Langcake on limb-threatening injuries

Cite this article as:
Tagg, A. Langcake on limb-threatening injuries, Don't Forget the Bubbles, 2015. Available at:
https://dontforgetthebubbles.com/pac-conference-langcake-on-limb-threatening-injuries/

The DFTB team are really excited to announce an upcoming video series…We have teamed up with APLS to share the videos from their Paediatric Acute Care Conferences. These videos have never been open access before, so if you weren’t able to attend the conferences, then now’s your chance to catch up.

The PAC Conference is run each year by APLS and consists of presentations on a range of topics relevant to paediatric acute and critical care.

Williams on Emerging Viral Infections

Cite this article as:
Davis, T. Williams on Emerging Viral Infections, Don't Forget the Bubbles, 2015. Available at:
https://dontforgetthebubbles.com/apls-pac-williams/

The DFTB team are really excited to announce an upcoming video series…We have teamed up with APLS to share the videos from their Paediatric Acute Care Conferences. These videos have never been open access before, so if you weren’t able to attend the conferences, then now’s your chance to catch up.

Kids in cars

Cite this article as:
Andrew Tagg. Kids in cars, Don't Forget the Bubbles, 2014. Available at:
https://doi.org/10.31440/DFTB.5062

The mercury on the outside thermometer is inching past 40oC for the third day in a row and for once you are grateful to be in the cool, air-conditioned emergency department.  The emergency phone snaps you back into alertness. The paramedics are bringing in a toddler that has been liberated from the back of a parked car.

Bottom Line

  •  Despite widespread public information campaigns children are still left alone in cars every heatwave.
  • Just 15 minutes unattended is enough to raise the temperature of the car to lethal levels.
  • Heat illness varies on a continuum from heat stress and cramps to heat exhaustion and then heatstroke.
  • Heatstroke is a medical emergency and is characterized by neurological deterioration, anhydrosis and a core temperature above 40oC

How big a problem is it?

During the recent heatwave in Melbourne, when the temperature topped 40 degrees for four days straight, Ambulance Victoria received 60 calls for children trapped in cars. Fortunately, there were no fatalities. During the 1995-2002 period in the United States, there were 171 entirely preventable deaths.

Studies have suggested that on a hot day the temperature in a locked vehicle can rise as high as 51-67oC within 15 minutes. 75% of this rise occurs within the first five minutes of the door closing, so even short periods of leaving a child unattended can be dangerous. There is some evidence that leaving the window cracked can make a difference but all the data suggests that it has to be open at least 20 cm to make an appreciable difference.

Why are children at particular risk?

Even though kids have a larger body surface area-to-mass ratio than adults, they have much less effective thermoregulation. They have a higher metabolic rate so are really little furnaces.  Unfortunately, they are less well able to regulate their cardiac output in response to heat stress and produce less sweat per apocrine gland compared to adults. Perhaps more importantly, unlike most adults, they cannot get out if they are left in the car seat on their own.

What’s the difference between heat stress, heat exhaustion, and heatstroke?

Words are important. What the lay public means when they say heatstroke is very different from what the medical professional means.

Heat stress is what we all feel when the mercury rises – we’re grumpy, irritable, sweaty and often listless but not unwell. The core temperature is unaffected.

Heat exhaustion occurs as a result of salt and/or water depletion.It may be compounded by nausea, vomiting and excessive sweating. The core temperature may or may not be up altered.

Heatstroke is a medical emergency and typically classified as either exertional (think running a marathon on a hot day)  or non-exertional (sitting in a hot car).  As the core temperature rises above 40oC the patient often becomes more lethargic and delirious. Seizures, then coma, eventually ensue.

How do children lose their excess heat?

Heat is lost via radiation, conduction, evaporation, and convection with these latter two being most amenable to change.

As with all potentially toxic exposures (to heat in this instance) removal from the source is vital. The child should be managed in a cool environment if possible and attention paid to their ABCs.

  • Airway – they may require intubation if clinically indicated
  • Breathing – if they need to be intubated then mechanical ventilation will need to be initiated
  • Circulation – children suffering from heatstroke are often profoundly dehydrated with challenging IV access. Don’t hesitate to break out your favourite intraosseous device. As peripheral cooling is instituted more blood is returned to the central circulation increasing the risk of pulmonary oedema.
  • Disability – seizures should be treated with benzodiazepines initially but you should check the UEC urgently and assess the sodium for hypo- or hypernatraemia depending on whether salt and water depletion or pure water depletion predominates.
  • Exposure – having discovered a high core temperature then it is time to do something about it. Techniques can range from the simple – remove clothes, ice packs in the axillae and groins, cool fans, cold IV fluids to the Macgyver – creating a cooling tent. This can be done by soaking a sheet in cold water and draping it, suspended, over the patient with a fan to push air through it. The aim is to maximize heat loss via convection, conduction, and evaporation.

They’ve got a temperature, shouldn’t you give them some paracetamol/Tylenol/acetaminophen?

There is no evidence that antipyretics lower the temperature in cases of heat-related illness.

Disposition for the sick patient is straight forward.  They need admission to HDU/ICU. But what should you do for the well-appearing child?

There is no consensus as to how long a patient should be observed but common sense would dictate that if their temperature has normalized and they are rehydrated then they are fit enough to go home.

Should you involve social services?

That is the million-dollar question. Certainly, in Australia, Section 231 of the Children and Young Persons (Care and Protection) Act 1998 clearly states:-

A person who leaves any child or young person in the person’s care in a motor vehicle without proper supervision for such a period or in such circumstances that :

(a) the child or young person becomes or is likely to become emotionally distressed, or
(b) the child’s or young persons health becomes or is likely to become permanently or temporarily impaired is guilty of an offence.

Hasn’t the distraught parent been through enough?  This excellent piece from the Washington Post, entitled Fatal Distraction eloquently puts parents struggle into words.

Outcome

Little Nelly is brought in, nearly naked and crying. Her rectal temperature is 38oC and she tolerates a delicious icy pole. Her mother is beside herself. You discuss the case with the local social services who agree to follow up.

Selected References

McLaren C, Null J, Quinn J. Heat stress from enclosed vehicles: moderate ambient temperatures cause significant temperature rise in enclosed vehicles. Pediatrics. 2005 Jul;116(1):e109-12. PubMed PMID: 15995010

King K, Negus K, Vance JC. Heat stress in motor vehicles: a problem in infancy. Pediatrics. 1981 Oct;68(4):579-82. PubMed PMID: 7322691.

Grubenhoff, Joseph A., Kelley du Ford, and Genie E. Roosevelt. “Heat-related illness.” Clinical Pediatric Emergency Medicine 8.1 (2007): 59-64.

Guard, A., and Susan Scavo Gallagher. “Heat related deaths to young children in parked cars: an analysis of 171 fatalities in the United States, 1995–2002.”Injury Prevention 11.1 (2005): 33-37.

https://lifeinthefastlane.com/education/ccc/heat-stroke/ accessed 21st January 2014

Bouchama, Abderrezak, and James P. Knochel. “Heat stroke.” New England Journal of Medicine 346.25 (2002): 1978-1988.

Wexler, Randell K. “Evaluation and treatment of heat-related illnesses.”American family physician 65.11 (2002): 2307-2313.

Asthma – medical management

Cite this article as:
Tessa Davis. Asthma – medical management, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.2815

A 9 year old boy is rushed into ED with what is clearly a severe exacerbation of his asthma. His sats are 80%, his RR is 60-70 and he is not looking great. You can hear some air entry with a bit of wheeze. He clearly needs some good treatment and he needs it quickly. Which drugs you choose? 

Traumatic brain injury - helmet

Traumatic brain injury

Cite this article as:
Adam Bartlett. Traumatic brain injury, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3381


An 8 year old boy is rushed into ED following a fall from a fourth story window.  He landed on concrete and has obvious signs of external damage to his skull and a GCS of 5.

He’s clearly sustained a serious traumatic brain injury – how is this best managed?

Inotropes and vasodilators

Cite this article as:
Marc Anders. Inotropes and vasodilators, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3934

Vasodilators:

Decreasing the pressures against which the heart works (systemic and pulmonary afterload); decreasing the work of the heart hence myocardial O2 demand.

Usual indications for vasodilator therapy are: systemic vasodilation (LV afterload reduction), pulmonary vasodilatation (RV afterload reduction), systemic hypertension, improving coronary blood flow.

Beware that infants, in response to low CO, increase afterload to maintain BP.

The use of vasodilators leads to increase in vascular capacitance and may require volume replacement. Avoid or use judiciously with lesions where there is obstruction to blood flow or fixed stroke volume.


Sodium-nitroprusside (SNP) via release of endogenous NO

Dosemcg/kg/min Clinical effect
0.2-6 Direct smooth muscle cell relaxationarterial > venous vasodilation
Side effects: severe hypotension (titrate slowly), worsening V/Q mismatch, cyanide and thiocyanate intoxication, methaemoglobinemia, tachyphylaxis

Glyceryl-trinitrate (GTN) via release of endogenous NO

Dosemcg/kg/min Clinical effect
1-10 Direct smooth muscle cell relaxationvenous > arterial vasodilationimproved coronary perfusion
Side effects: severe hypotension (titrate slowly)

Phenoxybenzamine via irreversible alpha-blockage

Dosemcg/kg/min Clinical effect
Load: 1 mg/kg over 1hr Vasodilation
TDS or BD:0.5mg/kg
Side effects: severe hypotension

Hydralazine via direct vasodilation by decreasing intracellular Ca++

Dosemcg/kg/min Clinical effect
10-50 Vasodilation
Side effects: reactive tachycardia

Prostacyclin = PGI2 (epoprostenol) via increase in NO

Doseng/kg/min Clinical effect
2-20 (40) Pulmonary vasodilation, treatment of PHT
Side effects: systemic hypotension, haemorrhagic diasthesis due to Platelet aggregation inhibition

Prostaglandin = Alprostadil = PGE1 via release of endogenous NO

Doseng/kg/min Clinical effect
5-100 Pulmonary vasodilationMaintaining PDA patency
Side effects: systemic hypotension, fever, hypoventilation and apnoea, antiplatelet function

Inhaled nitric oxide (iNO)


Sildenafil


Clonidine via presynaptic alpha 2 adrenergic action

Dosemcg/kg/hr Clinical effect
0.5-2 VasodilationSedationAnalgesia
Side effects: systemic hypotension, avoid in Porphyria, may decrease CO

Dexmedetomidine via presynaptic alpha 2 adrenergic action

Dosemcg/kg/hr Clinical effect
0.2-1 VasodilationBradycardia (can be used therapeutically)SedationAnalgesia
Side effects: systemic hypotension, decreases CO, avoid in LCOS

Captopril (ACE-I) via angiotensin converting enzyme inhibition

Dosemcg/kg Clinical effect
Test dose: 0.1 VasodilationImprove in CO
TDS or QID, increase dose by 0.1 mg/kg until clinical effect achieved
Side effects: systemic hypotension, renal dysfunction

All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Haemofiltration and dialysis

Cite this article as:
Marc Anders. Haemofiltration and dialysis, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3735

Indications:

  • Correction of water overload
  • To remove larger quantities of water from the body than the kidney is able to achieve in order to enable the administration of therapeutic fluids such as parenteral nutrition
  • To remove excess electrolytes
  • Correction of disorders of acid/base homeostasis, including inborn errors of metabolism, particularly metabolic acidosis
  • Liver failure (but it does not substitute liver function!)
  • Removal of urea and other waste products of metabolism in cases of renal failure or hypercatabolic state
  • Removal of ingested poisons, drugs or toxins in sepsis

Most common used: continuous veno-venous haemofiltration (CVVH or CVVHF) or continuos veno-venous haemodiafiltration (CVVHDF).

In CVVHF the filtrate depends on blood flow rate (aim for 3-5 ml/kg/min), the transmembrane pressure – TMP (change in oncotic pressure along the filter), prefilter dilution (decreases urea-/creatinine clearance) and the sieving coefficient (ratio between filtrate concentration and plasma concentration for a given molecule, e.g. urea=1, albumin=0).

The filtrate is replaced by a glucose/electrolyte solution (replacement fluid). In CVVHDF the clearance of small and middle sized molecules is enhanced by counter-current dialysate flow (diffusion).


Anticoagulation:

  • UFH/anticoagulation, aim ACT 160-180 secs
  • UFH/protamine: 1 mg protamine post-filter for every 100 U Heparin administered pre-filter
  • Citrate anticoagulation: 1ml citrate per 30 ml blood flow, aiming for pre-filter Ca++<0.4 mmol/l and replace post-filter with Ca++>1.2 mmol/l (Mg++, citrate accumulation → acidosis)

Replacement fluid:

  • For non-citrate anticoagulation: Na+ 140 mmol/l, Ca++ 2 mmol/l, Mg++ 0.5 mmol/l, Cl 110 mmol/l, HCO3 32 mmol/l, Lactate 3 mmol/l
  • For non-citrate anticoagulation and lactate free: Na+ 140 mmol/l, Ca++ 1.75 mmol/l, Mg++ 0.5 mmol/l, Cl 113.5 mmol/l, HCO3 35 mmol/l, K+ 4 mmol/l, glucose 5 mmol/l
  • For citrate anticoagulation: Na+ 136 mmol/l, Cl 106 mmol/l, citrate 10 mmol/l, citric acid 2 mmol/l

Catheter/blood Flow/filter:

Always aim blood flow/filtrate flow ratio > 5:1

Patient size Catheter Size Usual Blood Flow Rate Maximum
recommended
Blood Flow
Haemofilter
< 3 kg 5.0F 5 ml/kg/min 50 mL/min HF20; Filtrate 200-300mL/hr
< 8 kg 6.5F 5 ml/kg/min 75 mL/min HF20; Filtrate 200-300mL/hr
10 – 15 kg 8.0F 5 ml/kg/min 150 ml/min ST60; Filtrate 900-1400mL/hr
>15 kg 11F 5 ml/kg/min 300 ml/min ST100; Filtrate 6000mL/hr
Adult 14F 5 ml/kg/min 2000 ml/min ST150; Filtrate 6000mL/hr

Patient monitoring:

  • Electrolytes (glucose, Na+, K+, Cl, HCO3, Ca++) every 4 hrs, hourly for 1st 4 hours if they were abnormal
  • Magnesium and phosphate twice daily
  • Fluid balance per hour = IV fluids in per hour + enteral feeds per hour – urine – insensible losses – drain losses – patient Fluid removed per hour

Mode Clinical Use QDF (Diffusion) UFR (Convection) QRF Total Clearance
SCUF Water removal Nil =Filtrate flow Nil UFR
CVVH Clearance depends on TMP, QBF, Sieving Nil =Filtrate flow = QRF UFR
CVVHD Clearance depends on QBF, QDF QDF =QDF + UFR (small) Nil QD + UFR (small)
CVVHDF Improved clearance of small and middle size QDF =QDF + UFR = QRF QDF + UFR

References:

[1] Pediatr Nephrol 2012 Feb28: Sutherland et al: Continuous renal replacement therapy

[2] Curr Opin Pediatr 2011 Apr;23(2)181-5: Goldstein: Continuos renal replacement therapy: mechanism of clearance, fluid removal, indications and outcome

[3] Crit Care 2011 Jan 24;15(1)202: Oudemans-van-Straaten et al: Clinical review: anitocagulation for continuous renal replacement therapy – heparin or citrate?


All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Renal Failure

Cite this article as:
Marc Anders. Renal Failure, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3719

Definition: acute kidney injury (AKI) is failure of the kidneys to regulate electrolyte, acid-base and fluid homeostasis adequately with concomitant reduction in glomerular filtration rate (GFR). pRIFLE (paediatric Risk, Injury, Failure, Loss, End-Stage Criteria).

Chronic renal failure: hyperfiltration, estimated creatinine clearance <75 ml/min/1.73m2 , hypertension, microalbuminuria.