal tract – such as a neuropathic bladder. It is graded from 1 (mild) to 5 (severe.) Most mild to moderate reflux resolves by 5 years of age. However, surgery may be indicated if severe reflux is present, with worsening renal impairment or frequent pyelonephritis.

History and examination

As part of the history taking and examination, it is key to think about whether there could be underlying constipation, VUR or a neuropathic bladder. Asking about a family history of renal problems as well as considering antenatal renal scans is important to risk stratify for structural problems.

Ask about

  1. Constipation
  2. Urine flow
  3. Lower limb/back problems
  4. Antenatal renal abnormalities
  5. Family history of renal problems
  6. History of previous UTI/ fevers

Examine for

  1. Hypertension (complication)
  2. Poor growth
  3. Spine – for any spinal lesions
  4. Lower limb neurology
  5. Faecal masses
  6. Enlarged bladder / abdominal mass

What do we need to consider when further investigating UTIs?

NICE (the National Institute for Health and Care Excellence) ask the following three questions when considering a child’s risk of reflux and scarring:

How old is the child? Age is important. This may be a neonate or infant presenting with an infection as the first indicator of a possible underlying structural abnormality such as posterior urethral valves or VUR.

Is this an atypical UTI? 80% of paediatric UTIs are secondary to E.coli infection. An infection caused by an organism other than E.coli, or not responding within 48 hours of antibiotic therapy, is more unusual. Equally, if a child with a UTI looks unwell, has a palpable bladder, renal impairment or poor urine flow, your index of suspicion should be raised. These are uncharacteristic signs of a urinary tract infection.

Is this child having recurrent infections? Over 30% of children with UTIs will suffer from recurrent infections. Recurrent infections are defined as children who have either 2 or more upper UTIs (affecting the kidneys or ureters), 3 lower urinary tract infections (affecting the bladder or urethra) or 1 upper and 1 lower infection at any point up until the age of 16.

Investigations? Clear as M.U.D.

  • MCUG in 4 – 6 months
  • Ultrasound scan acutely or within 6 weeks
  • DMSA in 4 – 6 months

MCUG

An MCUG is a Micturating Cystourethrogram, which assesses for urinary reflux or obstruction. A catheter is inserted and radio-opaque contrast is administered via the catheter to fill up the bladder. X-rays are then taken during urination to see if urine is refluxing back towards the kidney.

Normal MCUG. Case courtesy of Dr Aditya Shetty, Radiopaedia.org. From the case rID: 27065
MCUG illustrating marked dilatation of the prostatic portion of the urethra consistent with posterior urethral valves. Case courtesy of Dr Andrew Dixon, Radiopaedia.org. From the case rID: 10432

DMSA

A DMSA scan is used to assess the function and location of the kidneys. An isotope that emits gamma rays is attached to ‘Dimercaptosuccinic acid’. This is administered via an intravenous cannula and is taken up by the kidneys a few hours later. If performed acutely it can show altered function consistent with pyelonephritis. In the UK, a DMSA scan is undertaken 4-6 months post-infection to assess for scarring.                       

A normal DMSA with equal isotope uptake in both kidneys. Case courtesy of Dr Yusra Sheikh, Radiopaedia.org. From the case rID: 69041

What does the guidance say?

In 2007, NICE published a guideline called “Urinary tract infection in the under 16s: diagnosis and management”, updated in 2018. When it comes to imaging, there are three main highlights.

1. Children under 6 months of age with a first typical UTI should have an ultrasound to assess for a structural cause. An MCUG is considered if this is abnormal.

2. All children with an atypical UTI, regardless of age, should have an ultrasound acutely. A DMSA is also performed if they are under 3 years of age to assess renal parenchyma. Children under 6 months are investigated more fully with an USS, DMSA and MCUG.

3. All recurrent UTIs require a DMSA scan within 4-6 months to assess for scarring.

This traditional approach for investigating children for reflux and scarring is safe yet adopts a different approach to imaging children with UTIs compared with other countries.

Controversial whizzarding….

The decision of who should be investigated further has caused great controversy. Different approaches are adopted around the world. This is due to conflicting evidence with clinicians balancing the risk of radiation, invasive imaging and cost with that of detecting children with an underlying congenital anomaly and preventing the development of chronic kidney disease.

There is conflicting data surrounding the risk factors for VUR in children with their first UTI. Ristola et al (2017) investigated risk factors for children with UTIs, finding the following 3 as the main risk factors for reflux: ultrasound abnormalities, recurrent infections and atypical infections. Interestingly, non-E. coli infections were the only statistically significant risk factor of infection recurrence.

Yılmaz et al (2016) were unable to identify risk factors associated with VUR, although did note that an abnormal renal scan at 6 months after the infection was closely related to the presence of VUR and recurrent UTIs.

In America, Canada, Poland and Italy, children up to 2 -3 years of age with their first UTI would be advised to have an ultrasound. The European Association of Urology advises every child presenting with a first UTI to be investigated with sonography. This is in comparison with the 6 month cut off advised by NICE, which is argued to be a more cost effective and risk stratified approach.

However, the American, Canadian and Italian guidelines do not investigate all children with recurrent UTIs as previously advised by the NICE guidance. Instead of all children with recurrent UTIs undergoing a DMSA scan, recent guidance suggests only performing a DMSA if there were concerns regarding an abnormal ultrasound or alternative diagnosis.

Therefore this makes me wonder, instead of investigating all children with recurrent UTIs, perhaps this decision should be made on an individual basis, using their ultrasound findings and considering risk factors.

How accurate are ultrasound scans in picking up VUR?

An ultrasound cannot exclude all cases of VUR as it is an observer-dependent investigation. Mahant et al (2002) reported low sensitivity of 40% and a specificity of 76% when diagnosing VUR, but the majority of these patients had lower grade reflux. There is now increasing awareness that low-grade reflux and mild scarring are unlikely to cause long term problems, therefore the argument presents itself: is there any benefit in investigating for them? Ultrasound scans are more likely to detect higher grade reflux and hence clinically significant cases, but further evidence is needed to support this approach.

The take homes

Some evidence suggests that children with ultrasound abnormalities or recurrent UTIS are at increased risk of complications from UTIs, regardless of their age or sex. There is no clear consensus on when to request a DMSA or MCUG but the latest evidence suggests that DMSA scans may not be necessary in all children with recurrent infections and a normal ultrasound scan. Clinicians should be aware of this existing controversy, weighing up the benefits and risks in order to make informed clinical decisions.

References

Craig J. Urinary tract infection: new perspectives on a common disease. Curr Opin Infect Dis 2001; 14 (3): 309–313.

Davis A, Obi B, Ingram M. Investigating Urinary tract infections in children BMJ 2013; 346 : e8654

Edlin RS, Shapiro DJ, Hersh AL, et al Antibiotic resistance patterns of outpatient pediatric urinary tract infections. J Urol2013;190:222–7.doi:10.1016/j.juro.2013.01.069

Kaufman J, Temple-Smith M, Sanci LUrinary tract infections in children: an overview of diagnosis and management BMJ Paediatrics Open 2019;3:e000487. doi: 10.1136/bmjpo-2019-000487

Mahant S, Friedman J, MacArthur C. Renal ultrasound findings and vesicoureteral reflux in children hospitalised with urinary tract infection. Arch Dis Child. 2002 Jun;86(6):419-20. doi: 10.1136/adc.86.6.419. PMID: 12023172; PMCID: PMC1762998.

Mori R, Lakhanpaul M, Verrier-Kones K. Diagnosis and management of urinary tract infection in children: summary of NICE guidance. Br Med J 2007; 335 (7616): 395–397.G

National Institute for Health and Care Excellence. Urinary tract infection in children: diagnosis, treatment and long-term management. Clinical guideline 54. London: NICE, 2007.

Newman DH, Shreves AE, Runde DP Pediatric urinary tract infection: does the evidence support aggressively pursuing the diagnosis?Ann Emerg Med2013;61:559–65.doi:10.1016/j.annemergmed.2012.10.034

O’Brien K, Edwards A, Hood K, et al Prevalence of urinary tract infection in acutely unwell children in general practice: a prospective study with systematic urine sampling. Br J Gen Pract2013;63:e156–64. doi:10.3399/bjgp13X663127

Okarska-Napierała M, Wasilewska A, Kuchar E Urinary tract infection in children: Diagnosis, treatment, imaging – Comparison of current guidelines. J Pediatr Urol2017;13:567–73.doi:10.1016/j.jpurol.2017.07.018

Ristola MT, Löyttyniemi E, Hurme T. Factors Associated with Abnormal Imaging and Infection Recurrence after a First Febrile Urinary Tract Infection in Children. Eur J Pediatr Surg. 2017 Apr;27(2):142-149. doi: 10.1055/s-0036-1572418. Epub 2016 Feb 8. PMID: 26855368.

Shaikh N, Craig JC, Rovers MM, et al. Identification of children and adolescents at risk for renal scarring after a first urinary tract infection: a meta-analysis with individual patient data. JAMA Pediatr2014;168:893–900.doi:10.1001/jamapediatrics.2014.637

Shaw KN, McGowan KL, Gorelick MH, Schwartz JS. Screening for Urinary Tract Infection in Infants in the Emergency Department: Which Test Is Best? Pediatrics. 1998;

Stein R, Dogan HS, Hoebeke P, et al Urinary tract infections in children: EAU/ESPU guidelines. Eur Urol2015;67:546–58.doi:10.1016/j.eururo.2014.11.007

Subcommittee on Urinary Tract Infection Reaffirmation of AAP clinical practice guideline: the diagnosis and management of the initial urinary tract infection in febrile infants and young children 2-24 months of age. Pediatrics 2016;138:e20163026.doi:10.1542/peds.2016-3026

Yılmaz S, Özçakar ZB, Kurt Şükür ED, Bulum B, Kavaz A, Elhan AH, Yalçınkaya F. Vesicoureteral Reflux and Renal Scarring Risk in Children after the First Febrile Urinary Tract Infection. Nephron. 2016;132(3):175-80. doi: 10.1159/000443536. Epub 2016 Feb 23. PMID: 26901769.

          

                                         

Paediatric pieces for Prehospital practitioners

Cite this article as:
Jason van der Velde. Paediatric pieces for Prehospital practitioners, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32110

I’m one of those that see little humans as little humans and big humans as big humans and don’t buy into the whole angst that children are different. Some humans require small bits of kits and some require rather large bits of kit….

Now before I get hissed at by a sizable proportion of readers, may I place my views into context? This may go some way into keeping you engaged, and, perhaps, convincing you that an alternative approach to equipment management might indeed be applicable to your practice. I’m a rural Prehospital Emergency Medicine and Critical Care Retrieval Physician. I grew up in the ambulance and rescue services in South Africa and have been engaged in looking after humans of all shapes and sizes since 1992. I currently work in stunningly beautiful West Cork, which despite being on the edge of Europe, can feel like being in the Australian Outback when you’re 3 hours away from a hospital with a post-arrest neonate or an 8-year-old with polytrauma. The Trauma Centre I’m attached to in Cork City is exceptionally busy, with a mixed adult and paediatric caseload. Approximately a third of my personal workload is paediatrics; oh and I have 5 children under the age of 14.

COVID has brutally shone a spotlight on the CRM issues we face every day in acute care specialities;  particularly with regards to equipment and consumables management. Overnight we decluttered many of our cubicles, creating isolation spaces. Rooms that are devoid of anything that might possibly become “contaminated”. Rooms are just “rooms” and no longer “clinical environments”.  We’ve had to adapt and conscientiously think about what consumables we bring to the bedside. Whatever we don’t use will need to be thrown out and whatever we don’t bring in will result in a potentially adverse delay, whilst a runner goes to fetch it from a distant storeroom. Folks, the latter is nothing new to the high visibility brigade… Welcome to Prehospital Care in the hospital! 

I’ve recently gone through a major upheaval, totally rethinking my equipment lists and layout whilst bringing a new 258 brake horsepower 4×4 into service. I manage circa 500 patients every year in the field. Kit logistics is everything, given the distant storeroom is a hospital up to 3 hours away and Gardai (the Irish word for police) don’t like to be used as runners. I must confess that I’m pretty old fashioned with what I use, and I don’t like change. It’s probably because I’m used to carrying what I need on my back and started my career in a system that at the time had very little. 

I’ve been motivated by the wealth of novel kit management ideas that have evolved from COVID preparation freely shared by colleagues on Social Media. In my own department, we’ve adopted various “Packs” to bring into  “COVID Rooms” to both reduce waste and to re-create our “clinical environment”, albeit one patient at a time.  

Pre-packaged kits ready to grab and go

I was asked to write a prehospital post on “adapting kit for children” and to highlight how I “improvise for children”. Sorry to disappoint, I certainly don’t “adapt kit” for children and I certainly don’t “improvise” either. What I do is innovate, putting hours and hours of iterative design and experience into safe equipment governance regardless of the size, shape or dilemma a human might find themselves in. 

How often have you reached for the simple in-hospital ward transfer bag, only to realise you probably should have been making use of that gym membership, let alone the health and safety implications of a ridiculously heavy bag stuffed to the gunnels? When you carry everything on your back as part of your daily routine, you get very used to minimising not only packaging but bulk. We’ve effectively been doing this in prehospital care for years without really thinking about it. Modulising equipment by clinical task reinforces a minimalistic approach and dramatically reduces both waste and weight. My new iteration of equipment bags takes this into account whilst also the addition of tackling the COVID infection control dilemma. 

Equipment ergonomics is nothing new to paediatric practice. For example, having everything to hand in a logical order is the hallmark of successful phlebotomy in a squirming toddler. The MOST important thing to start with is to ask yourself what you need a kit bag to achieve? I have evolved the primary platform on a comfortable army Bergen, which is equipped to ONLY provide life and limb threatening care to a human from preterm to centenarian a few hours hike through a mountain trail. To achieve this takes an immense amount of preplanning. For me, this latest iteration has built on a prehospital career of over 25 years, with 12 years of Irish practice to adapt, and there’s still so much more to do. The hallmark of quality prehospital care is not cutting corners and not improvising. I have the exact same standard of equipment, monitoring and drugs that you would expect available in a trauma unit. Innovation comes through layout and the principle of packaging everything into procedure based modules.

Experience has proven that it’s counterproductive to have a little bag full of syringes and needles. You’ll either have too many or not enough. Think about each and every life-saving procedure, for example, a chest drain then break it down into individual component parts. Do you have everything you need? With just one flap open on my bag, I have everything I need to pre-oxygenate an infant. There’s an Ayres T-piece, HME, angle piece, and one of each size 1 to 3 facemask, plus a single 10ml syringe for letting air into or out of the facemask seal. I consider airway adjuncts to be a separate module. 

In prehospital care, you do not have the luxury of knowing the size of the next patient. In the picture of my opened airway module, you will note I’ve everything required to manage a human airway. Spot the vacuum sealed hand suction if you can! You may notice a lack of toys. Airway cameras fail in the cold and wet. I’ve not yet met one that’s West Cork proof. 

Working repeatedly in  “COVID positive” homes really wakes you up to the realities of how poor our infection control practices were. In the new system, each module is vacuum-sealed in a clean room, before going into the main bag. If a module is opened, everything, regardless of if it’s used or not, is either discarded or re-sterilized as appropriate. The outside packaging of an unused module is easily decontaminated with a simple wipe or UV light. The bag itself is washable. 

Kit unused in a bag that’s been touched repeatedly by contaminated gloves should never have been a thing in the first place. Think about it! When you’re sucked into the moment of treating a sick child, the last thing you appreciate is infection control. Solutions need to be human proof. We can’t simply just do what we’ve always done. I call it the RNLI test. If your kit and all its contents reliably can survive a winter trip to an Irish offshore island, lying exposed in the hull of an open rescue boat, you’ve achieved infection control packaging! This means EVERYTHING, down to the stethoscope and SpO2 monitor requires vacuum sealing. 

Another advantage of having everything vacuum sealed is that when you prepare your kit, you’re not rushed, and everything can be meticulously checked with a colleague, using a challenge-response checklist. When you open your kit in chaos, you can be confident that everything you need is there, laid out exactly the same way on a nice clean piece of plastic – and not a dirty floor. Disposing excess packaging reduces clutter around the patient. Whilst there is a cost associated with setting up such a system, there are savings too. You don’t end up throwing as much away. By using a checklist , you also have the ability to record the expiry date of a piece of kit on the outside of the module.  You can either opt for having a store room with all the various modules vacuum sealed on a shelf to simply replace, or like me, you have a number of fully stocked bags always ready to go. I chose the latter, with three identical bergens allowing me the “luxury” of being able to offer one bag per polytrauma patient at a rural Road Traffic Collision.

Monitoring has always been a bulky problem. The solution has come about out of a novel community defibrillation project we initiated in West Cork. We wanted to equip every single off-duty member of the ambulance service with a patient monitor and defibrillator in the back of their private vehicle. With these professionals on a text alert system, we are able to go a long way to achieving a 10min response time in rural life or limb-threatening calls. Even the cheapest patient monitor, that conforms to the standards, costs €20k. By modularising everything into a sturdy waterproof case, ie purchasing SpO2, 12 lead ECG, defibrillator, BP cuff individually, we produced the same monitoring and defibrillation standard, in a far more rugged pack for a quarter of the price. 

Moving forward, my single kit bag now includes all the monitoring and drugs required for an RSI or cardiac arrest, including waveform capnography and ECG! These are not new technologies, but smaller, cheaper items such as EMMA Capnography and Bluetooth-to-iOS ECG devices. I no longer have the heavy monitor or hands so full of equipment that I can’t safely climb a flight of stairs, let alone reach a child trapped in a mindboggling place! It helps create that clinical environment in a non-clinical area. If further “next step” critical care retrieval paraphernalia is required, such as a ventilator, blood warmer or syringe driver,  this can be brought out from the car. 

But why on earth would all this be relevant to a paediatrician or paediatric nurse in an average hospital who may or may not ever have to retrieve or transport a sick child anywhere further than radiology? 

Around the corner, around the world” is a philosophy that defines risk in retrieval medicine. It’s not distance, but the very act of transferring a patient from one place to another that carries the risk. Most people are worried about a cardiac arrest en route. What will you do today if that cardiac arrest was caused by an infusion line, chest drain or endotracheal tube dislodging in transit in that unfamiliar, non-clinical space? The riskiest time is just transferring a patient across the bed to the trolley, radiology table or theatre table. After that, my least favourite place to be is an elevator or crowded corridor. Ask yourself the most basic and simple safety question… Is the equipment bag that accompanies me fit for purpose to provide critical care support to this little patient in an elevator? 

Head injury – the 4-hour observation clock…

Cite this article as:
Patrick Aldridge. Head injury – the 4-hour observation clock…, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32331

You have just seen a 3 year old boy who, one hour earlier, was running along the street, fell over and hit his head. There was no loss of consciousness, no vomiting and he’s running around the Emergency Department (ED) completely unaware of ‘social distancing’ practices. On examination he’s got a small forehead abrasion but nothing else concerning. The parent was initially concerned (so came to ED) and now wants to go home.

You think this is sensible and speak to your senior who advises that you observe him for 4 hours post-injury. You think he’s got a ’trivial head injury’ with no risk factors and ask why they need to wait a further 3 hours in ED. ‘That’s what we do’ comes the reply…

Paediatric head injuries, arguably, make up a significant proportion of children attending hospital. It’s been suggested and subsequently shown  that a fair proportion could be sent home by a competent nurse at triage even during a worldwide pandemic…

PREDICT have done some wonderful work recently with their ‘Guideline for Mild to Moderate Head injuries in Children – Algorithm’ (2021) – answering questions I have often wondered myself. However, I personally feel the two most ground-breaking of all these recommendations appear to have been glossed over. This may be because they are soooo obvious, simplistic and pragmatic but that makes me love them even more…

Trivial head injuries

Children with trivial head injuries do not need to attend hospital for assessment; they can be safely managed at home’. 

  • How many children in your own experience fall (boom boom) into this category and attended for review?
  • How much money and time (the families and the health services) could be saved if these children stayed at home?

A lot’ would be the assumption for both of these questions. However, this is currently an evidence void in need of answers.

Extended observation OR discharge

It is made very clear that children who do not fall into one of the assorted risk categories have ‘no need for observation’ aka discharge home.

  • No need to stop, pass go or take up sacred ED seating until 4 hours after their medically innocuous injury (agreed, to a parent an injury may not have been innocuous but by medical head injury rules it is).
  • The child stays for no longer than it took to see and assess them. This may be a hard practice to change in many ED’s.

4 hours

How many paediatric head injuries in your own clinical practice do you or someone else say/write the immortal words “Observe 4 hours from injury’? 

Do all the children observed for 4 hours across the world require this?

How many children, that you have seen in your practice, have deteriorated?

Why does this practice exist and what is the evidence base?

Well, there is a clear consensus on who should be observed for 4 hours from injury. In the UK, the National Institute for Health and Care Excellence (NICE) Head injury: assessment and early management CG176, 2014 – – suggests children with the following require observation for at least 4 hours from the injury:

  • Loss of consciousness lasting more than 5 minutes (witnessed)
  • Abnormal drowsiness
  • Three or more discrete episodes of vomiting
  • Dangerous mechanism of injury (high-speed road traffic accident either as pedestrian, cyclist or vehicle occupant, fall from a height of greater than 3 metres, high-speed injury from a projectile or other object)
  • Amnesia (antegrade or retrograde) lasting more than 5 minutes

The latest PREDICT guideline is slightly more prescriptive (especially around age groups) and suggests those with the following risk factors need observation for up to 4 hrs…

But why 4 hours? Why not 3 hours, as someone previously suggested with wheeze?  Why observe them at all and just CT the lot? Well, at the end of the day this is all about risk stratification. A CT scan is not without risk (that small thing called radiation?) and the actual number of abnormal CT’s (ciTBI/TBI-CT) has been shown to be quite low (2.3%) in a large group (19 920) of children with head injuries.  We want to scan those children deemed ‘high risk’ who are more likely to have an abnormal scan not those deemed medium/low risk who are less likely to have an abnormal scan.

The evidence for 4 hours

What evidence is 4 hrs observation based on? Umm, not a lot. Like many practices in medicine, it’s based on consensus and pragmatism. Many institutions follow a 4 hour target for patients to be admitted or discharged from the emergency department. Children with asthma/wheeze seem to require inhalers every 3-4 hours until discharge too and there are, no doubt, countless other examples within the medical world. Four hours observation post-injury is the consensus view and currently established practice from experts with specialist knowledge in this field. It probably came about when you had to sell your kidney to the Radiologist to get a CT scan and radiation doses delivered per scan were a lot higher than present ‘modern’ machines. It was easier to just observe the child and if they deteriorated you could then more easily argue for a scan. This is my best guess but is probably not far from the mark. Could this time be shortened in these at risk groups? Probably. But trying to research this would, no doubt, be an ethical minefield.

The clock is ticking…

There are a small select group of children with head injuries who require a period of observation post-injury, as suggested by national guidelines, decision rules and clinical gestalt. I would argue many children in ED’s across the world that are observed for ‘4 hours post-injury’ do not fall into any of the categories mentioned above and the root cause for observation being clinician preference based on defensive or outdated practice. This is understandable in those who see children infrequently, but should this be accepted going forward?

In the COVID-era we are living through, I believe there will be an increased focus on reducing unnecessary hospital footfall, ED crowding and time in a potentially risky environment. One potential quality improvement project would be to look at your own institution – how many children stay ‘4 hours post-injury’ and how many really needed to…?

High flow therapy – when and how?

Cite this article as:
Padmanabhan Ramnarayan. High flow therapy – when and how?, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31730

Isn’t nasal high flow just a fancy name for plain old high flow oxygen? Or is it CPAP-lite? For a therapy that has become so popular in less than a decade, amazingly, there is more opinion sloshing around than proper scientific evidence…

OK, back up, what is Nasal High Flow therapy?

Nasal high flow therapy (NHF), aka high flow nasal cannula therapy (HFNC), is a non-invasive mode of respiratory support, involving the delivery of heated (to 37° C) and humidified (to nearly 100% relative humidity) gas (oxygen and/or medical air) through nasal cannulae at high gas flow rates. What is a “high” gas flow rate is still not uniformly defined (some studies say >2 L/min and others >4 L/min). In physiological terms, to provide the true benefits of “high flow”, the gas flow rate should exceed the patient’s maximal peak inspiratory flow rate (roughly 8-10 x normal minute ventilation).

Makes sense, but what is a child’s peak inspiratory flow rate?

Short answer – it changes according to the age and the extent of respiratory distress. For example, a 4 kg baby breathing at 40 breaths/min and inhaling a tidal volume of 5 ml/kg (=20 ml) would have a minute ventilation of 0.8 L/min and a peak inspiratory flow (PIF) rate of nearly 3 L/min. However, the same infant would have a much higher PIF in respiratory distress. Matching the maximal PIF rate by aiming for roughly 8-10 x normal minute ventilation (in this case, 8-10 x 0.8 L/min = 7-8 L/min) is the key principle of NHF therapy. NB: Magically, the 8 L/min flow rate in this baby is also 2 L/kg/min (more on that later!)

Got it. But when should I start NHF in the ED?

Case 1. A previously healthy 4-month old infant is seen in the emergency department with a two-day history of coryza and poor feeding. On examination, he has mild/moderate subcostal recession and a respiratory rate of 60 bpm. His oxygen saturation in room air is 89%. Would you start nasal high flow?

This baby most likely has mild viral bronchiolitis and the main question is whether to start standard oxygen therapy (SOT) via nasal cannulae or NHF. The most useful clinical outcomes we are interested in are transfer to paediatric intensive care (PICU) and the need for endotracheal intubation.

What does the evidence say?

A recent systematic review (Lin J et al. Arch Dis Child 2019) is an obvious starting point. For the outcome of transfer to PICU, only two RCTs were included (Franklin et al. NEJM, 2018; Kepreotes et al. Lancet 2017). The overall risk ratio was 1.30 (95% CI 0.98, 1.72) indicating no significant difference between NHF and SOT, although there was a tendency to favour SOT.

Similarly, only two RCTs were included for the outcome of intubation (Franklin et al. NEJM, 2018; Yang et al. Chinese Pediatric Emergency Medicine, 2017). The overall risk ratio was 1.98 (95% CI 0.60, 6.56), again with no significant difference between NHF and SOT. So, not much joy from the systematic review…

Considering that Franklin et al dominated the systematic review in terms of sample size, it is useful to look at this RCT in a bit more detail, from a PICO point of view as well as the flow of patients through the RCT.

Population: Infants <12 months of age with bronchiolitis and needing supplemental oxygen

Intervention: NHF at 2 L/kg/min

Control: Standard oxygen therapy

Outcome: Escalation of care due to treatment failure (composite outcome)

A few reflections on the outcomes of infants in this RCT: although nearly double the number of infants randomised to SOT “failed treatment” compared to NHF, it is notable that over 75% of infants randomised to SOT did not “fail”; the majority of those who did “fail” SOT were rescued by NHF; and since NHF “failure” automatically led to PICU transfer, in effect, more infants were transferred to PICU in the NHF group than in the SOT group (12% vs 9%). Essentially, this RCT could be considered a trial of ‘immediate’ NHF versus ‘rescue’ NHF, as covered by us here previously.

Bottom line: There is no advantage to starting NHF as first-line therapy in an infant with mild bronchiolitis. A more clinically and cost-effective strategy would be to use NHF as ‘rescue’ therapy when standard oxygen therapy has failed.

Case 2. An ex-prem born at 24 weeks gestation, now 4 months old, is seen in the emergency department with a 24-hour history of coryza and cough. On examination, he has moderate/severe subcostal recession and a respiratory rate of 80 bpm. His oxygen saturation in room air is 85%. Would you start nasal high flow?

This baby is much sicker, with significant past medical history, and most likely has moderate/severe bronchiolitis. Would NHF be more useful as first-line therapy in this infant, where previously nasal CPAP would have been an option – can NHF be used as ‘CPAP-lite’? A really useful clinical outcome to focus on is endotracheal intubation.

What does the evidence say?

Lin et al summarise the evidence in their recent systematic review. For the outcome of intubation, 4 RCTs were included, but the total number of patients included were low (n=264). Intubation rates were identical in the NHF and CPAP groups (5.3%), with a risk ratio of 0.96 (95% CI 0.35, 2.61). So, there is not much evidence to support the use of NHF compared to CPAP, although quite notably, the rate of adverse events was lower in the NHF group (8% vs 21%).

Bottom line: There is no clinical advantage to starting NHF as first-line therapy in an infant with moderate to severe bronchiolitis to avoid intubation. However, its adverse event profile and tolerability by infants might make NHF more appealing as first-line therapy.

When should I start NHF in the HDU?

Case 3: A 5-year old boy with cerebral palsy and epilepsy is admitted to the paediatric HDU bed with fever, cough and respiratory distress. On examination, he has moderate subcostal and intercostal recession and a respiratory rate of 45 bpm. His oxygen saturation in room air is 88%. Would you start nasal high flow?

In this older child with a complex past medical history, is starting NHF, compared to either standard oxygen or CPAP, beneficial in terms of avoiding the need for endotracheal intubation?

What does the evidence say?

A recent systematic review (Luo J et al. Journal of Pediatrics, 2019) is an obvious starting point. In the comparison of NHF versus SOT, 5 RCTs were included, although 2 were focussed on bronchiolitis (previously covered – Franklin et al and Kepreotes et al). The other 3 RCTs were small (Chisti et al. Lancet, 2015; Ergul et al. Eur J Pediatrics, 2018; Sittikharnka et al. Indian J Crit Care Med 2018) with just 300 patients in total. The overall risk ratio for intubation from these 3 studies alone (calculated specifically for this post) was 0.72 (95% CI 0.38, 1.36). Similarly, in the comparison of NHF versus CPAP, 4 RCTs were included but 2 were in bronchiolitic infants (covered earlier). The other two RCTs (Ramnarayan et al. Crit Care 2018; Chisti et al. Lancet 2015) included just 187 children. The overall risk ratio for intubation based on these two RCTs (calculated for this post) was 2.14 (95% CI 0.93, 4.92) indicating a tendency for a higher intubation rate with NHF in older children.

Bottom line: In an older child, intubation was not less frequent when NHF was used compared to SOT as first line therapy. There was a tendency for NHF to be associated with a higher intubation rate compared to CPAP.

Great – what is the best way to provide NHF?

Starting gas flow rate

Milesi et al showed in physiological studies in infants aged <6 months with bronchiolitis that the work of breathing is reduced considerably when the gas flow rate is set at nearly 2 L/kg/min. In their cohort of 21 infants (mean weight 4.3 kg), the measured work of breathing was lowest at a flow rate of 7 L/min (compared to 1, 4 and 6 L/min). Similarly, in children up to the age of 3 years with pneumonia, work of breathing was reduced by nearly 20% at a flow rate of 1.5 L/kg/min compared to 0.5 L/kg/min (Weiler et al. Journal of Pediatrics 2017). Usual adult flow rates range from 50-60 L/min.

In summary, the optimal gas flow rate does not increase in a linear fashion with increasing age/weight, instead it goes from nearly 2 L/kg/min in infancy to nearly 1 L/kg/min in young adults.

RCTs of different starting flow rates

There have been two RCTs comparing NHF flow rates in bronchiolitis (Yurtseven A et al. Ped Pulm 2019; Milesi et al. Intens Care Med 2018). In the former, 1 L/kg/min (n=88) was compared to 2 L/kg/min (n=80) in infants <24 months with clinical severe bronchiolitis presenting to the emergency department. The primary outcome was ‘treatment failure’ within 24 hours. There was no significant difference in treatment failure between the two flow rates (1 L/kg/min: 11.4%; 2 L/kg/min: 10%). The second RCT compared 2 L/kg/min (n=142) with 3 L/kg/min (n=144) in infants aged <6 months with moderate/severe bronchiolitis. The primary outcome was treatment failure within 48 hours. There was no significant difference in treatment failure between the two groups (2 L/kg/min: 38.7%; 3 L/kg/min: 38.9%).

A useful chart with suggested starting flow rates based on weight is used in the ongoing FIRST ABC clinical trial of NHF versus CPAP.

Nasal cannula size

There are different nasal cannula sizes available based on the manufacturer. The general rule of thumb is that the cannula prongs should be no more than 50% of the diameter of the nostril to avoid inadvertent occlusion of the nasal passages. It is also advisable to start the gas flow rate at a low rate and then increase gradually over 10-15 min to avoid patient discomfort. Pacifiers may be useful in babies to prevent mouth opening.

Weaning NHF

There are no RCTs comparing weaning strategies for NHF. Clinical practice is also highly variable – in a global survey of practice in over 1000 PICU professionals by Kawaguchi et al, 68% weaned the FiO2 first to a threshold value (e.g. 0.40) and then weaned the flow rate gradually, 11% weaned the FiO2 first to a threshold value (e.g. 0.40) and then stopped NHF, and 4% weaned the flow rate alone without weaning the FiO2. The FIRST ABC RCT algorithm for the weaning of NHF provides a weight-based approach to a one-step weaning process and suggested clinical thresholds for weaning and stopping NHF.

The take homes

  • Nasal high flow is a form of non-invasive respiratory support that sits somewhere between standard oxygen therapy and nasal CPAP.
  • In infants with mild bronchiolitis, there is no clinical (or cost) benefit in starting NHF as first-line treatment – rather, NHF is best used as a ‘rescue’ therapy after standard oxygen.
  • In infants with moderate/severe bronchiolitis, NHF may be a useful first-line therapy owing to its ease of use and since it is better tolerated by infants, however there is no clinical benefit compared to nasal CPAP.
  • In older children with respiratory failure, there is little RCT evidence to guide practice – however, there is no clear benefit of starting NHF over and above standard oxygen. NHF may be associated with a higher intubation rate compared to CPAP in older children.
  • There is no RCT evidence to support either 1, 2 or 3 L/kg/min NHF flow rates in infants with bronchiolitis; however, physiological evidence suggests that nearly 2 L/kg/min is associated with reduction in work of breathing. Suitable flow rates in older children approximate 1.5 L/kg/min and in young adults, 1 L/kg/min.
  • There is no RCT evidence to support one way of weaning over another – the most common practice seems to be to reduce FiO2 to below 0.40, followed by a reduction in the NHF flow rate.
  • Ongoing RCTs such as the FIRST ABC trial will help address the question whether NHF is non-inferior to CPAP in critically ill children.

Carpal injuries

Cite this article as:
Sian Edwards. Carpal injuries, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.29050

Injuries to the hands are extremely common in children and are a frequent reason for their attending the ED. While common, their management can be limited by difficulties in proper assessment as well as a paucity of evidence to guide treatment. That said, documented outcomes remain typically excellent so it seems we must be doing something right! Generally, training is provided with an adult focus, and while some principles from adult trauma can be applied, it is not uniform. As our post on radiographic findings demonstrates, the bones of children are different. This is significant because we know that missed injuries or delays in appropriate treatment can lead to long term loss of function; further compounded by the science that children heal faster and therefore our window for intervention is considerably shorter. Therefore, accurate assessment coupled with appropriate initial management and timely referral if necessary are essential.

As is not uncommon in the paediatric arena, evidence specific to this population is limited although it is stated that carpal fractures in children are being increasingly reported . Perhaps this is as we, as clinicians, get better at diagnosis and radiologists therefore see more and so naturally become more adept at interpreting them. Regardless of radiographic findings, diagnosis is primarily through clinical examination. 

While not exclusive to the teenage population, we can expect the majority of carpal injuries to occur in the older child; as children age, become braver and take on more activities with an increased likelihood of higher velocity falls. Falling onto an outstretched hand, otherwise widely known as a FOOSH injury, is a common mechanism, accounting for 30% of non-scaphoid carpal injuries.

Before we get in to it, we can take a moment to re-familiarise ourselves with the bones of the hand and wrist.

The carpus

The carpal bones are the eight bones of the wrist that articulate the forearm with the hand – this in itself seems confusing as they are quite clearly situated in what we call the hand but go with it. They are divided into the proximal and distal rows, collectively known as the carpus. Proximally we have scaphoid, lunate, triquetrum, pisiform and distally, trapezium, trapezoid, capitate, hamate. The carpal bones develop through the course of childhood and should all be visible on X-ray by approximately 8 years of age.

Literature suggests that carpal fractures account for around 8-19% of all hand injuries worldwide; as we’ve already touched on, the majority will be scaphoid fractures and ED’s are pretty used to dealing with these – they even get their own series of x-rays – for that reason, this post will give some time to carpal fractures NOT including the scaphoid.

What are we looking for on x-ray?

While the AP view allows clear visualization of all of the carpal bones and would appear the ‘easier’ view, particularly to those less experienced with interpreting these x-rays, the lateral view is good for assessing the distal wrist, carpal bones and proximal metacarpals – it can appear confusing at first due to the overlapping bones. Regardless, both radiographs must be evaluated together. As always, we are tracing each individual bone looking for obvious breaks in the cortex before then looking for uniformity of the joint spaces; abnormally widened spaces are often indicative of ligamentous injury however abnormally narrow spaces are often the result of radiographic projection rather than injury. It is often helpful to sit back from the image and see it in its entirety as well as a close-up view.

Image adapted from a case courtesy of Dr Jeremy Jones, Radiopaedia.org. From the case rID: 37947

Recommended questions to ask when looking at the carpal bones:

  • Is the scapho-lunate distance less than 2mm wide? – if NO then suspect a tear of this ligament.
  • Is there a bony fragment lying posterior to the carpal bones? if YES, then suspect triquetral fracture.
  • Is there a bone sitting in the cup of the lunate? If NO, think carpal dislocation involving the lunate.

After the scaphoid bone, the triquetrum is the most commonly fractured bone in isolation with the trapezoid bone being the least frequently fractured. Each will now get it’s moment to shine as we take a minute to go through them.

Triquetral

Triquestral
Triquetral bone

Triquetral fractures usually occur on the dorsal aspect of the bone and are often the result of perilunate fracture dislocation as well as fracture of distal radius and ulna; they account for about 20% of all carpal fractures and are regularly missed.  These may occur by means of impingement from ulnar styloid, shear forces or avulsion from strong ligamentous attachments. The usual mechanism is a FOOSH whilst in ulnar deviation, and less commonly a direct blow to the dorsum of the hand. It is best seen on a lateral projection where the avulsed flake of bone may be seen lying posteriorly to the triquetrum – look for pooping duck sign on the image.

Image adapted from a case courtesy of Dr Maulik S Patel, Radiopaedia.org. From the case rID: 16046
Case courtesy of Dr Matt Skalski, Radiopaedia.org. From the case rID: 57109

Hamate

The hamate

Hamate fractures are rare, only accounting for approximately 2% of carpal fractures, potentially due to under reporting. They generally don’t happen in isolation, often being associated with dorsal fracture dislocation of 4th and 5th carpometacarpal (CMC) joints, ulnar nerve injury and flexor tendon rupture, especially of 4th and 5th fingers. Common mechanisms are from blunt trauma e.g. fist punch, falls and through impact from racquet sports.

Image adapted from a case courtesy of Andrew Murphy, Radiopaedia.org. From the case rID: 46110

Capitate

Capitate

Like hamate fractures, capitate fractures are also frequent injuries which seldom occur in isolation. A capitate fracture is uncommon, accounting for approximately 1.3% of carpal fractures and can be associated with a scaphoid fracture. It is uncommon to have a combined capitate-hamate fracture. The primary mechanism is a FOOSH with the wrist in hyperextension. Injury can result in ‘scaphoid capitate’ syndrome (1-2% incidence) where the capitate actually rotates by 180o – this latter presentation will need open reduction.

Image adapted from a case courtesy of Dr Bahman Rasuli, Radiopaedia.org. From the case rID: 65954

Lunate

Lunate

Lunate fractures account for about 1% of carpal fractures, and like its predecessors rarely occur independently. They are associated with injuries to the distal radius, carpus or metacarpals. Subluxations / dislocations of the carpus are most commonly centred around the lunate bone and key to their detection is the apple, cup, saucer analogy- the cup of the lunate should never be empty – the distal radius, lunate and capitate articulate with each other in a straight line on the lateral radiograph, so when examining the image, if the capitate (apple) is not sitting in the cup of the lunate on the saucer of the radius then injury is present. Failure to recognise this anatomy means that dislocations are often overlooked. Where scapho-lunate ligament injury has occurred, missed diagnosis can lead to chronic pain around the joint due to its instability. In the younger population, surgery will be considered to restore full function and relieve pain.

Normal capitate – lunate – radius alignment. Image adapted from a case courtesy of Dr Jeremy Jones, Radiopaedia.org. From the case rID: 37947
Perilunate dislocation. Image adapted from a case courtesy of Dr Ian Bickle, Radiopaedia.org. From the case rID: 46714
Image adapted from a case courtesy of Dr Henry Knipe, Radiopaedia.org. From the case rID: 70427

More commonly, injury can occur at the scapho-luncate ligament – on x-ray, expect to see a widened joint space which is often referred to as the “Terry Thomas” or “Madonna” sign (named for the gap between the front teeth) demonstrating such injury. While conservative management may often be trialled, surgical reconstruction can be needed.

Image adapted from a case courtesy of Dr Ian Bickle, Radiopaedia.org. From the case rID: 46695

Trapezium

Trapezium

Trapezium fractures comprise between 3% and 5% of all carpal fractures and <1% of all hand injuries; they can occur in isolation or in combination with another carpal bone e.g. fracture of the 1st metacarpal base and/or subluxation or dislocation of the 1st carpometacarpal (CMC) joint although this is extremely rare. They are often the result of high energy trauma, usually involving axial loading force. Isolated trapezium fractures can be easily missed on x-ray due to the overlying bones, particularly on AP view.

Image adapted from a case courtesy of Amanda Er, Radiopaedia.org. From the case rID: 74739

Pisiform

Pisiform

Pisiform fractures account for 0.2% of all carpal fractures and of those, half are in association with other carpal injuries; rarely it may dislocate without fracture and displace radially. Its rarity is attributed to the sturdy ligaments that encase it.

Image adapted from a case courtesy of Dr Garth Kruger, Radiopaedia.org. From the case rID: 29263

Trapezoid

Trapezoid bone

Trapezoid fractures are incredibly rare, with only about 10 cases reported in the literature. Their anatomic location and stable articulation with the 2nd metacarpal together with their strong ligamentous attachments to neighbouring carpal bones are thought to be responsible for the low incidence of fracture.

Image adapted from a case courtesy of Dr Bruno Di Muzio, Radiopaedia.org. From the case rID: 46412

So how do we manage these injuries?

Inevitably there will be some local differences, but the general principles are:

  • Closed manipulation can prove difficult and often unsuccessful so orthopaedic review is required if displacement exists.
  • If no displacement, and no concern about ligamentous injury, then conservative management is often indicated. There is frequently no requirement to formally immobilise so analgesia may be the only treatment. 
  • If carpal subluxation is suspected, always refer to the orthopaedic team for specialist evaluation. If you are unsure, the literature discusses obtaining a radiograph of the uninjured hand to use as comparison – this is not always a well received request so do consider utilising your local reporting radiologist, and if unavailable or in doubt then refer for follow up.

The take home

So, what essentially is our take home message? We need to keep in mind that carpal fractures, dislocations and ligamentous injuries do occur in children, albeit rarely. We need the ability to recognise the ‘normal’ so we can pick out the ‘abnormal’. As with all injuries, diagnosis should be mainly clinical with the x-ray being our confirmation. As cannot be said enough, if it presents like a fracture, or considerations of acute injury like swelling and pain inhibit your ability to confidently exclude it, then treat it as such and refer onwards to the specialists that can!

References

Armstrong M and Oyinkansola Adeogun BS (2009). Tendon injuries in the Pediatric Hand. The Journal of Craniofacial Injury. 20(4) : 1005-1010.

El-Feky M and Weerakkody Y (a). Trapezium fracture, accessed from https://radiopaedia.org/articles/trapezium-fracture?lang=gb accessed on 30/06/2020.

El-Feky M and Weerakkody Y (b). Pisiform fracture accessed from https://radiopaedia.org/articles/pisiform-fracture?lang=gb accessed on 30/06/2020.

Filho, R. L. R. et al. (2020). Capitate and Hamate Fracture. Case Study. Ortopedia, traumatologia, rehabilitacja. 22(2), pp. 143–149. doi: 10.5604/01.3001.0014.1185.

Foley K and Patel S (2012). Fractures of the scaphoid, capitate and triquetrum in a child: a case report. Journal of Orthopaedic Surgery. 20(1): pp 103-104.

Hacking C and Knipe H (). Carpometacarpal joint dislocation accessed from https://radiopaedia.org/articles/carpometacarpal-joint-dislocation?lang=gb accessed on 12/06/2020

Hacking C and Radswiki et al. Triquetral Fracture. Accessed from https://radiopaedia.org/articles/triquetral-fracture?lang=gb accessed on 30/06/2020.

Kam MLW, Sreedharan S, Teoh LC and Chew WYC (2011) ‘Severe Isolated Trapezoid Fracture:: A Case Report’, Hand Surgery, 16(2), pp. 185–187. doi: 10.1142/S0218810411005321.

Kose, O., Keskinbora, M. and Guler, F. (2015) ‘Carpometacarpal dislocation of the thumb associated with fracture of the trapezium’, Journal of orthopaedics and traumatology : official journal of the Italian Society of Orthopaedics and Traumatology, 16(2), pp. 161–165. doi: 10.1007/s10195-014-0288-9.

Maloney E, Zbojniewicz A, Nguyen J, Luo Y and Thapa M (2018). Anatomy and injuries of the paediatric wrist: beyond the basics. Pediatric Radiology. 48 : pp764-782.

Murphy A and Knipe H. Hamate fractures. Accessed from https://radiopaedia.org/articles/hook-of-hamate-fracture?lang=gb accessed on 30/06/2020.

Raghupathi AK, Kumar P (2014). Nonscaphoid Carpal Injuries – Incidence and associated injuries. Journal of Orthopaedics. II: 91-95.

Rasoli, S., Ricks, M. and Packer, G. (2012) ‘Isolated displaced non-union of a triquetral body fracture: a case report’, Journal of medical case reports, 6, p. 54. doi: 10.1186/1752-1947-6-54.

Shah S, Rochette L and Smith G (2012). Epidemiology of pediatric hand injuries presenting to United States emergency departments, 1990-2009. Journal of Trauma and Acute Care. 72(6) : pp 1688-1694.

Wahba G and Cheung K (2018). Paediatric hand injuries: clinical review. Canadian Family Physician. 64: pp 803-810.

Using your HEADS-ED

Cite this article as:
Sarah Edwards. Using your HEADS-ED, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31842

Paediatric mental health (MH) admissions to emergency departments and hospitals are increasing worldwide, including the UK, USA and Australia1–6. COVID-19 has changed this somewhat, at least in the UK, with a decrease in presentations in the first national lock down7. As the UK and the rest of the world return to the “new normal” in 2021, it is likely that paediatric MH presentations could rise back to pre-covid levels. 

These presentations can be challenging to manage in the emergency department. A variety of tools have been developed to help with history taking and disposition, including the HEEADSSS, HEADS-ED, Risk of Suicide Questionnaire (RSQ) and many others. Here we take look at a recent paper looking at the utility of one of these scoring systems, the HEADS-ED.

Cappelli M, Zemek R, Polihronis C, Thibedeau NR, Kennedy A, Gray C, Jabbour M, Reid S, Cloutier P. The HEADS-ED: Evaluating the Clinical Use of a Brief, Action-Oriented, Pediatric Mental Health Screening Tool. Pediatr Emerg Care. 2020 Jan;36(1):9-15. doi: 10.1097/PEC.0000000000001180. PMID: 28538605

What is HEADS-ED?

The HEADS- ED was developed in 2012 as a tool specifically to obtain a psychosocial history from adolescents in the ED, when it was found found to predict psychiatric consult and admission to inpatient psychiatry with a sensitivity of 82% and a specificity of 87% (area under the receiver operator characteristic curve of 0.82, P < .01). This was a promising finding. 

What was the aim of the paper?

There was a composite primary aim:

  1. To examine the utility and decision validity of the HEADS-ED tool for Paediatric Emergency Department (PED) physicians in guiding consultations to psychiatry and crisis services for patients presenting with mental health concerns.
  2. To examine the concordance between PED physicians and crisis intervention workers (CIWs) in communicating the level of need and action required amongst a sub-sample for the patients. 

Where was the paper set?

This study was conducted in the PED at the Children’s Hospital of Eastern Ontario, Ottawa, a tertiary hospital with 70,000 annual visits a year. 3100 (4.5%) of these are related to mental health concerns. Approximately two-thirds of the MH patients are seen by the PED physicians who either discharge to the community or request a consultation with specialised MH services. Those who don’t need any medical care (other 1/3rd ) are referred directly to the CIWs.

What did they do? 

The HEADS-ED was added to the charts of every child aged 12 to 17 presenting to the ED with a MH concern, completed by the PED physicians. 

Only adolescents who had a complete HEADS-ED were included in the study. If they were younger than 12 or older than 17, or if their presentation was not with a MH concern, then they were excluded from the study.

What did they find? 

There were 2704 mental health presentations during the study period. After various exclusions for wrong age or incomplete or no HEADS-ED assessment, 639 adolescents were included in the study. Of those 140 (22%) were seen by the CIWs.

How good is HEADS-ED at predicting consultation or admission?

The study team looked at how well the screening tool corresponded to consultation for full psychiatric assessment and subsequent admission to inpatient care. 254 (39.7%) children and young people required a consultation by the CIW or psychiatrist. 96 (15.3%) were admitted. 

Chi-squared was applied to each of the seven HEADS-ED items to examine whether the scores correlated to request for consultation and subsequent admission.

  • Inpatient admission was highly associated with higher scores in education, activities and suicidality
  • Consultations with CIW or psychiatry was associated with higher mean HEADS-ED score (mean 6.91)
  • Those who did not need a consultation had a mean score 4.70 (n=254)
  • Those who were discharged had a lower mean score than those admitted (5.28 vs 7.21).

As the HEADS-ED score increased, the likelihood of admission did also. 

How reliable is the score at predicting admission?

  • A HEADS-ED score of 8 or more and a suicidality score of 2 led to 164% more requests for consults from the PED team (relative risk, 2.64; confidence interval, 2.28–3.06) 

How well did the PED and CIW scores correlated?

140 patients had the HEADS-ED completed by both PED physicians and CIWs. The PED physicians rated patients higher on all HEADS-ED items and composite scores compared with CIW; however, not all were statistically significant. 

Agreement on ratings ranged from 61.7% to 92.9% with the highest agreement being suicidality and lowest agreement being activities and peers.

Bottom line – Should I change my clinical practice after reading this paper?

Maybe.

The HEADS-ED can be useful in helping take a psychosocial history in adolescents in the PED.

This may help confer concern when referring to the MH team. It cannot currently be used as a risk assessment as this was a single centre site, in Canada. More work is needed to understand its external validity.  

Final words from Andy Tagg

Patients with mental health concerns are increasing in numbers. Rather than skip over them for something easy it is important that we all get comfortable with asking uncomfortable questions. One of the challenges of formal tools is that they rend to direct the conversation and turn it into a tickbox exercise rather than a free-flowinng conversation. Clinicians need to be able to jump from topic to topic as they develop rapport with the child or young person in front of them.

With four times as many exclusions as inclusions I wonder how well the clinicians did if they did not use the tool. My first instinct would be that clinical gestalt, in experienced clinicians, would be as useful, if not better than the HEADS-ED tool. Where I see the potential value is for those healthcare workers with less experience, that might need a little guidance along the way.

References

1. Lo CB, Bridge JA, Bridge JA, et al. Children’s mental health emergency department visits: 2007-2016. Pediatrics [Internet] 2020;145(6). Available from: https://doi.org/10.1542/peds.2019-1536

2. Irteja Islam M, Khanam R, Kabir E. The use of mental health services by Australian adolescents with mental disorders and suicidality: Findings from a nationwide cross-sectional survey. PLoS One [Internet] 2020 [cited 2021 Jan 3];15(4). Available from: https://doi.org/10.1371/journal.pone.0231180

3. Lawrence D, Johnson S, Hafekost J, et al. The mental health of children and adolescents: Report on the second Australian child and adolescent survey of mental health and wellbeing [Internet]. Austrialian Government; 2015 [cited 2021 Jan 3]. Available from: https://www1.health.gov.au/internet/main/publishing.nsf/content/9DA8CA21306FE6EDCA257E2700016945/$File/child2.pdf

4. Tolentino A, Symington L, Jordan F, Kinnear F, Jarvis M. Mental health presentations to a paediatric emergency department. Emerg Med Australas [Internet] 2020 [cited 2021 Jan 3];1742-6723.13669. Available from: https://onlinelibrary.wiley.com/doi/10.1111/1742-6723.13669

5. Williamson A, Skinner A, Falster K, Clapham K, Eades SJ, Banks E. Mental health-related emergency department presentations and hospital admissions in a cohort of urban Aboriginal children and adolescents in New South Wales, Australia: findings from SEARCH. BMJ Open [Internet] 2018 [cited 2021 Jan 3];8:23544. Available from: http://bmjopen.bmj.com/

6. UKParliment. Written questions and answers – Written questions, answers and statements – UK Parliament [Internet]. UIN 181292. 2018 [cited 2021 Jan 3];Available from: https://questions-statements.parliament.uk/written-questions/detail/2018-10-18/181292

7. Ougrin D. Debate: Emergency mental health presentations of young people during the COVID-19 lockdown. Child Adolesc Ment Health [Internet] 2020;25(3):171–2. Available from: https://doi.org/10.1111/camh.12411

8. Cappelli M, Gray C, Zemek R, et al. The HEADS-ED: a rapid mental health screening tool for pediatric patients in the  emergency department. Pediatrics 2012;130(2):e321-7. 

Other useful resources 

Andrew Tagg. Mental Health Screening, Don’t Forget the Bubbles, 2019. Available at:

https://doi.org/10.31440/DFTB.21114

Henry Goldstein. Adolescent Inpatient Psychiatry, Don’t Forget the Bubbles, 2017. Available at: https://doi.org/10.31440/DFTB.11391 

Ester Sabel. The ABC of Self-Harm in Young People – A Psychiatric Approach to Resuscitation. 2019. https://www.rcemlearning.co.uk/foamed/the-abc-of-self-harm-in-young-people-a-psychiatric-approach-to-resuscitation/  

How to… set up the resuscitaire

Cite this article as:
Taryn Miller. How to… set up the resuscitaire, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31358

Check that the resuscitaire is plugged in and connected to the oxygen and air 

  • On button 
  • Light button 

Top to bottom run through 

Top panel  

  • Clock or timer to time your resuscitation – (start, stop and reset) 
  • Temperature settings 
    • Pre-warm – The machine will automatically set to pre-warm
    • Manual – Use the up button to change to manual 
    • Up and down buttons – Dial up the temperature using these buttons in the manual setting  
    • Baby – If using a manual continuous saturation monitor plug into here and then set to baby 

Key locks the settings so it cannot be changed again unless you press it again

Blender 1:13

This blender corresponds to the Fio2 of the gas coming out of the auxiliary gas port
You can dial it up or down
Most people set the initial FIO2 to 0.21 so that you are resuscitating on air 

Suction 1:25

Turn on suction using the switch
Increase pressure by turning the suction dial 
When you occlude the suction device the needle on the dial will move up and down to show how much negative pressure is exerted 

Ventilation settings 1:40

Autobreath

T piece is attached to auxiliary gas port shown 

Working from left to right 

  • Rate – most people start with an initial rate of 40 breaths per minute 
  • PEEP – If you are not setting the peep with valve on top of the T piece device you can set it using the PEEP dial 
  • On and off switch for autobreath 
  • Airway pressure relief – also known as the peak inspiratory pressure – most people like to set this at a maximum of 30 to begin with 

Testing pressures: 2:13 

To test the pressures when the T-piece is connected to the gas outlet:  

  • PEEP = Occlude the valve inside the mask, the needle will move to the desired level of peep 
  • Peak inspiratory pressure – occlude the valve at the top of the T-piece

Flow rate 2:31

  • This dial controls the flow rate through the gas outlet 
  • Most people set it at 8 litres per minute 

Gas outlet 

  • Below this you have an alternative gas outlet that always runs on 100% oxygen 
  • You can attach a water or anaesthetic circuit here and adjust the flow rate in the same way as above using this dial 

Gas Supply 

  • These dials show much how air and oxygen are in the tanks behind the resuscitaire 
  • This switch should be used whenever the gases are in use

Resuscitaire run through 

There is a baby being born – get your resuscitaire ready and primed 

  1. Plug the resuscitaire in 
  2. Connect to the gases – black to air, white to oxygen 
  3. Turn the resuscitaire on and turn the light on 
  4. Select manual and turn the temperature all the way up 
  5. Set your blender to an fi02 of 21 
  6. Check your suction – one end connects underneath the resuscitaire, the other end connects to the yanker. Check it is working by occluding the end 
  7. Set your Autobreath settings – 
    • Rate of 40 breaths per minute 
    • Peep of 4 or 5 and turn the peep on  
    • Flow rate of 8 
    • Connect the tubing to the outlet
  8. Test the pressures  
    • Occlude the mask to check PEEP isn’t too high 
    • Occlude the valve at the top of the T-piece to check your peak inspiratory pressure 
  9. You should have a 250ml bag-valve-mask to attach in case you need to manually bag the baby 
  10. Have lots of towels 
  11. Oxygen saturation probe and stick it to the edge of the resuscitaire  
  12. Airway trolley near by 

PEM adventures chapter 3

Cite this article as:
Team PEM Adventures. PEM adventures chapter 3, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31888

It’s time for another PEM adventure. Join us on another journey (with an inbuilt time travel machine) in managing Francesca, a teen who dreams of being a pop star…

Meet Francesca, a 15 year old girl who dreams of being a pop star.  She is making ripples in the world of teen music videos and has a HUGE audition tomorrow for a music video. But for the last 24 hours she’s been feeling a little shaky and pretty nauseous. Putting it down to nerves, her mother (who is also her agent) continued packing for the big trip. But Francesca vomited, had two episodes of diarrhoea and then spiked a fever and her mother knew she needed to get her fixed. Fast.

It’s the middle of a run of the mill shift for you. You’ve just fished a bead from a child’s ear, reduced a decently angulated forearm fracture and admitted a child with a pyelonephritis. When you take a look at Francesca though you know she’s sick. She is agitated, clammy and flushed, and febrile at 39.3°C. She’s tachycardic at 130, with a bounding pulse, blood pressure of 128/74 and normal heart sounds. She tachypnoeic at 24, with sats of 98% in air and a clear chest. Her abdomen is tender in the epigastric region, with no guarding or rigidity. Her GCS is 15 with no focal neurology. Her triage weight is 44kg.

You grab the sepsis trolley. Cannula in you, send some bloods: FBC, coagulation, CRP renal and liver function and blood cultures. You run a venous gas and this is what you see…

That lactate is horrific. You hastily prescribe a 20ml/kg bolus of 0.9% saline and a broad-spectrum third-generation cephalosporin. But, what’s your next step?

You prescribe some paracetamol. Easy enough. And then you go back and think about what to do next.

Close the tab and have a think about some more choices or move on to the next section.

You give another 20ml/kg of 0.9% saline and reassess.

Her heart rate drops down a couple of beats per minute but it bounces up again. So you give more saline. But her heart rate goes up a bit higher. And higher again. She begins to hyperventilate. Heart sinking, you repeat her gas. Her pH has dropped, her lactate has climbed and her potassium looks horribly high. This was NOT supposed to happen. The saline has done exactly the opposite of what you’d like it to do… how could that be? 

You wish you could go back in time and make that choice again. Luckily for you, that’s exactly what the inbuilt time travel machine is for.

Close the tab and take another look at the choices. If there’s nothing else you’d like to do then move on to the next section.

You give another 20ml/kg, but this time, instead of reaching for the saline, you go for Plasmalyte (or Hartmann’s, if that’s your fluid of choice). You reassess. Her heart rate drops down a couple of beats per minute but it bounces up again. Her pulses remain bounding, BP holds and JVP isn’t raised with no rales in her chest so you give another bolus and reassess. Same thing happens: a miniscule response but nothing substantial. You don’t make things worse, but you can’t seem to make things better either. Why isn’t fluid bringing down Francesca’s heart rate?

Close the tab and take another look at the choices. If there’s nothing else you’d like to do then move on to the next section.

Her ECG shows a sinus tachycardia. She’s in sinus rhythm with a p wave before each QRS and a normal p wave axis; her QRS axis is normal and intervals are normal too. There are no voltage criteria for ventricular hypertrophy and you can’t spot any subtle ST changes or delta waves. You use a handy ECG proforma to double check, but apart from the tachycardia, it all looks fine. So you go back to Francesca and have a think about what to do next.

Close the tab and take another look at the choices. If there’s nothing else you’d like to do then move on to the next section.

You have recently been on a POCUS course so you want to try out your ultrasound skills. You ultrasound her abdomen. It looks normal. The eminent professor of ultrasonography wanders by. You ask him to double check your findings. He agrees, ultrasound is normal. 

Close the tab and take another look at the choices. If there’s nothing else you’d like to do then move on to the next section.

While you’re pondering what to do, you receive a phone call from your bank. It’s noisy in ED so you pop into the corridor. The bank tells you they’ve just realised they owe you a couple of hundred pounds (*replace pounds with Euros, Dollars, Australian Dollars or any other local currency). That’s great news! Smiling, you type out a quick text to your best friend. “Epic windfall. Celebrate later in China Town?” You can almost smell the chow mein. Your stomach rumbles. It’s definitely time for some lunch. You let Francesca’s nurse know you’re going for a break.

Just as you’re finishing your sandwich, Francesca’s nurse comes rushing to find you. What with the phone call, the texting and the lunchtime queue in the canteen, it’s been almost three quarters of an hour since you last reviewed Francesca. She is far more agitated. The monitor is alarming. Her temperature is now 40.2°C and she’s very sweaty. She looks a little blue. With a heart rate of 159, BP of 108/72, respiratory rate of 32 and O2 saturations of 93% in air, things are not looking good.

Her mother wails, “Will she be better for her audition?!”

You repeat her gas. It’s not good – her lactate’s now 9.3 and her pH is down to 7.03.

Her nurse hands you an ECG. Scanning it you spy peaked T waves, wide QRS complexes and a prolonged PR.

Hang on! What was the potassium on that gas?! You snatch up her gas – her potassium’s 7.2! How are you going to bring that potassium down? What will you prescribe first?

This is a great first choice. Calcium gluconate stabilises Francesca’s cardiac membrane, buying you some time. The gluconate’s in. But that potassium still needs to come down. How are you going to do that?

Close the tab and choose a second drug or drug combination to bring that potassium down. If you’ve already done that and you’re happy with your choice then move on to the next section.

Fabulous! Sodium bicarbonate is an ideal drug in a child or young person who has hyperkalaemia AND acidosis (but you might want to stabilise the cardiac membrane first, if you haven’t done this already). You prescribe a sodium bicarbonate bolus once Francesca’s had her calcium gluconate and ask your amazing resus nurse to start to prepare for an insulin and dextrose infusion.

Close the tab and move on in the story.

On goes the salbutamol nebuliser while the infusion is drawn up. Up goes the infusion. But then something terrible happens. Francesca’s heart rate climbs higher and higher. And then higher again. Her pulse is thready, she’s more diaphoretic. You didn’t think it was possible but she looks even worse. A repeat ECG confirms your worst fears: she’s in SVT. 

Let’s jump back in that time machine and try that vote again. Close the tab and have a look at your other options.

Insulin and dextrose sounds like a good choice. But do you want to give it as your first line agent to bring Francesca’s potassium down? Or after something else?

You get out your phone – there must be an app there somewhere that tells you how to prescribe insulin dextrose infusions for hyperkalaemia. After much tapping and scrolling you find what you’re looking for and write it up. Your amazing resus nurse starts making up the infusion. 13 minutes later it’s up and running. But it’s too late. Francesca’s potassium has continued to climb and she’s going into a VT arrest. No!

It’s time for the time machine. Close this tab and click on “after something else”

This sounds very sensible. After all, insulin-dextrose infusions can take ages to draw up and you need to give something that will work quickly to stabilise her myocardium as well as something that will help drive the potassium back into the cells.

Close the insulin and dextrose tab and choose two drugs: one to stabilise the myocardium and one to bring down the potassium. Hint: she’s acidotic.

Phew! Francesca’s ECG rhythm is improving. Crisis averted. Or is it?

By now Francesca is so agitated, it’s becoming impossible to keep her in bed. “I have to rule out an intracranial infection”, you think to yourself. She needs a CT.

Her nurse begs you to give her a sedative. This makes you a little anxious (pun totally intended). You know that sedation in a sick child can be lethal. So, how will you manage her agitation?

You don’t want to risk giving her a sedative. You’re quite fond of being a doctor and this is a high stakes situation – you don’t want to lose your medical licence if she arrests. Her nurse rolls his eyes – you’re not the one trying to hold her in bed. But as Francesca rips out her cannula and throws herself against the wall you come to the realisation that you are going to have to prescribe something.

Close this tab and go back to choose a sedative.

You like ketamine, you use it a lot and it’s got an excellent safety profile, right? You give Francesca 1mg/kg. She drifts off into a dissociative state. Unfortunately you weren’t as right as you thought. Because it inhibits reuptake of catecholamines it tends to push heart rates up. Francesca becomes extremely tachycardic. After 20 minutes she starts to develop emergence phenomena and becomes even more agitated. She arrests. But don’t worry, we’ve given you a time travel machine for this very reason.

Close the tab and go back to make a different choice.

Unfortunately haloperidol, like Olanzepine, lowers seizure thresholds. You remember this just as it’s infused. Francesca starts fitting. And to make matters worse, it has also prolonged Francesca’s QTc. Her cardiac rhythm becomes unstable and she arrests. Not what you intended. You hop in your time travel machine and go back to make that choice again.

Close the tab and go back to make a different choice.

Unfortunately Olanzepine, like Haloperidol, lowers seizure thresholds. You remember this just as it’s infused. Francesca starts fitting. And to make matters worse, it has also further prolonged Francesca’s QTc. Her cardiac rhythm becomes unstable and she arrests. Not what you intended. You hop in your time travel machine and go back to make that choice again.

Close the tab and go back to make a different choice.

You give Francesca a nice calming benzodiazepine. She settles, buying you some time.

Close the tab and read on to the next part of the story.

You want Francesca out of ED – this is too stressful! Thankfully PICU have a bed. You compassionately explain to Francesca’s mum that the PICU team will work very hard to treat Francesca but she’s very, very sick. Her mum starts crying, “She’s such a beautiful girl! She was going to be famous! She’s worked so hard to lose weight for her audition!”

Internal alarm bells start ringing. “Hang on! How has she lost weight?” Eyes wide, you ask her mother, “Has she been taking something?!?”

Just as you garble this, Francesca’s dad arrives. He’s found a bottle of pills in Francesca’s room. The label says DNP. They were next to her exercise bike.

You ask switchboard to put you through to the national toxicology advice line. The toxicologist who answers the phone tells you that DNP, short for dinitrophenol, is a diet pill that’s illegal in most countries but quite freely available over the internet. It’s called a fat burner because DNP short circuits mitochondrial ATP production by uncoupling oxidative phosphorylation. Because ATP can’t be produced, metabolic rate increases and energy is instead released as heat. People who take it literally burn fat. But even a single pill can lead to uncontrolled hyperpyrexia and its toxic effects are increased with exercise.

They tell you that Francesca’s bloods must be monitored closely; her liver function will deteriorate as her liver literally cooks from within; she will become hypoglycaemic as her glycogen stores are consumed; and she’ll become hyperkalaemic. Monitor her methaemoglobin and if it reaches 30% or if there are signs of tissue hypoxia, give methylene blue.

They give you a long list of treatments including…

Cold intravenous fluids…

…ice packs…

…gastric and bladder cold fluid lavage with peritoneal cooling if you can…

…and Dantrolene…

…and if that fails… then a cooling heat-exchange central line… or ECMO if you’re really stuck.

That temperature just has to come down.

You thank toxicology and replace the handset and think to yourself, “Now where will I find Dantrolene?”

But while you’re pondering this, things go from bad to worse. Francesca’s temperature continues to climb. She’s now 41°C. She’s boiling. Sweat drips onto the sheets. She starts to have a generalised tonic-clonic seizure. You give her a dose of IV. Lorazepam but she continues to seize.

What will you give next?

But a second benzo doesn’t do the trick. She continues to seize. What will you give next?

Close the tab and have another look at the options.

Phenytoin seems like a sensible idea. It’s the second line anticonvulsant in APLS after all. You prescribe 20mg/kg and the infusion’s set up. But it wasn’t a sensible idea. In fact, it was a terrible idea. The phenytoin has exacerbated sodium channel blockade, making her QRS becomes extremely wide. Despite your best efforts to manage her arrhythmia she arrests. It’s time for the time machine. Let’s go back in time to try that one again.

Close the tab and take another look at the options.

You decide to avoid phenytoin because in the context of a toxin you were worried it would prolong her QTc and make her arrest. And ECLIPSE and CONSEPT showed it’s non-inferior to phenytoin in the management of seizures. It’s a good choice.  Her seizure stops.  What a relief.

Close the tab and move on in the story.

You decide to avoid phenytoin because you were worried its sodium channel blocking properties will widening her QRS complexes and make her arrest. And you’ve heard phenobarbital remains the second line recommended treatment in seizures secondary to recreational drugs. It’s a good choice.  Her seizure stops.  What a relief.

Close the tab and move on in the story.

Things can’t get any worse, right? Wrong. She is making a funny snoring noise. You’re really worried about her airway. You fast bleep the anaesthetist. Finally something’s going right, he’s just walking past, and he’s in resus in less time than you can say “dinitrophenol.” He’s up to speed in no time, and definitely agrees she needs a tube. Your RSI cocktail of choice is ketamine (1-2mg/kg), fentanyl (1mcg/kg) and rocuronium (1-2mg/kg). It’s the least cardio-unstable combination of drugs and you definitely don’t want to make things worse. (Take a look at ‘The curious incident of the wheeze in the night time’ for more on this.) But, luckily for you, the  anaesthetist is a clever guy and says, “Let’s avoid fentanyl since she’s hyperpyrexic as fentanyl’s serotonergic – we don’t want to raise her body temperature any higher than it is already.”

The resus nurse mishears his instruction and almost makes a fatal mistake. Spying a syringe labelled suxamethonium, the anaesthetist (who you decide is your new best friend) calmly says, “No suxamethonium. Her potassium is high. She’ll arrest with sux.”

He intubates successfully using midazolam, propofol and rocuronium.  She’s easy to ventilate.

Finally Francesca’s ready for PICU. With cold fluids, ice packs and Dantrolene her temperature comes down to 37.9 °C. You hand her over with clear instructions to avoid…

…serotonergic drugs (put away that fentanyl)

… or drugs that prolong QRS (don’t even think about phenytoin if she fits again)

…and to set up ECMO if her temperature climbs again.

18 months later you watch Francesca perform live in Eurovision. She receives “Douze points!” from every country, setting the record for the highest ever Eurovision score. She campaigns for better awareness of body image in girls and is vocal about the dangers of diet pills.

But let’s hop back in that time travel machine one last time and see what your learning was from her case…

You find this review article about DNP.

Grundlingh J, Dargan PI, El-Zanfaly M, Wood DM. 2,4-dinitrophenol (DNP): a weight loss agent with significant acute toxicity and risk of death. J Med Toxicol. 2011;7(3):205-212

Fascinatingly, as well as all the clinical management advice you received from your friendly toxicologist, it also tells you a bit about the history of DNP. You’re intrigued to read that the first death from DNP was over 100 years ago in 1918 secondary to occupational exposure of DNP powder.  It was used in France for the manufacture of munitions during the First World War.  In 1933 it was discovered that human consumption led to significant weight loss. It became very popular as a weight-loss drug but within 5 years it was recognised as being extremely dangerous and was labelled as “not for human consumption” by the FDA in 1938.  Anecdotally, it was prescribed to Russian soldiers during World War II to keep them warm.

It all went wrong in the 80s (didn’t it all?).  An American doctor prescribed DNP tablets to thousands of patients through his private weight loss clinic.  In 1986 he was convicted for drug law violations, fined and prohibited from dispensing DNP to patients.  But this didn’t stop him.  He was eventually jailed for fraud in 2008. But DNP is still out there and sadly widely available on the internet…

So, what has Francesca’s case taught us (aside from reminding us how very cool the Eurovision Song Contest is)?

1. Infection isn’t the only cause of fever

Keep your differentials open. You only need to Google ‘differentials fever + tachycardia’ and the first thing that pops up is a 2013 article titled, ‘Intoxications Associated With Agitation, Tachycardia, Hypertension, and Fever: Differential Diagnosis, Evaluation, and Management.’ (True as of 1st November 2020). Toxicological agents include drugs that cause:

  • Serotonin Syndrome: some antidepressants including SSRIs, SNRIs and lithium, anticonvulsants such as valproate, analgesics such as fentanyl, antiemetics such as ondansetron and street drugs such as cocaine, ecstasy, methamphetamine and LSD.
  • Neuroleptic Malignant Syndrome: ‘typical’ antipsychotics such as haloperidol, newer ‘atypicals’ such as risperidone and olanzepine, antiemetics such as metoclopramide and promethazine.
  • Malignant Hyperthermia: an inherited skeletal muscle disorder triggered by inhaled anaesthetics, succinylcholine, heat or exercise.
  • Sympathomimetics: cocaine, ketamine, ecstasy, amphetamines, synthetic cannabinoids.

Toxicology isn’t where it ends though. In our COVID world we’ll be used to including inflammatory syndromes like PIMS-TS to our list of differentials, but don’t forget other inflammatory syndromes including inflammatory bowel disease and rheumatological; oncological presentations; intracranial causes (bleed, tumour, basically anything that damages the hypothalamus can dysregulate temperature control); endocrine causes like thyroid storm, adrenal crisis… and the list goes on.

2. Engage your toxicology colleagues early

Even if you don’t think the primary cause is toxicological, as soon as it could be then pick up the phone to your regional / national toxicological service. Sedatives, anticonvulsants, anaesthetic induction cocktails… there are many ways things can go wrong. Ask a friend for advice before prescribing drugs in a potentially unstable situation.

3. Familiarise yourself with the management of acute behavioural disturbance

Acute behavioural disturbance can be a very challenging situation to manage. RCEM, the Royal College of Emergency Medicine in the UK, has a short guideline explaining the pros and cons of the different drugs of chemical restraint. Although not specifically tailored to paediatric presentations, the explanation of the drug side effects is a useful guide to frame your management. From a paediatric perspective, NICE (The National Institute of Health and Care Excellence, UK) have a pathway specific for children. If behavioural techniques don’t work and you need to move onto a pharmacological approach, NICE only advocates the use of IM lorazepam. The Royal Children’s Hospital in Melbourne’s ‘Acute Behavioural Disturbance: Acute Management’ CPG has an escalation ladder from behavioural management, to oral, then IM / IV medications, clearly stating antipsychotics should only be given to children who have previously taken antipsychotics or who have a normal ECG. Read it in conjunction with the RCEM guideline to understand the risks of each drug.

4. Think about the approaches to managing fever

We love a bit of paracetamol or ibuprofen to bring down a fever. But do you know how they work? Although paracetamol’s been used for over 100 years, we’re still not entirely sure how it works. Its antipyretic actions are thought to be due to inhibition of prostaglandin synthesis, resulting in a reset of the temperature centre in the hypothalamus. Nonsteroidals, such as ibuprofen, also inhibit prostaglandin production, although via a different cyclooxygenase (COX) pathway (all sounding vaguely familiar?).

However, fever caused by toxins is not caused by prostaglandin or COX inhibition and needs a different approach to resolve.

Start with non-pharmacological measures. Fans, ice packs in the groins and axillae, ice baths and internal techniques such as gastric and bladder cold fluid lavage, or, more invasively, Intravascular Heat Exchange Catheters (the ICY Catheter). The ICY catheter is placed in the inferior vena cava via the femoral vein, acting as an extracorporeal cooling device. Cold saline circulates through the catheter, which is closed so does not infuse saline into the bloodstream, instead returning the now-warmed saline back out of the body. The patient’s core temperature is measured via a thermometer in the bladder and an automated feedback loop between the thermometer and the ICY Catheter ensures the patient’s temperature is brought down to a target range, which can be adjusted by the treating clinician. Add benzodiazepines to prevent shivering and for sedation to help the child or young person tolerate these techniques.

There’s an extremely high mortality in severe hyperthermia – if these measures don’t work then RSI with muscle paralysis (but avoiding suxamethonium), with benzodiazepine infusions.

And reach for the antipyretic drugs. Dantrolene is frequently used in the management of anaesthetic-induced malignant hyperthermia and neuroleptic malignant syndrome. It works as a postsynaptic muscle relaxant, inhibiting calcium ion release and therefore decreasing the amount of excitation-contraction coupling from muscle cells. It’s usually found in theatre, to keep it ready to hand for the treatment of malignant hyperthermia. But, theatre is often far from the ED, and unless you know it’s there, it can take a while to hunt it down in the hospital – don’t let this delay you using it emergently in ED. Although the use of Dantrolene in DNP toxicity is currently under debate with only a few case reports citing its efficacy in DNP toxicity, its use is still recommended to bring down temperatures above 39-40 °C by Toxbase (the UK National Poisons Information Service) because of the high lethality of DNP.

Other options include Cyproheptadine, a first-generation antihistamine with additional anticholinergic properties and antagonist to serotonin, used in the treatment of serotonergic-driven hyperpyrexia (Serotonin Syndrome). To date, there are no case reports of cyproheptadine being used in DNP toxicity.

And don’t forget to monitor CK and renal function.

5. Consider your resuscitation fluid

You may have heard the phrase ‘(ab)normal saline’ before. Sure, one bolus with 0.9% saline is probably fine, but we should be reaching early for a balanced crystalloid like Hartmann’s or Plasmalyte, and probably from the outset.

Francesca has a pure metabolic acidosis and is trying to compensate by dropping her PaCO2. (Ab)normal saline is 0.9% NaCl – that’s one chloride ion for every sodium ion. Chloride binds with hydrogen to form HCl, hydrochloric acid. Giving Francesca more acid in the form of chloride will plunge her pH lower. This will cause her to hyperventilate to compensate further, which will tire her out faster.

And then Francesca becomes hyperkalaemic. Worsening Francesca’s acidosis by giving more saline will only serve to make the hyperkalaemia worse for a number of reasons, the simplest one being that acidosis drives intracellular potassium to the extracellular (intravascular) space. ‘Why is that?’ you might wonder. Remember, we use alkaline sodium bicarbonate to treat hyperkalaemia by driving potassium into the intracellular space. Giving acidic sodium chloride does the opposite: the hydrogen potassium pump exchanges extracellular hydrogen for intracellular potassium, pushing potassium out of the cell into the intravascular space. Giving acid, makes hyperkalaemia worse. Have a look at this Paediatric FOAM post, ‘Hartmanns in hyperkalaemia: Is that (O)K?’, for a more detailed account as to why we shouldn’t use saline in hyperkalaemic patients.

6. Have a strategy for your emergency treatment of hyperkalaemia

The treatment of life-threatening hyperkalaemia has three facets. All three are important but there is physiological and clinical  merit in doing these in order:

1) Membrane stabilisation

2) Shifting K+ into the cells

3) Reducing total body K+

The first two are the quick fix solutions for the ED. The last solution involves potassium diuresis and haemodialysis or haemofiltration and will traditionally be dealt with on the renal unit or PICU – we will expand on these in a separate blog.

IV Calcium Gluconate

Calcium is vital for stabilising the myocardium. Avoidance of a lethal arrhythmia is our primary concern in life threatening hyperkalemia and so giving calcium first is a priority.

Initial dose: Assuming we have peripheral access the dose is 0.1-0.3 ml/kg IV calcium gluconate 10%  over 10 minutes, diluted fivefold to 20mg/ml. Aim for an ionised calcium >1.15  and repeat if required, remembering that a one-off dose will usually last between 30 minutes to an hour. In the case of persistent arrhythmias or particularly resistant hypocalcaemic state further doses of calcium may be indicated or an infusion can be considered (0.2ml/kg/hr of calcium gluconate 10% diluted as above).

Bicarbonate

It is important to understand that bicarbonate will only work in hyperkalaemia if the patient is in an acidotic state. In this context not all bicarbonate solutions have been created equal.  8.4% bicarbonate is very hypertonic and a number of RCT’s suggest that, if given neat, it will not work in reducing serum potassium levels in hyperkalemic patients. This is thought to be due  to the phenomenon of solvent drag; the hypertonic fluid drags potassium ions to the extracellural compartment due to an osmotic shift. This essentially neutralises the effect a neutral or alkali pH has in the direction of movement of the K+ ions making the overall net shift minimal.

On the other hand, isotonic bicarbonate works in patients in an acidotic hyperkalemic state. Isotonic bicarbonate isn’t commercially available in most UK based hospitals but can be made by diluting each milliliter of 8.4% sodium bicarbonate with 4.6 ml of sterile water for injection or 5% dextrose.  A 1.5% solution of sodium bicarbonate is approximately isotonic. Isotonic bicarbonate can rapidly improve hyperkalemia if the patient is acidotic in three ways: a) by shifting potassium intro the intracellular compartment, b) by increasing potassium diuresis due to alkalosis and c) due to a dilutional effect.  1mmol/kg of isotonic bicarbonate can be given to alkalinise the pH and cause a K+ shift.

Insulin

Insulin shifts potassium into cells by stimulating the activity of the Na+– H+ channel on cell membranes. This in turn promotes the entry of sodium into cells, which leads to activation of the Na+– K+ ATPase, causing an influx of potassium. The decline in serum potassium levels by insulin is dose dependent. Due care must be taken to avoid hypoglycaemia, especially in infants and children with nephropathies.  The doses of IV insulin are as follows:

Neonates: 0.3 – 0.6 units/kg/hour

Children > 1 month: 0.05 – 0.2 units/kg/hour 

Run with glucose 0.5 – 1 g/kg/hour (5-10 ml/kg of glucose 10% via peripheral administration)

Salbutamol

Salbutamol causes a small shift of potassium into cells but a high dose is needed for an adequate effect, around 10-20mg on average. This equates to 4 to 8 back to back nebulised doses depending on the patient’s age. Salbutamol use comes with a caution however; it can both worsen a pre-existing acidosis by driving up lactate (essentially having a neutral effect  on potassium clearance) and will also cause a tachycardia, and in patients prone to arrhythmias, it can cause SVT’s or even VF. It should not be first line treatment, and certainly not before the membrane has been stabilised with calcium nor before the pH has been made less acidotic.

7. And DNP?

DNP toxicity is a well reported presentation to the ED, including a case report of a fatality in a teenage girl, using it as a weight-loss drug

Features usually occur within 4 hours, with agitation, flushing, hyperthermia and diaphoresis. As with Francesca, there may be abdominal pain, vomiting and diarrhoea. There may be yellow discolouration to the skin and urine, which can be confused with jaundice, and rash and desquamation can be a feature, (mis)leading you down the path of toxic shock. The deterioration can be very rapid with grossly elevated temperatures, heart rates and respiratory rates.

And the investigations? A metabolic acidosis secondary to raised lactate, methaemoglobinaemia, hyperkalaemia, hypocalcaemia and hyperglycaemia (at least until glycogen stores become depleted, when the blood sugar will drop).

Have a read of the letter to the editor in response to this case report, two case reports from the States, and a further report from London and decide for yourself whether you’ll be reaching for Dantrolene to treat DNP toxicity.

But, let’s finish on a cautionary tale. Dantrolene can be hepatotoxic so monitor liver function closely. This case report describes a child who developed hepatitis after dantrolene at a pretty low dose.

We would LOVE your feedback about these DFTB PEM adventures so if you can spare a minute, please complete our survey at www.tiny.cc/DFTBpemadventure or use your smartphone to let the QR code take you straight there. We timed ourselves completing it and it takes less than a minute. Thank you.

A HUGE thank you to Dr Laura Hunter, EM and Toxicology consultant at Guy’s and St Thomas’ NHS Foundation Trust in London, UK. As well as a wicked sense of humour, Laura has an encyclopedic knowledge of all things toxicological. Thank you Laura.

And we are absolutely delighted to announce that our friend, Costas Kanaris, has joined the PEM adventures team, bringing with him his wisdom of all things critical care and general brilliance.

References

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Blumberg A, Weidmann P, Ferrari P. Effect of prolonged bicarbonate administration on plasma potassium in terminal renal failure. Kidney Int. 1992;41(2):369-374.

Kim H. Acute therapy for hyperkalemia with the combined regimen of bicarbonate and beta(2)-adrenergic agonist (salbutamol) in chronic renal failure patients. J Korean Med Sci. 1997;12(2):111-116.

Kim H. Combined effect of bicarbonate and insulin with glucose in acute therapy of hyperkalemia in end-stage renal disease patients. Nephron. 1996;72(3):476-482.

Conte G, Dal C, Imperatore P, et al. Acute increase in plasma osmolality as a cause of hyperkalemia in patients with renal failure. Kidney Int. 1990;38(2):301-307.]

Fraley D, Adler S. Correction of hyperkalemia by bicarbonate despite constant blood pH. Kidney Int. 1977;12(5):354-360.

end-stage renal disease. Miner Electrolyte Metab. 1991;17(5):297-302.

Gutierrez R, Schlessinger F, Oster J, Rietberg B, Perez G. Effect of hypertonic versus isotonic sodium bicarbonate on plasma potassium concentration in patients with

DeFronzo RA, Felig P, Ferrannini E, et al. Effect of graded doses of insulin on splanchnic and peripheral potassium metabolism in man. Am J Physiol. 1980;238(5):E421–E427

Grundlingh J, Dargan PI, El-Zanfaly M, Wood DM. 2,4-dinitrophenol (DNP): a weight loss agent with significant acute toxicity and risk of death. J Med Toxicol. 2011;7(3):205-212. doi:10.1007/s13181-011-0162-6

Allen L. Hsiao, Karen A. Santucci, Patricia Seo-Mayer, M. Rajan Mariappan, Michael E. Hodsdon, Kenneth J. Banasiak & Carl R. Baum (2005) Pediatric Fatality Following Ingestion of Dinitrophenol: Postmortem Identification of a “Dietary Supplement”, Clinical Toxicology, 43:4, 281-285, DOI: 10.1081/CLT-58946

Kim Barker, Donna Seger & Suparna Kumar (2006) Letter To The Editor: “Comment on “Pediatric Fatality Following Ingestion of Dinitrophenol: Postmortem Identification of a ‘Dietary Supplement’””, Clinical Toxicology, 44:3, 351, DOI: 10.1080/15563650600584709

Siegmueller C, Narasimhaiah R. Fatal 2,4-dinitrophenol poisoning… coming to a hospital near you. Emergency Medicine Journal 2010;27:639-640.

Kopec KT, Kim T, Mowry J, Aks S, Kao L. Role of dantrolene in dinitrophenol (DNP) overdose: A continuing question? Am J Emerg Med. 2019 Jun;37(6):1216.e1-1216.e2. doi: 10.1016/j.ajem.2019.03.035. Epub 2019 Mar 23. PMID: 30948257.

Divij Pasrija, Shilpi Gupta, Amanda Hassinger. Dantrolene-Induced Hepatitis: A Rare Culprit in the PICU. J Pediatr Intensive Care 2020. DOI: 10.1055/s-0040-1710496

Van Schoor J, Khanderia E, Thorniley A. Dantrolene is not the answer to 2,4-dinitrophenol poisoning: more heated debate. BMJ Case Rep. 2018 Dec 19;11(1):e225323. doi: 10.1136/bcr-2018-225323. PMID: 30573533; PMCID: PMC6303589.