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ALL YOU NEED TO KNOW ABOUT THE SHORT OF BREATH CHILD Malvi Shah Here’s what we do: ■ Weekly tutorialsopen to all! ■ Focussed on core presentationsand teachingdiagnostictechnique If you’re new here… ■ By medicalstudents,for medical students Welcome to ■ Reviewed by doctors to ensure accuracy Teaching ■ We’ll keep you updated about our Things! upcomingevents via email and group chats!Learning objectives ■ Understandthe importanceof severity classificationsystemsin paediatric respiratoryconditionsand howto apply thesesystemsto real life scenarios ■ Understandhow themanagementof paediatric respiratoryconditions varies due to the aetiologyof each conditionand its severity ■ Understandthe basicprinciplesof paediatriccongenitalheartdefects ■ Understandhow themanagementof congenitalheartdefects linksto their aetiologyCONGENITAL HEART DISEASENote before we start ■ This is a pretty hard topic and can be confusing ■ Prioritiseotherpaeds stuff before thisas only goingto be max 2-3 qs in your AKT ■ My teachingtoday aims to go throughsome basic principles& guidesyou to pick out keywordsin SBAs ■ MLA contentmap- ‘congenitalabnormalities’:does not statespecific conditions,but I’ve gonethroughthe ones I thinkcome up most often ■ Key points in pinkFetal circulation- differences to adult 1. Very high pulmonary vascular resistance- so blood bypasses them, as lungs are not needed for oxygenation of blood 2. Foramen ovale- blood passes straight from RA → LA 3. Ductus arteriosus- blood in pulmonary artery goes straight to aortaChanges at birth 1. Baby takes first breath → lungs expand → pulmonaryvascular resistance drops → blood flows to lungs 2. Greater return of blood to the LA → pressure in LA increases → foramen ovale is forcedshut 3. Closureof ductusarteriosus-due to removal of placental prostaglandinRisk factors for congenital heart disease ● Advanced maternal age ● Maternal diabetes in pregnancy ● Rubella infection in pregnancy ● Maternal alcohol use in pregnancy Specific- lithiumuse causes Ebstein’s anomaly (atrialization of the RV- presents with tricuspid regurg & signs of right heart failure & systemic oedema)SBA You are shadowing the paediatric SHO on a night shift. The nurse has called the doctor urgently to see a 1 day old baby who has suddenly started deteriorating. The baby appears cyanosed and sats are 78% on air, these do not improve with high flow oxygen. The baby was born at 40+9 weeks by emergency caesarean section due to prolonged labour. The baby’s APGAR scores were 9 & 10 1 and 5 mins respectively. The mother was known to have insulin-dependent gestational diabetes but declined all antenatal scans. What is the most likelydiagnosis? 1. Tetralogy of Fallot 2. Transposition of great arteries 3. Total anomalous pulmonaryvenous drainage 4. Coarctation of the aorta 5. Tricuspid atresiaSBA You are shadowing the paediatric SHO on a night shift. The nurse has called the doctor urgently to see a 1 day old baby who has suddenly started deteriorating. The baby appears cyanosed and sats are 78% on air, these do not improve with high flow oxygen. The baby was born at 40+9 weeks by emergency caesarean section due to prolonged labour. The baby’s APGAR scores were 9 & 10 1 and 5 mins respectively. The mother was known to have insulin-dependent gestational diabetes but declined all antenatal scans. What is the most likelydiagnosis? 1. Tetralogy of Fallot 2. Transposition of great arteries 3. Total anomalous pulmonaryvenous drainage 4. Coarctation of the aorta 5. Tricuspid atresia CYANOTIC Transposition of the great arteries (TGA) ● Aorta and pulmonary artery swap places → 2 separate circuits of oxygenated and deoxygenated blood ● Cyanosis → deoxygenated blood in systemic circulation ● Symptoms & signs: ○ Cyanosis & tachypnoea after closure of DA ○ Loud single S2 ■ Attributed to the anterior positioning of the aorta (can’t auscultate pulmonary valve properly) ○ May be a murmur if VSD/ ASD ● Investigations ○ CXR- globular shaped heart- ‘egg on side’, if chronic ● Management: ○ Prostaglandin E- temporary ○ Surgical repair in first few days of life- 2 arteries are switched ● If symptoms unnoticed (due to presence of several shunts) → congestive heart failure ○ Right ventricular hypertrophy, left ventricular atrophySBA You are shadowing the paediatric SHO on a night shift. The nurse has called the doctor urgently to see a 2 hour old baby whose oxygen sats have been dropping constantly from birth, even when given high flow oxygen. The baby appears cyanosed and sats are 78% on high flow oxygen currently. On auscultation of the chest, there is a pansystolic murmur at the lower left sternal edge. The baby was born at 39+3 weeks. The mum moved to the UK just before delivery and all results from antenatal scans were lost, though she reports the pregnancy was normal and she has no health conditions. What is the most likely diagnosis? 1. AVSD 2. Isolated VSD 3. Tetralogy of Fallot 4. Tricuspid atresia 5. Pulmonary stenosisSBA You are shadowing the paediatric SHO on a night shift. The nurse has called the doctor urgently to see a 2 hour old baby whose oxygen sats have been dropping constantly from birth, even when given high flow oxygen. The baby appears cyanosed and sats are 78% on high flow oxygen currently. On auscultation of the chest, there is a pansystolic murmur at the lower left sternal edge. The baby was born at 39+3 weeks. The mum moved to the UK just before delivery and all results from antenatal scans were lost, though she reports the pregnancy was normal and she has no health conditions. What is the most likely diagnosis? 1. AVSD 2. Isolated VSD 3. Tetralogy of Fallot 4. Tricuspid atresia 5. Pulmonary stenosisTricuspid atresia ● The murmur is not DIRECTLY related to the heart defect ● What is this murmur? (type in chat)Tricuspid atresia ● Murmur of a VSD- described as a loud, harsh, pansystolic murmur ● In tricuspid atresia, the tricuspid valve does not form so no connection between RA & RV ● This has to co- exist with an ASD to be compatible with life! ● May also be a VSD, or a PDA CYANOTIC Tricuspid atresia ● Signs and symptoms ○ Progressive cyanosis from birth ○ VSD murmur, may also be a PDA murmur ● Investigations ○ CXR- increased RA & RV size ○ Echo- atretic tricuspid valve, flow across ASD ● Management ○ Temporary- prostaglandin, balloon atrial septostomy (if inta- atrial connection not large enough) ○ Long term- Fontan procedure (series of operations) ■ Overall end goal: to re- directs blood so venous return goes directly to the lungs and avoids the heart altogether ■ Purpose: to reduce blood flow to single functional ventricle and reduce risk of heart failure development ■ Palliative procedure only. Heart transplant would be curativeSBA You are shadowing the paediatric registrar in clinic. A 5 month old baby is brought in due to failure to thrive. He was born at 38+2 weeks to a 43 year old mother. He was well at birth and on the 73rd percentile for weight. Now he is on the 9th percentile for weight. Parents report he feeds very poorly. He appears to want to feed, but after a few sucks gets very breathless and has turned blue on occasion. Today he appears small for his age but is not cyanotic or tachypnoeic. He has an ejection systolic murmur at the upper right sternal border. What is the most likely diagnosis? 1. Coarctation of the aorta 2. Poor breastfeeding technique 3. Tetralogy of Fallot 4. Patent ductus arteriosus 5. Ventricular septal defectSBA You are shadowing the paediatric registrar in clinic. A 5 month old baby is brought in due to failure to thrive. He was born at 38+2 weeks to a 43 year old mother. He was well at birth and on the 73rd percentile for weight. Now he is on the 9th percentile for weight. Parents report he feeds very poorly. He appears to want to feed, but after a few sucks gets very breathless and has turned blue on occasion. Today he appears small for his age but is not cyanotic or tachypnoeic. He has an ejection systolic murmur at the upper right sternal border. What is the most likely diagnosis? 1. Coarctation of the aorta 2. Poor breastfeeding technique 3. Tetralogy of Fallot 4. Patent ductus arteriosus 5. Ventricular septal defect CYANOTICor ACYANOTIC Tetralogy of Fallot Four abnormalities: 1. Pulmonary stenosis/right ventricularoutflowtract obstruction(RVOTO)- means increased resistance to deoxygenated blood passing to the lungs. Presents as an ejection systolic murmur. 2. Right ventricularhypertrophy- in response to the above. Causes ‘boot- shaped’ heart on X- ray 3. VSD-Due to the RVH, pressure on right sided circulation is actually higher than on left side, so shunting of blood from RV→ LV. VSD does not cause a murmuras very large 4. Overridingaorta (aorta basically originates from the area of ventricles directly over the VSD) - means that deoxygenated blood can circulate through the body CYANOTICor ACYANOTIC Tetralogy of Fallot ● Signs & symptoms ○ Severity of the condition determined by degree of RVOTO: ■ More RVOTO → greater RV pressure → more shunting of blood R to L → more cyanosis ○ Severe case: ■ Cyanosis at birth (lips and fingertips) ■ VSD murmur ■ Clubbingof fingers and toes in a few months ○ Less severe case: ■ No cyanosis at birth- cyanosis only presents clinicallyif sats <80%. ■ VSD murmurat birth ■ May present with Tet spells later if untreated (more on this in next slide) CYANOTICor ACYANOTIC Tetralogy of Fallot Tet spells ● Any cause for increased oxygen demand- in babies this is essentially just feeding & crying ● Heart pumps more (deoxygenated) blood ● Cyanosis ● Management of Tet spells: ○ Things to increase systemic vascular resistance→ this reducesthe pressure difference between the R & L sides of the heart,reducingright → left shunting & improving cyanosis ■ Conservative- lie baby on back & flex knees- kinks femoral arteries, increasing SVR ■ Medical- phenylephrine (alpha blocker) ○ Beta blockers can also reduce RV outflow tract (infundibulum)spasm CYANOTICor ACYANOTIC Tetralogy of Fallot ● Investigations ○ CXR- boot shaped heart (due to RVH), decreased pulmonaryvascular markings due to reduced pulmonary flow ○ ECG- signs of RVH if untreated ● Management ○ Corrective surgery in 2 parts: part one is to widen the pulmonaryvalve, part two is to close the VSD ○ Done at age 3- 6 months ○ Why not earlier: baby too young to survive such a surgery ○ Why not later: irreversible RVH, tissue hypoxia leads to poor growth and development of the childSBA A 10 year old boy has been referred to the paediatric clinic due to suspected heart failure. PMH is unknown, though his parents report that he had a congenital heart defect at birth. In the last 2 years he has become more fatigued and is no longer able to run around as he gets very breathless and goes blue. He is on the 10th percentile for weight. On examination, he has a positive hepatojugular reflux and some ankle oedema though he is not currently cyanosed. There is a harsh pansystolic murmur at the lower left sternal edge. What is the underlying cause of the patient’s presentation? 1. Reversal of a left → right shunt 2. Coarctation of the aorta 3. Pulmonary stenosis 4. Left ventricular failure 5. Rheumatic feverSBA A 10 year old boy has been referred to the paediatric clinic due to suspected heart failure. PMH is unknown, though his parents report that he had a congenital heart defect at birth. In the last 2 years he has become more fatigued and is no longer able to run around as he gets very breathless and goes blue. He is on the 10th percentile for weight. On examination, he has a positive hepatojugular reflux and some ankle oedema though he is not currently cyanosed. There is a harsh pansystolic murmur at the lower left sternal edge. What is the underlying cause of the patient’s presentation? 1. Reversal of a left → right shunt 2. Coarctation of the aorta 3. Pulmonary stenosis Whatis the underlyingheart defect? 4. Left ventricular failure 5. Rheumatic fever Whathas happenednow?SBA A 10 year old boy has been referred to the paediatric clinic due to suspected heart failure. PMH is unknown, though his parents report that he had a congenital heart defect at birth. In the last 2 years he has become more fatigued and is no longer able to run around as he gets very breathless and goes blue. He is on the 10th percentile for weight. On examination, he has a positive hepatojugular reflux and some ankle oedema though he is not currently cyanosed. There is a harsh pansystolic murmur at the lower left sternal edge. What is the underlying cause of the patient’s presentation? 1. Reversal of a left → right shunt 2. Coarctation of the aorta 3. Pulmonary stenosis UntreatedVSD leadingto Eisenmenger’ssyndrome 4. Left ventricular failure 5. Rheumatic fever ACYANOTIC Left → Right shunts (VSD and PDA) ■ Signs and symptoms – PDA: continuous ‘machinery’ murmur at ULSE and under left clavicle +/- boundingpulses – Small VSD: asymptomatic with pansystolic harsh murmur at LLSE – Large VSD: biventricular heart failure (hepatomegaly, tachypnoea), failure to thrive – Heart failure occurs as so much blood is shunted into the RV, and returns back to the lungs and then LV, both the RV & LV get volume overloaded ■ Management – PDA- prostaglandin, or surgical ligation – Small VSD- no treatment needed, closes by itself – Large VSD- diuretics, calorie supplementation, surgical closure needed at 3- 6 months CYANOTIC Whathappens if largeVSDs or PDA Eisenmenger’s syndrome are NOT managed! but due to a differentoF, mechanismSBA A crash call is put out for a 2 day old baby girl in the postnatal ward who has suddenly become breathless. The baby was born at 38+2 weeks with no complications during pregnancy or delivery. The baby is responsive. O2 sats are 97% on room air. HR is 220 (110- 170) and RR is 90 (30- 60). Capillary refill is 2s in the hands, but 5s centrally and the lower limbs. Blood pressure is unrecordable in the lower limbs but normal in the upper limbs. Femoral pulses are not palpable. Temperature is 37.3. Given the most likely diagnosis, what is the best immediate management? 1. High flow oxygen 2. IV fluids 3. Indomethacin 4. Prostaglandin E1 5. Broad spectrum antibioticsSBA A crash call is put out for a 2 day old baby girl in the postnatal ward who has suddenly become breathless. The baby was born at 38+2 weeks with no complications during pregnancy or delivery. The baby is responsive. O2 sats are 97% on room air. HR is 220 (110- 170) and RR is 90 (30- 60). Capillary refill is 2s in the hands, but 5s centrally and the lower limbs. Blood pressure is unrecordable in the lower limbs but normal in the upper limbs. Femoral pulses are not palpable. Temperature is 37.3. Given the most likely diagnosis, what is the best immediate management? 1. High flow oxygen 2. IV fluids 3. Indomethacin 4. Prostaglandin E1 5. Broad spectrum antibiotics ACYANOTIC Coarctation of the aorta ● Pathophysiology ○ Arterial duct tissue encircling the aorta just above the point of insertion of the ductus arteriosus. ○ When the duct closes, the aorta constricts too ○ Blood flow to the lower part of the body suddenly cut off → shock and heart failure ● Signs & symptoms ○ Severe cases ○ Sudden shock and heart failure- tachypnoea, tachycardia, absent femoral pulses, metabolic acidosis ○ Less severe cases ○ Asymptomatic, systolic murmur between the scapulae, radio- femoral delay ● Management (severe cases) ○ Prostaglandins- keeps duct open so some blood can get into aorta past point of coarctation ○ Surgical correction soon after diagnosis- balloon angioplasty and stent insertion. ○ Mild cases can be monitored with regular echocardiograms. Congenital heart disease- cheat sheet CYANOTIC Name Whenandhow does itpresent? Key SBApoints Management TGA Cyanosishours- 24hrs post birth Globular heart on CXR- ‘egg on side’ Prostaglandins appearance Surgery soon after birth to swap positionof arteries Tricuspidatresia Progressive cyanosis from birth Prostaglandins VSD murmur, may also be a PDA Balloon atrial septostomy murmur Surgery- Fontanprocedure, series of operations (lung bypass) ToF No cyanosisat birth. 5-6m old baby ‘Boot- shaped’ hearton CXR Prostaglandins presents withfailure to thrive & ECG- right ventricular hypertrophy Surgery at 9 months-widen RVOT & close PDA episodes of cyanosis Pulmonary stenosis murmur ACYANOTIC Name Whenandhow does itpresent? Key SBApoints Management Coarctationof Mild: Asymptomatic withradio- Associated withTurner’s syndrome & Prostaglandins aorta femoral delay & hypertension bicuspid aortic valve Surgery soon after birth- balloon angioplasty & Severe: Heart failure & shock Mid systolic murmur, maximal over the stent insertion develops hours- 24 hours after back Mild cases- regular echo birth. Absent femoral pulses. Isolated VSD Small- asymptomatic Harsh pansystolicmurmur at LLSE Small VSDs- no management Large- heart failure Associated withchromosomal disorders- Large VSDs- surgical closure at 3- 6 months If not picked up- may present with Down’s (t21), Edwards (t18), Pautau (t13) & Eisenmenger’s → only mx is heart- lung transplant Eisenmenger’s syndrome congenitalinfections PDA If picked up early- may be Continuous‘machinery’ murmur under Indomethacinor ibuprofen (inhibitsprostaglandins) asymptomatic, with left clavicle If not picked up- may present with Associated withprematurity & maternal Eisenmenger’s syndrome rubella infectionin first trimester RESP CONDITIONSSBA 1 A 5 month old baby boy is brought to your GP surgery by his mother. She is really concerned as for the last 2 days he had sniffles and a runny nose but thinks that he has got worse today. On examination, he is alert and is crying constantly. His resp rate is 50/min (25- 55). He has mild intercostal and subcostal recessions and some tracheal tugging. There are no added sounds to his breathing. Central capillary refill is <2s. He has moist mucous membranes and a normally palpable anterior fontanelle. His temperature is 37.8, pupils are equally reactive to light. His abdomen is soft and there are no rashes visible. Mum reports that he is breastfeeding, though feeds are taking longer than usual as he is more irritable. He has had five wet and one dirty nappy in the last 24 hours. How would you advise the baby’s mother? 1. Discharge home telling parents that this is a self- limiting illness and they have nothing to worry about 2. Discharge home with supportive care and clear safety- netting advice 3. Discharge home with antibiotics and clear safety netting advice 4. Tell parents to take child to A&E 5. Call an ambulance and send to A&E immediatelySBA 1 A 5 month old baby boy is brought to your GP surgery by his mother. She is really concerned as for the last 2 days he had sniffles and a runny nose but thinks that he has got worse today. On examination, he is alert and is crying constantly. His resp rate is 50/min (25- 55). He has mild intercostal and subcostal recessions and some tracheal tugging. There are no added sounds to his breathing. Central capillary refill is <2s. He has moist mucous membranes and a normally palpable anterior fontanelle. His temperature is 37.8, pupils are equally reactive to light. His abdomen is soft and there are no rashes visible. Mum reports that he is breastfeeding, though feeds are taking longer than usual as he is more irritable. He has had five wet and one dirty nappy in the last 24 hours. How would you advise the baby’s mother? 1. Discharge home telling parents that this is a self- limiting illness and they have nothing to worry about 2. Discharge home with supportive care and clear safety- netting advice 3. Discharge home with antibiotics and clear safety netting advice 4. Tell parents to take child to A&E 5. Call an ambulance and send to A&E immediatelyWhat is bronchiolitis? ■ Epidemiology: commonestin babies 1- 9 months(thoughnote canlast until up to 2 years in ex- prem babies) ■ Pathophysiology - Babies have tiny bronchioles to begin with. - Even a small amount of inflammationreduces the space for airflow significantly. - Flow rate ∝ radius which means a small change in radius greatly changes the flow rateSigns and symptoms - What happens if a child can’t get enough oxygen into their lungs? - Resp- signs of respiratory distress - Dehydration- struggling to breathe - Tachypnoea so can’t feed properly - Accessory muscle use - reduced oral intake - Intercostal recessions - sunken fontanelle - Subcostal recessions - dry mucous membrane - Tracheal tugging - increased skin turgor - Nasal flaring - prolonged cap refill - Pursed lip breathing - Grunting - Cyanosis - Abnormal airway noises - General- reducedenergy - Irritability → Lethargy → DrowsinessAssessing severity of bronchiolitis From NICE guidelinesfor bronchiolitis Immediately refer babies and children with Consider referring babies and children with bronchiolitis to bronchiolitis for emergency hospital care (usually by hospital if they have any of the following: 999 ambulance) if they have any of the following: ● apnoea (observed or reported) ● a respiratory rate of over 60 breaths/minute [2015] ● baby or child looks seriously unwell to a healthcare professional ● difficulty with breastfeeding or inadequate oral ● severe respiratory distress, for example fluid intake (50% to 75% of usual volume, taking account of risk factors [see recommendation grunting, marked chest recession, or a 1.3.3] and using clinical judgement) [2015] respiratory rate of over 70 ● clinical dehydration [2015] breaths/minute ● persistent oxygen saturation of less than 92%, ● central cyanosis. [2015] when breathing air. [2021] Going back to SBA 1, we can see that the child had noneof thesefeaturesWhat safety netting advice would you provide? Type in chat ■ This could be a good integratedOSCE station-resp exam on a doll/ bronchiolitishistorytaking+ parentalcounsellingSafety netting advice ■ how to recognise developing 'red flag' symptoms: – worsening work of breathing (for example grunting, nasal flaring, marked chest recession) – fluid intake is 50% to 75% of normal or no wet nappy for 12 hours – apnoea or cyanosis – exhaustion (for example, not responding normally to social cues, wakes only with prolonged stimulation). ■ that people should not smoke in the baby or child's home because it increases the risk of more severe symptoms in bronchiolitis ■ how to get immediate help from an appropriate professional if any red flag symptoms developSBA 2 What is bronchiolitiscaused by? 1. Parainfluenza virus 2. Respiratory syncytial virus 3. Parvovirus B19 4. Streptococcus pneumoniae 5. Haemophilus influenzaeSBA 2 What is bronchiolitiscaused by? 1. Parainfluenza virus 2. Respiratory syncytial virus 3. Parvovirus B19 4. Streptococcus pneumoniae 5. Haemophilus influenzaeCauses & treatment - Caused by RSV- in adults and older children this normallycauses a mild self- limiting illness, but in babies causes resp problems - No medications to directly treat it. - Management involves supporting babies with anything that is compromised (feeding, breathing) - Supplemental oxygen - Insertion of NG tube for feedingTrue or false? - All babies with bronchiolitisneed a capillary blood gas if they are requiring oxygen. -True or false? - All babies with bronchiolitisneed a capillary blood gas if they are requiring oxygen. - FALSE - We try to minimiseupsetting babies unnecessarily. - A blood gas will not give us any information that will change the management. - Assessing the severity of bronchiolitisand its resolution is done using clinical assessment mainly. - NB- NICE guidelines do state - Consider carrying out capillary blood gas testing in babies and children with severe worsening respiratory distress (when supplemental oxygen concentration is greater than 50%) or suspected impending respiratory failure (see recommendation 1.1.10). [2015]True or false? - There is a vaccine against bronchiolitis.True or false? - There is a vaccine against bronchiolitis. - False. There is a monoclonalantibody, Pavilizumab, that can be given as injections to babies with a high risk of developing bronchiolitis (e.g. Down’s syndrome, congenital heart defects). - This is not a vaccine as it does not stimulate the body to develop its own antibodies against RSVSBA 3 You are a FY2 doctorin paediatrics A&E. The next child is an 18 monthold boy presenting because his parents are concernedthat he has beenunwell for 3 days and it is getting worse. He is verydistressedand crying loudly and youcan see markedsubcostal and intercostal recessions in betweencries and he has a loud barking cough and stridorous breathing. What is the most likely diagnosis? 1. Epiglottitis 2. Croup 3. Bronchiolitis 4. Inhaledforeign body 5. Asthma exacerbationSBA 3 You are a FY2 doctorin paediatrics A&E. The next child is an 18 monthold boy presenting because his parents are concernedthat he has beenunwell for 3 days and it is getting worse. He is verydistressedand crying loudly and youcan see markedsubcostal and intercostal recessions in betweencries and he has a loud barking cough and stridorous breathing. What is the most likely diagnosis? 1. Epiglottitis 2. Croup 3. Bronchiolitis 4. Inhaledforeign body 5. Asthma exacerbationWhat is croup? - Pathophysiology: - Inflammatory response to a parainfluenza virus infection causes ‘laryngotracheobronchitis’. - Children have smaller airways than adults and a small amount of swelling leads to severe symptoms - Occurs in children mainly between 6 months- 2 yearsSigns & symptoms and severity classification - Westley croupMildssification- all things in Moderatee logical! Severe - Happy, content, playingchild → Distressed, lethargic, stridor at rest ● Occasional barking cough ● Frequent barking cough ● Frequent barking cough ● No audible stridor at rest ● Easily audible stridor at rest● Prominent inspiratory (and ● No or mild suprasternal ● Suprasternal and sternal occasionally, expiratory) stridor and/or intercostal wall retraction at rest at rest recession ● No or little distress or ● Marked sternal wall retractions ● The child is happy and is agitation ● Significant distress and prepared to eat, drink, and ● The child can be placated agitation, or lethargy or play and is interested in its restlessness (a sign of surroundings hypoxaemia) ● Tachycardia occurs with more severe obstructive symptoms and hypoxaemiaTrue or false? ■ True or false? Steroids are the mainstay of management in croup.True or false? ■ True or false? Steroids are the mainstay of management in croup. ■ TRUE ■ Normallygive dexamethasone orally to children with croup of any severity. ■ In more severe croup, nebulisedbudesonide is used if children cannot swallow easily ■ Know how to prescribe this as a stat dose- could get an A- E station croup with dexamethasone prescribing.Prescribing case Jimmyis a 2 year old boy presenting to paediatric A&E with mild croup. Obs are as follows- temp 38, sats- 97% RA, RR- 35, HR- 130, BP- not measured. He has no known drug allergies. Weight: 12kg Please prescribe him any appropriate medications on the Good Hospital drug chart. (2 mins)Prescribing case - answers We give 150 micrograms/kg of dexamethasone Dose = 150 x child’s weight in kg. Dose = 150 x 12 = 1800 micrograms = Scroll to the ‘medicinal forms and pricing’ section → make sure you give this as an oral solution 1800/ 400 = 4.5mlSBA 4 You are a paeds FY2. A 2 year old presents with stridor, severe respiratory distress and drooling, onset over 5 hours. What is the most likely diagnosis & what do you do? 1. Croup → give oral dex 2. Anaphylaxis → give IM adrenaline 3. Epiglottitis → call for urgent anaesthetics help 4. Quinsy→ call for urgent ENT help 5. Asthma → give nebulised salbutamolSBA 4 A 2 year old presents with stridor, severe respiratory distress and drooling,onset over 5 hours. What is the most likely diagnosis & what do you do? 1. Croup → give oral dex (croup would have stridor, and a barking cough, but not drooling- this indicates severe upper airway obstruction) 2. Anaphylaxis → IM adrenaline (comes on more rapidly, over minutes) 3. Epiglottitis→ call for urgentanaestheticshelp 4. Quinsy→ call for urgent ENT help (would present with droolingbut not stridor. May also have trismus & difficulty opening mouth.) 5. Asthma → give nebulisedsalbutamol (would have wheeze, not stridor)What is epiglottitis? - Inflammation of the epiglottis causing marked obstruction of the airway: - Causes: - Due to H. influenzae type b (Hib) infection- question stems may mention that the child is unvaccinated - Epidemiology - Can affect children of any age - It’s actually more common in adults than children now due to the introduction of a vaccine against H. influenzae type b in the 1990s in the UKSigns & Symptoms and management Presents with: Investigations - Tripoding(why?) - If high degree of suspicion, no Ix needed - Drooling - If ?foreign body in larynx, - Stridor may do cervical XR → thumb - Sore throat - High fever sign (v v swollen epiglottis) Management - NEVER examine the airway or move the child about as this could distress the child and cause a full obstruction. - Since all the obstruction is behind the tonsils, the mouth may look normal and be falsely reassuring - Quinsyalso presents with very similar symptoms (drooling,high fever, sore throat), but quinsy less typically has resp distress and o/e of the mouth there will be uvula deviation - Call for anaesthetic support immediatelyas the child may need to be intubated.Bonus point When is the Haemophilus influenzae b (Hib) vaccine given? Type in chatBonus point When is the Haemophilus influenzae type b (Hib) vaccine given? 2, 3, and 4 months as part of 6 in 1, and then at 12- 13 months as part of Hib/ MenC combinedvaccineTrue or false? Milly, a 3 year old girl, is brought to the GP as her mum is concerned about her child’s breathing. In the last 6 months, Millyhas had 4x 5 day episodes of wheezing which is worse in the early morning and night, difficulty in breathing, a runny nose, reduced appetite and low- grade fever. Mum says Millystarted nursery 6 months ago. True or false: the most likely diagnosis is asthmaTrue or false? FALSE Episodes are accompanied by signs of viral illness- viral induced wheeze. This is much more common in young children <=5 years than asthma. Some children with recurrent VIW episodes may go on to develop asthma. VIW is managed in a similar way to acute asthmaSBA 5 What is the first line diagnostic test/ method for diagnosingasthma in children aged 5- 16? 1. Clinicaldiagnosis from symptom history 2. 2 week peak flow diary showing diurnal variation 3. Spirometry with bronchodilatorreversibility 4. FeNO measurementSBA 5 What is the first line diagnostic test/ method for diagnosingasthma in children aged 5- 16? 1. Clinicaldiagnosis from symptom history (this is for children under 5. In general, though, asthma diagnosis is not made in children this young) 2. 2 week peak flow diary showing diurnal variation (this would be helpful but is not diagnostic) 3. Spirometrywith bronchodilatorreversibility(thisis the first- line approach) 4. FeNO measurement (this is done if the spirometry is normal or does not display bronchodilatorreversibility)Asthma in children ■ Generally diagnosis/ management follows similarprinciples to those in adults ■ Diagnosis in children: ■ Spirometry with bronchodilatorreversibility- measurement of lung function before and after giving inhaled salbutamol. FEV1 shouldimprove by at least 12% ■ FeNO testing. Should be >= 35ppb of NOSBA James is an 8 year old boy brought into A&E with breathing difficulties. He was playing football at school whenhe started struggling to breathe and wheezing.On examination,he is alert, but struggles to completesentencesin onebreath.There is widespreadwheeze on auscultation of his chest and use of accessory neck muscles & intercostal recessions.He appears well- perfusedwith no cyanosis. HR 140, RR 45, BP 110/70, Temp37.1, O2 sats 96% (on 15L O2 via NRB mask) What is the next best step in management? 1. Administer10 puffs of salbutamol via an inhaler + spacer (100 microgram/ puff) 2. Administera single dose of 5mg nebulisedsalbutamol over5 mins 3. Administer30mg of nebulisedsalbutamol over2 hours, reassessing the patient at 20 min intervals 4. Administerdoses of 5mg nebulisedsalbutamol at 20 min intervals for 2 hours, re- assessing the patient after each dose 5. Administer24mg oral prednisoloneSBA James is an 8 year old boy brought into A&E with breathing difficulties. He was playing football at school whenhe started struggling to breathe and wheezing.On examination,he is alert, but struggles to completesentencesin onebreath.There is widespreadwheeze on auscultation of his chest and use of accessory neck muscles & intercostal recessions.He appears well- perfusedwith no cyanosis. HR 140, RR 45, BP 110/70, Temp37.1, O2 sats 96% (on 15L O2 via NRB mask) What is the next best step in management? 1. Administer10 puffs of salbutamol via an inhaler + spacer (100 microgram/ puff) 2. Administera single dose of 5mg nebulisedsalbutamol over5 mins 3. Administer30mg of nebulisedsalbutamol over2 hours, reassessing the patient at 20 min intervals 4. Administer doses of 5mg nebulised salbutamol at 20min intervals for 2 hours,re- assessingthe patient after each dose 5. Administer24mg oral prednisoloneAsthma: assessment of severity Similar systemas to adults,but some key differences: Moderate attack Severe attack Life-threatening attack SpO2 > 92% SpO2 < 92% (unlike in adults, SpO2 < 92% SpO2 < 92% PEF > 50% best or may be consistent with a 'severe' attack in PEF < 33% best or predicted children) predicted No clinical features PEF 33-50% best or predicted Silent chest of Can't complete sentences in one breath or Poor respiratory severe asthma too breathless to talk or feed effort Heart rate > 125/min Altered Respiratory rate > 30/min consciousness Use of accessory neck muscles Cyanosis PEFR assessmentfor over5s only, or for children who are able to take a peak flow reading What is the severity of James’ asthma attack in the last question? Management of asthma attacks ‘Burst therapy’: short bursts of salbutamol and ipratropium every 20 min I have not includedsalbutamol & ipratropium doses as they vary slightly by age: always check doses per age and/ or weight in the BNF for children! Learn this well, comesup frequently as a prescribing station in OSCEs MILD MODERATE SEVERE Refer toPICU straight away Oxygen Start with 15L via NRB, then Start with 15L via NRB, then Start with 15L via NRB, then step down if able, titrate to step down if able, titrate to step down if able, titrate to target sats 94- 98% target sats 94- 98% target sats 94- 98% Salbutamol Inhaled, 2- 10 puffs every 20-Nebulisedin O2every 20- 30 Nebulisedin O2,every 20- 30 30 mins mins mins Ipratropium bromide Inhaled, every 20- 30 mins Nebulisedin O2,every 20- 30 Nebulisedin O2,every 20- 30 for up to 2h only mins for up to 2h only mins for up to 2h only Prednisolone (note this is 1-2mg/kg od, max 40mg 1-2mg/kg od, max 40mg 1-2mg/kg od, max 40mg the BNF dose, I would stick with this for exams) Other Consider IV magnesium and IV magnesium IV aminophylline Consider IV aminophylline and IV salbutamolResus council guidelines for acute asthmaBack to the SBA What is the next best step in management? 1. Administer10 puffs of salbutamol via an inhaler + spacer (100 microgram/ puff)- would only do this for a moderate exacerbation 2. Administera single dose of 5mg nebulisedsalbutamol over5 mins- not enough 3. Administer30mg of nebulisedsalbutamol over2 hours, reassessing the patient at 20 min intervals- according to BTS guidelines, in children, continuous nebulisedβ2 agonists are of no greater benefit than the use of frequent intermittentdosesin the same total hourly dosage 4. Administer doses of 5mg nebulised salbutamol at 20min intervals for 2 hours,re- assessingthe patient after each dose- Describes burst therapy 5. Administer24mg oral prednisolone-this is needed,but is not the next best stepOther paeds resp & cardio things to know (not covered today) ■ Anaphylaxis! ■ Managementof stable asthma ■ Cystic fibrosis ■ Supraventriculartachycardias ■ Paediatriccardiac arrest THANKS FOR WATCHIN G! PMedall and see you next week!orm on Name for feedback form: Malvi Shah