Back to School

Cite this article as:
Andrew Tagg. Back to School, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.23086

It’s the first day of school here in Australia and parents and carers are waving their young children off with a kiss for their first day.  When I first saw the size of school bags I was amazed. How can children carry so much? Surely they will just fall over and lie on their backs waving their little legs in the air like distressed turtles? What on earth are they carrying in there that needs the Bag of Holding?*

 

 

What’s the problem?

Barbosa J, Marques MC, Izquierdo M, Neiva HP, Barbosa TM, Ramírez-Vélez R, Alonso-Martínez AM, García-Hermoso A, Aguado-Jimenez R, Marinho DA. Schoolbag weight carriage in Portuguese children and adolescents: a cross-sectional study comparing possible influencing factors. BMC pediatrics. 2019 Dec;19(1):157.

With reduced access to lockers, it seems that children are taking the weight of the world on their shoulders. Surprisingly, this Portuguese group found that Grade 5 children carried more than Grade 9 kids. This trend has been replicated in New Zealand with Grade 3 kids carrying around 7kg (13.2% of their body weight) and Grade 6 leavers bearing only 6.3Kg (10.3% body weight). Most school items have a set weight, no matter what grade you are in, but one might have thought that as the educational load increases over the years so might the weight of the textbooks. Perhaps an increase in the use of personal electronic devices and e-books accounts for some of this difference.

Surely carrying those giant bags can’t be good for the growing body? Neck, back, and shoulder pain are prevalent in adolescents and are closely linked by carrying heavy school bags. These effects take place when the bag weighs more than 10% of their body weight. In nearly every study girls carry more than boys. This makes sense as although they may carry exactly the same things in their rucksacks girls are generally lighter and so the weight of their bag, as a percentage of their total body weight, is higher.

 

Mandrekar S, Chavhan D, Shyam AK, Sancheti PK. Effects of carrying school bags on cervical and shoulder posture in static and dynamic conditions in adolescent students. International journal of adolescent medicine and health. 2019 Oct 30.

This group looked at how they carry their bags. Trying to be cool and swinging your bag over just one shoulder changes one’s static biomechanics.  The head and neck move forward to compensate and the carrying shoulder rises. Then, because the centre of gravity is shifted the subject would tilt their torso away. Could this be the cause of the stereotypical teenage posture? It took just five minutes of bag wearing for any postural changes to become evident. It has also been suggested that a heavier bag weight is associated with an increased incidence of lower back pain in teens and this, in turn, is linked with an increased risk of lower back pain as an adult.

If they are not wearing their back slung over one shoulder they are wearing it slung low, rather than high and tight on their shoulders, and most of the biomechanic data suggests this puts a lower degree of stress on their lumbar spines than letting it ride high. The higher position also lends itself to more forward rotation of the pelvis and greater hip flexion. And, of course, wearing your bag on the front, instead of on the back, causes a whole new range of issues.

Harmless?

Whilst this post is focusing on just one potential downside of heavy school bags, Wierseema et al. found 247 children with injuries related to backpack use between 1999-2000. These were due to tripping over them (28%), getting hit by one (13%) or just trying to put them on (8%). Actually wearing the thing was associated with another 13% of complaints – specifically back pain.

There is also a condition called backpack palsy or, to be more accurate, backpack brachial plexus palsy. It is much more common in military recruits but can occur in children. Often unilateral, the paraesthesia, pain and sensory loss in addition to possible muscle wasting are due to neuropraxia of the brachial plexus.

Losing weight?

Does it make a difference if teenagers take some of the rubbish out of their bags?

Rodríguez-Oviedo P, Santiago-Pérez MI, Pérez-Ríos M, Gómez-Fernández D, Fernández-Alonso A, Carreira-Núñez I, García-Pacios P, Ruano-Ravina A. Backpack weight and back pain reduction: effect of an intervention in adolescents. Pediatric research. 2018 Jul;84(1):34.

This Spanish group targetted teenagers with an educational intervention. This comprised of a one-hour session on posture, the effects of backpack weight and some healthy lifestyle advice. They found that the intervention arm of the trial did indeed have (statistically significant) lighter bags moving forward in the younger cohorts but not in the older ones.

Strapping in?

Mathur H, Desai A, Khan SA. To determine the efficacy of addition of horizontal waist strap to the traditional double shoulder strap school backpack loading on cervical and shoulder posture in Indian school-going children. Int J Phys Med Rehabil. 2017;5(434):2.

If you want to reduce the usual bag-induced postural slump these authors, looking at 60 children, suggest that adding a waist strap to the usual two shoulder straps could make all the difference.

So what does this all mean?

As parents, we need to keep an eye on what our children are actually putting in their bags (compared to what they say they are putting in there). Perhaps we should weigh the bags as often as the children and limit the number of keyrings and Beanie Boos attached to the outside? Perhaps we need to further embrace technology and allow for the increased use of electronic devices coupled with a much, much older technology and let them use bags on wheels, similar to carry on luggage?

There have been a number of initiatives to make the wearing of school backpacks healthier. Sri Lanka introduced a National Healthy Schoolbag Campaign aimed at improving the lives of children. Large textbooks were split into smaller volumes to make it easier to carry just one small book around and a multidisciplinary schoolbag regulatory council was set up to liaise with industry partners to help regulate bags. In the US the “Pack it light, wear it right” initiative focussed on what the individual could do.

 

*If you really want to know what is in their bags you need to look inside. This wonderful paper from Archives suggests that the vast majority (96%) of parents had never checked the weight of their children’s bags and 34% had never even looked inside

Forjuoh SN, Little D, Schuchmann JA, Lane BL. Parental knowledge of school backpack weight and contents. Archives of disease in childhood. 2003 Jan 1;88(1):18-9.

 

Other Selected References:

American Academy of Pediatrics. How not to wear a school backpack. AAP Grand Rounds. 2008 Nov 1;20(5):58-9.

Brackley HM, Stevenson JM. Are children’s backpack weight limits enough?: A critical review of the relevant literature. Spine. 2004 Oct 1;29(19):2184-90.

Kim KE, Kim EJ. Incidence and risk factors for backpack palsy in young Korean soldiers. Journal of the Royal Army Medical Corps. 2016 Feb 1;162(1):35-8.

Goodgold S, Corcoran M, Gamache D, Gillis J, Guerin J, Coyle JQ. Backpack use in children. Pediatric physical therapy: the official publication of the Section on Pediatrics of the American Physical Therapy Association. 2002;14(3):122-31.

Jayaratne K, Jacobs K, Fernando D. Global healthy backpack initiatives. Work. 2012 Jan 1;41(Supplement 1):5553-7.

Maurya S, Singh M, Bhandari PS, Bhatti TS. Backpack brachial plexus palsy. Indian Journal of Neurotrauma. 2009 Dec;6(02):153-4.

Rose K, Davies A, Pitt M, Ratnasinghe D, D’Argenzio L. Backpack palsy: A rare complication of backpack use in children and young adults–A new case report. european journal of paediatric neurology. 2016 Sep 1;20(5):750-3.

Talbott NR, Bhattacharya A, Davis KG, Shukla R, Levin L. School backpacks: it’s more than just a weight problem. Work. 2009 Jan 1;34(4):481-94.

Weir E. Avoiding the back-to-school backache. CMAJ: Canadian Medical Association journal= journal de l’Association medicale canadienne. 2002 Sep;167(6):669-.

Wiersema BM, Wall EJ, Foad SL. Acute backpack injuries in children. Pediatrics. 2003 Jan 1;111(1):163-6.

Diabetic Ketoacidosis

Cite this article as:
Dani Hall. Diabetic Ketoacidosis, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22689

Maisie is 2 years old. Apart from a few coughs and colds, she is usually a very well, happy little girl. She’s been a bit poorly for the last 48 hours – a bit off colour, off her food, lethargic and just not her usual cheeky self.

She’s been drinking though and has had good wet nappies. In triage she has a runny nose and slight cough. She is pretty tachycardic and tachypnoeic and doesn’t look well and so she’s moved to majors.

Maisie is put on a monitor and immediately you can see that her respiratory rate is elevated at 40 breaths per minute with saturations of 97% in air. Her heart rate is also elevated at 150 beats per minute with a normal blood pressure of 105/65. Her capillary refill time is 3 seconds peripherally and she is afebrile.

Her heart sounds are normal, her chest is clear and her abdomen is soft although mildly tender throughout.

The only objective thing you have is the tachypnoea with a bit of a runny nose. You wonder if she has viral induced wheeze and is just too tight for the wheeze to be audible so you prescribe salbutamol and review after 10 minutes. But that’s made no difference to her respiratory rate, and her chest is still completely clear.

Things just don’t add up. She’s holding her tummy – perhaps her tachypnoea and tachycardia are secondary to pain. Her abdomen remains soft with no guarding, but she doesn’t like you palpating it. Could this be appendicitis? Or even worse an intussusception? You speak to the paediatric surgeon who asks you to cannulate Maisie and send some blood. They’ll be down to review her shortly.

You cannulate Maisie and take a venous gas. The results seem to take an age. And your heart sinks when you see them…

She’s acidotic at 7.15 and it looks metabolic with a bicarbonate of 13.9 and base deficit of minus 8.7. Her lactate is 2.9 and her glucose is very high at 29.5. You run a drop of Maisie’s blood through the bedside ketone monitor. Her blood beta-hydroxybutyrate is. 5.1.

This is diabetic ketoacidosis.

 

DKA can be really difficult to diagnose in toddlers

Classically children with DKA present with polyuria and polydipsia with abdominal pain, nausea, and vomiting. This can progress to dehydration, weakness, and in severe cases, they may be lethargic. Blood tests show a raised white cell count as a physiological response to the raised stress hormones, cortisol and catecholamines, and so are not a reliable indicator of infection. But, and this is a big but, an infection can precipitate DKA so it is important it is considered.

Although ketoacidosis may result in a classic ‘pear drop/acetone’ smell to the breath, not everyone has the chemoreceptors to detect it.

Common misdiagnoses include dehydration secondary to infection or respiratory presentations. Ketoacids stimulate the respiratory centre resulting in rapid fast breathing – Kussmaul breathing – blowing off carbon dioxide to compensate for the metabolic acidosis. It may also present as an acute abdomen as abdominal pain and ileus can result from hypokalaemia, acidosis, and poor gut perfusion. If opioids are given for pain this can suppress the Kussmaul breathing leading to worsening acidosis

The BSPED (2020), and ISPAD definitions of DKA are:

acidotic with a bicarbonate of <15 mmol/l or a pH <7.3 and ketones of >3.0 mmol per litre

However… just when you starting thinking it was easy… children with known diabetes may develop DKA with normal glucose and so you must keep a high index of suspicion and check pH and ketones in an unwell child with diabetes.

Lack of insulin leads to rising blood glucose levels in the bloodstream. However, this glucose is not transported into the cells and so the body needs to produce an alternative energy source for cellular activity. Three processes occur:

  • muscle is broken down to mobilise amino acids which are then used to create glucose (catabolism)
  • fat is broken down to produce glycol and ketones (lipolysis)
  • the liver uses lactate, glycol and amino acids to create more glucose (gluconeogenesis)

High ketone levels lead to metabolic acidosis.

Hyperglycaemia leads to glucose spilling into the urine (glycosuria). These glucose molecules exert an osmotic pull, dragging water, cations, and anions such as phosphate, potassium, and sodium into the urine (osmotic diuresis). The child becomes dehydrated with physiologically low levels of potassium and phosphate. Ketones also spill into the urine (ketonuria) in preference to chloride, which is retained in the plasma, leading to a worsening chloride-driven acidosis.

Maisie is dehydrated because of the osmotic diuresis exerted by the glucose in her urine. And she’s acidotic because of the ketones circulating in her bloodstream. The question is, what are we going to do about this?

The complications of DKA have incredibly high mortality and morbidity, so we’re going to start here.

Cerebral oedema

Cerebral oedema occurs in approximately 1% of children with DKA. While relatively rare, it can have devastating consequences with mortality of approximately 25%. In fact, more than half of all diabetes-related deaths in children are caused by cerebral injury.

Cerebral oedema usually occurs within the first four to 12 hours of starting treatment for DKA, suggesting that it’s the treatment itself that precipitates cerebral oedema.

Risk factors for cerebral oedema in DKA can be split into two groups.

The first group is characterised by children who have a longer duration of symptoms and are therefore more severely dehydrated at presentation. Younger children, particularly toddlers, and children who present in DKA without a previous diagnosis of diabetes mellitus, fall into this group, most likely because they have been in DKA for a long period of time before the diagnosis is made.

The second group is children who develop cerebral oedema because of the treatment they have received. Giving insulin within the first hour of treatment increases the risk of cerebral oedema – the theory is that the usually inactive sodium-hydrogen ion exchange pump is activated by the double hit of high intracellular hydrogen ions early in treatment while children are more acidotic plus insulin crossing the leaky blood-brain-barrier. The exchange pump transports sodium into the intracellular fluid, which then drags water with it due to its osmotic effect, leading to cerebral oedema.

Giving bicarbonate also increases the risk of cerebral oedema. The physiological mechanism of this is unclear but there is some thought that giving bicarbonate to correct acidosis can worsen tissue hypoxia due to effects on 2,3-DPG in erythrocytes (remember acidosis shifts the oxygen dissociation curve to the right, increasing the affinity of haemoglobin and oxygen) or that giving bicarbonate may lead to preferential movement of carbon dioxide across the blood-brain barrier, both of which will promote acidosis and poor oxygen offload in the CSF. However, whatever the cause, it is clear from a systematic review published in 2011 by Chua et al that giving bicarbonate to children with DKA is linked with increased rates of cerebral oedema. The guidance, therefore, mandates that bicarbonate should not be used routinely to correct acidosis. Fluids and insulin will do that by improving skin perfusion and reducing ketosis. Only give bicarbonate if the acidosis is resulting in reduced cardiac function, and then give very carefully…

So, with that in mind, how are we going to treat Maisie?

ABC resuscitation

The initial management of a child with DKA follows the principles laid out in APLS: ABC resuscitation.

If a child is obtunded and not protecting their own airway then they should be intubated because of the risk of airway obstruction. However, intubation in DKA is risky… both sedation and the resultant hypercarbia can cause cerebral herniation. Central lines are also risky in these children because of the increased risk of thrombosis. Only use them if absolutely necessary and remove them as soon as possible.

Luckily, Maisie is maintaining her own airway, her GCS is 15 and she is not obtunded. The airway is not a problem for her.

After managing the airway and breathing we move onto circulation. So the question is: should we give Maisie a fluid bolus?

This is a big question.  We are taught that children with cardiovascular compromise should receive fluid boluses to support their circulation.  But assessing cardiovascular compromise in children with DKA can be very challenging. Clinical evaluation of hydration and shock is very difficult in children with DKA. Acidosis drives tachycardia and reduces peripheral skin perfusion.

Koves et al set out to look at this by studying a group of 37 children under 18 presenting with DKA.

Emergency Department doctors recorded heart rate, respiratory rate, blood pressure, cool peripheries, capillary refill time, skin turgor, the presence or absence of sunken eyes and dry mucous membranes to provide a clinical estimate of dehydration. A second emergency department doctor, blinded to the clinical interpretations of the primary doctor, was asked to review the patient before treatment and record their assessment of the same clinical variables. There was a good clinical correlation between the two assessments. Following admission, the children’s weights were measured daily until discharge and percentage dehydration was calculated from the weight gain from admission to discharge.

There was no agreement between assessed and measured dehydration. There was a tendency to overestimate dehydration in children with <6% measured dehydration and underestimate in children >6% dehydrated.

It’s a tricky business and these same parameters clearly won’t be of use in estimating shock in these children.

A true assessment of shock in DKA should rely on assessment on blood pressure measurements and peripheral pulse volume. So that doesn’t really help us. Maisie’s blood pressure and pulse volumes are normal so she’s not shocked. But she clearly is dehydrated. 

BSPED (2020) uses pH and bicarbonate to classify the severity of DKA:

  • pH 7.2–7.29 or bicarbonate <15 mmol/l is mild DKA with 5% dehydration
  • pH 7.1–7.19 or bicarbonate <10 mmol/l is moderate DKA with 7% dehydration
  • pH < 7.1 or bicarbonate <5 mmol/l is severe DKA with 10% dehydration

So, are we going to give her a fluid bolus?  Let’s turn to the guidelines…

BSPED 2020 states:

Any child in DKA presenting with shock (as per the APLS definition of tachycardia and prolonged capillary refill time) should receive a 20 ml/kg bolus of 0.9% saline over 15 minutes. Let’s call this a ‘resuscitation bolus’.

Further 10 ml/kg boluses may be given if required up to a total of 40 ml/kg. Then add inotropes if the child remains shocked.

Boluses given to treat shock should NOT be subtracted from the calculated fluid deficit.

All children with DKA, whether mild, moderate or severe, who require IV fluids should receive an initial 10 ml/kg bolus over 60 minutes. Let’s call this a ‘rehydration bolus’. This bolus SHOULD be subtracted from the calculated fluid deficit.

The American Academy of Pediatrics, agrees that all children with DKA should have a bolus of 10ml/kg over 30 minutes to an hour. If a child is critically unwell with hypovolaemic shock, then additional boluses of 20ml/kg of 0.9% saline should be given.

Australian guidelines vary depending on region – from no routine fluid boluses to 10-20 ml/kg 0.9% saline for the sickest. Some say subtract fluid boluses from rehydration calculations, others don’t. There is no clear consensus.

So why is there so much international variation?

Traditionally, we have been warned about the danger of causing cerebral oedema in children with DKA by giving them too much fluid, reducing serum osmolality and literally flooding the brain. This is based, on the most part, by an old paper that showed an association between large volume fluid resuscitation in DKA and cerebral oedema. Note the word association, not causation.

Fluid management in DKA

Dogma has been to restrict fluids in paediatric DKA. It is widely thought that the rapid administration of intravenous fluids reduces serum osmolality, resulting in cerebral oedema. Guidelines traditionally have, therefore, advised slow fluid replacement using isotonic fluids as using hypotonic fluids was thought to cause further drops in osmolality. 

And the evidence seemed to support this.  Retrospective reviews showed better outcomes in children with DKA who received less fluid.

But…

  • only an association had been demonstrated, not causality.
  • and it is reasonable to suspect a confounder in that those with more severe DKA could be expected to be both at higher risk of cerebral oedema and more likely to receive large volumes of fluid resuscitation based on their clinical presentation.

And then along came this paper by Kupperman et al published in the New England Journal of Medicine in 2018, which has shifted thinking a bit, as well as causing some controversy…

Lead authors Nate Kupperman and Nicole Glaser suggested the causal effect of fluid resuscitation and cerebral oedema was a myth in Glaser’s 2001 retrospective case-control study that gave us the list of risk factors for cerebral oedema in DKA.

Kupperman’s team wanted to look specifically at the relationship between fluids and cerebral oedema (defined in the study as a drop in GCS, or longer-term evidence of neurological injury defined as a drop in IQ or short-term memory difficulties 2-6 months later) in DKA in children. They looked at 1255 children with DKA presenting to 13 hospitals in the States over a 9 year period, which, because 101 children presented twice, equated to 1389 episodes of DKA. Children were excluded if their GCS was less than 12, or if they had already received significant DKA management prior to assessment. 289 were withdrawn by the treating physician. The mean age was 11. It’s important to think about all of this as these exclusion criteria mean that the very sick and the very young, two groups who are at significantly increased risk of cerebral oedema, were probably lost in this cohort.

Children were randomized into 4 groups. All patients in both groups received IV insulin at 0.1u/kg/hr. Dextrose was added to the saline solution when blood glucose dropped to 11.1 to 16.7 mmol/l.

Children were randomized into 4 groups:

  • FAST rehydration with 0.45% sodium chloride
  • FAST rehydration with 0.9% sodium chloride
  • SLOW rehydration with 0.45% sodium chloride
  • SLOW rehydration with 0.9% sodium chloride

In short, Kupperman’s team found no difference between the groups. There was no significant difference in GCS, or longer-term evidence of neurological injury. The endpoint that many of us are most concerned about, clinically apparent brain injury (deterioration in neurological status requiring hyperosmolar therapy or endotracheal intubation or resulting in death) was a secondary outcome, presumably due to its rarity and hence difficulty in showing statistically significant differences between groups. But again, there was no significant difference between groups.

There was a 0.9% rate of brain injury overall and it didn’t matter which type of fluids or how fast. Patients were more likely to get hyperchloraemic acidosis in the 0.9% NaCl group but this is of debatable clinical significance.

The evidence does not seem to support our traditionally cautious approach to DKA. The speed of IV fluids does not seem to be the cause of brain injury in DKA. But… and this is a big but… don’t forget the youngest and sickest patients weren’t included. All we can probably really conclude is that children who are not in the at-risk group for cerebral oedema are probably more resilient to higher volumes of fluids delivered at faster rates.

Ok… back to Maisie. How are we going to manage her fluids

Well, again it depends where in the world Maisie presents. 

BSPED 2020 advises to calculate maintenance fluids the same way as they’re normally calculated for children in the UK:

  • 100 ml/kg/day for the first 10kg
  • plus 50ml/kg/day for each kg between 10 and 20kg
  • plus 20ml/kg/day for each kg above 20kg

(A maximum weight of 80kg should be used for fluid calculations)

The International Society for Pediatric and Adolescent Diabetes guidance is as follows:

ISPAD says

  • Shock is rare in DKA but if present should be treated with 20ml/kg fluid boluses, repeated as necessary to achieve tissue perfusion.
  • Give all children a 10ml/kg bolus over an hour to rehydrate them.
  • Calculate maintenance fluids in the normal way using the simplified Holliday-Segar formula.
  • Replace rehydration fluids over 24-48 hours, using clinical signs of dehydration to estimate the degree of dehydration. 2 or 3 signs would constitute to 5% dehydration, more signs would equate to 7% dehydration and weak pulses, hypotension or oliguria would indicate the child is 10% dehydrated.

Managing electrolytes

Once you’ve navigated the quagmire of fluid management in DKA, you need to think about adding electrolytes. Remember, glucose molecules in the urine exert an osmotic pull, dragging water, cations, and anions such as phosphate, potassium, and sodium into the urine: the child becomes dehydrated with physiologically low levels of the electrolytes potassium and phosphate.

Always assume whole body potassium depletion in DKA. This is compounded by the treatment you give which causes potassium to move intracellularly. Replace potassium as soon as the patient has urine outpatient and labs confirm the child is not hyperkalaemic.

An ECG will give you clues about clinically significant hypokalaemia:

  • Prominent U waves (an extra positive deflection at the end of the T wave)
  • Flat or biphasic T waves
  • ST-segment depression
  • Prolonged PR interval

Although phosphate is lost in the urine as part of the osmotic diuresis in DKA, prospective studies involving relatively small numbers of subjects and with limited statistical power have not shown clinical benefit from phosphate replacement. Administrating phosphate can be dangerous, by causing calcium levels to drop. However, symptomatic severe hypophosphataemia, when serum phosphate levels drop below 1 mg/dL with an ensuing metabolic encephalopathy or depressed cardiorespiratory function, can be dangerous, albeit very rare. A sensible approach is to monitor phosphate levels alongside regular potassium level checks and, if a child is hypophosphataemic and symptomatic, replace phosphate whilst carefully monitoring serum calcium levels.

Back to Maisie. We’ve managed her fluids according to our local guidelines. But how can we tell if we’ve got the balance right?

We can’t monitor urine output as Maisie is going to be polyuric anyway because of the osmotic effect of glycosuria. Her capillary refill time will be prolonged because she’s acidotic and therefore skin perfusion will be reduced.

And her serum sodium and osmolality won’t be reliable indicators of fluid balance because of the effect of plasma glucose on her electrolytes. On top of this, her kidneys will preferentially excrete chloride from any saline and potassium chloride over ketones so there’s limited value to monitoring the anion gap because it doesn’t differentiate between hyperchloraemia or ketones. Instead, we should measure Maisie’s corrected sodium.

Because of its osmotic effect, glucose drags water with it into the intravascular compartment diluting the other osmols – 1mmol rise in glucose will drop sodium and chloride by 1mmol/L.  If Maisie’s glucose goes up by 1 the other osmols will go down by 1.  If glucose goes down by 1 the other osmols will go up by 1.

The corrected sodium must rise with therapy at a rate of 0.5-1 mmol/h

  • Falling corrected sodium means too much water gain: we’ve been overzealous the fluids.
  • A rapidly rising corrected sodium means too much water loss: we’ve been too fluid restrictive.

The Evelina London South Thames Retrieval Service has a great corrected sodium calculator on their website. You plug in her numbers – her initial sodium was 148 with glucose of 29.5, giving her a corrected sodium of 157.6. A couple of hours have passed and her latest gas shows that her glucose has come down to 24.5 – great – and her sodium has improved slightly to 144. You press calculate…

… and your heart sinks as you see her second corrected sodium has fallen by 6 points to 151.6 as you know that the corrected sodium must rise with treatment.

You go back to Maisie’s bedside to review her.

Maisie has dropped her GCS to 12 (E3, V4, M5).  This is incredibly worrying – her GCS was 15 when you last checked on her.  You move her round to resus and ask your nurse to grab some hypertonic saline.

Clinical features of cerebral oedema

  • Headache
  • Slowing heart rate
  • Rising blood pressure
  • Focal neurology such as cranial nerve palsies
  • Falling oxygen saturations
  • Change in neurological status including restlessness, irritability, drowsiness, confusion, incontinence

Treat cerebral oedema with either hypertonic saline or mannitol.

Calculate your dose of hypertonic saline or mannitol before you need it and know where it’s kept. If a child has an acute deterioration, treat it.

Mannitol is an osmotic diuretic and can be given at 0.5 – 1 g/kg over 10-15 minutes. The effects should be apparent after 15 minutes. Mannitol lasts about 2 hours and can be repeated at this point if needed.

Hypertonic saline is a good alternative to mannitol or can be used after mannitol if a second agent is needed.

Don’t forget other neuroprotective measures like elevating the head of the bed to 30 degrees and intubation if concern regarding airway protection.

If there’s no improvement in GCS, do a CT, but not until the child is stable. CT is used to identify any potential lesion that would warrant neurosurgery – intracranial haemorrhage, or a lesion that would warrant anticoagulation such as thrombosis.

Hypertonic saline or mannitol?

DeCourcey et al (2013) conducted a retrospective cohort study over a 10 year period to see whether the increase in the use of hypertonic saline had had any effect on mortality in DKA. They looked at over 43,000 children under the age of 19 with DKA presenting to 41 children’s hospitals in America and found that the use of hypertonic saline replaced mannitol as the most commonly used agent in many of the participating hospitals. Controversially, their data suggested that hypertonic saline may not have benefits over mannitol and may be associated with a higher mortality rate.

However, this does remain controversial, with a counter-argument published as a letter to the editor a few months later arguing that (1) the fact that mortality from cerebral oedema in DKA had decreased by 83% over the same time period that use of hypertonic saline had increased, along with (2) the fact that DeCourcey’s paper only found a statistically significant difference in mortality between hypertonic saline and mannitol once age and race were removed from analyses (two factors that, themselves, have a significant influence on mortality in DKA-related cerebral oedema), meant that we shouldn’t be rushing to conclude that hypertonic saline is less safe than mannitol in the treatment of cerebral oedema.

No guidelines are yet to recommend mannitol over hypertonic saline. This seems to be one of those situations where a prospective study is needed to really answer the question of whether mannitol is superior, or at least non-inferior to hypertonic saline.

Back to Maisie. You give Maisie 3ml / kg 3% saline over 15 minutes and are relieved to see her wake up.  You decrease her fluid prescription and thankfully from that point on her corrected sodium starts to slowly rise.

Insulin

Finally, you’re ready to give Maisie some insulin. Insulin will control Maisie’s glucose and switch off ketosis, therefore improving her acidosis.  Some departments use 0.1 units/kg/hr and some use 0.05 units/kg/hr.  The question is, what is the optimal dose? 

Nasllasamy’s team set out to compare the efficacy and safety of low-dose and standard-dose insulin infusions. They randomized 50 children under the age of 13 with DKA presenting over a 12 month period to receive insulin infused at either 0.05 units/kg/hr or 0.1 units/kg/h. They found that the rate of decrease in blood glucose and time to resolution of acidosis were similar in each group. There was no statistical difference in complication rates of hypokalaemia, hypoglycaemia or cerebral oedema.

This study suggests that low dose insulin is non-inferior to standard-dose insulin in managing children with DKA.  It’s important to note that this was a non-inferiority trial and a larger study, powered to show superiority would be helpful. However, many units have been using lower doses of insulin at 0.05 units/kg/hr safely for some time and this study supports the use of lower dose insulin.

BSPED 2020 states:

Insulin can be given at 0.05units/kg/hr or 0.1 units/kg/hr, although ‘0.05 units/kg/hr would probably be sufficient in most cases except perhaps severe DKA’.

Children under 5 years should be given 0.05 units/kg/hr.

And so, as Maisie is young and therefore in the higher risk group of children with DKA, you opt to start her on insulin at 0.05 units/kg/hr.

In children who are already on long-acting insulin, BSPED 2020 states that it should be continued, or if they are newly diagnosed, they advise to consider starting long-acting subcutaneous insulin alongside intravenous insulin.<

 

Manage high-risk children in PICU

  • pH <7.1
  • young (under 2s or under 5s depending which guideline you read)
  • cardiovascular shock
  • corrected sodium >150 or <130
  • hyper or hypokalaemia
  • altered conscious state
  • glucose >50

Maisie has multiple risk factors: she’s young and she developed clinically apparent cerebral oedema.  You admit her to PICU where she makes stable progress and is discharged home 4 days later on a subcutaneous insulin regime.

Selected references

Take a read of Chris Gray’s take for St Emlyns here

Lawrence SE, Cummings EA, Gaboury I, Daneman D. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr 2005; 146:688

Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med 2001; 344:264

Edge JA, Jakes RW, Roy Y, et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006; 49:2002

Marcin JP, Glaser N, Barnett P, et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. J Pediatr 2002; 141:793

Scibilia J, Finegold D, Dorman J, et al. Why do children with diabetes die? Acta Endocrinol Suppl (Copenh) 1986; 279:326

Edge JA, Hawkins MM, Winter DL, Dunger DB. The risk and outcome of cerebral oedema developing during diabetic ketoacidosis. Arch Dis Child 2001; 85:16

Chua HR, Schneider A and Bellomo R. Bicarbonate in diabetic ketoacidosis – a systematic review. Ann Intensive Care. 2011; 1:23

Koves IH et al. The Accuracy of Clinical Assessment of Dehydration During Diabetic Ketoacidosis in Childhood. Diabetes Care 2004:27(10);2485-2487

Kuppermann N et al. Clinical Trial of Fluid Infusion Rates  for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018;378:2275-87

DeCourcey et al. Increasing use of hypertonic saline over mannitol in the treatment of symptomatic cerebral edema in pediatric diabetic ketoacidosis: an 11-year retrospective analysis of mortality. Pediatr Crit Care Med. 2013; 14(7):694-700

Tasker RC, Burns J. Hypertonic saline therapy for cerebral edema in diabetic ketoacidosis: no change yet, please. Pediatr Crit Care Med. 2014;15(3):284-285

Nallasamy K et al. Low-Dose vs Standard-Dose Insulin in Pediatric Diabetic Ketoacidosis. A Randomized Clinical Trial. JAMA Pediatr. 2014; 168(11): 999 – 1005

ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidodis and the hyperglycaemic hyperosmlar state. Pediatric Diabetes 2018; 19 (Suppl. 27): 155–177

Hot Garbage: Mythbusting fever in children

Cite this article as:
Alasdair Munro. Hot Garbage: Mythbusting fever in children, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22916

Juniper is a 3yr old girl brought in with her mother, with a 48hr history of fever. Her mum is particularly concerned because her fever was up to 39.8°C, didn’t come down with paracetamol and she describes an episode which sounds like a rigor. On examination, she has a temperature of 39.3°C, a runny nose and bright red tonsils, and looks otherwise well. You go to discharge her, but your colleague asks if you should wait to see if her temperature comes down with ibuprofen before sending her home?

 

Introduction

Febrile illnesses are the most common cause of presentation to acute paediatric medical services. This means that fever is the most common presenting symptom seen by paediatricians, and it is clearly a huge cause of concern for parents. Despite this fact, it is clear that in day-to-day practice that there is a widespread misunderstanding about fever, its purpose, and its clinical interpretation.

Well, no longer! Once you have finished reading, you will be a master of all things related to fevers in children. We will start with some basic understanding of the processes surrounding fever, and finish off with some mega myth-busting!

What is fever?

Fever is an elevated core body temperature, as part of a physiological response to infection regulated by the hypothalamus. This is crucial to understand – your body is in control of your temperature. This is not something an infection is doing to your body; it is something your body is doing to the infection. This is different from pathological hyperthermia, where your temperature is elevated by either hypothalamic dysfunction or external heat. These are extremely rare.

Note: there are other, non-infectious causes of fever, such as cancer, Kawasakis, and autoinflammatory conditions, but these are rare in comparison to infectious fever and are covered elsewhere.

 

What temperature counts as a fever?

At what threshold do we say a child has an elevated body temperature? This is more controversial than one might think, as actually the data from which we derive “normal” body temperature is extremely poor. The most common cut off for defining a fever is 38°C – but it is important to remember that there is nothing magic about 38°C compared to 37.9°C, and temperature is better taken in context or a trend, if possible.

How do we get fevers?

The process of developing fever is extremely complex, and our understanding is still developing. At present, our best explanation is that the process is triggered by the presence of chemicals referred to as pyrogens. Pyrogens can either be exogenous (such as parts of the microbe itself, like the lipopolysaccharide on the outside of bacteria), or endogenous, such as cytokines like IL1, TNF, Prostaglandin E2 and importantly IL6, which are released by immune cells when they detect an invader. These pyrogens act to increase body temperature peripherally, but importantly also trigger receptors in the preoptic nucleus in the brain. This releases PGE2 into the hypothalamus, which then sets a new target temperature. This target is met by many facets designed to increase heat, including:

  • Release of noradrenaline by the sympathetic nervous system, increasing thermogenesis in brown adipose tissue and causing peripheral vasoconstriction and piloerection (reducing heat loss)
  • Acetylcholine release stimulating muscle myocytes to induce shivering
  • Feeling cold”, inducing heat-seeking behaviours (warm clothes and blankets)

It is important to remember that the body is trying to get hotter. If you intervene with non-medicinal efforts to cool it down, it will work even harder to try to heat up.

Why do we get fevers?

The process of having a fever has been conserved across species from lizards to mammals, and even plants! This is because it is a beneficial response to an infection. The mechanisms by which a fever helps protect you from infection include:

  1. Higher temperatures inhibiting growth/replication of pathogens
  2. Higher temperatures promoting the immune response to infection

It is also worth noting that bacteria are killed more easily by antibiotics at higher temperatures, so there is also a potential third mechanism.

 

Summary

Fever is beneficial. When a pathogen causes infection, pyrogens stimulate the hypothalamus to increase the body temperature through several mechanisms, and this increased temperature helps inhibit the growth of the pathogen AND stimulates the immune system to fight it.

That was a lot of science. Don’t worry – it’s time to get clinical! All this science stuff is lovely, but what does this mean for our patients?

Clinical significance of fever

As we have ascertained, fever is beneficial. For this reason, when a child presents with fever, the fever itself is actually of no concern. What we are interested in is the reason for the fever. Is this fever the result of a benign, self-limiting, childhood infection – or is it associated with a serious bacterial infection? Trying to determine this is enough for its own blog article (the most important thing is the end of the bed assessment – see Andy Tagg’s excellent breakdown of the paediatric assessment triangle).

Ignore the fever itself – what’s important is ascertaining its cause.

Now, let’s get on and bust some myths that persist surrounding fever in children!

 

Myth 1 – Higher temperature indicates a serious infection

This is one of the most common concerns amongst parents. The particular height of temperature may be what prompts them to come to hospital, or even what prompts the health care provider to initiate more aggressive management or investigations.

The truth is that the relationship between the height of temperature and risk of serious illness is at best complicated, and at worst a dangerous distraction. There is a very poor correlation, with such woeful sensitivity and specificity that it will both grossly over and under-call serious infections (either if the high temperature is used to rule in, or lower temperature to rule out). The caveat to this is in younger infants (particularly under 60 or 90 days), who have a higher baseline risk of serious infections (and more to the point – once they spike a temperature will be managed aggressively regardless of how high it was). Some studies have shown an extremely weak association in older children, but not enough for it to have any meaningful influence on our management. A fever is a fever – higher temperatures should not be managed any differently than lower ones.

 

Myth 2 – Temperature not relieved by antipyretics indicates a serious infection

Another common misconception also linked to the myth above. Some fevers respond well to antipyretics, and some do not. We do not understand why this is the case, however, studies have not demonstrated that failure to respond to antipyretics is a useful indicator of a more serious infection. It is not very pleasant for the child to remain hot, but it does not mean they are at any higher risk. A child whose temperature does not respond to antipyretics should not be treated any differently to one that does.

Myth 3 – Rigors indicated a serious infection

This has been covered in-depth in a separate blog post – but to summarise; there is extremely weak evidence that rigors are associated with an increased risk of bacterial infection in children, which is irrelevant when factors that are more important are taken into account. There is also evidence of no increased risk. The presence or absence of rigors should not be a deciding factor in the management of febrile children.

Myth 4 – You must wait for a fever to come down before discharge

This may seem common practice for many of you working in acute paediatrics. If a child is febrile on arrival, people often want to wait to see the temperature come down before allowing them to be discharged (this should be differentiated from seeing observations normalize in the absence of fever – which is a more understandable if still slightly questionable practice). As we have seen, a fever merely indicates the presence of an infection. If you have ascertained the cause of the fever, or at least ruled out any red flags for serious causes, the ongoing presence or absence of a fever means nothing for the child. If it comes down before discharge, it will probably just go up again once they are home! There is no need to make them wait around for hours for no reason.

Myth 5 – Fever should be treated with antipyretics

We have established that fever is beneficial. Therefore, there is essentially no reason to treat a fever in and of itself. It will not cause harm, and it is probably helping. Some children tolerate having higher temperatures extremely well, so if they are playing happily or do not seem terribly bothered about their temperature of 39°C then you leave them well alone.

Treat the child, not the fever.

Myth 6 – Fever should not be treated with antipyretics

There is an opposing school of thought, which says that since fevers are beneficial, we should not treat them at all. Given how absolutely dreadful it can feel to have a fever (which many of us adults should be able to vouch for), many of us give medicines to try to bring the temperature down and make the child more comfortable. This is the right thing to do. Despite the potential benefits having a fever confers, there is no evidence of any clinically meaningful harms to treating temperatures in unwell children, or even in adults in ICU. If the child is distressed by the temperature, they should have antipyretics to make them feel more comfortable.

Summary

  • Fever helps your body to fight infection and is not dangerous (no matter how high)
  • The fever itself is not important. The cause of the fever is what matters
  • There is little to no evidence that higher temperatures, temperatures that don’t respond to antipyretics, or rigors indicate an increased risk of serious infection
  • Persisting fever on its own is not a reason to postpone discharge
  • Only treat fevers if they are causing distress. Treat the child, not the fever

 

Postscript: Febrile convulsions

When I posted my initial thread on twitter about fevers, there were many comments asking why I didn’t address febrile convulsions. This was mainly because these are worth a post to themselves (which they have here). In brief, febrile convulsions are extremely distressing for parents to observe, but they are common and they are very benign. We do not advise treating fevers to prevent febrile convulsions, and until recently, this was because there was no evidence that they had any effect in preventing them. A recent study from Japan did demonstrate a decrease in recurrence of febrile convulsions in children who had already had one if given regular PR paracetamol, however, there are major caveats to this study discussed in depth here.

 

For the more visual oriented, the talented Emma Buxton has created an infographic of the key reminders from this blog post:

Idiopathic anaphylaxis

Cite this article as:
Abbey Ward. Idiopathic anaphylaxis, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.21876

A fifteen year old boy came into ED, brought in by his parents after having to use his EpiPen at home. He was at school, he was well in the morning. Suddenly while walking between classes he started to feel nauseous, sort of breath and tight chested. Once again he was having an anaphylactic reaction, but he did not know what he was reacting to.

 

Anaphylaxis

Anaphylaxis is a common severe allergic reaction to an allergen. IgE binds to the allergen which causes degranulation of mast cells and basophils leading to histamine release.  This in turn causes smooth muscle constriction and bronchoconstriction as well as angioedema. This is a type 1 immunological reaction.

This reaction leads to facial swelling, bronchoconstriction, airway obstruction, rash, vomiting, diarrhoea and fluid redistribution leading to shock and respiratory failure. Anaphylaxis is a life-threatening medical emergency and needs prompt treatment as well as education to prevent further anaphylactic attacks. So the prevention of anaphylactic shocks is highly important, and usually this can be done by tracing common allergens that the patient was exposed to right before they develop a reaction. However, in some cases this is more difficult to determine and may not be obvious.

In our case there was no identifiable allergen at all.

 

Idiopathic anaphylaxis

Idiopathic anaphylaxis is a condition where patients develops an anaphylactic reaction without a causative agent. The patient develops an anaphylactic reaction without any form of trigger. This can be dangerous, as patients can spontaneously develop anaphylaxis without any warning, putting them in life threatening situations regularly and without warning. It is unclear what causes this and although patients are commonly very atopic and will have other atopic conditions and allergies.

 

Treatment

Treatment for idiopathic anaphylaxis is the same as for any other cause of anaphylaxis in the acute setting. Patients need treatment with adrenaline and steroids. However, in the long term they need to be well educated and prepared, including education on what anaphylaxis is and how important it is, using EpiPen’s and how important it is to always carry one in case of a reaction developing.

The child in out case, underwent multiple allergen and immunological investigations and although multiple allergens were identified, he continued to have anaphylactic reactions without apparent triggers.

 

Key learning points

  • Anaphylaxis can occasionally be idiopathic although this is rare
  • Idiopathic anaphylaxis has the same pathology and presentation to allergen mediated anaphylaxis
  • Patients with idiopathic anaphylaxis need the same acute treatment
  • Long term treatment involves a lot of education around the condition

A better discharge summary

Cite this article as:
Beckie Singer. A better discharge summary, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.21995

Discharge summaries, often considered the bane of every junior doctor and ED physician’s existence. But what if we took a step back and considered these as a clinical handover to primary care – similar in nature to the clinical handover that occurs in the transfer of care documents that you would send with a patient you are transferring to another hospital? They suddenly take on a whole other level of importance. Studies from the ‘adult medicine world‘ have shown that roughly 20% of patients experience an adverse event during the hospital-to-home transition, many of which could be mitigated by good handover between the hospital and the primary care provider.

I am Sam

Cite this article as:
Dani Hall. I am Sam, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.21781

This post is based on a talk Dani presented at the Irish Association of Emergency Medicine conference in November 2019. The talk wouldn’t have been possible without the extraordinary help and inspiration from Mike Farqhuar from the Evelina London Children’s Hospital and Mike Healy from the Linn Dara CAMHS Unit.

Monteggia fracture dislocations

Cite this article as:
Rie Yoshida. Monteggia fracture dislocations, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.21141

Emiko is an 8-year-old girl who presents to the ED with a swollen and painful left arm. She is a keen mixed martial arts enthusiast and has suffered a direct blow to the arm whilst practising earlier today. On examination, her left proximal forearm and elbow joint are swollen and tender. She has limited movement of her elbow joint. The arm is neurovascularly intact.

Paediatric ophthalmology: Siobhan Wren at DFTB19

Cite this article as:
Team DFTB. Paediatric ophthalmology: Siobhan Wren at DFTB19, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.21733

Siobhan Wren is an ophthalmologist based at Imperial College in London. It’s a rotation that most of us skipped out on in medical school but with paediatric ocular trauma accounting for a third of all ocular trauma it is something that needs to be on our radar.

In this talk she focuses on the first sixty minutes after the injury – keeping the patient comfortable and safe, not making things worse and a stepwise approach to the basic examination.

 

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal. DFTB20 will be held in Brisbane, Australia.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

iTunes Button
 

Selected References

Sii F, Barry RJ, Abbott J, Blanch RJ, MacEwen CJ, Shah P. The UK Paediatric Ocular Trauma Study 2 (POTS2): demographics and mechanisms of injuries. Clinical ophthalmology (Auckland, NZ). 2018;12:105.

Breastfeeding Basics

Cite this article as:
Annabel Smith. Breastfeeding Basics, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.21681

“If breastfeeding did not already exist, someone who invented it today would deserve a dual Nobel Prize in medicine and economics… Breastfeeding is a child’s first inoculation against death, disease, and poverty, but also their most enduring investment in physical, cognitive, and social capacity.”

Wrist torus and greenstick fractures

Cite this article as:
Emily Cadman. Wrist torus and greenstick fractures, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.21125

Forearm fractures (torus and greenstick fractures combined) are very common in children and happen in about 1 in 100 children. Wrist and forearm fractures account for half of all paediatric fractures.

They are often discussed alongside each other as they have several things in common. They are both almost exclusively seen in children due to the cartilaginous, compressible, soft nature of young bones. Which means you will often hear people say “they are the same thing” (in fact, if you google “buckle fractures” they often offer up beautiful examples of…greenstick fractures!) . But that just isn’t true; while they have things in common, they also have significant differences. Read on to find out…