Download paediatric emergencies

PAEDIATRIC EMERGENCIES
Alice Keyte
[email protected]
AIMS
 Recognition of seriously ill child
 ABCDE
 Management of different severe clinical cases
Curriculum
 Paediatric emergencies (all E)
 Diabetic ketoacidosis (3)
 Severe sepsis including meningococcal septicaemia
(3)
 Severe asthma (3)
 Upper airway obstruction (3)
 Anaphylaxis (3)
(E) = Outline emergency management of condition
(3) = Good working knowledge
ABCDE
 D – Danger
 R – Response
(shout for help)
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A – Airway
B – Breathing
C – Circulation
D – Disability (conscious level, pupils, posture)
E – Expose (rashes, trauma, burns)
How do you assess each of these?
Airway
 Maintaining airway?
 Head tilt, chin lift – sniffing the morning air
 OPA – Oropharangeal Airway (GCS <8) - midline to jaw
angle
 Nasopharyngeal - nose tip to tragus
 Obstructed – Anaesthetic team
 Oxygen
 Appropriate mask
Breathing
Respiratory Distress
Tachypnoea
Recession
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Rate
Rhythm
Symmetry – seesaw breathing
Effort
Age
RR
Effectiveness
SILENT CHEST
HYPOXIA
<1
1-2
2-5
5-12
>12
30-40
25-35
25-30
20-25
15-20
Tracheal tug
Accessory muscles
Head bobbing
Grunting
Nasal Flare
Circulation
Tachycardia
Pain
Temperature
 Effort = Heart Rate
 Effectiveness:
Fear/ Anxiety
SHOCK
 Capillary Refill (<2secs)
 Cyanosis
 BP
HYPOTENSION
Arrhythmia
Age
<1
1-2
2-5
5-12
>12
HR
110–160
100–150
95-140
80-120
60–100
Disability
 Conscious Level (AVPU)
 Pupils (fixed and dilated?)
Alert
Responds to Voice
--------------(GCS 8/9 i.e.?airway
threat)--------- ---Responds to Pain only
Unresponsive
 Posture (frog?)
 DEFG – DON’T EVER FORGET GLUCOSE
EXHAUSTION
Exposure
 Rashes – anaphylaxis? Meningitis?
 Trauma
 Burns – dehydration = hypovolaemic shock
(Standard bolus = 10/20ml/kg of 0.9% saline)
Preterminal Signs
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SILENT CHEST
HYPOXIA
HYPOTENSION
EXHAUSTION (limp frog position)
RESPIRATORY DISTRESS (tracheal tug, cyanosis,
reduced cap refill, head bobbing, intercostal
recession)
Aren’t Small grown ups
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Anatomy
Surface area and weight
Development
Parents
Pathology
Child protection
Causes of collapse
Conditions
 Asthma and allergy
 Infection
 Respiratory
 Sepsis
 Other
 Neurological
 Fits
 Altered consciousness
 DKA
 Trauma
 Burns
 Drowning
DKA
 Mostly seen in DM type 1
 High glucose + NO insulin.
 Osmotic diuresis, dehydration + electrolyte loss (Na +
K)
 Tissues + fat = alternative energy source as cannot
utilise glucose → KETONES + metabolic acidosis.
Clinical
 Smell of acetone on breath (pear drops)
 Hyperventilation due to acidosis → Kussmaul
breathing
 Nausea + vomiting
 Signs of dehydration – reduced skin turgor, dry
mucous membranes, tachycardia/hypotension
 Hypovolaemic shock
 Drowsiness + lethargy
 Coma
 Polyuria
 Polydipsia
Investigations
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Blood glucose > 15mmol/l
FBC, U&E’s to assess dehydration
ABG to assess for severe metabolic acidosis
Urinalysis
 Glucose and ketones
 Evidence of precipitating cause
Management
(SLOW!)
As they are cotransported!
 Fluids
 If in shocked → saline bolus (10-20ml/kg 0.9% Saline)
 Maintain rehydration – 0.9% saline + potassium initially
- 0.45% saline once glucose <15mmol/l
 GRADUAL REHYDRATION OVER 18 TO 72 HOURS → RISK OF CEREBRAL
OEDEMA AND HERNIATION WITH RAPID FLUID SHIFTS (Manitol)
 Monitoring fluid input, output, U&E’s and neurological state aids progress
 Insulin
 IV infusion at 0.1units/kg/hr
 titrating dose according to blood glucose ‘INSULIN SLIDING SCALE’
 Avoid drops >5mmol/l/hr
Cont.
 Acidosis
 Self corrects with insulin and fluids
 Re-establish oral fluids, diet and insulin
subcutaneously
 Identify and treat underlying cause
 Careful monitoring
Complications
 Cerebral oedema (headache, reduced consciousness,
fits, irritability)
 Avoided by slow restoration of fluids and electrolytes
 Cardiac dysrhythmias
 Secondary to potassium imbalances
SEPTICAEMIA
 Bacteria → blood.
 Host response to bacterial toxins = release inflammatory
cytokines + activate endothelial cells
 vasodilatation/vasoconstriction
 Depress cardiac function
 Disturb cellular oxygen consumption
 Cause capillary leak with resulting hypovolemia
 Promote DIC = Disseminated intravascular coagulation.
 Activation of coagulation.
 Small blood clots in vessels = consume coagulation proteins and
platelets ---- disrupting normal coagulations = bleeding
SHOCK = An acute failure of circulatory function that leads to
inadequate tissue perfusion
Causes
 Meningococcal infection (Neisseria Menigitidis) ±
meningitis
 pneumococci
 Neonates = group B strep from birth canal
Clinical
HISTORY
EXAMINATION

Fever

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Poor feeding
Lethargy

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History of focal infection
o Gastroenteritis
o Osteomyelitis
o Cellulitis

Organ failure

Predisposing factors
o Immunocompromised

Non-blanching purpuric rash
(meningococcal) if suspected =
immediate injection of benzylpenicillin)
Irritability
Shock (early = increased CO, warm
extremities, high fever, confusion)
(late = reduced CO, hypotension,
cool peripheries, metabolic acidosis)
Management
 SEPTIC SCREEN:
 FBC, CRP, Blood and Urine cultures, LP and CXR
 Oxygen – 100% via face mask
 Fluid 20ml/kg colloid or crystalloid - due to increased
vascular permeability and loss of proteins/fluids
 Antibiotics IV Ceftriaxone – then tailor to culture
results
 DIC (Disseminated intravascular coagulation)
 Microvascular blood clots and depletion of clotting
factors = bleeding
 May require fresh frozen plasma
SEVERE ASTHMA
 Severe
 Too breathless to talk or feed
 Respiration >50 per minute
 Pulse > 140 bpm
 PEFR < 50% predicted
 Life threatening
 PEFR < 33% predicted
 Fatigue, drowsiness
 Cyanosis
STATUS ASTMATICUS
Assess Severity
 Marked pulsus paradoxus
 different BP on inspiration and expiration → indication of
airway obstruction
 PaO2
 PEFR – Peak Expiratory Flow Rate
Management
 Immediate treatment
 O2 via face mask
 Salbutamol and ipratropium nebulised
 Oral prednisolone
 If there are life threatening features
 IV aminophylline (competitive nonselective
phosphodiesterase inhibitor)
 IV hydrocortisone (steroid)
Together = greater
bronchodilation than a
β2 agonist alone,
leading to a faster
recovery and shorter
duration
of admission.
Cont.
 Subsequent management
 O2
 Β2 agonist – Examples?
 Maintain
UPPER AIRWAY OBSTRUCTION
 CROUP
 EPIGLOTITIS
 Def: Mucosal inflammation and swelling which can
rapidly cause life-threatening obstruction
Clinical
 Stridor – Inspiratory noise due to obstruction to
breathing in the larynx or trachea
 Hoarseness
 Barking cough
Classification
CROUP
EPIGLOTTITIS
HiB type 2 → incidence decreasing because
due to widespread immuinisation & uptake
AETIOLOGY
Parainfluenza virus
PATHOPHYSIOLGY
Oedema of the subglottic area = potentially
dangerous because of narrowing of the
trachea
Emergency due to respiratory obstruction →
intense swelling of the epiglottis and
surrounding tissues associated with
septicaemia
ONSET
Days
Hours
PRODROME
Coryza
None
COUGH
Barking
Slight if any
FEEDJNG
Can drink
NO!
MOUTH
Closed
Drooling saliva
TOXIC
No
Yes
FEVER
< 38.5⁰C
>38.5⁰C
STRIDOR
Rasping
Soft
VOICE
Hoarse
Weal or silent
MANAGEMENT
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Managed at home
Oral steroids
Nebulised adrenaline as inpatient if low
oxygen saturations
Don’t examine throat
Senior staff
Intubate
IV Abx
Rifamapcin to close household contacts
Dos and DON’Ts
 DON’T take the baby/child away from their mother!
 In epiglottitis DON’T examine the throat
 DO call for HELP!
ANAPHYLAXIS
 Severe allergic reaction
 Allergens: Nuts, Eggs, Milk
 prior antigen exposure sensitizing mast cells and
basophils
 systemic release of inflammatory mediators
 capillary leak, mucosal oedema and smooth muscle
contraction
Clinical
 Uticaria and angiodema – facial swelling
 Respiratory:
 Cough, stridor, hoarseness and drooling
 Wheeze
 Laryngeal oedema, bronchoconstriction
 Cardiovascular:
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Lightheaded/dizziness
Syncope
Pallor
Tachycardia
Management
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ABC + remove allergen if possible
IM adrenaline 10 micrograms/kg
20 ml/kg fluid if shocked
Repeat adrenaline and fluids every 5 min if no
improvement
 Once stable
 IV hydrocortisone – little immediate effect,
but prevents later reaction (biphasic) - STEROID
 IV chlorpheniramine – limit ongoing
inflammation - ANTIHISTIMINE
QUESTION 1
 Chelsea, aged 3 months, is brought into the accident
and emergency department by her parents with a 2day history of feeding difficulties preceded by coryzal
symptoms. On examination she is pyrexial and
appears dehydrated. Furthermore she has signs of
respiratory distress with a widespread expiratory
wheeze; her arterial oxygen saturation in 90% on air.
 Give 6 causes of wheezing or stridor in an infant?
 Asthma, bronchiolitis, inhalation of foreign body, croup,
upper airway obstruction, cardiac failure, CF,
 Give 6 signs of respiratory distress in an infant?
 Tachypnoea (>50rpm), nasal flaring, subcostal recession,
intercostal recession, chest hyperinflation, use of
accessory muscles, grunting, head bobbing, feeding
difficulties, tachycardia.
 What is the normal heart rate and respiratory rate in
infants?
 Infant = <1 year of age
 HR = 110-160
 BR = 30-40
 List eight signs of dehydration in an infant?
 Dry mucous membranes + tongue, dull, dry + sunken
eyes, sunken anterior fontanelle, reduced skin turgor,
delayed cap refill, irritability, dry nappy, weak pulse,
reduced BP.
QUESTION 3
 A 15 year old female pupil at a mixed sex Comprehensive
school was sent home early with a complaint of severe
headache. When she returned home she vomited twice and
her mother noted a red rash on her leg. She called an
ambulance and the patient was admitted with a presumed
diagnosis of meningitis. The rash rapidly became more
extensive and she was admitted to the Paediatric Intensive
Care Unit. A lumbar puncture was performed and antibiotic
therapy was commenced. She made a slow recovery and was
discharged 16 days later.
 a) Describe the features of this rash.
 Non-blanching, purpuric rash. Generalised all over the
leg.
 b) What simple test would you use if you saw a similar
rash?
 Tumbler test
 c) In a patient with severe meningitis the rash may
become haemorrhagic. Explain why this might occur.
 DIC
When this patient was admitted to PICU her blood pressure
was 90/55 but she had bounding pulses and warm
peripheries. Septic shock was diagnosed.
 What is the definition of shock?
 Shock = An acute failure of circulatory function that leads to inadequate
tissue perfusion
 List three other forms of shock and briefly explain the underlying
pathophysiological changes in each.
 Cardiogenic, anaphylactic, hypoxic, hypovolaemic
 Why is meningitis a particular problem in schools and halls of
residence?
 Close contact
 What vaccination programs are available in the United Kingdom for
the prevention of meningitis?
 NO Men B
 Men C = at 3month, 12-13months and 13-15 years
 Briefly discuss the problems associated with vaccination programmes
(in general).
QUESTION 2
 Arterial Blood Gas Results:
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PH 7.20 (7.35 – 7.45)
PO2 5.0 kPa (12 – 14 kPa)
PCO2 10.0 kPa (4.5 – 5.5 kPa)
HCO3- 36.0 mmol/l (12 – 26 mmol/l)
Base Excess + 10 mmol/l (1-2 to +2 mmol/l)
You are provided with these results taken during the patient’s
terminal admission, 24 hours before death
 a) What are the major abnormalities, and how do you
account for these in pathophysiological terms?
 b) What changes would you expect in the blood gas analysis
in a patient with a severe diabetic ketoacidosis? Circle the
correct answer.
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•
•
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P02 Decreased/Increased/Normal
PC02 Decreased/Increased/Normal
pH Decreased/Increased/Normal
Base excess Negative/Positive/Unchanged
CONCLUSION
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Children cope well, but then quickly deteriorate
They’re not small adults
Get expert help if there are signs of serious illness
Do the simple things well, and early
Reassess
Don’t panic!