PICU Protocol of EHA

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PICU Protocol of EHA

Egyptian Clinical Practice Protocols

in
Pediatric Intensive Care Units
for
Egypt Healthcare Authority
First Edition
2022
Produced by
Working Group for Development of
Egyptian Clinical Practice Protocols
in
Pediatric Intensive Care Units
for
Egypt Healthcare Authority

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 PICU Protocol of EHA

Executive Committee

1. Prof. Dr. Hanan Ibrahim: (Head of the Committee) Professor of pediatrics-

ASU, Head of PICUs-ASU, Head of Egyptian Society of Pediatrics and pediatric
Critical Care (ESPPCC).
2. Prof. Dr. Hafez Bazaraa: Professor of pediatrics, Head of PICU, Cairo
University. Pediatrics Armed Forces College Of Medicine.
3. Prof. Dr. Azza Ahmed El-Tayeb: Professor of pediatrics, Assiut University.
4. Prof. Dr. Khaled Talaat: Professor of pediatrics, Tanta University.
5. Prof. Dr. Soha Adly Hashem: Consultant of Pediatrics, Neonatology, Emergency
Cases and PICU. International Coordinator and Trainer of PALS, American Heart
Association.
6. Dr. Sondos Mohamed Magdy: Lecturer of Pediatrics and PICU, Ain Shams
University.
7. Dr. Huda Karam: (Moderator of the Committee) Pediatric Specialist, Moderator
& coordinator of Medical Advisory Council of Egypt Healthcare Authority (EHA)

Disclaimer
Protocols and guidelines outline the recommended or suggested clinical practice;
however, they cannot replace sound clinical judgment by appropriately trained and
licensed physicians.
The physician is ultimately responsible for management of individual patients
under their care.

Intellectual Property Rights

All Intellectual Property Rights are reserved to EHA. No part of this publication
can be reproduced or transmitted in any form or by any means without written
permission from the EHA and authors.

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PICU Protocol of EHA

Supervised & Revised By

➢ General Doctor/ Mourad Alfy Ramzy Tadros

• MD, FRCPCH(UK), MRCPI(Dublin)

• Consultant Paediatrician of Egyptian Military Medical Services.
• Professors of Paediatrics Military Medical Academy
• Head of Training Committee of Paediatrics of Egyptian Military Medical Board
• Consultant Paediatrician of the Medical Advisory Council of Egypt Healthcare
Authority (EHA).

Reviewed By

1. Dr. Hala Adel: Pediatric Consultant, Moderator & coordinator of Medical

Advisory Council of Egypt Healthcare Authority (EHA)

2. Dr. Huda Karam: Pediatric Specialist, Moderator & coordinator of Medical

Advisory Council of Egypt Healthcare Authority (EHA)

Cover Designed & Edited By

➢ Mr. Bassam Sayed: Technical Officer at Egypt Healthcare Authority (EHA)

Chairman's Office

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 PICU Protocol of EHA

PREFACE
Recently, there is an increasing need to provide programs with accurate
competency-based assessments to ensure the delivery of high-quality healthcare. The
aim of developing these Egyptian Clinical Practice Protocols in Pediatric Intensive
Care Units is to unify and standardize the delivery of healthcare to any child at all
health facilities.

The current status of healthcare in which avoidable failures are abound. “We
train longer, specialize more, use ever-advancing technologies, and still we fail.” Part
of the problem, is that the ever-increasing complexity of medicine makes uniform care
delivery impractical or impossible. That is, unless there are protocols, checklists, or
care paths that are readily available to providers.
Regarding Pediatric Intensive Care Units, busy clinicians have all felt the need
for a concise, easy-to-use resource at the bedside for evidence-based protocols, or
consensus-driven care paths.
In this protocol, we offer comprehensive reviews of selected topics and
comprehensive advice about management approaches based on the highest level of
evidence available in each case. Our goal is to provide an authoritative practical
medical resource for pediatricians.

We hope that such an approach will encourage clinicians to apply available

evidence to their practice and also track compliance with desired practices. We hope
that practicing pediatricians, fellows and practitioners will find this protocol useful in
delivering high-quality clinical care to their patients. We remain open to feedback and
suggestions about how to improve this resource and how to make it maximally useful
to those delivering care at the bedside in for patients in Pediatric Intensive Care Units.

Members of the Working Group

For Development of the Egyptian Clinical Practice Guideline

In Pediatric Intensive Care Units

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PICU Protocol of EHA

Table of Contents

Page
Title
Number
Executive Committee 3
Preface 5
Standards for PICU Preparation 7
Pediatric Resuscitation 9
Basic Fluid Therapy 17
Shock 27
Acute Severe Asthma 42
Status Epilepticus 53
Diabetic ketoacidosis 62
Hypoglycemia 75
Adrenal Crisis 77
Acute kidney Injury (AKI) 81
Comatose Child 88
Cerebral Oedema 89
Blood Product Prescription 93
Clinical Practice Guidelines on Prevention and 99
Management of Pain
Basic Mechanical Ventilation 107
Poisoning Protocol 117

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 PICU Protocol of EHA

Standards for PICU Preparation

Human resources needed for every five beds:

✓ Doctors; one consultant, one specialist and four residents
✓ Clinical pharmacy; one
✓ Nurses; one head nurse, three nurses and three assistant nurses
✓ Two porters
✓ One infection control specialist

PICU structural composition:

1-Take in consideration the proximity to OR
2-also to be near to ER
3-8 meters are the area needed for each ICU bed
4-PICU should contain: procedure room, operating room and preparatory room
5-AC system with hepa filter
6-Entrance different from exit
7-Central sterilization unit

Laboratory requirements for any PICU

• Emergency lab 24 hours 7days or lab to lab deal
• CBC, blood gases, electrolytes coagulation profile, LFT, KFT

Pharmacy:
• Emergency stock of medication for each unit
• Internal pharmacy 24 hours /7 days
• Each governorate should contain TPN center preferred to be in largest hospital
• Blood bank for each governorate

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PICU Protocol of EHA

Security cameras for PICU beds

Doctors& nurse rooms with toilet and for each five beds one toilet
Store room
For each five beds one sterilization basin
Equipment:
1-Central station
2- Portable x ray and U/S with duplex probe
3-For each PICU bed;
Monitor +4 syringe +2 infusion pump+ 1 warmer+ 2 oxygen outlets +1 air outlet
+1 suction outlet +12 electric outlets on UPS with stabilizer
4-For every five beds we need 5 MV +2 high frequency MV +2 noninvasive
ventilation +1 crash car with D/C unit +ECG + augmented EEG
5- Air mattress

Transportation:
• Separate portable ventilator or one of the unit ventilators if it also could be
used as portable ventilator
• Four oxygen cylinders
• Two portable monitors
• Two incubators

NB:
▪ Two CRRT machines for each governorate in same place or if there is a
dialysis unit it should be in it

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 PICU Protocol of EHA

Pediatric Resuscitation
Scope:
• Applicable to individuals up to 12 years of age
• Resuscitation of neonates in the delivery room is NOT within the scope of this protocol
• This protocol applies to healthcare settings. Basic life support by lay by-standers is not
the intended scope

Recognition:
• CPR is indicated when there is no reliable central pulse with a rate of at least
60/min. in a patient who is unconscious and unresponsive
• Central pulse may be assessed in the Carotid, Brachial or Femoral arteries
• Duration of assessment may NOT exceed 10 seconds
• Hospitalized critical patients will be already on continuous monitoring. Note that
those with pulseless electrical activity will show cardiac electrical activity (ECG
pattern) on the monitor in absence of a central pulse. CPR is still necessary
• Hemodynamically stable patients with HR less than 60/min may require
alternative approaches
• Rescue breathing is indicated
(a) Together with chest compressions during CPR
(b) In patients with absent or grossly ineffective (eg gasping) breathing even if there is a
reliable pulse Airway opening is necessary for rescue breathing
• Immediate defibrillation is needed for those with recognized pulseless shockable
rhythm (VF, VT) once it is available.
• CPR should be performed until a shockable rhythm is recognized and a
defibrillator is ready
o CPR is not indicated when there are obvious signs of life such as a reliable
central pulse ≥60/min., regular breathing, eye opening, speech, cough, etc.
o However, this does not rule out a critical or unstable condition. System
support may be required. Recognition and management of system failures
before cardiac arrest occurs and after return of spontaneous circulation are
keys to survival
• CPR is a team process; Pre-assignment of teams and appropriate training
improve outcomes. While CPR can and should be initiated by a single
individual, calling for help is then necessary to continue effective management.
Required equipment, medications and supplies must be readily available and
checked regularly and after each use

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PICU Protocol of EHA

Sequence of Actions:

1. Recognize the case, ensure safety, call for help and position the patient

• It is important to ensure the patient is not in ongoing danger and it is important

that the rescuer approach safely so he would not be endangered. Approach with
care
• Inside the hospital, scene safety should be easy to maintain
• A sole rescuer may initiate a cycle of CPR first if calling for help requires him
to leave the patient
• A defibrillator/ monitor should be available or brought with coming help
• Patient should be positioned supine on a flat hard surface. A bed mattress is too
soft; a board may be used under the patient, but make sure it can take the force
of chest compressions and its edge is away from the patient’s back
• If the patient needs to be moved or turned, do that with care to avoid injury

2. If there is no central pulse ≥60/min., start chest compressions

3. Open airway, check breathing and start rescue breaths

• If there is no pulse, starting chest compressions immediately, followed by

airway-breathing support is recommended (C-AB). If there is a pulse, the usual
ABC approach; starting with airway & breathing, is recommended. Conscious
patients with a FB airway obstruction will require specific management

4. Identify a shockable rhythm (VF/VT) & give DC shock

5. Immediate vascular access for drug ± fluid administration

• Shockable rhythms are not the commonest causes of pediatric cardiac arrest;
however, early recognition & treatment could markedly improve outcome. Do
NOT unnecessarily interrupt CPR but identify rhythm as soon as available.
When cardiac arrest is associated with an attended VF/VT (in a monitored
patient), an immediate DC shock is given if available

6. Check and correct correctable factors

• This should occur throughout resuscitation

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 PICU Protocol of EHA

• EMD (electromechanical dissociation) = pulseless electrical activity

• The first DC shock may be 2-4J/Kg

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PICU Protocol of EHA

Chest Compressions
Site: midline on the lower sternum
• NOT the xiphisternum, NOT on the left precordium

Rate: 100-120/min
Depth/ force: need to depress 1/3 the AP chest diameter
• Two hands for older children
• One hand for younger children
• Only use the heel of the hand(s), fingers should NOT be applied to the chest
• Two fingers for infants
• Both thumbs with hands encircling the chest
• Index and middle fingers (preferred for single rescuer)

Quality: compression NOT rocking motion, allow FULL RECOIL between

compressions, MINIMAL INTERRUPTION (preplan before you interrupt)

Airway-Breathing Support
Airway
• Head tilt chin lift to open airway. Cannot use this technique if there is a need to
immobilize the cervical spine. Only jaw thrust can be used in this case
• Check for breathing (look, listen and feel). Remove obvious FB. Suction
secretions, blood, etc.
• Maintain airway
• Oropharyngeal, nasopharyngeal or laryngeal mask airways may be helpful
• Endotracheal intubation once possible
• ETT position must be confirmed
• Surgical airway is rarely necessary

Breathing

• With airway open, use bag & mask to ventilate

• Use the highest possible oxygen (100%)
• Check for a visible chest rise during ventilation
• Use bag and ETT once placed
• If you started with breathing & are not doing CPR, give 5 initial breaths then
reassess circulation
• Oxygen recommendations are different in neonatal resuscitation
• Lack of adequate chest rise: verify airway, proper mask seal, absence of a leak
or FB obstruction

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 PICU Protocol of EHA

Synchronizing breaths & chest compressions

• Generally, 15:2 (2 breaths after every 15 chest compressions). Five such

sequences represent one cycle (1-2min)
• 30:2 has been suggested for child CPR with a single rescuer, although 15:2 can
still be used
• With advanced airway (ETT): no need. Provide breaths continuously at 12/min.
Increase to 20/min. if there is (return of) spontaneous circulation
• Hyperventilation during cardiac arrest is not beneficial and may be harmful

In case of choking/ FB obstruction

• An obvious FB can be removed, blind finger sweeps should be avoided

• A conscious patient with effective cough should be allowed to cough &
monitored
• If there is no/ loss of effective cough in a conscious patient, apply alternately 5
back blows, 5 abdominal thrusts (children NOT infants), 5 chest thrusts (can use
in infants)
• If patient unconscious/ lost consciousness start CPR
• Direct laryngoscopy & removal under vision may be possible

VASCULAR ACCESS
• The best time to establish vascular access is before cardiac arrest
• Peripheral lines can be used during resuscitation. A small bolus of normal saline
can be given after each injection to improve drug delivery to the central
circulation
• In absence of an alternative, intraosseous or femoral vein access will not
significantly interfere with resuscitation. All resuscitation medications can be
given intraosseous
• Volume (10-20mL/Kg isotonic crystalloid) is given in hypovolemic patients.
This should not delay CPR, adrenaline administration or defibrillation
• Endotracheal and intracardiac routes for medications are no longer
recommended

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PICU Protocol of EHA

DRUGS

Adrenaline
• During CPR for cardiac arrest, give 10μg/ Kg adrenaline IV and repeat every 2
cycles (3-5min)
• For pulseless VT/VF, give adrenaline after the third shock (if patient still
pulseless in shockable rhythm) and repeat every 2 cycles
• 10μg/ Kg equals 0.01 mg/Kg or 0.1mL/Kg using diluted solution (1/10,000 or 1
ampoule of 1 mg in 10mL). The max. adult dose is 1 mg
• There is NO evidence to support higher single doses
• Following return of spontaneous circulation, consider starting an adrenaline
infusion and titrate rate to response

Amiodarone
• Used for pulseless VT/VF that has not responded after the third DC shock
• Dose: 5mg/Kg, may be repeated ONCE after the 5th shock
• Lidocaine (1mg/Kg followed by 20-50μg/ Kg/min) may be an alternative

“Glucose, Ca, Mg, bicarbonate and atropine are not routinely recommended
during CPR”

Glucose
• Should be avoided except if there is hypoglycemia

Calcium
• Is indicated for hypocalcemia, massive transfusion, hyperkalemia,
hypermagnesemia and calcium channel blocker toxicity

Magnesium
• Is indicated for hypomagnesemia and torsade de pointes

Sodium bicarbonate
• May be considered after establishment of adequate ventilation, chest
compressions and giving adrenaline if there is severe metabolic acidosis,
hyperkalemia, tricyclic antidepressant toxicity or prolonged CPR

“Naloxone reverses opioid-induced CNS depression but it cannot substitute

breathing support and can precipitate withdrawal in opioid-dependent patients”

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 PICU Protocol of EHA

Shockable Rhythms

• Patients with cardiac arrest and a shockable rhythm (VT or VF) must receive
immediate DC shock
• CPR must start/ continue until the rhythm is identified and defibrillator is ready
• Check rhythm after every CPR cycle if available
• DC may be delivered manually or using AED

Manual: use 2-4J/Kg for the first shock and 4J/Kg for all subsequent shocks.
Make sure the Synchronize button is not accidentally on with VF as it will lead
to failure of giving the shock

AED: when attached, it will analyze rhythm and display if a shock is needed.
You still need to press the shock button to have it delivered. For children 1-
8years of age, use an attenuator. For infants, use a manual defibrillator. If
unavailable, use whatever is available.

Either case, paddles must be properly positioned and must not contact each
other. Smaller sized paddles are needed for those <10Kg. Apply conducting gel/
cream if available

• Confirm all is clear, with no one touching the patient or bed, before delivering
the shock
• Once delivered, immediately remove paddles and resume CPR. do not stop to
check response. Provide 1 cycle of CPR first.
• Make interruptions of CPR for checking rhythm as brief as possible. If another
shock is needed, continue CPR until defibrillator charged and ready.
• If the patient is still in cardiac arrest:

And rhythm still shockable➔ repeat a shock after every CPR cycle, give
adrenaline & amiodarone after the 3rd shock, repeat adrenaline every 2 cycles
and amiodarone only once after the 5th shock
And rhythm changed to non-shockable➔ give adrenaline and continue CPR

• Antiarrhythmic drugs cannot replace a DC shock in the context of cardiac arrest

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PICU Protocol of EHA

Correctable Factors

✓ Hypoxia
✓ Hypovolemia
✓ Hypothermia
✓ Hypo/hyperkalemia (& other metabolic)
✓ Tension pneumothorax
✓ Tamponade
✓ Thrombosis (PE, coronary)
✓ Toxic

Post-Resuscitation Management

• Assess and support for any system dysfunction, correct any correctable factors,
address the underlying disease. Continue to monitor patient and determine the
appropriate location for care (eg ICU). Key points include:

Respiration: maintain adequate ventilation and oxygenation. Most patients will

require an ETT and positive pressure ventilation. Obtain blood gases and use
pulse oximetry to guide oxygen therapy.

Circulation: assess cardiac rate and rhythm, pulses, BP and perfusion (capillary
refill, peripheral temperature & color, distal pulses, etc). Apply shock protocol
if needed. Patients may have myocardial dysfunction

Neurological: patients may develop convulsions or cerebral oedema

Metabolic: normothermia, glucose, fluid, electrolyte & acid-base status

Surgery or interventions may be needed to manage trauma, achieve hemostasis

or address other life-threatening emergencies. The correct timing and patient
support are necessary to maximize benefit and minimize risk

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 PICU Protocol of EHA

Basic Fluid Therapy

Scope:
• This protocol addresses intravenous fluid therapy in infants and children.
• Neonates are not specifically covered.
• Although the overall principles are similar, some conditions may have different
fluid requirements; such as diabetic ketoacidosis, perioperative fluid
management, burns, etc.
• For details of fluid management in shock, refer to shock protocol.

Disclaimer:
• Protocols and guidelines outline the recommended or suggested clinical practice;
however, they cannot replace sound clinical judgment by appropriately trained
and licensed physicians. The physician is ultimately responsible for management
of individual patients under their care.

Objectives:
✓ Provision of maintenance requirements
✓ Replacement of ongoing (excessive/ abnormal) losses
✓ Correction of deficit/ dehydration
✓ Volume expansion (mainly shock)

Maintenance Requirements:
Normal maintenance per 24hrs

Weight Calculation Max.

-10 Kg (excludes neonates) 100 mL/Kg 1000 mL/ 10Kg
>10- 20 Kg + 50 mL/kg 1500 mL/ 20 Kg
>20 Kg + 20 mL/Kg 2400 mL
All patients 1500 mL/m2
• Insensible losses are 400mL/m2/day
• Normal maintenance replaces normal urine and insensible losses; since sweat,
stool and abnormal losses are normally negligible
• This calculation tends to overestimate requirements of most acutely ill patients
after the resuscitation phase. It is suggested to use 70% of this as a starting point
in these cases.

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PICU Protocol of EHA

Normal maintenance applies provided that:

• Patient is normally hydrated (not dehydrated or oedematous; in which case a +ve

or –ve ‘respectively’ balance relative to maintenance is required)
• No fluid restriction is necessary eg HF, SIADH, etc
o Generally, 60-70% of normal maintenance is given in such cases
• There are no abnormal losses (radiant warmer, fever, diarrhea, drains, 3rd space,
burns, etc). Measured or estimated non-urinary abnormal losses need to be added
to normal maintenance.
• Urine output is normal
o In anuric, oliguric or polyuric patients; maintenance shall equal insensible
losses + patient’s urine output + abnormal losses if present.
Amount and type of fluids:
Condition Amount Type Example
Normal Normally 1500 mL/m2/day 0.5NS(a), glucose-saline
maintenance hydrated, no Or check table above 5-10% 1:1 with KCl
restrictions, glucose(b), (0.5-
normal urine 10-20mEq/L 1mL/100mL)
&no K
abnormal
losses
Restricted Oedema, HF, Generally 60-70%, 0.5NS-NS(c), Glucose-saline
maintenance SIADH, etc higher restrictions 5-10% 1:1 or NS, with
may apply glucose(b), KCl
10-20mEq/L (0.5-
K 1mL/100mL)
Dehydration Maintenance + 0.5NS-NS, Glucose-saline
deficit 2.5-5%(b) 1:1 or NS, with
glucose, 20- KCl
40mEq/L K (1-2mL/100mL)
Insensible Anuria 400mL/m2, may ≥10% glucose
loss only omit in case of
overload
Insensible Oliguria 400mL/m2/day As normal maintenance,
loss + urine Plus actual patient’s with/without K
output urine output per
1,4,12 or 24h(d)
Polyuria 0.5NS, Glucose-saline
≤5%glucose, 1:1 with KCl
20mEq/L K(e) (1mL/100mL)
Abnormal Other than in Add amount equal to Depends on type of fluid lost(f)
losses urine losses in 1,4,12 or
24hrs(d)
PD/ CRRT Consider patient & therapy balance together

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 PICU Protocol of EHA

NOTES:
• Oral/ enteral fluids, medications, drug infusions, blood products, etc are part of
maintenance/ replacement fluids. Only 85% of milk is fluid.
• Na, K should be monitored and adjusted accordingly. Do Not add maintenance
potassium in anuric patients. All stated Na, K, glucose requirements are starting points.
Modify based on actual level monitoring.
(a) In critically-ill children (not small infants), 0.5NS is be preferable in the first 24hrs,
rather than lower Na (eg Neomaint, 4:1 glucose-saline used in neonates & small
infants). Normal saline may be preferred with hyponatremia or CNS injury. Na content
must be adjusted based on at least daily serum electrolyte checks.
(b) Many acutely ill children (>6Mo) will not require glucose initially. If needed to
maintain blood glucose, prevent catabolism & ketosis, 10% glucose in maintenance
fluids may be necessary if tolerated. Higher concentrations require central access
unless for a very short term. Blood glucose should not consistently exceed 180-200
mg/dL. Higher infusion rates (eg in dehydrated patients) require reducing glucose
concentration. Patients with liver cell failure, adrenal insufficiency or metabolic crisis
should receive at least 10% glucose, even if insulin is required. Very rapid replacement
(eg severly polyuric patients) may not tolerate even 2.5% so use glucose-free fluids (±
low rate glucose 10% as a separate infusion).
(c) Unless sodium restriction is also necessary
(d) Interval depends on patient’s condition and how changing it is. As a start, use 1hr
for immediate postcardiac surgery, posttransplantation and those on CRRT; use 12-
24h for values close to normal maintenance (i.e. slight increase or decrease) and 4h for
most other cases. Increase interval when stable
(e) Extremely polyuric patients are expected to need higher Na and lower K content
(f) For example, upper GI losses by Ringer plus 20 mEq/l potassium, diarrhea by usual
rehydration solutions, drains with Ringer lactate, etc

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PICU Protocol of EHA

Dehydration & Deficit Therapy

Dehydration Mild Moderate Severe

Description History of ECF Significant Hypovolemic shock,
loss, acute wt loss, dehydration: score 3- lethargy* or severe
just detectable 7, or TWO of metabolic acidosis*
dehydration, score (sunken eyes, poor Score 8+ two of (sunken
1-2 skin turgor, thirst, eyes, very poor skin turgor,
irritability) lethargy* or inability to
drink*)
*of no other cause
Deficit (mL/Kg) 30-50 60-90 100-150
‘higher values for
smaller patients’

• Score allocates 2 points (0=normal, 1=mild, 2=severe) for each of fontanel,

tongue, eyes & skin turgor. Two points are added for each of shock, lethargy and
metabolic acidosis if present.

Deficit Therapy:
• Shock should be treated as needed. Patients with severe dehydration who are not
shocked may still be given a rapid bolus of 10-20mL/Kg isotonic crystalloid
(normal saline) over 30-60 min; which is then subtracted from deficit
There are rapid, slow & very slow methods for correction of dehydration:

Rate Rapid Slow Very slow

Duration ≤ 6hrs 24hrs ≥48 hrs
of
correction
Indications - Rapid fluid losses Most hospitalized Concerns of osmotic
- Acute severe dehydration (eg cases shifts
GE) (eg DKA,
In children with no concerns hypernatremia)
from rapid hydration (eg HF,
electrolyte disturbance, etc)
Technique Give deficit over 6h Give 24h maintenance Give maintenance +
(? 3-4h in children >2yrs) + deficit over 24hrs 30-50 mL/kg/day until
Other approaches: corrected (typically
- Give ½ deficit (+1/3 will take 2-3 days)
daily maint.) in 8h,
then ½ deficit (+2/3
daily maint) in 16h
- Give deficit + (½
daily maint) over 12h

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 PICU Protocol of EHA

• Type of fluid: 0.5NS –NS with glucose 2.5% (rapid)-5% (slow) and 20 mEq/l
potassium (more if needed). Premixed rehydration fluids with 77—142mEq/L
Na may be used (care of K content)
• Potassium should not be added in anuric or hyperkalemic patients although
hypokalemia may still be corrected (by formula, without maintenance K) in
anuric patients if needed.
• Dehydration should be reassessed frequently.

o Severity may be different from initial assessment and patients may have
abnormal losses or have/ develop acute kidney injury.

Hyponatremia
Hyponatremia denotes a free water excess relative to Na content; however, ECF
volume may be increased, normal or decreased
ECF volume Pathophysiology Examples Management strategy
Reduced Na loss > GE, diuretics, Rehydrate with higher Na
(hyponatremic water loss adrenal
dehydration) insufficiency, Crude: use NS or 3/4NS
salt-losing & modify according to
nephropathies, rate of Na rise
etc
Accurate: add 10 ml/kg
hypertonic saline to total
daily fluids
Normal Free water gain SIADH Water restriction (60-
Increased Water> salt Congestive HF, 70%)
retention hepatic failure,
nephrotic Use 0.5NS - NS (unless
syndrome Na restriction is also
needed)
• NS, 3/4NS & ½ NS refer to Na content. Appropriate glucose & K should be
added.
• Correction rate at no more than 0.5 mEq/Kg hourly (12/day), preferably even
slower (8/day). Check & modify rate of rise after 6h.
• Severe symptomatic cases may warrant initial partial correction with 5-10 ml/Kg
hypertonic saline to raise Na 4-8 mEq/L which is adequate to reverse acute
symptoms), followed by more gradual correction. Approaches include 5mL/kg
over 1-2 h (30 min for severe brain oedema) which may be repeated once.
Alternatively, 2mL/Kg over 15-30 min, which may be repeated once if
symptoms persist and for a 3rd time after checking serum Na if symptoms still
persist.

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PICU Protocol of EHA

Hypernatremia
Hypernatremia denotes a free water deficit relative to Na content; however, ECF
volume may be increased, normal or decreased

ECF volume Pathophysiology Examples Management strategy

Reduced Water loss> GE Give maintenance +
(hypernatremic Na loss 40mL/Kg/day with 1/3NS-
dehydration) ½ NS

Modify according to rate

of Na drop:
- If too slow: ↑rate or ↓Na
content, & vice versa
Normal Free water loss DI Give 40mL/Kg free water
Increased Hypertonic Na Concentrated (eg G5%) per 24h and the
intake formula, sea remaining fluids as usual
water, Na
bicarbonate, etc

• ½ NS & 1/3NS refer to Na content. Appropriate glucose & K should be added.

• Na content can be given as bicarbonate in acidotic patients (eg 30mL bicarbonate

in 500 mL glucose 5% + 5mL KCl will be 60meq/L Na – between 1/3NS & ½
NS)

• Correction rate at no more than 0.5 mEq/Kg hourly (12/day). Check & modify
rate of drop after 6h.

• An accurate calculation is possible, based on urine vol, urine Na, insensible loss
& current ECF volume status to determine 24h maintenance water & Na
requirements separately. Then, allocate 40 mL/kg of the total volume as free
water and give the remainder with the proportional amount of calculated Na.

• PD is needed for refractory hyperNa, intractable acidosis or associated AKI with

need for dialysis

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 PICU Protocol of EHA

Hypokalemia

• Interpret K together with pH (a low pH ➔ extracellular shift of K so level will

increase; correction will lower K correspondingly)

• Mild hypokalemia which is non-progressive may be corrected by increasing K

intake.
• Otherwise, correction can be achieved using the formula:

"Body weight X deficit (target-actual K) X 0.6 mEq (0.3 mL)"

• Amount to be diluted in normal saline & given over few hrs (correct 0.5mEq/l
per hr).

• Never give concentrated KCL.

• Target K is 3.0 for chronic hypokalemia & where complete correction is risky
or not necessary, 4.0 for those with or at risk for arrhythmia or during correction
of acidosis & 3.5 for most cases

• An empiric correction using 0.5mEq/Kg (0.25mL/Kg), DILUTED and given

over 1-2 hr may be used

Hyperkalemia
• Interpret K together with pH (correction of acidosis could correct hyperkalemia)
• Emergency measures for hyperkalemia: (K> 7 mEq/L, rising or with ECG
changes)
(all may be temporary & K can rebound so if hyperkalemia is severe and K
cannot be eliminated from the body, dialysis will be needed)
• Calcium gluconate IV to reverse membrane effects of K
• Intracellular shift with bicarbonate, iv or nebulized salbutamol &/or glucose-
insulin
• Potassium removal can be achieved using loop diuretics, cation exchange resin
(Ca or Na polystyrene sulfonate) or dialysis. The administration of
corticosteroids & fluids in cases of hyperkalemia secondary to adrenal
insufficiency is also effective.

23
PICU Protocol of EHA

Fluids & mixtures by sodium content

Na (mEq/L) Examples Glucose & K content

Isotonic ±150 Normal saline None K (4-5 mEq/L) in
Ringer & lactated Ringer (Na ringer & LR
slightly less)
3/4 NS ±110 Glucose: saline 1:3 1/4th source glucose (2.5%
if using 10%), No K
80-90 IV rehydration premixed Glucose <5%
solutions K varies by brand (8-
30mEq/L)
½ NS 77 Glucose: saline 1:1 ½ source glucose (5% if
Half normal saline using 10%, 2.5% if 5%),
No K
1/3 NS ±50 No K. Using 5%, final
glucose:
Glucose: saline 2:1 3.3% (6.7% with 10%)
Glucose: ½ NS 1:2 1.7%
1:19 bicarb: glucose 5%
(25mL/500) 5% & higher Na(60mEq/L)
1:16 bicarb: glucose
(30mL/500)
0.2NS ±30 Glucose 10%: saline 4:1 8%, No K
Glucose 10%: 25%: saline 11%, No K
3:1:1 12%, K 10mEq/L
Neomaint 10%, K 20mEq/L, higher
Pedimaint Na (37)
0 Glucose (all conc.)
Glucose 25% can be used to increase final mixture glucose concentration. Kadalex is
glucose 5% with 27mEq/L potassium. To increase K by 20 mEq/L add 5mL KCl per
500 mL, or 1 mL/100Ml

Formulae & Calculations

Body surface area (m2) = weight (kg) x 4 + 7

weight (Kg)+90
10 Kg ≈ 0.5m , 20 Kg ≈ 0.8m2, 30 Kg ≈1m2, adult ≈1.7m2
2

mL/day to drops/ min: divide by 100

eg 10 Kg with maintenance 100 mL/Kg/d = 1000 mL/day

Rate (drops per min. by ordinary IV set) = 1000 (mL/day)/ 100 = 10 (drops/ min.)

24
 PICU Protocol of EHA

Limit of oliguria:
-400 mL/m2/day
-25% normal maintenance
-1mL/Kg/hr up to 10 Kg, 0.5mL/Kg/hr >10Kg, 20mL/hr in those >40kg

eg 10 Kg: 1 mL/kg/h = 10 mL/h = 240 mL/day

30 Kg= 1 m2 body surface area = 400 mL/day

Limit of polyuria:
-2000 mL/1.7m2/d
- 0.8-1.0 x normal maintenance
- 3mL/kg/hr up to 10 Kg

eg 10 Kg: 30 mL/hr= 720 mL/day

30 Kg= 1m2 body surface area = 1200 mL/day (2000mL/1.7m2)

Universal fluid balance formula:

Obligatory intake (medications, infusions, transfusions) + enteral*&parenteral

nutrition + IV fluids= Insensible loss + Urine output + Abnormal losses +
Ultrafiltration
*only calculate oral/enteral fluids and water content of foods (eg 85% of milk formula)

Metabolic acidosis:
Weight x deficit x 0.33 = mEq NaHCO3 (or mL 8.4% solution)

Deficit= base deficit -5, also ½ base deficit or 15- patient bicarbonate
eg 10 Kg, base excess -20 mEq/L
Deficit (base deficit - 5) = 20 - 5 = 15
Amount of 8.4% bicarbonate: 10 (weight) X 15 (deficit) X 0.33 = 50 mL

Hypokalemia:

Weight x deficit x 0.6 = mEq KCl (or 0.3 = mL KCl)

KCl MUST BE DILUTED in normal saline

Deficit= target K – patient K , Target K can be 3-4 meq/L depending on the condition
Correct a deficit of 0.5/hr

Hyponatremia:
Rapid correction 5-10 mL/ Kg hypertonic saline in 2hrs

25
PICU Protocol of EHA

Glucose: insulin for hyperkalemia:

MIX 0.5g/kg glucose (eg 5ml/kg glucose 10%, 2mL/Kg 25%) with 0.1 u/kg soluble
insulin & give over ½ hr. May double both, i.e. 1g/kg glucose & 0.2 u/Kg insulin

eg 20 Kg
GLUCOSE: 40 mL of 25% or 100 mL of 10%
INSULIN: 2 u soluble insulin

24-hr infusion calculation:

Basic formula 1.44 mg/Kg/day (or 1.5 mg/25hrs) = 1 mcg/Kg/min
Body weight (Kg) x target dose (mcg/Kg/min.) x 1.44 mg ➔ dilute to 24mL & give
at 1 mL/hr

eg 20 Kg, Noradrenaline 0.1 μg/Kg/min

20 (body weight) X 0.1 (target dose) X 1.44 ≈ 3 mg
3 mg diluted to 24 mL and give at 1 mL/hr
1 mL/hr = 0.1 μg/Kg/min. Adjust rate according (eg 1.5mL/hr= 0.15 μg/Kg/min.)

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 PICU Protocol of EHA

Shock
Definition:

Shock is an acute process characterized by the body’s inability to deliver

adequate oxygen to meet the metabolic demands of vital organs and tissues.

Table (1): Types of Shock (Nelson 20th edition)

Hypovolemic Cardiogenic Distributive Septic Obstructive
Decreased Cardiac pump Abnormalitie Encompasses Decreased
preload failure secondary s of multiple forms of cardiac output
secondary to to poor vasomotor shock secondary to
internal or myocardial tone from Hypovolemic; direct
external losses function loss of third spacing of impediment
venous and fluids into the to right- or
arterial extracellular, left- heart
capacitance interstitial space outflow or
Distributive: early restriction of
shock with all cardiac
decreased afterload chambers
Cardiogenic;
depression of
myocardial function
by endotoxins
Potential Congenital heart Anaphylaxis Bacterial Viral Fungal Tension
etiologies disease Neurologic: (Immunocompromise pneumothora
Blood loss: Cardiomyopathies loss d patients are at x Pericardial
hemorrhage; : infectious or of increased risk) tamponade
Plasma loss: acquired, dilated sympathetic Pulmonary
burns, nephrotic or restrictive vascular tone embolism
syndrome; Ischemia secondary to Anterior
Water/electrolyt Arrhythmias spinal cord or mediastinal
e loss: vomiting brainstem masses
diarrhea injury Critical
Drugs coarctation of
the aorta

27
PICU Protocol of EHA

Table (2): Hemodynamic variables in different shock states

(nelson 20th edition)

Type of Cardiac Systemic Mean Capillary Central

shock output vascular arterial wedge venous
resistance pressure pressure pressure
Hypovolemic ↓ ↑ ↔ or ↓ ↓↓↓ ↓↓↓
Cardiogenic*
Systolic ↓↓ ↑↑↑ ↔ or ↓ ↑↑ ↑↑
Diastolic ↔ ↑↑ ↔ ↑↑ ↑
♦ ♦
Obstructive ↓ ↑ ↔ or ↓ ↑↑ ↑↑
Distributive ↑↑ ↓↓↓ ↔ or ↓ ↔ or ↓ ↔ or ↓
Septic
Early ↑↑↑ ↓↓↓ ↔ or ↓□ ↓ ↓
Late ↓↓ ↓↓ ↓↓ ↑ ↑ or ↔
Systolic or diastolic dysfunction
Wedge pressure, central venous pressure, and pulmonary artery diastolic
pressures are equal
Wide pulse pressure

Sepsis:
• Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host
response to infection (new definition JAMA 2016).
• Organ dysfunction can be identified as an acute change in total SOFA score 2 points
consequent to the infection.
• The baseline SOFA score can be assumed to be zero in patients not known to have
preexisting organ dysfunction.

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 PICU Protocol of EHA

SOFA Score:
Table (3): Sequential [Sepsis-related] organ failure assessment score
(JAMA 2017)

qSOFA Score:
• Patients with suspected infection who are likely to have a prolonged ICU stay or to
die in the hospital can be promptly identified at the bedside with qSOFA, ie, alteration
in mental status, systolic blood pressure 100 mm Hg, or respiratory rate 22/min.

Box 4. qSOFA (Quick SOFA) Criteria (JAMA 2016)

- Respiratory rate ≥ 22/min.
- Altered mentation
- Systolic blood pressure ≤ 100 mmHg

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PICU Protocol of EHA

Septic shock
• Septic shock is a subset of sepsis in which underlying circulatory and cellular/
metabolic abnormalities are profound enough to substantially increase mortality.

Patients with septic shock can be identified

• With a clinical construct of sepsis with persisting hypotension requiring
vasopressors to maintain MAP 65 mm Hg and having a serum lactate level >2 mmol/L
(18 mg/dL) despite adequate volume resuscitation. With these criteria, hospital
mortality is in excess of 40%.

How to differentiate between cold and warm shock?

Cold shock Warm shock

Capillary refill > 2 seconds Flash capillary refill
Peripheral pulses Diminished Bounding
Mottling of skin Present Absent
Pulse pressure Narrow Wide
How to proceed? (JAMA 2016)

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 PICU Protocol of EHA

Management of Septic Shock (nelson 21th edition)

31
PICU Protocol of EHA

Early Goal Directed Therapy: (The 2012 Surviving Sepsis Campaign

Guidelines)
During the first 6 hours of resuscitation, the goals of initial resuscitation of
sepsis-induced hypoperfusion should include all of the following as one part of a
treatment protocol:
● Central venous pressure (CVP) 8-12 mm Hg
● Mean arterial pressure (MAP) ≥65 mm Hg
● Urine output ≥0.5 mL/kg/hr
● Cardiac index > 3.3 < 6.0L/min/m2 in PICU
● Central venous (superior vena cava) or mixed venous oxygen saturation
● ≥70 percent or ≥65 percent, respectively

Therapeutic Endpoints
Clinical
● Heart Rate normalized for age
● Capillary refill < 2sec
● Normal pulse quality
● Warm extremities
● Blood pressure normal for age
● Urine output >1 mL/kg/h
● Normal mental status
● CVP >8 mmHg
● No difference in central and peripheral pulses

Threshold rates Heart rate (bpm) Mean arterial pressure

Term newborn 120-180 55
Up to 1 yr 120-180 60
Up to 2 yrs 120-160 65
Up to 7 yrs 100-140 65
Up to 15 yrs 90-140 65

Laboratory:
● Decreasing lactate
● SvO2 >70%

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 PICU Protocol of EHA

Table (4): Vasodilators/Afterload Reducers (nelson 20th edition)

Drug Effect(s) Dosing range Comment(s)
Nitroprusside Vasodilator (mainly 0.5-4.0 µg/kg/min Rapid effect
arterial) Risk of cyanide
toxicity with
prolonged use (>
96 hr)
Nitroglycerin Vasodilator (mainly 1-20 µg /kg/min Rapid effect Risk of
venous) increased
intracranial pressure
Prostaglandin E1 Vasodilator 0.01-0.2 µg /kg/min Can lead to
Maintains an open hypotension Risk of
ductus arteriosus in the apnea
newborn with ductal-
dependent congenital
heart disease
Milrinone Increased cardiac Load 50 µg /kg over Phosphoodiesterase
contractility Improves 15 min inhibitor
cardiac diastolic function 0.5-1.0 µg/kg/min – slows cyclic
Peripheral vasodilation adenosine
monophosphate
breakdown

33
PICU Protocol of EHA

Table (5): Cardiovascular Drug Treatment of Shock (nelson 20th edition)

Drug Effect(s) Dosing range Comment(s)
Dopamine ↑ Cardiac contractility 3-20 µg/kg/min ↑ Risk of
arrhythmias at high
doses
Significant peripheral
vasoconstriction at > 10
g/kg/min
Epinephrine ↑ Heart rate and ↑ cardiac 0.05-3.0 µg/kg/min May ↓ renal
contractility perfusion at high
Potent vasoconstrictor doses
↑ Myocardial O2
consumption
Risk of arrhythmia at
high doses
Dobutamine ↑ Cardiac contractility
Peripheral vasodilator
Norepinephrine Potent vasoconstriction 0.05-1.5 µg/kg/min ↑ Blood pressure
secondary to ↑
No significant effect on systemic vascular
cardiac contractility resistance
↑ Left ventricular
afterload
Phenylephrine Potent vasoconstriction 0.05-2.0 µg/kg/min Can cause sudden
hypertension
↑ O2 consumption

Terlipressin dose in septic shock:

● Loading dose 20 mic/kg/ dose followed by continuous infusion 4- 20 mic/ kg/ hour

34
 PICU Protocol of EHA

REFERENCES:

▪ David A. Turner and Ira M. Cheifetz, shock Chapter 70 Part IX

516:528 nelson textbook of pediatrics 20th edition 2015
▪ Mervyn Singer, Clifford S. Deutschman, Christopher Warren
Seymour, Manu Shankar-Hari, Djillali Annane, Michael Bauer et
al., The Third International Consensus Definitions for Sepsis and
Septic Shock(Sepsis-3) JAMA.2016; 315(8):801-810.
▪ Rodriguez-Nunez A, Lopez-Herce J, GilAntonJ, et al: Rescue
treatment with terlipressin in children with refractory septic shock:
A clinical study. Crit Care 2006; 10: R20 (doi:10.1186/cc3984)

35
PICU Protocol of EHA

Anaphylactic Shock:
Emergency Treatment:

• Patients with anaphylaxis should be placed on their back with lower extremities
elevated. If short-of-breath and/or vomiting, patient should be placed semi-upright in
a position of comfort with the lower extremities elevated.

➢ Intramuscular epinephrine 1: 1000 (1 mg/ml) at a dose of 0.01 mg/kg body

weight up to a maximum dose of 0.3 mg injected into the lateral thigh (vastus
lateralis).
➢ The dose can be repeated at 5-15 min intervals.
➢ The intramuscular route is preferred because epinephrine has a vasodilator
effect in skeletal muscle. After IM injection into the vastus lateralis, absorption
is rapid, and epinephrine reaches the central circulation rapidly.
➢ The maximum dose of epinephrine in anaphylaxis is lower than the dose used
in cardiopulmonary resuscitation.
➢ Failure to inject it promptly before the patient gets acute cardio-respiratory
failure and shock potentially increases the risk of death and the risk of biphasic
anaphylaxis (late phase reaction).

• Support the airway and ventilation

• Give supplementary oxygen 6-8 L/min

• Resuscitate with intravenous saline 0.9% (20 ml/kg body weight, repeated up to a
total of 50 ml/kg over the first half an hour.

• Other lines of treatment:

➢ Nebulized beta-2 stimulants: Decrease wheeze but are not life-saving H1-
antihistamines: Decrease itch and hives but not life saving
➢ Dose of diphenhydramine (Pirafene 50 mg/ml):
✓ 2-6 years: 6.25 mg 6-12 years: 12.2-25 mg > 12 years: 25-50 mg
➢ Corticosteroids: effects take several hours: not lifesaving. Used to prevent
biphasic; however, there is no evidence that this occurs.
➢ Dose of Hydrocortisone : 2.5- 5mg / kg

36
 PICU Protocol of EHA

Refractory Cases:

• IV epinephrine: central line – 1:10,000 solution – infusion pump ⁻ Intubation

• Cricothyrotomy

• Vasopressors

• Glucagon: exerts positive inotropic and chronotropic effects on the heart,

independent of catecholamines. Therefore, glucagon, 1 mg intravenous bolus, followed
by an infusion of 1 to 5 mg per hour, may improve hypotension in one to five minutes,
with a maximal benefit at five to 15 minutes. (The U.S. Food and Drug Administration
have not approved glucagon for this use.) Nausea and vomiting may limit therapy with
glucagon.

Duration of Monitoring:

• Protracted or biphasic anaphylaxis (up to 72 hours; usually within 10 hours) occurs

in up to 20% of adults and 6% of children. ⁻ Patients should ideally be monitored for
at least 4, and preferably 8-10 hr.

• Some cases require monitoring for ≥ 24 hours.

37
PICU Protocol of EHA

• IV epinephrine: central line – 1:10,000 solution – infusion pump

• Intubation
• Cricothyrotomy
• Vasopressors: noradrenaline or dopamine
• Glucagon

Acknowledgment:
▪ Thanks to Prof. Dr. Elham Hosni, for participating in this chapter.

38
 PICU Protocol of EHA

REFERENCE:
▪ Simons FER et al., for the WAO. J Allergy Clin Immunol 2011; 127: 587-
93-e22 and WAO Journal 2011; 4: 13-36. Illustrator: J Schaffer

39
PICU Protocol of EHA

40
 PICU Protocol of EHA

41
PICU Protocol of EHA

Acute Severe Asthma

42
 PICU Protocol of EHA

Managing exacerbations in acute care settings

43
PICU Protocol of EHA

Primary care management of acute asthma or wheezing in pre-schoolers

44
 PICU Protocol of EHA

Treatment of Acute Severe Asthma in PICU:

1. Monitoring:
• Noninvasive blood pressure and oxygen saturations (SpO2). Those with respiratory
failure requiring mechanical ventilation should undergo the placement of central
venous, arterial, and urinary bladder catheters.
2. Oxygen:
• Oxygen should be used as carrier gas for intermittent or continuous nebulization and
to keep oxygen saturation above 92%.
3. Steroids:
• Methylprednisolone loading dose of 2 mg/kg followed by 0.5 to 1 mg/kg every 6
hours.
4. Bronchodilator:
• The usual dose for continuous albuterol nebulization ranges from 0.15 to 0.5
mg/kg/h.
• Nebulized ipratropium, in 0.25 to 0.50 mg doses, can be used every 20 minutes
during the first hour, followed by the same dose range every 6 hours.
5. Magnesium Sulfate:
• The dose of magnesium sulfate is 25 to 50 mg/ kg/dose (maximum 2 g), infused for
20 to 30 minutes, and followed by continuous infusion dependent on the patient’s
weight.
• Children weighing < 30 kg: of 25 mg/kg/h
• Children weighing > 30 kg may receive 20 mg/kg/h,
• Infusion rates must not exceed 2 g/h in any patient. Titration to the desired clinical
effect should be based on serum magnesium concentrations and tolerability.

Keep serum magnesium level below 6 mg /dl

• Observation of magnesium sulphate side effects:

Serum magnesium concentrations above 9 mg/dL causes:

Nausea, flushing, somnolence, vision changes, muscle weakness and hypotension

Serum magnesium concentrations above 12 mg/dL causes:

Respiratory depression and arrhythmias

45
PICU Protocol of EHA

6. Methylxanthines:

• The theophylline dose is 80% of the aminophylline dose.

• A loading intravenous dose, 5mg/kg of theophylline or 6 mg/kg of aminophylline,
given during 20 minutes is needed to achieve a therapeutic concentration.
• After the loading dose, a continuous infusion should be started. Infants younger than
6 months are 0.5 mg/kg/h
• Infants 6 months to 1 year 0.85 to 1 mg/kg/h
• Children 1 to 9 years, 1 mg/ kg/h
• Children older than 9 years, 0.75 mg/kg/h.

Serum drug concentrations should be obtained:

• 30 to 60 minutes after the loading dose is finished

• At 12 hours after the beginning of the continuous infusion
• Every 12 to 24 hours or when toxicity is suspected.

7. Mechanical ventilation of asthmatic patients:

Bilevel Positive Airway Pressure

• Noninvasive positive pressure ventilation (NPPV) in addition to conventional

therapy showed clinical improvement and correction of gas exchange abnormalities in
children and adults with asthma. NPPV was well tolerated in children, including
patients as young as 1 year
• Typically, recommended settings include an inspiratory positive airway pressure of
10 cm H2O, an expiratory positive airway pressure of 5 cm H2O, with or without a
low back-up ventilation rate.

Criteria for selecting severe asthmatic patients for NPPV trial

✓ Tachypnea above normal limit of age
✓ Tachycardia above normal limit of age
✓ Use of accessory muscles of respiration
✓ Hypoxia with a Pa,O2/FI,O2 ratio >200 mmHg
✓ Hypercapnia with Pa, CO2, 60 mmHg FEV1< 50% pred"

46
 PICU Protocol of EHA

Absolute and relative contraindication for noninvasive positive pressure

ventilation (NPPV) trial

Absolute contraindications:
✓ Need for immediate endotracheal intubation
✓ Decreased level of consciousness
✓ Excess respiratory secretions and risk of aspiration
✓ Past facial surgery precluding mask fitting

Relative contraindication:

✓ Hemodynamic instability
✓ Severe hypoxia and/or hypercapnia, Po2/Fio2 ratio of [ 200 mmHg,
Pco2 ] 60 mmHg
✓ Poor patient cooperation
✓ Severe agitation
✓ Lack of trained or experienced staff

Invasive Mechanical Ventilation:

1. Criteria for intubation

2. Recommendations for intubation technique
3. Recommendations for appropriate ventilator settings
4. Management in the immediate postintubation period
5. Medical management of asthma in the ventilated patient 6- Prevention
and treatment of complications.
6. Prevention and treatment of complications.

47
PICU Protocol of EHA

48
 PICU Protocol of EHA

Criteria for Intubation:

Clinical:

• Cardiac arrest
• Respiratory arrest
• Progressive exhaustion
• Altered sensorium such as lethargy or agitation, interfering with oxygen delivery or
anti-asthma therapy.

Laboratory:

• pH less than 7.2, carbon dioxide pressure increasing by more than 5 mm Hg/h or
greater than 55 to 70 mm Hg, or oxygen pressure less than 60 mm Hg on 100% oxygen
delivered through a mask.

• Failure to reverse severe respiratory acidosis despite intensive therap.

1. Recommendation for intubation:

✓ Orotracheal intubation with sedation and neuromuscular

blockade are preferred for asthmatic patients in critical respiratory
distress.
✓ Intubation medication

• Atropine at a dose of 0.02 mg/kg IV (minimum 0.1 mg, maximum 0.5 mg child, 1
mg adolescent) used to attenuate the vagal reflexes that lead to laryngospasm and
worsen bronchospasm

• Ketamine: 1.0 to 1.5 mg/kg I.V and 1.0 to 1.5 mg/kg succinylcholine I.V
o It stimulates the release of catecholamines leading to bronchodilation; Side
effects include hypersecretion, hypotension and hypertension, arrhythmias,
and hallucinations

• Or propofol 2 mg/kg administered I.V over 2 minutes with succinylcholine,

preferred in patients with hypertension, and succinylcholine should be avoided in
patients with hyperkalemia.

49
PICU Protocol of EHA

2. Mechanical ventilation recommendations:

➢ Low rate
➢ Low PEEP
➢ Prolonged expiratory time
➢ Allow hypercapnia: till pH as low as 7.15 and a Pa CO2 of up to 80 mmHg

All these settings to avoid hyperinflation and auto-PEEP

1. Deal with expected complications:

❖ Hypotension:

Look for:
✓ Pneumothorax
✓ Hypovolemia
✓ High auto PEEP

❖ Cardiac arrest:

Look for:
✓ Hypoxia
✓ Exclude right mainstem intubation (21 cm at incisors)
✓ Exclude pneumothorax and place pleural drain
✓ Exclude pneumonia and other lung disease
✓ Pneumothorax

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 PICU Protocol of EHA

Mechanical ventilation algorithm

51
PICU Protocol of EHA

References:
▪ Nievas IF, Anand KJ, Severe acute asthma exacerbation in children: a
stepwise approach for escalating therapy in a pediatric intensive care unit.
J Pediatr Pharmacol Ther. 2013 Apr;18(2):88-104. doi: 10.5863/1551-6776-
18.2.88.

▪ Barry Brenner, Thomas Corbridge, and Antoine Kazzi Intubation and

Mechanical Ventilation of the Asthmatic Patient in Respiratory Failure
Proc Am Thorac Soc Vol 6. pp 371–379, 2009

▪ A. Soroksky, E. Klinowski, E. Ilgyev, A. Mizrachi, A. Miller, T. M. Ben

Yehuda, I. Shpirer, Y. Leonov Noninvasive positive pressure ventilation in
acute asthmatic attack Eur Respir Rev 2010; 19: 115, 39–45.

▪ Asthma clinical care guidelines, Children’s Hospital Colorado

▪ Soroksky, E. Klinowski, E. Ilgyev, A. Mizrachi, A. Miller, T. M. Ben

Yehuda, I. Shpirer, Y. Leonov 2010 Noninvasive positive pressure
ventilation in acute asthmatic attack, Eur Respir Rev 2010; 19: 115, 39–45

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 PICU Protocol of EHA

Status Epilepticus
Definition:
5 min or more of (i) continuous clinical and/or electrographic seizure activity or (ii)
recurrent seizure activity without recovery (returning to baseline) between seizures.

53
PICU Protocol of EHA

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 PICU Protocol of EHA

Table (6): Intermittent drug dosing in SE (Brophy et al., 2012)

55
PICU Protocol of EHA

Table (7): Pharmacological and non-pharmacological therapies

for the treatment of RSE/SRSE (A. Vasquez, et al., 2018)
Mechanism of Adverse Clinical Level of
dose
action events considerations evidence
Pharmacological therapies
Benzodiazepines
Midazolam Positive Loading Hypotensi Prolonged use Class
allosteric dose: 0.2 on, may cause IIA,
modulation of mg/kg; respiratory tachyphylaxis Level B
administer at depressio and drug Class IV
GABA- A
an infusion n accumulation
receptors, rate of 2
Increases mg/min
frequency of CI Infusion rate:
channel 0.05– 2
opening mg/kg/h
Breakthrough
SE: 0.1–0.2
mg/kg bolus,
increase
rate by 0.05–
0.1
mg/kg/h.
every 3–4 h
IV anesthetic Activation of Long half-life
Loading Hypotension, Class
GABA (15–
agents Barbiturates Receptors
dose: 5– 15 cardiac and 50 h) Requires IIB,
increase
Pentobarbital mean CI
mg/kg; respiratory mechanical Level B
channel
opening
infusion rate depression, ventilation. Can Class IV
duration,
inhibition of paralytic
≤ 50 mg/min exacerbate
NMDA ileus,
receptors, porphyria
Infusion rate: infection
alteration in Hepatic
conductance of
0.5– 5 enzyme inducer
Cl, K+
, Ca2+ ion Drug
mg/kg/h
channels. accumulation
Same as with prolonged
Breakthrough
Pentobarbital use
SE: 5 mg/kg
bolus,
increase rate
by 0.5– 1
mg/kg/h.

every 12 h

56
 PICU Protocol of EHA

Mechanism of Adverse Clinical Level of

dose
action events considerations evidence
Pharmacological therapies

Thiopental Same as the 2–7 mg/kg, Hypotension, Requires Class IV

mechanism
infusion rate cardiac and mechanical
described
ventilation,
Above ≤ 50 mg/min respiratory
titrate
Infusion/ depression infusion rates to
EEG burst-

maintenance

rate: 0.5–5 suppression

mg/kg/h
Breakthrough
SE:1– 2
mg/kg bolus,
titrate by 0.5–
1 mg/ kg/h.

every 12 h
Propofol Chloride channel Initial loading PRIS, Requires Class
mechanical
conductance, dose: 1–2 hypotension, ventilation IIB,
enhances
GABA-A receptor mg/kg Initial cardiac and Prolonged Level B
infusion
infusion rate respiratory of propofol is a Class IV
20 depression relative
mcg/kg/min contraindication
in
titrated by 5– children (due to
risk
10 of PRIS) and in
mcg/kg/min patients with
Use with metabolic
acidosis,
caution with mitochondrial
doses > 65 disorders or
mcg/kg/min hypertriglyceride
mia
Breakthrough Reduces ICP
SE: Increase Caution with
infusion rate concomitant use
of
by 5–10 mcg/ steroid or
kg/min every catecholamine
5 min therapy

57
PICU Protocol of EHA

Mechanism of Clinical Level of

Dose Adverse effects
action considerations evidence
Ketamine Noncompetitive 0.5–3 mg/kg Tachycardia, Relative Class IV
NMDA glutamate Infusion rate: hypertension, contraindication in
receptor antagonist 1–10 mg/kg/h ICP elevation patients with ICP.
reduces neuronal Ketamine is an
excitability enzyme inducer and
inhibitor (CYP2C9)
Inhalational Enhancement of Concentration Hypotension High seizure Class IV
Anesthesia GABA-A receptors, 1–5% Titrate requiring use recurrence rate
of
Isoflurane noncompetitive to achieve vasopressors,
antagonist of NMDA burst- atelectasis,
receptor suppression paralytic ileus,
on
EEG infection, deep
vein
thrombosis
Immunomodulatory Alteration of IgG- 1–2 g/kg Hypersensitivit Immunomodulatory Class IV
y
therapy IVIG specific receptors divided over reactions, therapies may be
(FcgR) expression 3–5 days transfusion considered in
and
function (decreases related acute patients with
cytokine lung injury, cryptogenic,
production),
attenuation of thromboemboli autoimmune
c
complement events, renal etiologies of
mediated
cell damage dysfunction RSE/SRSE.
with
concentrated
solutions,
aseptic
meningitis
Corticosteroids: Inhibition of Glucose Class IV
Methyl inflammation 1 g/day for 3– intolerance,
Prednisolone associated proteins 5 days psychiatric
(e.g.
cytokines, disturbances,
chemokines)
and altered
immune
immunosuppressive function,
adrenal
action suppression

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 PICU Protocol of EHA

Mechanism of Clinical Level of

Dose Adverse effects
action considerations evidence

Non-pharmacological alternatives
Ketogenic diet Ketosis 4:1 (ratio fat Hypoglycemia, Contraindicated Class
mediated to hyperlipidemia, in pyruvate IV
decreased carbohydrates weight loss, carboxylase
glycolysis, and proteins) acute deficiency,
increase in free
pancreatitis, disorders of
and
polyunsaturated metabolic fatty acid
fattyacids, anti- acidosis oxidation and
inflammatory metabolism,
action, orporphyria
stabilization of
neuronal
membrane
Hypothermia Reduction of Na+ 32–35C x Deep venous Requires EEG Class
IV
exchange, 24h thrombosis, monitoring
decreased
K+ conductance, Rewarming ≤ infections,
regulation of 0.5 C/ h cardiac
glutamatergic arrhythmias,
synaptic
transmission, electrolyte
disruption of disturbances,
synchronized acute intestinal
discharges ischemia,
coagulation
disorders
Electroconvulsive Enhancement of Variable May induce Relative Class
IV
Therapy GABA protocols seizures and contraindication in
neurotransmission, non-convulsive patients with
increase of seizure SE after cardiovascular
threshold and treatment, conditions
Requires
reduction of neural amnesia, EEG monitoring
metabolic activity headache,
cognitive
impairment
Vagus nerve Modulation of the Surgical Hoarseness, Class
IV
Stimulation locus coeruleus, implantation surgical
thalamus and infection, rarely
limbic
circuit through asystole or
noradrenergic and bradycardia
serotoninergic
projections,
elevation
of GABA levels in
brainstem

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PICU Protocol of EHA

N.B:
• If patient is less than 18 months give pyridoxine 100 mg i.v

• As regards thiopental infusion:

➢ If thiopental infusion is started stop midazolam infusion

➢ Increase thiopental infusion by 1mg/kg/hour every 30 min and give 2mg/kg

bolus as needed if seizures is occurred on infusion

➢ If convulsion is controlled Taper thiopental infusion after 24- 48hours by 25%

decrease every 12 hours

• As regard propofol infusion:

➢ When seizures have been controlled for 12 hours, the drug dosage should be
slowly reduced over a further 12 hours. If seizures recur, the drug infusion should
be given again for another 12 hours, and then withdrawal attempted again. This
cycle may need to be repeated every 24 hours until seizure control is achieved.

• When to do EEG:
➢ After clinical control of convulsion to diagnose subclinical status epilepticus

➢ After midazolam or thiopental or propofol infusion to document burst

suppression

Acknowledgment:
▪ Thanks to Prof. Dr. Hoda Tomom, and Pediatric Neurology Team for
their help and participation in this chapter.

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 PICU Protocol of EHA

References:
▪ Proposed Algorithm for Convulsive Status Epilepticus From “Treatment
of Convulsive Status Epilepticus in Children and Adults,” Epilepsy
Currents 16.1 - Jan/Feb 2016

▪ Nicholas S. Abend, MD and Dennis J. Dlugos, MD, MSCE, Treatment of

Refractory Status Epilepticus: Literature Review and a Proposed Protocol
PEDIATRIC NEUROLOGY Vol. 38 No. 6 june 2008

▪ Alejandra Vasqueza, Raquel Farias-Moellerb, William Tatumc, Pediatric

refractory and super-refractory status epilepticus, Eur J Epilepsy (2018)

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PICU Protocol of EHA

Diabetic ketoacidosis
Definition:
Diabetic Ketoacidosis is one of two serious, acute life-threatening complications
of Type I diabetes mellitus (IDDM), or Type II, insulin insufficient diabetes mellitus,
the other being severe hypoglycemia.

The biochemical criteria:

Blood glucose > 200 mg/dL

Venous pH < 7.3
bicarbonate < 15 mmol/L
Ketonemia or Ketonuria

The severity of DKA is categorized by the degree of acidosis

Degree pH HCO3
Mild < 7.3 <15 mmol/L
Moderate < 7.2 <10 mmol/L
Severe < 7.1 <5 mmol/L

Clinical Signs:
1. Dehydration (which may be difficult to detect)

2. Tachycardia

3. Tachypnea (which may be mistaken for pneumonia or asthma)

4. Deep, sighing (Kussmaul) respiration; breath has the smell of acetone

5. Nausea, vomiting (which may be mistaken for gastroenteritis)

6. Abdominal pain that may mimic an acute abdominal condition

7. Confusion, drowsiness, progressive reduction in level of consciousness

and, eventually, loss of consciousness.

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 PICU Protocol of EHA

Management:
Acute management should follow the general guidelines for PALS with
particular attention to the following aspects for the child who presents in DKA.

1. Immediately measure BG and urine ketone concentrations with bedside

meters.
2. Perform a clinical evaluation to identify a possible infection
3. Weigh the patient
4. Assess severity of dehydration:

5% dehydration Prolonged capillary refill time (normal

capillary refill is ≤1.5–2 s)
Abnormal skin turgor (‘tenting’ or inelastic skin)
Abnormal respiratory pattern (hyperpnea).
Dry mucus membranes, sunken eyes, absent tears,
weak pulses, and cool extremities.

≥10% dehydration weak or impalpable peripheral pulses

hypotension
oliguria

5. Assess level of consciousness using Glasgow coma scale (GCS).

6. Additional measures is done of unconscious patient Secure the airway and
empty the stomach by continuous nasogastric suction to prevent pulmonary
aspiration
7. Give oxygen to patients with severe circulatory impairment or shock.
8. A cardiac monitor should be used for continuous electrocardiographic
monitoring to assess T waves for evidence of hyper- or hypokalemia
9. Obtain a blood sample for laboratory measurement of:

✓ Serum or plasma glucose

✓ Electrolytes (including Na, K)
✓ Blood urea nitrogen, creatinine
✓ Serum osmolality
✓ Venous pH, pCO2

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PICU Protocol of EHA

✓ Complete blood count. Note that an increased white blood cell count
in response to stress is characteristic of DKA and is not indicative of
infection.
✓ Albumin, calcium, phosphorus, magnesium concentrations.
✓ Urine analysis
✓ Cultures (blood, urinary, sputum) only if evidence of infection
✓ HbA1c to assess duration of hyperglycemia
✓ ECG is done if serum measurement of K is delayed

10. Give antibiotics to febrile patients after obtaining appropriate cultures of

body fluids
11. Catheterization of the bladder usually is not necessary, but if the child is
unconscious or unable to void on demand (e.g., infants and very ill young
children) the bladder should be catheterized

Goals of therapy:

a. Correct dehydration

b. Correct acidosis and reverse ketosis

c. Restore BG to near normal

d. Monitor for complications of DKA and its treatment

e. Identify and treat any precipitating event

Calculations:

Anion gap = Na − (Cl + HCO3): normal is 12 ± 2 mmol/L.

o In DKA, the anion gap is typically 20–30 mmol/L; an anion gap >35 mmol/L
suggests concomitant lactic acidosis.
Corrected sodium = measured Na + 2 [(plasma glucose − 100)/100] mg/dL. Patients
with DKA are liable for hyponatremia due to:
Glucose largely restricted to the extracellular space, causes osmotic movement of water
into the extracellular space thereby causing dilutional hyponatremia
the low sodium content of the elevated lipid fraction of the serum in DKA

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 PICU Protocol of EHA

1-Fluid therapy:
Fluid replacement should begin before starting insulin therapy.

I. Antishock therapy:

It is given as required, to restore peripheral circulation.

o Patients not in shock but with volume depletion 0: 20 ml /kg over 1: 2
hours may need to be repeated until tissue perfusion is adequate.
o Patient with DKA in shock: rapidly restore circulatory volume with isotonic
saline in 20 mL/kg boluses infused as quickly as possible through a large
bore cannula with reassessment after each bolus.

II. Deficit therapy:

✓ In moderate DKA 5- 7% (50:70 ml/ kg)

✓ In severe DKA 7-10% (70:100 ml/kg)

o Calculate the subsequent rate of fluid administration, including the provision of

maintenance fluid requirements, aiming to replace the estimated fluid deficit
evenly over 48 h.

o Maintenance fluid: to be calculated based on body weight.

o 100cc/kg for the first 10kg, 50cc/kg for the next 10kg, and 20 cc/kg thereafter

“The rate of fluid administration should seldom exceed 1.5–2 times the usual
daily maintenance requirement.”

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PICU Protocol of EHA

Table 1: showing maintenance volumes, also after subtraction of initial boluses

given for the patient assuming it was 10-20 ml/

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 PICU Protocol of EHA

Duration of IV fluid therapy:

Divide fluids over remainder of time for replacement: This is calculated based
on serum osmolality (mosmol/kg H2O):

o If s-osmolality 300 - < 320 correct over 24 hours

o If s-osmolality > 320 - < 340 correct over 36 hours.
o If s-osmolality > 340 or initial sNa+>150 meq/L correct over 48hours.

2-Insulin therapy:

Insulin therapy: begin with 0.1 U/kg/h in patients above five years

0.05 U/Kg/h in patients below five years

Insulin drip start 1–2 h AFTER starting fluid replacement therapy.

Dilute 50 units regular human insulin in 500 mL normal saline, (0.1 unit insulin =1 mL).

3-Potassium replacement:
If immediate serum potassium measurements are unavailable, an ECG may
help to determine whether the child has hyper- or hypokalemia.
Signs of hypokalemia in ECG: Prolongation of the PR interval
T-wave flattening and inversion ST
depression, prominent U waves
apparent long QT interval (due to fusion
of the T and U waves)

Signs of hyperkalemia in Tall, peaked, and symmetrical T waves

ECG: shortening of the QT interval

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PICU Protocol of EHA

4. Bicarbonate Administration:
Bicarbonate administration is not recommended except for treatment of life
threatening hyperkalemia.

Bicarbonate is NOT recommended and has potential hazards in patients with DKA:

1. HCO3 diffuses slowly through BBB

(HCO3 + H+ CO2 + H2O)

CO2 diffuses rapidly paradoxical CNS acidosis * ↑ risk of cerebral edema.

2. Alkalosis is associated with hypokalemia.

3. May ↑ s-Na+ in a patient with hyperosmolar dehydration.
4. HCO3ˉ therapy shifts the OxyHb dissociation curve to the left (decreases O2
release to the tissues) ↑ tissue hypoxia.

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 PICU Protocol of EHA

Indication for bicarbonate therapy in patients with DKA:

(1) A patient with pH < 6.9 who is in shock with decreased cardiac contractility and
peripheral vasodilatation with poor tissue perfusion.

(2) Patients with LIFE THREATENING Hyperkalemia.

In these cases only Give NaHCO3 1-2 meq/kg or 80 meq/m2 body surface area added
to 0.45% saline over 1 hour (never by bolus).

Be careful about s-K+ and DO NOT stop K+ infusion while bicarbonate is being given.

Reassess after 1 hour of finishing bicarbonate infusion.

Rate of I.V fluid administration:

Rate of I.V fluid and insulin drips depend on RBS and rate of decent of RBS/
Hour which should not exceed 90 mg/dL.

RBS level Type of I.V fluid Rate of insulin drip

> 300 mg/dL Saline 0.9 % > 5 years 0.1 IU/kg/h
< 5 years 0.05 IU/kg/h
140 :300 mg/dL Saline 0.9%: glu 5% Same rate
Or rate of decrease
> 90 mg/dL
80: 140 mg/dL Saline 0.9%: glu 10% Same rate
Or rate of decrease
> 90 mg/dL
> 80 mg/dL Saline 0.9%: glu Same rate
Or rate of decrease 12.5%
> 90 mg/dL

> 80 mg/dL Saline 0.9%: glu Decrease to half rate

Or rate of decrease 12.5%
> 90 mg/dL

If rate of blood sugar decrease less than 30 mg/dL or acidosis is not corrected so you
should revaluate:
1. IV fluid calculations
2. Insulin delivery system & dose
3. Need for additional resuscitation
4. Consider sepsis

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PICU Protocol of EHA

Clinical and biochemical monitoring

There should be documentation on a flow chart of hour-by-hour clinical

observations, IV and oral medications, fluids, and laboratory results. Monitoring
should include the
Following:

• Hourly (or more frequently as indicated) vital signs (heart rate, respiratory rate,
blood pressure).

• Hourly (or more frequently as indicated) neurological observations (GCS) for

warning signs and symptoms of cerebral edema that include:

1) Headache
2) Inappropriate slowing of heart rate
3) Recurrence of vomiting
4) Change in neurological status (restlessness, irritability, increased drowsiness,
incontinence)
5) Specific neurologic signs (e.g., cranial nerve palsies, abnormal pupillary
responses)
6) Rising blood pressure
7) Decreased oxygen saturation
8) Rapidly increasing serum sodium concentration suggesting loss of urinary free
water as a manifestation of diabetes insipidus (from interruption of blood flow to the
pituitary gland due to cerebral herniation)
9) Failure of measured serum sodium levels to rise or a further decline in serum
sodium levels with therapy is thought to be a potentially ominous sign of impending
cerebral edema. Too rapid and ongoing rise in serum sodium concentration may also
indicate possible cerebral edema as a result of loss of free water in the urine from
diabetes insipidus.

• Amount of administered insulin.

• Hourly (or more frequently as indicated) accurate fluid input (including all oral
• fluid) and output.
• Capillary blood glucose concentration should be measured hourly (but must be
cross-checked against laboratory venous glucose, as capillary methods may be
inaccurate in the presence of poor peripheral circulation and acidosis).
• Laboratory tests: serum electrolytes, glucose, blood urea nitrogen, calcium,
magnesium, phosphorus, hematocrit, and blood gases should be repeated 2–4
h, or more frequently, as clinically indicated, in more severe cases.

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 PICU Protocol of EHA

Where Should the Patient be treated? Indications for ICU admission:

1. Patients with severe DKA: (pH < 7.1, shock, or with long duration of symptoms).
2. Patients with altered level of consciousness.
3. DKA in children below 5 years (are at increased risk of cerebral edema).
4. Patients with high BUN, possible oliguria & acute tubular necrosis (for need of a
central venous catheter & dialysis).
5.If cerebral edema develops as a complication of treatment.

Introduction of oral fluids and shift to S.C. insulin

• Can introduce oral fluids after substantial clinical improvement (mild

acidosis/ketosis may still be present).
• Plan to change to SC insulin when ketoacidosis has resolved (pH > 7.3, HCO3>
15, anion gap is normal) + oral fluids are tolerated.
• Best is to shift before a meal time.
• Start S.C. intermediate acting + short acting insulin.

To prevent rebound hyperglycemia, the first SC injection should be given 15–30

min (with rapid acting insulin) or 1–2 h (with regular insulin) before stopping the
insulin infusion to allow sufficient time for the insulin to be absorbed. With
intermediate or long-acting insulin, the overlap should be longer and the rate of IV
insulin infusion gradually lowered.

Calculate insulin dose as:

0.7 U/kg/d in prepubertal children with long standing DM (may need IU/kg/d in
new cases).
1.0 U/kg/d at mid puberty.

1.2 U/kg/d by the end of puberty.

Give the first dose of rapid-acting insulin analogue 15 minutes before stopping
insulin infusion and of regular insulin 1 hour before stopping it.

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PICU Protocol of EHA

Cerebral edema:

The incidence of clinically overt cerebral edema in national population studies

is 0.5–0.9% and the mortality rate is 21–24%

Diagnosis is established by:

1. One diagnostic criterion or

2. two major criteria or
3. one major and two minor criteria

These have a sensitivity of 92% and a false positive rate of only 4%. Signs that
occur before treatment should not be considered in the diagnosis of cerebral edema.

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 PICU Protocol of EHA

Treatment of cerebral edema:

Initiate treatment as soon as the condition is suspected.

I.Reduce the rate of fluid administration by one-third.

II.Give mannitol, 0.5–1 g/kg IV over 10–15 min, and repeat if there is no
initial response in 30 min to 2 h.
III.Hypertonic saline (3%), suggested dose 2.5–5 mL/kg over 10–15 min, may be
used as an alternative to mannitol, especially if there is no initial response to
mannitol
IV.Hyperosmolar agents should be readily available at the bedside.

V.Elevate the head of the bed to 30.◦

VI.Intubation may be necessary for the patient with impending respiratory

failure.
VII.After treatment for cerebral edema has been started cranial imaging may be
considered as with any critically ill patient with encephalopathy or acute focal
neurologic deficit. The primary concern is whether the patient has a lesion
requiring emergency neurosurgery (e.g., intracranial hemorrhage) or a lesion
that may necessitate anticoagulation (e.g cerebrovascular thrombosis)

References:

▪ ISPAD Clinical Practice Consensus Guidelines 2018 Compendium

▪ Protocol of Management of Type 1 Diabetes Mellitus, the Diabetes Clinic
Children's Hospital - Ain Shams Universit

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PICU Protocol of EHA

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 PICU Protocol of EHA

Hypoglycemia
Diagnosis:
In addition to the measured glucose concentration thresholds listed below,
symptomatic hypoglycemia is defined by the presence of clinical signs such as:
➢ Tachycardia
➢ Sweating
➢ Altered level of consciousness (agitation, lethargy, or seizures)

Approach for Diagnosis

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PICU Protocol of EHA

Management of Hypoglycemia:
A. Emergency Treatment:

If hypoglycemia is treated with IV dextrose (0.5 to 1 g/kg), administer one of the

following:
✓ D25W (25% dextrose in water): 2 to 4 mL/kg
✓ D10W (10% dextrose in water): 5 to 10 mL/kg

B. Continuous Treatment for persistent Hypoglycemia:

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 PICU Protocol of EHA

Adrenal Crisis
Definition
it is a physiological event caused by an acute relative insufficiency of adrenal
hormones.
Etiology
• May be precipitated by physiological stress in a susceptible patient.
• Should be considered in patients with congenital adrenal hyperplasia.
• Hypopituitarism on replacement therapy.
• Those previously or currently on prolonged steroid therapy.

Assessment:
A) History and physical examination – look for:

• Glucocorticoid deficiency:

➢ Weakness, anorexia, nausea and/or vomiting, hypoglycemia, hypotension

(particularly postural) and shock.

• Mineralocorticoid deficiency:

➢ Dehydration, hyperkaliemia, hyponatremia, acidosis and prerenal renal failure.

B) Investigations

• Immediate blood glucose.

• Serum glucose, urea, sodium and potassium.
• Arterial or capillary acid base.

“Where the underlying diagnosis not known, collect at least 2 ml of

clotted blood for later analysis (cortisol and 17 hydroxyprogesterone).”

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PICU Protocol of EHA

Management:

Susceptible patients who present with vomiting but who are not otherwise
unwell should be considered to have incipient adrenal crisis. To attempt to
prevent this from developing further:
• Administer I.M hydrocortisone 2 mg/kg.
• Give oral fluids and observe for 4–6 hours before considering discharge.
• Discuss with appropriate consultant.

For all other children:

1. Give intravenous fluids.

Shock or severe dehydration:

• Normal saline 20 ml/kg I.V. bolus. Repeat until circulation is restored.
• Administer remaining deficit plus maintenance fluid volume as normal saline in
• 5% dextrose evenly over 24 hours.
• Check electrolytes and glucose frequently.
• After the first few hours, if serum sodium is greater than 130 mmol/L, change
to half normal saline.
• 10% dextrose may be needed to maintain normoglycaemia.

Moderate dehydration:
• Normal saline 10 ml/kg i.v. bolus. Repeat until circulation is restored.
• Administer remaining deficit plus maintenance fluid volume as normal saline in
• 5% dextrose evenly over 24 hours.

Mild or no dehydration:

• No bolus.
• 1.5 times maintenance fluid volume administered evenly over 24 hours.

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 PICU Protocol of EHA

2. Give hydrocortisone
Administer hydrocortisone intravenously. If I.V access is difficult, give I.M
while establishing intravenous line.

• 10 mg for infants
• 25 mg for toddlers
• 50 mg for older children
• 100 mg for adolescents
Should be administered as a bolus and a similar total amount given in divided
doses at 6 hr intervals for the 1st 24 hr. These doses may be reduced during the next
24 hr if progress is satisfactory

When stable reduce I.V. hydrocortisone dose, then switch to triple dose oral
hydrocortisone therapy, gradually reducing to maintenance levels (10–15 mg/m2/day).

Equivalent doses (20-25% of the hydrocortisone dose) of prednisone or

prednisolone may be divided and given twice daily.

In patients with mineralocorticoid deficiency, start fludrocortisone at

maintenance doses (0.05-0.2 mg daily) as soon as the patient is able to tolerate oral
fluids.

3. Treat hypoglycemia
• Hypoglycemia is common in infants and small children.
• Treat with I.V. bolus of 5 ml/kg 10% dextrose in a neonate or infant and 2
ml/kg of 25% dextrose in an older child or adolescent.
• Maintenance fluids should contain 5–10% dextrose.

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PICU Protocol of EHA

4. Treat hyperkalemia
• Hyperkalemia usually normalizes with fluid and electrolyte replacement.
• If potassium is above 6 mmol/L perform an ECG and apply cardiac monitor as
arrhythmias and cardiac arrest may occur.
• If potassium is above 7 mmol/L and hyperkalemic ECG changes are present:
(eg. peaked T waves, wide QRS complex)
Give:

➢ 10 % calcium gluconate 0.5 ml/kg I.V over 3–5 mins.

➢ Commence infusion of insulin 0.1 units/kg/hr I.V together with an infusion of 50%
dextrose 2 ml/kg/hr.
• If the potassium is above 7 mmol/L with a normal ECG :

Give sodium bicarbonate 1–2 mmol/kg I.V over 20 mins, with an infusion of 10%
dextrose at 5 ml/kg/hr.

5. Identify and treat potential precipitating causes such as sepsis.

6. Admit to appropriate inpatient facility.

Prevention
Prevention of a crisis if possible, is essential and may involve:
• Anticipating problems in susceptible patients.
• Giving triple normal oral maintenance steroid dose for 2–3 days during stress (eg.
fever, fracture, laceration requiring suture).
• Giving intramuscular hydrocortisone when absorption of oral medication is
doubtful eg. In vomiting or severe diarrhea.
• Increasing parenteral hydrocortisone (1–2 mg/kg) before anesthesia, with or
without an increased dose postoperatively.

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 PICU Protocol of EHA

Acute kidney Injury (AKI)

Background
AKI =
• A recent increase of >1.5x in creatinine from a previous baseline or a value of >
1.5 x upper limit of the reference interval for age.
• Usually associated with a fall in urine output <0.5ml/kg/hour for 8 hours.
• Creatinine results should be interpreted in the context of age, body and muscle mass,
and ethnicity.

Creatinine Reference Ranges

• Neonates (premature) 0.33-0.98 mg/L 29 - 87 µmol/L

• Neonates (full-term) 0.31-0.87 mg/L 27 - 77 µmol/L
• to 12 months 0.16-0.38 mg/L 14 - 34 µmol/L
• 1to <3 years 0.17-0.35 mg/L 15 - 31 µmol/L
• to <5 years 0.26-0.42 mg/L 23 - 37 µmol/L
• 5 to <7 years 0.32-0.59 mg/L 28 - 52 µmol/L
• 7 to <9 years 0.4-0.6 mg/L 35 - 53 µmol/L
• 9 to <11 years 0.38-0.74 mg/L 34 - 65 µmol/L
• 11 to <13 years 0.52-0.79 mg/L 46 - 70 µmol/L
• 13 to <15 years 0.57-0.87 mg/L 50 - 77 µmol/L
• 15 years and over
• Male: 0.7 – 1.2 mg/L 62 - 106 µmol/L
Female: 0.5 – 0.9 mg/L 44 - 80 µmol/L

AKI Warning Score

AKI stage Creatinine change from baseline/ upper limit Urine

or eGFR (mL/min/1.73m2) output
1 >1.5-2x or
eGFR < 75
2 2-3x or <0.5mL/kg for
8 hours
eGFR < 50
3 >3x or
eGFR < 35

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PICU Protocol of EHA

Assessment

Causes Considerations in the history

Pre-renal
• Hypovolemia • Signs and symptoms of
• Impaired Cardiac output hypovolemia e.g. vomiting or
diarrhea, decreased UO,
• Renal vessel occlusion
dizziness, lethargy
• Hepatorenal syndrome
• renal artery stenosis
• Past history: biliary atresia,
cardiac disease

Intrinsic renal disease

• Glomerulonephritis • Recent viral illness
• Involvement of renal • Change in urine color e.g.
microvasculature- HUS, HSP red or “coca cola” colored
• Interstitial nephritis • History of transplant or
• Drugs nephrotoxic drugs
• Acute Tubular necrosis
• Tumour lysis syndrome

Post-renal or obstructive

• Posterior urethral valves

• Abdominal pain Reduced UO
• Bilateral ureteric obstruction
• History of trauma
(trauma, calculi)
• History of kidney stones
• Urethral obstruction (trauma,
• Frequent UTI’s
calculus)

GFR Calculation

In children, eGFR is calculated using the following formula, in which:

k = 30 µmol/L for children <1 year
k = 40 µmol/L for children >1 year

eGFR (mL/min/1.73m2) = k x height(cm)

Serum creatinine (µmol/L)
N.B
(1mg/dl = 88 µmol/L)

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 PICU Protocol of EHA

Management

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PICU Protocol of EHA

Pediatric nephrology referral to the Renal Team

o Immediate referral for any stage AKI where
▪ K+ >6.5mmol/L
▪ Oligo/anuria and plasma Na+ <125 mmol/L
▪ Pulmonary edema of hypertension unresponsive to diuretics
▪ Plasma urea >40mmol/L unresponsive to fluid challenge
▪ Persistent or worsening metabolic acidosis
o AKI stage 2 or 3 and consider for stage 1
o Any AKI
▪ in CKD patient or patient with a renal transplant
▪ Suspected intrinsic renal disease (e.g. nephritis / HUS)

If any concerns outside of this list, please discuss with ECHL

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 PICU Protocol of EHA

Fluid management in AKI

Clinical Assessment of Fluid Status
• Fluid assessment- peripheral circulation, edema, urine output
• Signs of cardiac failure- raised JVP, hepatomegaly, peripheral pitting edema,
bilateral lung crepitations.
• Blood pressure (changes are late and measurements in isolation not usually helpful)
• Low BP with cool peripheries -> intravascular depletion and shock
• High BP with warm peripheries -> fluid overload

Hypovolemia Overloaded
• Furosemide IV
Initial management

1. Fluid challenge 10
Euvolemia
mL/kg0.9% infusion 3-5
sodium chloride • Fluid challenge 10 mg/kg up to 4
STAT mL/kg 0.9% sodium times
2. Initial fluid chloride over 1 hour a day (max dose
replacement = 250mg;max
insensible losses 1g/day) may be
(400ml/m2/day) + considered but
UO (last24h) this should be a
decision by a
senior clinician
• Replace UO and
Ongoing management

insensiblelosses for
at least 24-48h
Replace ongoing fluid losses
▪ Beware of (insensible at 400ml/m2/d,
increased urine, GI losses)
losses in fever,
Insensible losses are higher
profuseD&V,
in febrile children and lower in Fluid restrict to
hyperventilating ventilated children 50-75%of UO
• Beware of polyuric
recoveryphase

“If renal function continues to improve, set a fluid target.

Ongoing management “Monitor, Maintain, Minimize”

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PICU Protocol of EHA

Monitor
Strict and Accurate Input / Output

✓ At least daily weights

✓ Always plot height and weight on a growth chart
✓ Ideally at the same time each day, especially for small children
✓ Blood pressure at least four hourly

Nutrition
✓ Children with AKI are in a catabolic state and therefore need monitoring to
ensure meeting adequate calorie requirement

Investigations
✓ Bloods: daily U&E. Management of electrolyte abnormalities especially

Hyperkalemia

✓ Urinalysis at least daily

Maintain

✓ Ensure adequate circulatory volume – address hypoperfusion urgently with fluid

boluses (10 mL/kg) and inotropic support once the volume is restored.

Minimize

✓ Further harm should be reduced by stopping nephrotoxic drugs and restarting

when appropriate with dose adjustments
✓ Intravenous contrast should also be avoided

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 PICU Protocol of EHA

ABBREVIATIONS
ACE-I Angiotensin-Converting Enzyme Inhibitor
AKI Acute Kidney Injury
ANA Antinuclear Antibody
ANCA Antineutrophil Cytoplasmic Antibodies
anti-GBM Anti–Glomerular Basement Membrane
ARB Angiotensin II Receptor Blocker
ASOT Antistreptolysin O Titer
C3/4 Complement 3/4
CK Creatine Kinase
CKD Chronic Kidney Disease
D&V Diarrhea and Vomiting
GI Gastrointestinal
HSP Henoch-Schönlein Purpura
HUS Hemolytic Uremic Syndrome
Hx History
JVP Jugular Venous Pulse
LDH Lactate Dehydrogenase
NSAID Non-Steroidal Anti-Inflammatory Drugs
PEWS Pediatric Early Warning Signs
sCr Serum Creatinine
STAT To Be Performed Immediately
U&E Urea and Electrolytes (Sodium “Salt”, Potassium, And
Magnesium)
ULRI Upper Limit Of The Reference Interval
UO Urine Output
USS Ultrasound Scan

References
▪ https://www.grepmed.com/images/3937/differential-nephrology-postrenal-
diagnosis-prerenal-failure- kidney
▪ https://www.thinkkidneys.nhs.uk/aki/wp-
content/uploads/sites/2/2016/05/Guidance_for_paediatric_patients_final.pdf
▪ https://www.nuh.nhs.uk/download.cfm?doc=docm93jijm4n840 Source
▪ O - 5 yeam Roche Cobas® Enzymatic Creatmme lat insen 09-2014 V7 O
▪ 5yeam and over Roche Cobas® Jaffe Creatmme kit insen 10-2015 V11.0
▪ https://bihsoc.org/wp-content/uploads/2017/11/GOSH-BP-flowsheet-
Children-E-Brennan-May-2017-1.pdf

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PICU Protocol of EHA

Comatose Child

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 PICU Protocol of EHA

Cerebral Oedema
Scope
Applicable to cerebral oedema in infants, children and adolescents
This protocol is NOT intended to address the management of specific etiologies
of cerebral oedema/ increased intracranial pressure

Disclaimer
Protocols and guidelines outline the recommended or suggested clinical practice;
however, they cannot replace sound clinical judgment by appropriately trained and
licensed physicians. The physician is ultimately responsible for management of
individual patients under their care.

Recognition
Cerebral oedema needs a high index of suspicion and must be actively checked
for in any acute neurological condition and in case of neurological deterioration in any
patient.

The most common underlying conditions are:

✓ Traumatic brain injury
✓ Hypoxic/ ischemic brain injury
✓ Intracerebral & subarachnoid hemorrhage
✓ Cerebrovascular stroke
✓ Hypertensive encephalopathy
✓ CNS infectious and inflammatory conditions
✓ Intracranial space-occupying lesions
✓ Hyponatremic encephalopathy
✓ Hepatic encephalopathy
✓ In-born errors of metabolism during acute crisis
✓ During treatment of DKA and severe hypernatremia
✓ Dialysis disequilibrium syndrome
The most important clinical manifestations include:
✓ Altered consciousness; irritability or deteriorating consciousness
✓ Sluggish pupillary reaction and hyperreflexia
✓ Focal neurological abnormalities
✓ Bradycardia and hypertension
✓ Abnormal respiration

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PICU Protocol of EHA

NB. CT findings are NOT essential before starting therapy. CT may be needed to
evaluate etiology. Assess patient stability and initiate indicated emergency
measures before transfer for imaging.
NB. Increased ICP may also be evaluated through the presence of papilloedema and
CSF pressure measurement.

Treatment of Cerebral Oedema

➢ Ventilation, Oxygenation and Circulation

➢ Control of cerebral metabolism
➢ Fluid and hyperosmolar therapy
➢ Dexamethasone
➢ Specific treatment of the underlying cause
➢ CSF diversion procedures and decompressive craniotomy

Ventilation, Oxygenation and Circulation

Ensure/ secure adequate airway and breathing
• Intubation may be necessary for GCS<8, inability to maintain airway or
hypoventilation
• Consider cervical spine immobilization in trauma victims

Maintain normal ventilation and oxygenation

• Oxygen, keeping patients with borderline oxygen or CO2 is NOT sufficient
• In patients with acute severe increase in ICP, a BRIEF period of MILD
hyperventilation (PaCO2 30mmHg) can be implemented.

“Avoid prolonged or excessive hyperventilation as it can

exaggerate cerebral ischemia”

Maintain adequate B.P. for cerebral perfusion

• Use volume and vasoactive drugs as necessary
• Hypotension can exacerbate cerebral ischemia
Ensure adequate cerebral venous drainage:
• Elevate the head of the bed 30 degrees in neutral position if not contraindicated
• Avoid neck compression
• Wide, bilateral and unnecessary jugular venous lines are not recommended

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 PICU Protocol of EHA

Control of Cerebral Metabolism

Increased cerebral energy requirement in the context of compromised perfusion

can increase cerebral damage:

• Control of any clinical or subclinical (bedside EEG) seizure activity

• Even if this would mean the need for intubation and MV in an ICU setting
• Active normothermia : aggressive management of fever or hyperthermia
• Monitor and correct hypoglycemia

Fluid and Hyperosmolar Therapy

In absence of (or after correcting) hypovolemia or hypotension, a restricted fluid

management is necessary:
• Provide 50-70% of normal maintenance requirements
• If correcting dehydration as in hypernatremia or DKA, reduce the fluid rate by
1/3 provided there is no hypovolemia or hypotension

Avoid rapid reduction or subnormal serum sodium levels, modify sodium content
of fluids
Avoid rapid reduction of blood glucose or urea levels

Hyperosmolar Therapy

IV hypertonic saline (5 mL/Kg of 2.7% NaCl over 30 min & may be repeated
once)
• Treatment may be repeated after several hours as clinically indicated
• Increasing serum Na beyond 155-160mmol/L is not recommended
• Continuous hypertonic saline at a low rate may be used to maintain serum Na
>145mmol/L but is not routine
IV mannitol (0.5-1g/Kg, 20% better than 10%, over 20min)
• Mannitol is effective even in those who cannot receive hypertonic saline
• Mannitol has a higher nephrotoxic potential than hypertonic saline
• Hypertonic saline improves systemic and cerebral perfusion compared to
mannitol
• Both may be given in the same patient
• Repeated regular (eg q6h) doses of mannitol are not recommended

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PICU Protocol of EHA

Dexamethasone:

• The main value is in cases of inflammatory vasogenic cerebral oedema; as in

cases with vasculitis, cerebral infarctions, infectious, inflammatory and
neoplastic lesions

• In bacterial meningitis, it is initiated with the first dose of antibiotics

• It is not recommended in cases of intracerebral hemorrhage

• Dose: 0.15 mg/kg/6h; a higher initial dose (0.5 mg/Kg) may be used

Specific Treatment of The Underlying Cause

CSF Diversion Procedures and Decompressive Craniotomy

• These should be considered case by case; weighing risks and benefits

• They non-specifically reduce ICP but do not address cerebral oedema itself

• CSF diversion is the specific treatment of acute hydrocephalus

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 PICU Protocol of EHA

Blood Product Prescription

Key Points
• All blood transfusion activity must occur in compliance with the relevant
hospital procedures and guidelines.
• All patients should have consent for blood product administration recorded in
the medical record prior to transfusion.
• A blood transfusion should only be given when the expected benefits to the
patient are likely to outweigh the potential hazards.
• A blood product transfusion may be required to treat acute blood loss associated
with surgery or trauma, or when the body cannot make enough blood cells in the
case of bone marrow failure, cancer or bone marrow suppression.
Background
This guideline is adapted from the National Blood Authority (NBA) Patient
Blood Management Guidelines: Module 6 Neonatal and Pediatrics (2016) as well as
the British Society for Hematology Guidelines on transfusion for fetuses, neonates and
older children (2016). Local procedures or guidelines may vary.

Indications for Red Blood Cell (RBC) transfusion

Table 1: Indications for red blood cell transfusion

Hb Indication
Red Blood Cell (RBC) transfusion is often indicated, however lower
Hb <7 g/dL
thresholds may be acceptable in patients without symptoms (symptoms
may include – tachycardia, flow murmur, lethargy, dizziness, shortness
of breath, and cardiac failure) and where specific therapy (e.g. iron) is
available.
Hb 7-9 g/dL RBC transfusion may be indicated, depending on the clinical setting e.g.
presence of bleeding or hemolysis and clinical signs and symptoms of
anemia.
Hb >9 g/dL RBC transfusion is often unnecessary and may be inappropriate
Transfusion may be indicated at higher thresholds for specific situations:
Children with cyanotic congenital heart disease or on Extra Corporeal Life Support
(ECLS)
Children with Hemoglobinopathies (thalassemia or sickle cell disease) or congenital
anemia on a chronic transfusion program

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PICU Protocol of EHA

Indications for Platelet Transfusion

Table 2: Indications for platelet transfusion in infants and children

Platelet Indication to trigger platelet transfusions in infants and children

count
(x10^9/L)
<10 ✓ Clinically stable pediatric patients receiving chemotherapy for
leukemia or post hematopoietic stem cell transplantation (HSCT)
(prophylactic).*
✓ Clinically stable patients with solid tumors (prophylactic).*
✓ Critically ill patients with no bleeding.
* Transfusions at higher levels may be required for bladder, brain or
necrotic tumors.
<20 Chemotherapy, HSCT & risk factors (e.g. fever, sepsis, minor
bleeding, mucositis, disseminated intravascular coagulopathy
(DIC) without bleeding)
Critically ill patients with risk factors for bleeding (e.g. sepsis, renal
failure, medications) Nasogastric tube insertion
Intramuscular injections e.g. Erwinia asparaginase
Insertion of a non-tunneled central venous line
<30 ✓ Lumbar puncture (LP) and ongoing chemotherapy-induced
thrombocytopenia
✓ Central nervous system (CNS) tumor and:
• A VP shunt or Ommaya reservoir
• Has a gross total resection and is receiving chemotherapy and/or
radiation
• Has residual tumor and is receiving chemotherapy and/or radiation
<50 LP and new disease induced thrombocytopenia
Patient undergoing invasive procedure (including tunneled central
venous line insertion) Moderate active bleeding (including bleeding
associated with DIC)
CNS tumour and:
A past history of intracranial hemorrhage
Is receiving an anti- angiogenesis agent such as bevacizumab
<75 Major hemorrhage due to trauma or significant post-operative bleeding

<100 Patient undergoing high risk invasive procedure (e.g.

neurosurgery/ophthalmology) ECLS (lower platelets may be
acceptable in stable patients)

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 PICU Protocol of EHA

Platelet transfusion is NOT indicated for the following

• Stable patients with chronic, stable, severe thrombocytopenia due to:

Alloimmunization
• Immune thrombocytopenia (ITP)
• Thrombotic thrombocytopenic purpura (TTP) Aplastic anemia or
myelodysplastic syndrome (MDS)
• These patients should be observed without prophylactic platelet transfusions and
should receive platelet transfusions only with clinically significant bleeding
• Bone marrow aspirate and trephine biopsy Intravenous cannula insertion

Indications for Fresh Frozen Plasma (FFP)

FFP is appropriate for the following

• Acute bleeding in the setting of significant coagulopathy.

• Warfarin reversal, in the presence of significant or life-threatening bleeding or
prior to emergency surgical procedures
• Given in addition to vitamin K

Note:
✓ Vitamin-K dependent clotting factor concentrates (e.g. prothrombinex) may be
given instead of FFP for bleeding secondary to warfarin or emergency warfarin
reversal.
✓ Liver disease, with clinically significant bleeding in the context of coagulopathy
post liver transplantation. Acute disseminated intravascular coagulopathy (DIC)
with bleeding and significant coagulopathy
✓ During massive transfusion or cardiac bypass for the treatment of bleeding
Plasma exchange for the treatment of TTP
✓ Specific factor deficiencies where a factor concentrate is not available

FFP is NOT indicated for the following

✓ The correction of minor coagulation abnormalities (minor prolongation of the

INR/APTT) in the non- bleeding child
✓ Liver disease when there are minor coagulation abnormalities and no-bleeding
✓ For reversal of a INR <2.0 in patients undergoing minor procedures

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PICU Protocol of EHA

Indications for Cryoprecipitate

✓ Active bleeding and fibrinogen level <1.5 g/L

✓ During massive transfusion or cardiac bypass, for the treatment bleeding when
the fibrinogen level <1.5 g/L or there is hyperfibrinolysis
✓ Acquired fibrinogen deficiency or acute DIC when there is significant bleeding
and the fibrinogen <1.0 g/L
✓ Prior to an invasive procedure when the fibrinogen <1.0 g/L and there is a risk
of significant bleeding associated with the surgery or it is at a critical site (e.g.
neurosurgery or eye surgery)

Cryoprecipitate is NOT indicated for the following

✓ Non-bleeding children with mildly reduced fibrinogen levels

✓ Liver disease when there are minor coagulation abnormalities and no active
bleeding

Management - Transfusion volumes and rates

In children less than 20 kg, transfusion volumes should be calculated based on

weight and prescribed in mLs In children greater than 20 kg, calculate and prescribe
the transfusion volume with consideration to pack sizes for RBC transfusion, prescribe
a single unit followed by clinical reassessment to determine additional transfusion
requirements for platelet transfusions, the usual platelet dose in an adult is one adult
unit All transfusions must be completed within 4 hours of spiking a pack

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 PICU Protocol of EHA

Table 3: Transfusion Volumes and Rates

Blood product RBC Platelets FFP Cryoprecipitate

The formula for Children <20 Children <20 kg: 10 – 20 5 – 10 mL/kg

kg: mL/kg
Calculating Pooled platelets 10
Transfusion mL = wt (kg) x
Hb (g/L) rise mL/kg Apheresis
Volume
(desired Hb – platelets
(mL) 5 – 10 mL/kg
actual Hb) x 0.5
e.g.10 kg child Children >20 kg:
requiring Hb to 1 unit for /10 kg
child
rise from 60 to
80g/L:
10 x 20 x 0.5 =
100mL
Children >20
kg:
1 unit for >20 kg
child
Typical unit Red cell unit ~ Pooled platelet ~ FFP ~284 Cryoprecipitate
Volume 258 ml 334 mL mL
~ 36 mL
Pediatric red Apheresis platelet Pediatric
cells (pedipak) ~181 mL FFP
~ 61 mL (pedipak)
~69 mL

Transfusion Rate 5 mL/kg/hr. 10 – 20 mL/kg/hr. 10 – 20 10 – 20

mL/kg/hr. mL/kg/hr.
Commence at a Faster infusion
slower rate (e.g. rates (e.g. given
half the over
prescribed rate) 30 minutes) may
for the first 15 result in a
minutes (Usual transfusion
maximum rate reaction
150
ml/hr.)

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PICU Protocol of EHA

Blood product modifications

• Request the appropriate blood component and special requirements:
• Irradiated blood products should be given to:
✓ All immunocompromised patients, including all immunology patients,
oncology patients, children with cardiac disease, and directed blood
donations to prevent graft-versus-host disease.

CMV negative products:

• Leucocyte-depleted blood products are considered an acceptable alternative to

CMV seronegative products.
• CMV-negative products are only indicated for exchange transfusion, pregnant
adolescents and patients with Severe Combined Immunodeficiency Disease
(SCID) who are CMV negative.

Phenotype matched red blood cells:

• Indicated for chronically transfused patients or patients with red cell

alloantibodies

Cryodepleted FFP

• May be requested for patients with Thrombotic Thrombocytopenic Purpura

(TTP), although FFP may be as effective.

IgA deficient products

• Patients with IgA deficiency who have developed an anti-IgA antibody

HLA matched

• For children with immunological refractory thrombocytopenia

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 PICU Protocol of EHA

Clinical Practice Guidelines on Prevention and Management of Pain

Recommendations Strength of Quality of
Recommendation Evidence
Analgesia
1) We suggest that, in critically ill pediatric patients 6 yr. old
and older who are capable of communicating, pain
assessment via self-report be routinely performed using the Conditional Low
Visual Analog Scale, Numeric Rating Scale, Oucher Scale,
or Wong-Baker Faces pain scale.
2) We recommend the use of either the Faces, Legs,
Activity, Cry, and Consolability or COMFORT-B scales Strong Moderate
for assessing pain in non-communicative critically ill
pediatric patients.
3) We recommend the use of observational pain assessment Strong Moderate
tools rather than vital signs alone for assessment of
postoperative pain in critically ill pediatric patients.
4) We suggest the use of observational pain assessment tools
Conditional Low
rather than vital signs alone for assessment of procedure-
related pain in critically ill pediatric patients.
5) We recommend that IV opioids be used as the primary
Strong Moderate
analgesic for treating moderate to severe pain in critically
ill pediatric patients.
6) We recommend the addition of an adjunct NSAID (IV or
oral) to improve early postoperative analgesia in
Strong Moderate
critically ill pediatric patients.
7) We suggest the addition of an adjunct NSAID agent (IV or
Conditional Low
oral) to decrease opioid requirements in the immediate
postoperative period in critically ill pediatric patients.
8) We suggest the addition of adjunct acetaminophen (IV or
Conditional Low
oral) to improve early post-operative analgesia in
critically ill pediatric patients.
9) We suggest the addition of adjunct acetaminophen (IV or
Conditional Low
oral) to decrease opioid requirements intermediate
postoperative period in critically ill pediatric patients.
10) We recommend that music therapy be offered to Strong Moderate
augment analgesia in critically ill postoperative pediatric
patients.
11) We recommend that nonnutritive sucking with oral Strong High
sucrose be offered to neonates and young infants prior to
performing invasive procedures.

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PICU Protocol of EHA

Quality
Recommendations Strength of
of
Recommendation
Evidence
Sedation
1) We recommend the use of the COMFORT-B Scale or Strong Moderate
the State Behavioral Scale, to assess level of sedation Conditional Low
in mechanically ventilated pediatric patients.
2) We suggest the use of the Richmond Agitation- Conditional Low
Sedation Scale to assess the level of sedation in Conditional Low
mechanically ventilated pediatric patients.
3) We suggest that all pediatric patients requiring MV Conditional Low
are assigned a target depth of sedation using a Conditional Low
validated sedation assessment tool at least once daily.
4) We suggest the use of protocolized sedation in all
critically ill pediatric patients requiring sedation
and/or analgesia during MV.
5) The addition of daily sedation interruption to sedation
protocolization is not suggested due to lack of Conditional Low
improvement in outcomes.
6) During the periextubation period when sedation is
typically lightened, we suggest the following bundle
strategies to decrease the risk of inadvertent device
removal:
a) Assign a target depth of sedation at an increasing
frequency to adapt to changes in patient clinical status
and communication strategies to reach the titration
goal.
b) Consider a sedation weaning protocol.
c) Consider unit standards for securement of
endotracheal tubes and safety plan.
d) Restrict nursing workload to facilitate frequent
patient monitoring, and decrease sedation
requirements, and risk of self-harm.
7) We suggest the use of alpha2-agonists as the primary
sedative class in critically ill pediatric patients
requiring MV.

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 PICU Protocol of EHA

Quality
Strength of
Recommendations of
Recommendation
Evidence
8) We recommend that dexmedetomidine be considered Strong Moderate
as a primary agent for sedation in critically ill
pediatric postoperative cardiac surgical patients
with expected early extubation.
9) We suggest the use of dexmedetomidine for
Conditional Low
sedation in critically ill pediatric postoperative
cardiac surgical patients to decrease the risk of
tachyarrhythmias.
10) We suggest that continuous protocol sedation at
doses less than 4 mg/kg/hr. (67 µg/ kg/min) and Conditional Low
administered for less than 48hr may be a safe
sedation alternative to minimize the risk of protocol-
related infusion syndrome development.
11) Short-term (< 48 hr.) continuous protocol
sedation may be a useful adjunct during the Good practice
periextubation period to facilitate the weaning of
other analog-sedative agents prior to extubation.
12) We suggest consideration of adjunct sedation
with ketamine in patients who are not otherwise at an Conditional Low
optimal sedation depth.
13) During the periextubation period when sedation
Conditional Low
is typically lightened, we suggest the following
bundle strategies to decrease risk of inadvertent
device removal:
a) Assign a target depth of sedation at increasing
frequency to adapt to changes in- patient clinical
status and communicate strategies to reach
titration goal.
b) Consider a sedation weaning protocol.
c) Consider unit standards for securement of
endotracheal tubes and safety plan.
d) Restrict nursing workload to facilitate frequent
patient monitoring, decrease sedation
requirements, and risk of self-harm.

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PICU Protocol of EHA

Quality
Strength of
Recommendations of
Recommendation
Evidence
Neuromuscular blockade
1) We suggest that train-of-four monitoring be used in Conditional Low
concert with clinical assessment to determine the depth of
neuromuscular blockade.
2) We suggest using the lowest dose of NMBAs required to
achieve desired clinical effects and manage undesired Conditional Low
breakthrough movement.
3) Electroencephalogram-based monitoring maybea useful
adjunct forthe assessment of sedation depth in critically ill Good practice
pediatric patients receiving NMBAs.
4) We suggest that sedation and analgesia should be adequate
Conditional Low
to prevent awareness prior to and throughout NMBA use.
5) We recommend routine use of passive eyelid closure and
eye lubrication for the prevention of corneal abrasions in Strong Moderate
critically ill pediatric patients receiving NMBAs.
ICU delirium
1) We recommend the use of the preschool and pediatric Strong High
Confusion Assessment Methods for the ICU or the
Cornell Assessment for Pediatric Delirium as the most
valid and reliable delirium monitoring tools in critically
ill pediatric patients.
2) We recommend routine screening for ICU delirium using
a validated tool in critically ill pediatric patients upon Strong High
admission through ICU discharge or transfer.
3) Given low patient risk, and possible patient benefit to
reduce the incidence and/or decrease duration or severity
Conditional Low
of delirium we suggest the following non-pharmacologic
strategies: optimization of sleep hygiene, use of
interdisciplinary rounds, family engagement on rounds,
and family involvement with direct-patient care.
4) We suggest performing EM, when feasible, to reduce the
development of delirium. Conditional Low
5) We recommend minimizing benzodiazepine-based Strong Moderate
sedation when feasible in critically ill pediatric
patients to decrease incidence and/or duration or
severity of delirium.

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 PICU Protocol of EHA

Strength of Quality of
Recommendations
Recommendation Evidence
6) We suggest strategies to minimize overall sedation exposure
whenever feasible to reduce coma and the incidence and/or Conditional Low
severity of delirium in critically ill children.
7) We do not suggest routine use of haloperidol or atypical
antipsychotics for the prevention of or decrease in duration Conditional Low
of delirium in critically ill pediatric patients.
8) We suggest that in critically ill pediatric patients with refractory
delirium, haloperidol or atypical antipsychotics be considered Conditional Moderate
for management of severe delirium manifestations, with
consideration of possible adverse drug effects.
9) We recommend a baseline electrocardiogram followed by
routine electrolyte and QTc interval monitoring for patients Strong Moderate
receiving haloperidol or atypical antipsychotics
iatrogenic withdrawal syndrome (iws)
1) We recommend use of either the Withdrawal Assessment Strong Moderate
Tool-1or Sophia Observation Scale for the assessment of
IWS due to opioid or benzodiazepine withdrawal in
critically ill pediatric patients.
2) We suggest routine IWS screening after a shorter duration
(3–5 d) when higher opioid or benzodiazepine doses are Conditional Moderate
used.
Good practice
3) Until a validated screening tool is developed, monitoring
for IWS from alpha2-agonists should be performed using a
combination of associated symptoms (unexplained
hypertension or tachycardia) with adjunct use of a validated
benzodiazepine or opioid screening tool.
4) We suggest that opioid-related IWS be treated with opioid Conditional Low
replacement therapy to attenuate symptoms, irrespective of
preceding dose and /or duration or opioid exposure.
5) Benzodiazepine-related IWS should be treated with
Good practice
benzodiazepine replacement therapy to attenuate
symptoms, irrespective of preceding dose and/or duration
of benzodiazepine exposure.
6) Alpha2-agonist–related IWS should be treated with IV
Good practice
and/or or enteral alpha2-agonist replacement therapy to
attenuate symptoms, irrespective of preceding dose and/or
duration of alpha2-agonist exposure.
7) We suggest use of a standardized protocol for
sedation/analgesia weaning to decrease duration of Conditional Low
sedation taper and attenuate emergence of IWS.

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PICU Protocol of EHA

Strength Quality
Recommendations of of
Recommendation Evidence
Optimizing Environment
1) We suggest facilitation of parental or caregiver Conditional Low
presence in the PICU during routine care and
interventional procedures to a) provide comfort to
the child, b) decrease pa- rental levels of stress and
anxiety and c) increase level of satisfaction of care.
2) We suggest offering patients the use of noise
reducing devices such as ear plugs or headphones Conditional Low
to reduce the impact of non-modifiable ambient
noise (conditional, low-level evidence).
3) We suggest that PICU teams make environmental
and/orbehavioral changes to reduce excessive Conditional Low
noise and therefore improve sleep hygiene and
comfort, in critically ill pediatric patients.
4) We suggest performing EM to minimize the
effects of immobility in critically ill pediatric Conditional Low
patients.
Conditional Low
5) We suggest the use of a standardized EM
protocol that outlines readiness criteria,
contraindications, developmentally appropriate
mobility activities and goals, and safety thresholds
guided by the multidisciplinary team and family
decision-making.

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 PICU Protocol of EHA

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PICU Protocol of EHA

Schematic summary of the key Pain, Agitation, Neuromuscular Blockade, and

Delirium in critically ill pediatric patients with consideration of the PICU Environment
and Early Mobility (PANDEM) recommendations and representation of the interplay
between sedative and analgesic choice on unintended but related outcomes.

BRAIN MAPS = Bring oxygen, Remove/Reduce deliriogenic drugs, patient Atmosphere,

Immobilization, New organ dysfunction, Metabolic disturbances, Awake, Pain, Sedation
CAPD = Cornell Assessment of Pediatric Delirium
COMFORT-B = COMFORT-Behavior
EEG = electroencephalogram
ETT = endotracheal tube
FLACC = Faces, Legs, Activity, Cry, and Consolability
IWS = iatrogenic withdrawal syndrome
MV = mechanical ventilation
NMBA = neuromuscular blocking agent
NSAID = nonsteroidal anti-inflammatory drug
pCAM- ICU = pediatric Confusion Assessment Method for the ICU
PRIS = propofol-related infusion syndrome
psCAM-ICU = preschool Confusion Assessment Method for the ICU
RASS = Richmond Agitation-Sedation Scale
SBS = State Behavioral Scale
SOS= Sophia Observation Scale
TOF=train-of-four
WAT-I=WithdrawalAssessmentTool-1

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 PICU Protocol of EHA

Basic Mechanical Ventilation

Scope:

MV is a respiratory support modality. Patients requiring MV are likely to require

other therapies; for the underlying disease, for respiratory care (eg physiotherapy,
suction, nebulized medications) and possibly for other system support. This protocol
addresses the MV part; however all aspects of patient care are equally important. MV
is not a contraindication for enteral feeding.

This protocol addresses mechanical ventilation of pediatric patients; beyond the

neonatal period, in the pediatric critical care setting.

Disclaimer:
Protocols and guidelines outline the recommended or suggested clinical practice;
however, they cannot replace sound clinical judgment by appropriately trained and
licensed physicians. The physician is ultimately responsible for management of
individual patients under their care.

Concept Definitions

Ventilation: gas exchange between alveolar and surrounding gas. The volume inspired
(normally = expired) each breath is the tidal volume (Vt). Minute volume is the amount
of ventilation per minute and equals tidal volume x respiratory rate.

RR: respiratory rate is the number of breaths per minute

Cycle: in the context of MV, a respiratory cycle is a breath (inspiration & expiration)

Cycling: in the context of MV, cycling is the end of inspiration. Cycling occurs when
the ventilator ends inspiration allowing passive expiration by the patient

Ti: inspiratory time is the time interval from the beginning of inspiration till the
beginning of expiration

Rise time: the time interval between the beginning of inspiration and reaching the
plateau; during which pressure is rising. It can be expressed in seconds or a percentage
of inspiratory time

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PICU Protocol of EHA

Oxygenation: (arterial oxygenation) the amount of oxygen reaching arterial blood,

measured as partial pressure (PaO2; normally 80-100mmHg) or as oxygen saturation
(SaO2 or SpO2; normally 95-97%); which is the percentage of oxyhemoglobin.
Arterial oxygenation depends on ventilation, FiO2 and pulmonary gas exchange.

FiO2: The percentage of oxygen in inspired gas. Room air has 21% oxygen.

Compliance: change in volume for change in pressure (∆V/∆P). Low compliance

means more change in pressure is required to achieve a volume change (stiff lungs; as
in pneumonia, collapse, ARDS)

Resistance: airway resistance is the force opposing air flow into or outside the lungs.
Bronchospasm increases airway resistance and this increases the effort necessary to
move air into/ outside the alveoli

Work of Breathing: the energy used (essentially the amount of effort used) in
breathing; aiming to achieve normal ventilation.

PIP: the peak inspiratory pressure; the highest pressure reached during inspiration

PEEP: the positive end-expiratory pressure; during expiration, an amount of +ve

pressure is maintained and it does not drop to zero. The main purpose is to prevent
alveolar collapse during expiration.

MAP: mean airway pressure. The average pressure throughout the respiratory cycle
(inspiration & expiration)

P plateau: the plateau pressure is the pressure at the plateau phase towards the end of
inspiration, measured in an inspiratory pause when there is no air flow. It is correlated
to the alveolar peak pressure; by excluding the pressure gradient needed to overcome
airway resistance.

AP: the pressure difference between plateau pressure and PEEP

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 PICU Protocol of EHA

Indications
• Post CPR management
• Severe hypoxemia (PaO2< 50-55mmHg) despite oxygen therapy. An
SpO2<85% by pulse oximeter is highly suggestive of PaO2<50-55mmHg
• Severe hypoventilation (PaCO2 >60mmHg with respiratory acidosis)
• Sustained or frequent apnea with desaturation
• Unacceptable work of breathing (most common indication in PICU)
• Excessively slow, shallow or irregular breathing
• Severe or increasing respiratory distress (impending exhaustion)
• Airway compromise requiring intubation
• Severe refractory shock
• CNS: deep coma with respiratory weakness or airway compromise, severe
cerebral oedema especially with (even mild) hypoventilation, refractory
status epilepticus needing anesthetic drugs
• Surgery under general anesthesia with neuromuscular blockade (most
common indication)

Objectives of MV
• Normal/ acceptable ventilation
• Normal/ acceptable oxygenation
• Acceptable work of breathing. Eliminating patient effort is not the objective,
but increased WOB on MV is not acceptable either.
• Lung protection. Avoidance of ventilator-induced lung injury

Initiation
Airway Establishment

• Non-invasive ventilation through a face mask may be used for those with
adequate airway and adequate circulation. Response should be assessed after
1hr and invasive MV initiated if response is inadequate.
• ET intubation is the most common approach. Bag-mask ventilation is
effective until preparations are made for intubation and ventilation.
• Tracheostomy should be considered when anticipated duration of MV exceeds
2-4weeks

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Primary settings

1. Mode:

There are different modes of MV and they are all acceptable provided they are
appropriate to the ventilator specs, user experience and patient’s condition

CMV: Only acceptable when the patient either

(a) Can provide no significant work of breathing due to disease condition or necessary
sedation/ neuromuscular blockade; or
(b) Has severe ARDS or very severe bronchial obstruction and cannot be adequately
ventilated except after eliminating patient efforts by neuromuscular blockade. This
should be employed for the shortest time necessary

SIMV: The strategy is to share the effort between the ventilator and the patient based
on rate. Reducing set ventilator rate can increase patient’s spontaneous rate and vice
versa. The total rate (ventilator + patient) should be appropriate for age and condition.
Weaning depends on reducing set rate.

Assist-Control: The strategy is to assist every breath initiated by the patient.

Ventilatory support is based on patient’s rate, the set rate should be below the patient’s
respiratory rate and acts as a backup. It is important that the given pressure/volume per
breath is sufficient to achieve an acceptable minute volume; without discrepancy
between set Ti and patient Ti and without excessively high respiratory rate. Improved
lung condition is associated with lower PIP achieving normal Vt. Further weaning
requires shift to PSV or SIMV.

Pressure Support: The strategy is also to assist every breath initiated by the patient,
who also determines the inspiratory time. This is pressure controlled. Reducing
pressure support (∆P above PEEP) increases patient work and vice versa. PS can be
applied alone for patients who have a good respiratory drive, or combined with SIMV
to assist breaths above the set rate.

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2. Primary Control Variable:

• Ventilators give a breath based on delivering a certain tidal volume (volume

controlled) or on increasing pressure to a certain value (pressure controlled) for
the duration of inspiration, followed by a passive expiration.
• Normal Vt is 6 -8mL/Kg. VC may use constant or decelerating (recommended)
flow. The resulting PIP will depend on lung mechanics and is measured
• PC depends on raising pressure to a certain PIP (in some ventilators ∆P above
PEEP). The Vt delivered depends on lung mechanics and is measured
• Both VC and PC aim to provide an appropriate Vt
• There are modes that attempt to combine both methods (Dual modes eg PRVC,
VG, VC+, etc). The principle is setting a target Vt and adjusting pressure based
on actual measured Vt; with many variations. Proportional assist ventilation
depends on giving a variable support depending on patient’s effort aiming to
achieve normal ventilation without increasing patient WOB. These modes can
be helpful and improve patient synchronization when used appropriately. Each
device has its own principles and users should be aware of these before using
such modes.
3. PIP or Vt:
• Other than dual modes, you will set one and monitor the other
• The plateau pressure (pressure at the end of inspiration) should not exceed 28-
30cmH2O to avoid lung injury. Patients with near normal compliance can
achieve normal Vt with MUCH lower pressures; while those with severe ARDS
may not be able to achieve normal Vt at this pressure and a lower Vt (4-5mL/kg)
may be accepted. Both high volume and high pressure should be avoided.
• Note: Plateau pressure is normally close to PIP but can be considerably less in
presence of airway obstruction. Some ventilators set ∆P not PIP (so you need to
add PEEP to get PIP)
• All modern ventilators can measure both delivered Vt and peak/plateau P.
4. Inspiratory Time Ti:
Other than PS and similar modes, you set the Ti after which the ventilator allows
the patient to expire. Setting must consider:
(a) For an I/E ratio near 2 (initially used), the Ti should be 20/ total (patient +
ventilator) rate
(b) Without changing rate, a longer Ti leads to a higher MAP in PC (& you can then
lower PIP if tolerated) and a lower PIP for a given Vt in volume control (both
are favorable). A too short Ti can lead to inadequate Vt or excessive PIP.
(c) Increasing Ti is limited by the need for adequate time for expiration to avoid air
trapping. While stiff lungs can usually tolerate I/E ratio 1:1, those with
obstructive pathology need great caution
(d) A set Ti greatly different from the patient’s own Ti can lead to asynchrony

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5. Ventilator Rate:
In CMV and SIMV, this is the rate per min. the ventilator should provide.
Initially, a normal rate for age should be set.

6. PEEP:
This prevents end-expiratory collapse and optimizes tidal breaths to a favorable
segment of lung compliance. A starting PEEP can be 5cmH2O and note:
• Those with stiff lungs may need considerably higher PEEP to maintain lung
recruitment
• The best PEEP is that which improves oxygenation and Vt at a relatively low ∆P
• Excessive PEEP can lead to alveolar overstretch, increasing an air leak, reduced
venous return and increased intracranial pressure

7. FiO2 :
• Initially set 100% if the patient is unstable, cyanosed or severely hypoxic with
lung pathology; otherwise set 40-50%. Adjust based on pulse-oximetry to the
FiO2 achieving acceptable oxygenation (saturation around 94%).
• Neonates and especially preterms are more susceptible to the adverse effects of
excessive oxygen
• Those with brain injury, refractory shock, pulmonary hypertensive crisis & CO
poisoning require high FiO2 and maintaining a higher degree of arterial
oxygenation
• The maximum safe duration by FiO2 is as follows:
✓ 100% 3-4h
✓ 80% 24h
✓ 60% 3-4days
✓ 40% 3-4 weeks

8.Flow or Rise Time:

Changing these settings alter how rapidly the peak pressure is attained during
inspiration.

9.Trigger Sensitivity:
Correct setting is associated with:
(a) The ventilator recognizing most patient efforts (no missed triggers); and
(b) There are no false triggers
NB:
▪ Humidifier must be used with appropriate temperature, necessary bacterial
filters must be installed, flow sensor must be installed and calibrated for any
mode other than CMV/IMV, alarm limits must be checked and backup power
must be operational (ventilator battery or UPS).
▪ Interrupting the ventilator circuit should be minimized. ET suction is a sterile
procedure and should be done when necessary. Unnecessary injections of saline
into the ETT should be avoided.

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Initial Settings Summary

Mode & control CMV only when patient not breathing or with
variable neuromuscular blockade
SIMV, with or without PS, or AC
PC and VC (with decelerating flow) both acceptable
Dual modes when applicable & user experienced in them
PIP or Vt Initial PIP: 15 for normal lungs, 20 for pathological lungs
Check chest expansion/air entry/ expired Vt and adjust PIP
up or down targeting a normal Vt (while beside patient)
Neonates & preterms need lower pressures
Generally will not exceed 30. In severe obstruction Pplateau
should not exceed 30 (PIP might be higher)
VC: set a normal Vt 6-8mL/min. Check resulting airway
pressure and if it exceeds above limits, reduce Vt to 4-
6mL/min. to achieve safe pressure.
Ti Rate Start at an I/E of 1:2 (Ti= 20/ total rate). At age-appropriate
rates:
Infants: Ti 0.5 at a rate of 40
Small children: Ti 0.6-0.7 at a rate of 30
Older children: Ti 1.0 at a rate of 20

Longer Ti may be helpful with stiff lungs

I/E may reach 1:1 with a longer Ti or high RR but ensure
complete expiration before next cycle (auscultation, vent.
Curves). Not recommended with bronchial obstruction.
PEEP Generally 5. Those with stiff lungs may need considerably
higher
FiO2 Start 100% if cyanosed, severely hypoxic or otherwise
unstable
Else, start around 50%
Adjust targeting SpO2 ≥92%; not necessarily close to 100%
(there are some exceptions needing higher SpO2)
Flow or rise time Mostly don’t change ventilator preset

Trigger sensitivity If patient initiating breaths, adjust to avoid missed efforts

and false triggers

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Monitoring and Adjustment

Monitoring of MV

• Patient monitoring is essential; including continuous ECG, pulse oximetry and

non-invasive blood pressure. Useful data can be obtained by clinical
examination, from ventilator measurements and graphics, blood gases and
imaging studies.
• The patient should be monitored for the objectives of MV.

Note:

▪ Ventilation and oxygenation can be assessed from blood gases; however,

pulse oximetry can be used to assess oxygenation, the ventilator can usually
measure minute volume and capnography may be used for end-tidal CO2.
▪ Pulmonary gas exchange is assessed using oxygen-derived pulmonary
indices:
(1) Oxygenation index (OI) = FiO2 (%) x MAP / PaO2
Higher value ➔ more severe pathology
Above 20 ➔ severe lung pathology
Below 5 ➔ necessary to consider extubation
Cannot apply in patients without positive pressure support (MV or CPAP)
(2) Oxygen saturation index. Uses SpO2 instead of PaO2. Values are
somewhat lower than OI
(3) Arterial/ inspired oxygen ratio= PaO2/ FiO2(fraction 0.21-1.00)
Can be applied with or without positive pressure support
Normally >300. Lower values ➔ more severe pathology
<100 ➔ severe ARDS

▪ The ventilator can usually measure compliance and resistance

▪ Work of breathing is generally assessed clinically. It is also important to
identify patient-ventilator asynchrony (ventilator graphics can help) and
determine the appropriate level of sedation (patient calm and synchronized
but not oversedated)
▪ NB Proper settings and synchronization can be associated with less need
for sedation in many patients. No patient may receive neuromuscular
blockade without deep sedation.
▪ Patients should be monitored for ventilator induced lung injury, including
ventilator parameters that denote overdistension, barotrauma or
atelectrauma, as well as the development of VAP.

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Adjustment of Settings
Ventilation:
• Increasing tidal volume increases ventilation, but avoid overdistension &
observe ∆P limits
• Increasing rate increases ventilation, but observe for Te adequacy

Oxygenation:
• Ventilation affects oxygenation
• Increasing FiO2 increases oxygenation
• Increasing MAP (PEEP, I/E ratio, lastly PIP) increases oxygenation
• A successful lung recruitment improves oxygenation

WOB:
• Patient work of breathing can be decreased by increasing ventilation provided
by the ventilator, as well as by improving patient-ventilator synchronization
• Where possible and tolerated, reducing ventilation provided by the ventilator,
with equivalent increase in patient contribution, corresponds to lowering the
level of support
NB:
▪ It is acceptable to increase settings during a procedure or in response to
deterioration (particularly FiO2 and ventilator rate). However, it is
mandatory to identify & correct the cause of deterioration. After the reason
is over, aim to return to the preceding settings relatively rapidly.
Acute deterioration on MV:
• The most common causes
✓ Equipment failure: inlet gases, ventilator, circuit leak or obstruction, etc
✓ ETT blockage (secretions, blood) or displacement
✓ Patient (most notably pneumothorax; also bronchospasm, asynchrony,
pulmonary hemorrhage, pulmonary oedema, pulmonary embolism and
collapse. Some of these may cause less sudden deterioration
• If the cause is not immediately obvious, a trial of bag & tube ventilation will
immediately by-pass ventilator, circuit or source gas failure. Further, it will
enable assessment of resistance, chest rise and auscultation.
• A blocked tube should be removed and patient ventilated by bag and mask
until reintubation is done.
• An obvious tension pneumothorax with failure of ventilation should be
immediately drained (using needle thoracentesis if appropriate) without
unnecessary delays. A chest tube will then be required (needle will not be
enough during on-going MV)

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Beyond adjustment of settings:

• If the patient’s condition is deteriorating/ not responsive despite

increasing/high settings in absence of a rapidly correctable factor, also
consider

Lung Recruitment Maneuver

More conservative goals:
• Permissive hypercapnia or hypoxemia. Accepting lower than usual goals of
ventilation & oxygenation (eg PaCO2 60-65 provided pH>7.15, SpO2 86-
88%) may be appropriate in those with severe lung pathology so long they do
not lead to a decompensation.
Note:
▪ Permissive hypercapnia requires heavy sedation & frequently paralysis.
These goals are NOT TO BE USED in those with CNS injury

Using a different mode:

• As CMV, HFV, ECMO

WEANING
The following general principles apply:
• Once the patient is ventilated and stable, assess readiness for weaning
(decreasing support) at least daily. Based on
(a) Improvement of the underlying cause
(b) Condition of other systems eg hemodynamics, metabolic, neurological
(c) Absence of neuromuscular blockade and absence of heavy sedation. It is
helpful to interrupt sedation for 1-3hrs daily to judge consciousness and
respiratory drive
(d) Patient’s ability to tolerate a reduction in support (eg rate in SIMV, ∆P in
PS) without excessive RR or effort
• When settings are low enough, a spontaneous breathing trial (without
ventilator support) can be used to judge the patient’s ability to breathe
spontaneously. Judge based on ventilation, oxygenation and WOB. Trials
should not be prolonged (1-2h are usually enough)
• FiO2 <40%, PEEP ≤5, PS ≤10, OI<5
• Patients on long-term MV are more difficult to wean so a more gradual
process is needed
• Any correctable factors should be addressed before extubation (volume, BP,
temp, electrolytes, P, Mg, hemoglobin, etc)
• Be prepared to manage laryngeal oedema and to reintubate if necessary. Those
on MV for significant periods may be weaned to mask CPAP

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Poisoning Protocol

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