PAEDIATRIC EMERGENCIES

1. PAEDIATRIC EMERGENCIES Alice Keyteajk1g10@soton.ac.uk

2. AIMS Recognition of seriously ill child ABCDE Management of different severe clinical cases

3. 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

4. ABCDE D – Danger R – Response (shout for help) A – Airway B – Breathing C – Circulation D – Disability (conscious level, pupils, posture) E – Expose (rashes, trauma, burns) How do you assess each of these?

5. 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

6. Breathing Respiratory Distress Tachypnoea Recession Tracheal tug Accessory muscles Head bobbing Grunting Nasal Flare Age RR <1 30-40 1-2 25-35 2-5 25-30 5-12 20-25 >12 15-20 Rate Rhythm Symmetry – seesaw breathing Effort Effectiveness SILENT CHESTHYPOXIA

7. Circulation Tachycardia Pain Temperature Fear/ Anxiety SHOCK Arrhythmia Age HR <1 110–160 1-2 100–150 2-5 95-140 5-12 80-120 >12 60–100 • Effort = Heart Rate • Effectiveness: • Capillary Refill (<2secs) • Cyanosis • BP HYPOTENSION

8. Disability Alert Responds to Voice --------------(GCS 8/9 i.e.?airway threat)--------- ---- Responds to Pain only Unresponsive Conscious Level (AVPU) Pupils (fixed and dilated?) Posture (frog?) DEFG – DON’T EVER FORGET GLUCOSE EXHAUSTION

9. Exposure Rashes – anaphylaxis? Meningitis? Trauma Burns – dehydration = hypovolaemic shock(Standard bolus = 10/20ml/kg of 0.9% saline)

10. Preterminal Signs SILENT CHEST HYPOXIA HYPOTENSION EXHAUSTION (limp frog position) RESPIRATORY DISTRESS (tracheal tug, cyanosis, reduced cap refill, head bobbing, intercostal recession)

11. Aren’t Small grown ups Anatomy Surface area and weight Development Parents Pathology Child protection

12. Causes of collapse

13. Conditions • Asthma and allergy • Infection • Respiratory • Sepsis • Other • Neurological • Fits • Altered consciousness • DKA • Trauma • Burns • Drowning

14. 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.

15. Clinical • Smell of acetone on breath (pear drops) • Hyperventilation due to acidosis →Kussmaulbreathing • Nausea + vomiting • Signs of dehydration – reduced skin turgor, dry mucous membranes, tachycardia/hypotension • Hypovolaemic shock • Drowsiness + lethargy • Coma • Polyuria • Polydipsia

16. Investigations • 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

17. Management(SLOW!) As they are co-transported! • 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

18. Cont. • Acidosis • Self corrects with insulin and fluids • Re-establish oral fluids, diet and insulin subcutaneously • Identify and treat underlying cause • Careful monitoring

19. Complications • Cerebral oedema (headache, reduced consciousness, fits, irritability) • Avoided by slow restoration of fluids and electrolytes • Cardiac dysrhythmias • Secondary to potassium imbalances

20. 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

21. Causes Meningococcal infection (Neisseria Menigitidis) ± meningitis pneumococci Neonates = group B strep from birth canal

22. Clinical

23. 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

24. 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

25. Assess Severity • Marked pulsusparadoxus • different BP on inspiration and expiration → indication of airway obstruction • PaO2 • PEFR – Peak Expiratory Flow Rate

26. Management Together = greater bronchodilationthan a β2 agonist alone, leading to a faster recovery and shorter duration of admission. • 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)

27. Cont. • Subsequent management • O2 • Β2agonist – Examples? • Maintain

28. UPPER AIRWAY OBSTRUCTION CROUP EPIGLOTITIS Def: Mucosal inflammation and swelling which can rapidly cause life-threatening obstruction

29. Clinical Stridor – Inspiratory noise due to obstruction to breathing in the larynx or trachea Hoarseness Barking cough

30. Classification

31. 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!

32. 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

34. Clinical • Uticaria and angiodema – facial swelling • Respiratory: • Cough, stridor, hoarseness and drooling • Wheeze • Laryngeal oedema, bronchoconstriction • Cardiovascular: • Lightheaded/dizziness • Syncope • Pallor • Tachycardia

36. Management • 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

37. QUESTION 1 Chelsea, aged 3 months, is brought into the accident and emergency department by her parents with a 2-day 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.

38. 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.

39. 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.

40. 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.

41. 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

42. 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).

43. QUESTION 2 • Arterial Blood Gas Results: • 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

44. 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. • P02 Decreased/Increased/Normal • PC02 Decreased/Increased/Normal • pH Decreased/Increased/Normal • Base excess Negative/Positive/Unchanged

45. CONCLUSION 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!