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YEAR 4 PAEDS > Emergency Paeds > Flashcards

Emergency Paeds Flashcards

1
Q
  1. What is croup?
  2. what time of year is it most common?
  3. what causes the majority of cases?
A
  1. upper respiratory tract infection commonly caused by a viral infection.
  2. Common in winter months
  3. Parainfluenza viruses account for the majority of cases (RSV can cause too, as well as influenza and adenovirus)
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2
Q

Epidemiology of croup?

A

peak incidence at 6 months - 3 years

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3
Q

What are the charachteristic presenting features of croup ?

A

Characteristic :
* barking cough - occurs in clusters
* inspiratory stridor
* respiratory distress - increased work of breathing
Hoarse voice
Low grade fever
Coryza

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4
Q

Why do you get stridor?

A

stridor is caused by combination of laryngeal oedema and secretions. This causes airway obstructoin, leading to turbulent airflow and reuslting in audible stridor .

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5
Q

Risk factors for Croup?

A
  • Age: croup most commonly occurs in children aged 6-36 months
  • Family history
  • Male (the male:female ratio is approximately 1.4:1)
  • Congenital airway narrowing
  • Hyperactive airways
  • Acquired airway narrowing
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6
Q

Clincial features in history: symptoms in Croup?

A
  • Upper respiratory tract symptoms including coryza and nasal congestion/discharge
  • Fever
  • Hoarse voice
  • Barking cough (often described as ‘seal-like’)
  • Inspiratory stridor
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7
Q

What is important to remember before examine a child with suspected croup? What is the focus of the examination?

A

Focus:
* confirm diagnosis
* assess severity

KEY TO REMEMBER IF SUSPECT CROUP:
* do not agitate child - worsen resp distress
* guidelines say minnimal handling - throat exam rarerly needed (rarely considered but never if suspect epiglottitis)

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8
Q

Walk through clinical examination of a child with suspected croup and typical findings

A

EXAM:
* A rapid ABCDE assessment should be performed to identify and manage any life-threatening features, for example, impending respiratory failure or significant airway obstruction.

Typical findings
* Increased work of breathing: intercostal and sternal recession
* Agitation: in severe croup
* Lethargy: in severe croup

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9
Q

CKS suggest what cirteria to grade severity of Croup?
(Categories based on Mild, Moderate, Severe )

A
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10
Q

When do CKS advise you should admit a child with Croup?

A

ADMIT
* any child with moderate or severe croup.

Other features to prompt admission include:
* < 6 months of age
* known upper airway abnormalities (e.g. Laryngomalacia, Down’s syndrome)
* uncertainty about diagnosis

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11
Q

Differencials for Croup? try and think of differenciators for a few

A

Epiglottitis:
* cause: Haemophilus influenzae
* NO barking cough
* child = appear anxious, pale and ‘toxic’.
* difficulty swallowing causes drooling, fever, and ‘tripod’
* don’t examine the mouth / upset the child - risk of airway complete obstruction.

Upper airway abscess:
* (e.g. peritonsillar, parapharyngeal and retropharyngeal):
* fevers, stiff neck, torticollis, drooling and ‘hot potato voice’.
* NO barking cough.

Foreign body inhalation:
* sudden onset stridor and respiratory distress often w/ hx of choking.
* May be a barking cough and stridor depending on the location of the obstruction.
* Importantly- no fever.

Other:
allergic reaction
injury to the airway
congenital airway anomalies
bronchogenic cyst
early Guillain-Barré syndrome.

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12
Q

Investigations for Croup?

imaging

A

Mostly diagnosed clinically

Imaging - Chest x-ray:
* a posterior-anterior view will show subglottic narrowing, commonly called the ‘steeple sign’ (see pic)
* in contrast, a lateral view in acute epiglottis will show swelling of the epiglottis - the ‘thumb sign’
* A lateral airway X-ray in children may be considered to rule out foreign body inhalation.

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13
Q

What is management for Croup?

A
  • Croup is a self-limiting illness and treatment depends on severity
  • Aim is to reduce the severity and avoid the need for intubation.
  • Corticosteroids (e.g. dexamethasone) are the first-line pharmacological option to reduce the severity of symptoms.
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14
Q

What is management of mild Croup?

A
  • Oral dexamethasone 0.15 mg/kg as a single dose
  • If otherwise well, discharge home with a written advice sheet, safety netting and early follow up in the community (within 24 hours)
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15
Q

What is management of moderate Croup?

A
  • Oral dexamethasone 0.15-0.3 mg/kg as a single dose
  • Observe for improvement and no deterioration.
  • Discharge criteria include: no stridor at rest, normal 02 sats, normal colour, normal activity, able to tolerate fluids orally and caregivers understand when to return.
  • If the patient worsens during observation, may need nebulised adrenaline 5ml of 1:1000 and further observation.
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16
Q

Management of severe Croup?

A
  • Nebulised adrenaline 0.5ml/kg (up to 5ml) of 1:1000 undiluted (this can be repeated if required)
  • O2 to correct hypoxia (if present)
  • Oral or IV/IM dexamethasone 0.3-0.6 mg/kg
  • Monitoring for min 4 hours after giving adrenaline - risk of rebound of symptoms after the adrenaline wears off.

If children with severe croup require two or more doses of adrenaline, consider paediatric critical care review. An early review by the intensive care team is important as the patient may require intubation to protect the airway.

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17
Q

What are criteria for hospital admission with Croup ?

A
  • Severe croup
  • Moderate to severe croup but with deterioration or repeated doses of adrenaline
  • Toxic appearing child
  • Oxygen requirement
  • Inability to tolerate oral fluid intake.

Additional factors to consider include young age, number of healthcare attendances, carer anxiety or an inability for carers to bring the child back to the hospital in case of deterioration.

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18
Q

When should Croup resolve?

A

In most children, croup resolves within 3 days.

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19
Q

What are complications of Croup?

A
  • Secondary bacterial infections (including bacterial tracheitis, bronchopneumonia and pneumonia)
  • Post-obstructive pulmonary oedema
  • Pneumothorax
  • Pneumomediastinum
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20
Q

Recognising an acutely ill child is important to triage and treat

Fever is a common presentation of infectious diseases in young children.

Thinking about ‘red flag’ signs, what can you recall of the NICE ‘green, amber, red’ guidance on feverish children <5 years?

A

From pass med:

Amber signs include:
Nasal flaring
Lung crackles on auscultation
Not responding normally to social cues
Reduced nappy wetting
Dry mucous membranes
Pallor reported by parent or carer

Red signs include:
Moderate or severe chest wall recession
Does not wake if roused
Reduced skin turgor
Mottled or blue appearance
Grunting

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21
Q

What are some common presentations of an acutely unwell child?

A
  • High fever (often sudden onset)
  • non blanching rash (sepsis)
  • Altered level of consciousness
  • anaphlyaxis
  • poisoning
  • inhaled foreign body / choking
  • severe dehydration
  • acute asthma attack
  • burns and scalds
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22
Q

If early signs of acute illness in children are missed, the child can progress to cardio-respiratory arrest.

Cardiac arrest often follows which 2 things ?

(as opposed to being due to a primary cardiac problem)

A
  1. Circulatory failure (shock)
  2. Respiratory failure

thus recognising signs early can prevent cardiac failure

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23
Q

We know that cardiac arrest in children is caused most often by either 1. Circulatory failure or 2. Respiratory failure.

Use these as your schema to think of broad causes of cardiac arrest

1. Fluid loss / fluid maldistribution 2. resp distress / resp depression

A
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24
Q

What are causes of circulatory failure / shock?

A
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25
Q

What are clinical features of circulatory failure / shock?

What clinical signs suggest what cause?

A

Clinical features:
* Tacchycadia
* thready pulse
* delayed Cap refil (<2 sec) check centrally as more reliable
* Cool extremeties
* hypotension (late sign)
* Tachypnoea
* Restlessness
* reduced urine output
* metabolic acidosis

Signs that suggest a cause
* Fever in sepsis
* purpuric rash (meningococcus)
* Hepatomegaly (Heart failure)
* Focus of infection

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26
Q

How is circulatory failure / shock managed?

A
  • high flow 02, resp support
  • IV fluid bolus
  • Consider inotropic support
  • Anitbiotics for septic shock
  • adrenaline and hydrocortisone for anaphylaxis
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27
Q

What are causes of respiratory failure?

A
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28
Q

What are clincial features of Respiratory failure ?

A
  • SOB
  • Tachypnoea
  • Cyanosis
  • Nasal flaring
  • grunting
  • Intercostal muscle recession
  • Restlessness or confusion

Zero to finals signs of resp distress:
* Raised respiratory rate
* Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
* Intercostal and subcostal recessions
* Nasal flaring
* Head bobbing
* Tracheal tugging
* Cyanosis (due to low oxygen saturation)
* Abnormal airway noises

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29
Q

What are clincial findings / signs on examination that point to different causes of respiratory failure?

A
  • Colour: pallor or cyanosis.
  • Respiratory drive: pattern and timing of breathing think central or brainstem cause.
  • Inspiration: upper airway obstruction produces stridor e.g. croup / epiglottitis
  • Expiration: lower airway obstruction leads to cough, wheeze, and a prolonged expiratory phase e.g asthma, pnuemonia.
  • Chest wall movement: chest and abdominal wall dynamics may indicate flail chest, diaphragmatic palsy, pneumothorax, FB inhalation (asymmetrical chest wall movement).
  • Position and level of agitation e.g. tripod epiglottitis
  • Mental state - neurological
  • HR and perfusion -impending arrest.
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30
Q

Investigations for respiratory failure ?

A

Non-invasive / bedside:
* pulse oximetry: SpO2.
* (PEFR) or spirometry: assessment of severity of asthma.

Lab:
* ABG: assessment of acid–base, PP 02 and C02
* capillary blood sample is a good alternative for pH and pCO2 if extremity is warm and blood
flows freely.
* Blood tests: FBC, U&E, glucose, cultures.

Imaging
* CXR: for diagnosis (e.g. severe pneumonia); for assessment of complications (e.g. pulmonary oedema, pneumothorax)
* POCUS of thorax: for diagnosis (e.g. pulmonary effusion).

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31
Q

Management of respiratory failure?

A
  • assess severity by examination, blood gases / 02 sats
  • Give high flow 02
  • intubate an ventilate if rising C02
  • Treat underlying cause e.g. antibiotics for infection, bronchodilators and steroids for asthma, remove FB
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32
Q

The collapsed child: what are common causes of cardiorespiratory arrest?

A
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33
Q

Not all children who collpse proceed to fill respiratory or cardiac arrest. What are some other cuases of sudden collapse in children?

A
  • Syncope
  • epilepsy
  • choking
  • cardiac arrythmias (rare)
  • factitious illness (rare)
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34
Q

What are the principals of paediatric basic life support?

Flow chart of what do

A

ratio of 15:2 breaths for all except newborns, where ratio is 3:1.

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35
Q

How to give chest compressions

Hint: age dependant

A

Compress lower ½ of sternum to ⅓ of the chest’s depth

  • Infants, 2 fingers or place both thumbs on sternum and encircle the entire thorax with your hands
  • Smaller children: use the heel of 1 hand in the middle of a line joining the nipples
  • Children (>8yrs), use adult 2-handed method
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36
Q

How do you immediately manage a child who is choking?

A
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37
Q

What are the principals of ADVANCED paediatric life support ?

Flow chart of steps, immediate treatment, during CPR

A

IV adrenaline 10 micrograms/kg (0.1 mL / kg-1 of 1 in 10,000 solution).

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38
Q

What are reversible causes of cardiac arrest in children?

A
  • hypoxia
  • hypovolaemia
  • hypo/hyperkalaemia / metabolic
  • tension pneumothorax
  • toxins
  • tamponade - cardiac
  • thromboembolism
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39
Q

Why is Intraosseous transufion useful? give examples of times it is used

A
  • useful for immediate vascular access in life threatening emergencies where rapid IV access cant be obtained.
  • rapid, safe and effective way of gaining vascualr access
  • Cardio-pulmonary arrest, severe burns, prolonged status epilepticus, hypovolameic and septic shock
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40
Q

What can you do with intraossues transfusion / acess?

i.e. give meds etc

A
  • safe to administer all IV medicines
  • give fluids
  • give blood products
  • take bloods: crossmatch, FBC, U&E, blood cultures
  • NOTE: need to tell lab they are marow samples as blood gas can be taken but need to let lab know its marrow)
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41
Q

Contraindications for interosseus access?

A

Osteoporosis, osteogenesis imperfecta, infection at insertion site, vascular injury proximal to the insertion site, fracture in target bone, or previous IO insertion at site within 48 hours.

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42
Q

Site for interosseus access?

A

The proximal tibia is the preferred site; anteromedial surface of the tibia, 1–2cm medial to and 1–2cm distal to the tibial tuberosity.

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43
Q

What are causes of convulsions in a child ?

think broad differencials to this presentation

A
44
Q

A child presents with convulsions. Think about what you will need from your evaluation:

What will you ask in history?
What will look for on examination?
What investigations could you order and what would they tell you?

A
45
Q

What is a febrile convulsion?

A
  • a single tonic–clonic, symmetrical generalized seizure lasting <15min, when temp rises rapidly in a febrile illnes (e.g. viral URTI) in a normally developing child
  • Age 6 months - 6 years ( 3% children)
  • happens no more than 1 x in 24 hours
46
Q

Differenciate between different typs of febrile convulsions

A
47
Q

What to do when examining a child with febrile convulsions?

What investigations?

A

Find the source of infection, look for signs of meningitis as risk is meningoencephalitis

Investigations:
MSU, CXR, ENT swabs

48
Q

Treatment of febrile convulsions?

A
  • Give o2
  • put in recovery position
  • check glucose
  • if fit lasting >5min treat as status epilepticus
  • antipyretics may reduce discomfort but do not treat nor prevent fits
  • if recurrent febrile convulsions occur then benzodiazepine rescue medication may be considered
    this should only be started on the advice of a paediatrician)
49
Q

Prognosis of further febrile convulsions?

A

Overall risk of further febrile convulsion = 1 in 3.
This varies widely depending on risk factors for further seizure, including:
* age of onset < 18 months
* fever < 39ºC
* shorter duration of fever before the seizure
* a family history of febrile convulsions

50
Q

Link of febrile convulsions to epilepsy?

A

Risk factors for epilepsy:
* FHx of epilepsy
* complex febrile seizures
* background of neurodevelopmental disorder

  • Children with no RF have a 2.5% risk of developing epilepsy
  • Children with all 3 features the risk of developing epilepsy is much higher (e.g. 50%)
51
Q

Acute malnutrition manifests as what 2 clincial syndromes?

A

marasmus and
kwashiorkor

although there can be overlap

52
Q

Signs of Marasmus?

A

Signs:
* ‘old man’ appearance
* emaciated
* thin
* flaccid skin
* prominent bones
* alert
* irritable
* distended abdomen

53
Q

Signs of Kwashiorkor?

A

has higher mortality than marasmus.

Signs:
* bilateral pitting oedema
* apathy
* anorexia
* skin/hair depigmentation and fragility;
* distended abdomen

54
Q

What happnes in both Marasmus and Kwashikor?

A

Both forms are associated with failure of physiological and metabolic processes,
reduced immunity, reduced gut absorption, and a vicious cycle leading to death.

55
Q

Treatment of acute malnutrition?

A
  • re-educate child, family and politicians.

Food;
* Gradually increasing, high-protein diet + vitamins.
* Most can be treated at home with fortified ready-to-use foods if >6 months, no serious medical complications, and able to eat.
* if complications / too weak to eat need a period of stabilization to restore physiological and metabolic
processes while avoiding refeeding syndrome (↓k ; ↓mg ; ↓po4 –; oedema, seizures) before continuing
treatment at home.

56
Q

What can dehydration lead to in a child?

A

Dehydration can lead to shock, severe metabolic acidosis, and death, particularly in infants.

57
Q

How can you assess severity of dehydration in a child?

A

By assessing acute changes in body weight and looking at following signs

58
Q

What are different types of dehydration ?

think of electrolyte i.e salt

A
  • Isotonic dehydration (Na 130–150mmol/L)
  • Hyponatraemic dehydration (Na <130mmol/L)
  • Hypernatraemic dehydration (Na >150mmol/L)
59
Q

approach to Isotonic / hyponatraemic dehydration:

1) Assessment 2) calculate 3 ) investigations 4) management / monitoring

A

1) assess the degree of dehydration (use weight change and signs).
2) Calculate the fluid deficit (e.g. 10% dehydration when weight is 15kg suggests a 1500mL fluid deficit)
3) Check U&E - urea may be high in dehydration -(Na , K , Ca ), creatinine and glucose.
4) Monitoring : vital signs, losses (urine, stool, vomit, NG) daily weight, BP
4) Rehydrate ove 24 hours : image

60
Q

Approach / complications / montoring for hypernatraemic dehydration?

A

(Water losses exceed Na loss.)

  • Complications: Cerebral oedema is a risk during rehydration, so correction of the defecit should be achieved slowly and evenly, over 48h.
  • Check U&E (at least 8-hourly blood U&E) creatinine and glucose.
  • Monitoring : vital signs, losses (urine, stool, vomit, NG) daily weight, BP
  • Use normal saline, so that Na correction occurs slowly.

Seizures and cerebral oedema may complicate rehydration in hypernatraemic dehydration. Treat
symptomatically and refer to an ICU.

61
Q

Common cause of dehydration in children?

A

Gastroenteritis causing diarrhoea and vommitting

rotavirus is most common cause of gastroenteritis in children in UK

62
Q

What kind of dehydration do you get from gastroenteritis?

iso / hypo / hyper natraemic?

A

Hypernatraemic due to water loss

63
Q

what features suggest hypernatraemic dehydration:

A
  • jittery movements
  • increased muscle tone
  • hyperreflexia
  • convulsions
  • drowsiness or coma
64
Q

what children are at increased risk of dehydration?

A
  • < 1 year, especially <6 months
  • infants who were of low birth weight
  • children who have passed six or more diarrhoeal stools in the past 24 hours
  • children who have vomited three times or more in the past 24 hours
  • children who have not been offered or have not been able to tolerate supplementary fluids before presentation
  • infants who have stopped breastfeeding during the illness
  • children with signs of malnutrition
65
Q

What could you give if you suspect dehydration?

Not super serious dehydration

A
  • give 50 ml/kg low osmolarity oral rehydration solution (ORS) solution over 4 hours, plus ORS solution for maintenance, often and in small amounts
  • continue breastfeeding
  • consider supplementing with usual fluids (including milk feeds or water, but not fruit juices or carbonated drinks)
66
Q

Normal HR, BP, RR, Urine output for different ages

reminder from intro lec

A
67
Q

Paediatric fluid prescribing rules

reminder from intro lec

A
68
Q

Poisoning / accidental injestion in a youg child

  1. common casues
  2. history points to cover
  3. examination points to cover
A
69
Q

Compare and contrast poisoning and overdose

A

Poisoning
* commonly 2-3 yrs
* accidental

Overdose
* older children / teens
* self harm and intentional

70
Q

What do you need to determine / clarify in poisoning / overdose?

A

How much, when, and what exactly was injested.
* e.g.the number of tablets dispensed is often on the pack—count what remains and calculate the
maximum dose ingested

other medicines/chemicals
* Ask if other medicines are kept in the same place and could the child have taken more than one type? Was this child playing with
any?

71
Q

What are the principals of management for poisoning ?

A
  • ABC priority but never forget DEFG (glucose!)
  • Consider intubation if GCS<8
  • maintain BP, correct hypoglycaemia, monitor urine
  • baseline studies: FBC, U&E, gluocse, ECG
  • Serum measurement: e.g paracetemol, salicyates, iron, anticonvulsants, lithium, carboxyhaemoglobin
  • supportive manageent is mainstay
  • is there a specific antidote? e.g. naloxone, atropine
72
Q

What is iron poisoning?

how common / pathophysiology

A

Iron is a common childhood poison.

It is absorbed as fe2+, oxidized to fe3+, and bound to transferrin.

Toxicity occurs when transferrin binding capacity is exceeded.

73
Q

Different formulations contain differnout amounts of iron. What doses of elemental iron are potentially fatal?

A

mild toxicity : >20mg/kg of elemental iron.
Moderate–severe toxicity: >60mg/kg.
potentially fatal: 200–250mg/kg

74
Q

Presentation of iron poisoning

initial, over hours, potential complication if survive

A
  • Nausea, vomiting, abdo pain, haematemesis, diarrhoea, altered mental status, or hypotension.
  • 6-12 hours - apparent improvement
  • 12 & 24 hours cardiovascular collapse and massive GI bleeding.
  • Severe metabolic acidosis with raised anion gap may develop as each Fe ion combines with water to produce 3H and Fe(OH)3 causing renal and hepatic failure.
    Hepatotoxicity is a marker of severity and is a common cause of death.

complications for survivors
* may develop pyloric strictures after 4–6 weeks due to scarring.

75
Q

investigations for iron poisoning

A
  • Blood gas (metabolic acidosis), serum iron concentration, U&E, FBC,LFTS, clotting, glucose, ECG.

Iron levels at 4–6h indicate severity.
* Levels of <3mg/L (~55μmol/L) are associated with minimal symptoms and >5mg/L (~90μmol/L) serious toxicity.

  • Abdominal X-ray may show tablets within the gut and reveal a bezoar (a mass within the
    gastrointestinal system).
76
Q

How to manage iron toxicity?

A
  • severe: do not wait for tests start desferrioxamine (Chelation with IV desferrioxamine (15mg/kg/h until 80mg/kg given then discuss with national poisons service). stop when acidosis improves
  • expert help (sometimes gastric lavage is used)
  • whole-bowel irrigation can be used
  • activated charcoal (not used as doesnt bind iron)
  • supportive care - IV fluids and bicarbonate to correct acidosis
77
Q

1) What happens to urine when give desferrioxamine?
2) complications / SE of giving desferrioxamine

A

1) makes wee orangey-red -demonstrates that free iron has been bound to the desferrioxamine.

2) desferrioxamine: associated with hypotension, rashes, pulmonary oedema, and acute respiratory distress syndrome.

78
Q

Intentional overdose in older children and adolescents:
* agents used ?
* risk factors ?
* general management principals?

A
79
Q

What is theraputic dose of paracetemol?
what dose can cause hepatotoxicity?

A

therapeutic:
* 15mg/kg.

Hepatotoxicity can occur if:
* ≥150mg/kg

80
Q

Features of paracetemol poisoning

include, initial, time course, complications

A

initial:
* minimal: nausea and vomitting which settle <24 hours

24 hours:
* hepatic enzymes rise

> 48 hours
* jaundice, enlarged tender liver

3-4 days post ingestion
* maximal liver damage occurs

Complications:
Hypoglycaemia, hypotension, encephalopathy, coagulopathy, coma, and death (liver failure)

81
Q

Management of single oral paracetamol overdose

A

Admit:
* taken >75mg/kg (or an unknown amount) and do a serum paracetamol concentration.
* ≥4h post ingestion, do venous gas, U&E, bicarbonate, FBC, LFTS and clotting.
* If presenting <1h, and >150mg/kg ingested, and no contraindication (eg vomiting; ↓GCS), give activated charcoal.

  • Plot on nomogram- If plasma paracetamol level is on or above the line, or the patient has an abnormal INR, ALT, or creatinine, treat with acetylcysteine (NAC).
82
Q

What doese of NAC for paracetemol overdose?

A
  • 150mg/kg in up to 200ml (depending on weight; see bnfc) of 5% glucose infused over 1h
  • followed by 50mg/kg IVI over the next 4h
  • 100mg/kg IVI over the next 16h. It is
  • Effective in preventing liver damage if started <8h after overdose.
83
Q

Management of paracetemol poisoning in a pt who presents 8-24 hours after injestion?

A
  • start NAC immediately if ingested dose is
    >150mg/kg, or dose is unknown.
  • NAC can be stopped if paracetamol level is below the treatment line or if patient is asymptomatic, and INR, LFTS, and creatinine are normal.
84
Q

Management of paracetemol poisoning in a pt who presents 8-24 hours after injestion?

A
  • start NAC immediately if ingested dose is
    >150mg/kg, or dose is unknown.
  • NAC can be stopped if paracetamol level is below the treatment line or if patient is asymptomatic, and INR, LFTS, and creatinine are normal.
85
Q

Why is aspirin (i.ie acetylsalicylic acid) not recommended in children <16 years?

A

Association with Reye syndrome

86
Q

Salicylate poisoning: when does toxicity occur (i.e. dose) form aspirin?

A

Toxicity occurs at ~100mg/kg aspirin.

87
Q

What is the presentation of salicylate / aspirin poisoning?

early signs, resp, metabolic, central, GI, renal and electrolyte

A

Early signs
* tinnitus and hearing loss.

Resp:
Stimulation of resp centres - tachypnoea + Resp alkalosis. pulmonary oedema

Metabolic:
Interference with aerobic metabolism leads to the metabolic (lactic) acidosis which is characteristic of salicylate poisoning.

GI:
irritation (nausea, vomiting, abdominal pain is common).

Central effects:
agitation, delirium, and seizures.

Renal and electrolyte:
Rhabdomyolysis, electrolyte disturbances - particularly hypokalaemia.

88
Q

Investigations and tests for salicylate / aspirin poisoning ?

A

Bedside:
* Blood gas, glucose, ECG

Lab:
* FBC; U&E, clotting,
* Salicylate levels are best obtained at 6h (peak level);
do initial level to confirm diagnosis, then levels every 2h to confirm levels are decreasing—
* NOTE enteric coated (EC) preparations can lead to delayed absorption.

Imaging:
abdominal Xray - large bezoars of EC aspirin can be seen

Bezoars - accumulations of indigestible contents w/in GI tract.

89
Q

Management of aspirin poisoning ?

A
  • Avoid intubation unless in resp failure, sudden loss of hyperventilatory drive can lead to decompensation and death.
  • Resuscitate : bolus of 10–20ml/kg of 0.9% nacl.
  • Correct hypokalaemia.
  • Severe toxicity (levels (5.1mmol/L)— urinary alkalinization with IV sodium bicarbonate to enhance elimination (under expert guidance in ITU).
  • Activated charcoal is effective in adsorbing aspirin, give via NGT.
  • Haemodialysis is definitive treatment: use
    when evidence of end-organ injury (seizures, severe acidosis, rhabdomyolysis, renal failure, pulmonary
    oedema). Seek expert help.
90
Q

How is hypoglycaemia defined in children and infants?

A

This emergency is defined as a blood value <2.6mmol/L or <3.0mmol/L if symptomatic.

91
Q

Causes of hypoglycaemia in children?
i.e. endocrine (big headings)

carb intake or absorption,
gluconeogenesis, or glycogenolysis

A

Endocrine
* Hyperinsulinism.
* Hypopituitarism.
* Growth hormone (GH) deficiency.
* Hypothyroidism.
* Congenital adrenal hyperplasia (CAH).

Metabolic
* glycogen storage disease
* galactoseamiea
* acyl CoA dehydrogenase deficiency

Toxic:
* salicylates
* alcohol
* insulin
* valporate

Hepatic :
* hepatitis
* cirrhosis
* reye syndrome

Systemic:
* starvation
* malnutrition
* spesis
* malabsorption

92
Q

Hx and examination of hypoglycaemia?

A

History:
* identify timing of hypo in relation to feeding and medication

Examination:
* short stature?
* failure to thrive ?
* hepatomeglay ?
* features of generalised metabolic disorder?

93
Q

Investigations of hypoglycaemia in an acute episode?

A
  • Save blood and urine for metabolic and endocrine testing.
  • Check blood glucose.
  • Blood U&E, LFTs, and osmolality.
  • ABG.
  • Blood ketones.
  • Toxicology screen.
94
Q

Treatment of hypoglycaemia?

A

Asymptomatic:
* PO glucose drink or gel

Symptomatic:
* glucose 2ml/kg 10% dextrose IV
* continuous infusion of IV dextrose (6-8kg/min) e.g, normal saline with 5% dextrose at normal maintenace rate
* if no response - specialsit advice consider glucagon, hydrocortisone

95
Q

What are some of the reasons why paediatric patients are predisposed to hypothermia?

A
  • radiation (large surface area to volume ratio, large head)
  • convective (repeated examinations with exposure to atmosphere)
  • conductive (loss of heat into bed)
  • thermoregulatory response altered (sedation or paralysis, neurological injury)
96
Q

How do you prevent hypothermia in children in an emergency ?
Clinical and Environmental prevention

A

Environmental
* adequate ambient temperature
* maintain dry skin
* cover head with a cap or beanie
* warm blankets
* heating blanket
* forced air warmers
* infra-red radiant heaters

Clinical
* minimise exposure to environment during clinical examination
* continuous or intermittent thermal monitoring
* avoiding cold fluids
* giving warm fluids (39 degrees) to prevent further heat loss
* warm ventilator gases (37 degrees if normothermic, 42 degrees if hypothermic)

97
Q

What are some emergency paediatric rewarming strategies ?

A
  • gastric or bladder lavage with 42 degrees normal saline
  • peritoneal lavage with 42 degrees potassium free dialysate (20mL/kg at 15/60 cycles)
  • pleural or pericardial lavage
  • endovascular warming
  • extracorporeal blood rewarming (ECMO or dialysis)

https://litfl.com/paediatric-hypothermia/

98
Q

What are some differencials for hyperthermia or heat illness?

A

Infection
* (e.g. Brain abscess, Encephalitis, Meningitis)

CNS
* Status Epilepticus

Toxicology
* Aspirin overdose
* illicit drugs (including PCP, MDMA, Cocaine and Amphetamines),
* medications (e.g. neuroleptics)
* Neuroleptic Malignant Syndrome

Endocrine:
* Phaeochromocytoma
* Thyroid Storm
* Malignant Hyperthermia.

chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://www.bsuh.nhs.uk/library/wp-content/uploads/sites/8/2021/01/Paediatric-guidelines-Heat-Illness.pdf

99
Q

Assessment of hyperthermia : What are 3 stages ?

A

Heat stress : temp normal

Heat exhaustion : temp >38

Heat stroke: temp > 40

100
Q

Assessment of hyperthermia: what to do if suspect hypthermia?

A

once suspect:
* document rectal temp

if suspect heat exhaustion / heat stroke :
* do capillary blood gas
* urine dip

101
Q

Signs, symptoms and some investigation findings of the 3 stage of hyperthermia / heat illness?

A
102
Q

How to manage heat stress?

chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://www.bsuh.nhs.uk/library/wp-content/uploads/sites/8/2021/01/Paediatric-guidelines-Heat-Illness.pdf

A

Discharge with safety-netting advice
* Rest, stretch or massage affected muscle groups
* hydrate (water +/- Dioralyte)
* avoid exposure to heat & sun until asymptomatic

103
Q

How to manage heat exhaustion?

may progress rapdily to life threatening heat stroke

chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://www.bsuh.nhs.uk/library/wp-content/uploads/sites/8/2021/01/Paediatric-guidelines-Heat-Illness.pdf

A
  • Admit
  • IV access
  • Bloods - FBC, U&E, LFT, Clotting, Calcium, Phosphate, Creatine Kinase and Blood Gas
  • 12-lead ECG if significant electrolyte abnormalities
  • Hydrate oral - Dioralyteor or IV fluids
    Cooling pt:
  • Remove clothing
  • Lie pt down and consider elevating legs
  • Evaporative cooling most effective initial cooling strategy (tepid water sprayed over skin whilst fanning)
  • wrap ice-packs in towels and place around neck, axilla and groin OR cover in towels soaked in ice-water OR cooling blankets (if available)

NOTE: Avoid cold water immersion in children (risk of discomfort, agitation, shivering, combativeness, overshoot hypothermia and bradycardia)

104
Q

Heat stroke is an emergency - what is a key differenciator to determine if heat stroke or heat exhaustion?

A

In heat stroke get altered mental state

105
Q

How to manage heat stroke in a child?

A
  • manage as for heat exhaustion
  • assess and stabalise of ABCDE
  • hypovolaemia - IV fluid bolus 20 ml / kg room temp crystalloid
  • seizures ? lorazepam 0.1 mg /kg/ IV
  • aim to cool to 39 degress (avoid overshoot hypothermia)
  • urinary catheter to monitor urine output
  • admit to HDU
  • CT brain if persistent CNS symptoms / signs of raised ICP
106
Q

Lightening learning Paed emergencies: Spontaenous pneumothorax

Types of spontaenous pnuemothorax and treatment

A
107
Q

Lightning learning Spontaneous pneumothorax

A

YEAR 4 PAEDS (19 decks)

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