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Nephrology Chapter 5: Paediatrics 147
https://t.me/med1917
Acute kidney injury (AKI)
→ sudden, potentially reversible drop in renal function = oliguria <0.5ml/kg/h
Pre-renal Renal Post-renal
Causes Hypovolaemia
• Gastroenteritis
• Sepsis
• Burns
• Haemorrhage
• Nephrotic syndrome
Circulatory failure
Symptoms Shock:
• Pallor
• Cool peripheries
• HR, RR
Management
31
Urgent
• IV fluids
• Circulatory support
Vascular
• HUS
• Vasculitis
• Embolus
• Renal vein thrombosis
Tubular
• Acute tubular necrosis (ATN)
• Ischaemic
• Toxic
• Obstructive
renal causes
= most common
Glomerular: glomerulonephritis
Interstitial
• Interstitial nephritis
• Pyelonephritis
• Haematuria
• Oedema
• Metabolic acidosis ( HR, RR, confusion)
• Hyperkalaemia (palpitations, weakness)
• Hypocalcaemia (cramps, tingling, numb)
• Hyperphosphataemia
Correct fluid and electrolyte balance / metabolic acidosis
Monitor weight + U&Es, record fluid input & output
Fluid balance:
• Fluid restriction & diuretics
Prevent catabolism:
• High calorie, normal protein diet
→ Immunosuppression if rapidly progressive
glomerulonephritis
Obstruction
• Congenital
e.g. posterior urethral valves
• Acquired
e.g. blocked catheter
• Bladder fullness & pain
• Urinary dribbling
Urine drainage:
• Nephrostomy
• Bladder catheterisation
Urology referral
Haemolytic uraemic syndrome (HUS)
Triad of:
1. Renal failure
2. Thrombocytopenia → may have purpura/bruising
3. Microangiopathic haemolytic anaemia (damaged RBCs due to small vessel
occlusion)
CAUSE
↱ Diarrhoeal prodrome
→ 2° to gastroenteric infection with verocytotoxin-producing E. coli 0157:H7
(from farm animals / uncooked beef)
→ toxin causes intravascular thrombogenesis in renal endothelial cells →
clotting cascade activated
→ platelets are consumed & haemolytic anaemia occurs
INVESTIGATIONS
• FBC – Hb, plts, fragmented blood
film
• U&Es
• Stool culture
31
Cho MH (2020) Pediatric acute kidney injury: focusing on diagnosis and management.
Child Kidney Dis 24:19–26
(95%) typical (diarrhoeal): good prognosis
↳
(5%) atypical (non-diarrhoeal): poor prognosis
MANAGEMENT: supportive →
manage fluid balance
• Dialysis & plasma exchange
• Follow up: for persistent proteinuria,
HTN, progressive CKD
Indications for dialysis
→ Failed conservative Mx
→ Hyperkalaemia or hypo-/hypernatraemia
→ Severe acidosis
→ Pulmonary HTN or oedema
→ Multisystem failure
148 Chapter 5: Paediatrics Nephrology
https://t.me/med1917
Chronic kidney disease (CKD)
→ progressive loss of renal function → rare in kids (10 in 1 million)
renal osteodystrophy = poor mineralisation
due to renal failure → like rickets
Dialysis & transplantation
• For end-stage CKD
• Ideally child gets transplant before dialysis
is needed
• Needs immunosuppression with transplant
CLINICAL FEATURES
• Anorexia & lethargy
• Polydipsia & polyuria
• Hypertension
• Bone deformities →
renal osteodystrophy
• FTT / poor or delayed growth
(despite high GH levels)
• Anaemia (unexplained normochromic, normocytic) – due to EPO
MANAGEMENT
→ By specialist paediatric nephrologist & MDT
→ AIM: prevent metabolic complications & allow normal growth &
development
1. Diet – combat losses from
anorexia and vomiting
• Calorie supplements
• NG tube / gastrostomy
2. Prevent renal osteodystrophy
• Calcium & phosphate restriction
– e.g. dairy
• Vit D supplements if deficiency
3. Salt & water balance
• Salt supplements
32
CAUSES: most = familial/
congenital
• Structural malformation (40%)
• Glomerulonephritis (25%)
• Hereditary nephropathies (20%)
• Systemic diseases (10%)
• Unknown (5%)
• Bicarbonate supplements
if metabolic acidosis
4. Anaemia
• Recombinant
EPO / erythropoietic stimulating
agent
• Iron replacement
5. Hormone abnormalities
• Recombinant human growth
hormone
All children with a renal abnormality
should have annual BP checks throughout their life
Further Ix to consider
ECHO, ECG, CXR, renal USS, renal artery
Doppler
Hypertension
→ BP >95th percentile for age, height & sex
CAUSES: usually secondary in children
1. Renal
• Renal parenchymal disease
• Renal artery stenosis
• PKD
• Renal tumours
2. Endocrine
• Congenital adrenal hyperplasia
• Cushing’s / steroid therapy
• Hyperthyroidism
CLINICAL PRESENTATION
→ Failure to thrive
→ Vomiting
→ Headaches
→ Cardiac failure
INVESTIGATIONS: for 2° cause
• 24h BP monitoring
• FBC, U&Es, renal function
• Blood glucose & fasting lipids
• TFTs
• Plasma renin & aldosterone
• Urinalysis
• Urine catecholamines
32
NICE (2021) Chronic kidney disease [NG203]
3. Catecholamine excess
• Phaeochromocytoma
• Neuroblastoma
4. Coarctation of the aorta
5. Essential HTN (diagnosis
of exclusion)
6. Obesity
→ Retinopathy
→ Facial palsy
→ Convulsions
→ Proteinuria
MANAGEMENT
• Tx underlying cause if possible
• Antihypertensives
• Regular BP monitoring
• Lifestyle advice if essential HTN
Cardiovascular
https://t.me/med1917
Antenatal circulation
• LA pressure low as little return from lungs
• RA pressure high as receives all
systemic blood (including from placenta)
• Keeps foramen ovale open & blood
flows from RA → LA
• Blood also bypasses lungs by flowing
through ductus arteriosus
CHANGES AT BIRTH
• pulmonary resistance means more
blood into LA so LA pressure
• Loss of placental circulation causes
RA pressure
• Foramen ovale closes
• Ductus arteriosus closes within first
few hours/days
Foramen ovale
(open)
Fig. 5.31
Fetal heart
RA
Ductus arteriosus
(open)
Foramen ovale
(closed)
Chapter 5: Paediatrics 149
= left atrium
= right atrium
Newborn heart
Ductus arteriosus
(closed)
Congenital heart disease
→ 1% of live births
PRESENTATION
1. Antenatal cardiac USS diagnosis (at 20w)
2. Detection of a heart murmur (most common presentation)
→ BUT 30% of children have an innocent murmur at some point, often during
febrile illness/anaemia
3. Heart failure
Symptoms: SOB, sweating, poor feeding, FTT, recurrent chest infections
Signs: RR, HR, murmur, crackles, enlarged heart, hepatomegaly, cool peripheries
Causes
Tx: diuretics, inotropes, treat cause
Neonates: duct-dependent
(obstructed LHS)
• Hypoplastic left heart
syndrome
• Critical aortic valve stenosis
• Severe coarctation of the aorta
• Interrupted aortic arch
4. Cyanosis
Peripheral (hands & feet): if cold, unwell from any cause or polycythaemia
Central (tongue): if arterial O2 tension drops
5. Shock & collapse
Symptoms: pallor, impalpable pulses, metabolic acidosis
DDx: congenital heart disease, infection, inherited metabolic disorder
Ix: Blood tests, blood & urine cultures, ECHO
Infants: high pulmonary flow
(causing left → right shunt)
• VSD
• AVSD
• Persistent ductus arteriosus
↱
DDx = sepsis
Children/adolescents:
RHS or LHS heart failure
• Eisenmenger syndrome
(RHS heart failure)
• Rheumatic heart disease
• Cardiomyopathy
Duct-dependent lesions: in severe left-sided
obstructive lesions, blood flow through duct =
critical for survival → dramatic deterioration in
condition when duct closes
e.g. TOF, TGA, HLHS, aortic stenosis/
coarctation
Mx: prostaglandin to maintain duct
patency
Features of innocent murmurs
• aSymptomatic patient
• Soft blowing murmur
• Systolic murmur only
• left Sternal edge
No parasternal thrill/radiation
May vary with posture
DDx of cyanosis in newborn PLUS
respiratory distress (RR >60bpm)
• Cyanotic congenital heart disease
• Infection, e.g. GBS, septicaemia
• Respiratory disorder, e.g. RDS, meconium
• Persistent pulmonary HTN of newborn
• Inborn metabolic error = acidosis & shock
SUMMARY OF CONGENITAL HEART DISEASE PRESENTATIONS
Symptoms Type of lesion
Breathless (acyanotic)
Blue (cyanotic)
Collapse & shock Obstruction: Coarctation, HLHS
Asymptomatic Obstruction: Aortic/pulm. stenosis
L→R shunts: VSD, ASD, PDA
R→L shunts: TOF, TGA
May be mixed Sx in AVSD, complex
congenital heart disease
Blue = cyanotic conditions
Persistent cyanosis in otherwise well infant =
nearly always structural heart disease
PDA: Patent ductus arteriosus
TGA: Transposition of great arteries
HLHS: Hypoplastic left heart syndrome
TOF: Tetralogy of Fallot
150 Chapter 5: Paediatrics Cardiovascular
https://t.me/med1917
↱
Left → right shunts
→ acyanotic
Atrial septal defect
(ASD)
Fig. 5.32
ECG findings in ASD
• Secundum ASD: partial RBBB (RSR pattern)
& right axis deviation (due to RV hypertrophy)
• Partial AVSD: superior QRS axis (= –ve AVF
deflection due to displaced sinoatrial node)
ATRIAL SEPTAL DEFECT (ASD)
Types
• Secundum ASD (80%) – defect in centre of atrial septum, involving foramen
ovale
• Primum ASD/partial AVSD (20%) – defect of AV septum, allowing
communication between the atria & AV valves
Symptoms
• Normally asymptomatic
• Recurrent chest infections, wheeze, SOB
• Arrhythmias (from 40y onwards)
Signs
• Ejection systolic murmur – at ULSE (blood through pulmonary valve)
• Fixed, widely split 2nd heart sound
• Pansystolic murmur – at apex (in AVSD due to AV valve regurgitation)
Investigations
• CXR – cardiomegaly, enlarged pulmonary arteries, pulmonary vascular
markings
• ECHO – visualise abnormal anatomy
• ECG
Management
Small defects: monitor – often close spontaneously
Secundum ASD: cardiac catheterisation to insert occlusion device
Partial AVSD: surgical correction at 3–5y
Ventricular septal defect
(VSD)
Fig. 5.33
VENTRICULAR SEPTAL DEFECT VSD = defect anywhere in ventricular
septum (30% cases of congenital heart disease)
Small (<3mm) Large (>3mm)
Symptoms Asymptomatic
Signs
• Loud pansystolic murmur
• At LLSE
• Quiet 2nd pulmonary sound
Ix • CXR = normal
• ECG = normal
• ECHO = visualise defect
Mx Often close spontaneously but may
persist to adulthood
(if asymptomatic, no Tx needed)
• Heart failure: HR, RR (SOB & active
precordium), hepatomegaly
• Failure to thrive
• Recurrent chest infections
• Soft pansystolic / no murmur
• Mid-diastolic murmur – at apex
• Loud 2nd pulmonary sound (due to
pulm. aorta pressure)
• CXR = cardiomegaly, pulm. artery/
markings, pulm. oedema
• ECG = biventricular hypertrophy
(T upright in V1, inverted in V6)
• ECHO = visualise defect
Heart failure: diuretics + ACEi
Failure to thrive: additional calorie intake
Surgery before 1y
Cardiovascular Chapter 5: Paediatrics 151
https://t.me/med1917
PERSISTENT DUCTUS ARTERIOSUS → failure of duct closure by 1m after
EDD (not pathological if preterm)
Symptoms
• Normally asymptomatic
• Heart failure & pulmonary HTN (if duct is large)
Signs
• Continuous murmur – below left clavicle/ULSE
• Collapsing/bounding pulse
• Swinging O2 saturations
Investigations
• ECHO – readily shows patent duct
• CXR & ECG = usually normal
Management
• Ibuprofen / surgical tying
• Closure with coil or occlusion device (via catheter at 1y)
So blood still able to
↳
flow from aorta →
pulmonary artery
RF = preterm
Right → left shunts
→ CYANOSIS in 1stweek of life
TETRALOGY OF FALLOT (TOF)
Four cardinal features
1. Large VSD
2. Aorta overriding the ventricular septum (receives blood from both ventricles)
3. Subpulmonary stenosis = RV outflow obstruction
4. RV hypertrophy as a result of RV outflow obstruction
Signs
• Cyanosis in 1st week – usually diagnosed before cyanosis is obvious
• Loud, harsh ejection systolic murmur – at LLSE
Investigations
1. ECHO: shows cardinal features
2. CXR:
• Small ‘boot-shaped’ heart
• Pulmonary artery ‘bay’
• pulmonary markings
3. ECG: RV hypertrophy (upright T in V1 & no S)
Management
• Maintain duct patency: prostaglandin infusion
• Surgery at 6m: close VSD & relieve RV outflow obstruction
• Blalock–Taussig shunt: between subclavian artery & pulmonary artery to
pulmonary flow (if very cyanosed)
• Tx hypercyanotic spells >15min ‘TET SPELLS’
▶ Knees to chest + sedation & pain relief (morphine)
▶ O2 ± ventilation
▶ IV propranolol (relaxes right ventricle)
▶ IV fluids (+ HCO
–
for acidosis)
3
(antenatally or due
↳
to early murmur)
Fig. 5.34 Persistent ductus arteriosus.
blue, O2 <94%, collapse
TOF = most common cyanotic congenital heart
disease (10%)
Tetralogy of Fallot
(TOF)
Fig. 5.35
‘TET SPELLS’ = worsening of right to left
shunt during exertion/crying/agitation causing
increased pulmonary resistance = cyanotic
episodes
If severe = drowsy, seizures, death
152 Chapter 5: Paediatrics Cardiovascular
https://t.me/med1917
TRANSPOSITION OF THE GREAT ARTERIES TGA = 5% of congenital
heart disease
Aetiology
• Aorta connected to RV & pulmonary artery connected to LV
• Incompatible with life unless blood can mix (e.g. via VSD/ASD)
Transposition of the great
vessels (TGV)
Fig. 5.36
Signs
• CYANOSIS – on day 2 when ductus arteriosus closes
• Loud, single 2nd heart sound
• May be murmur if another abnormality present
Investigations
• ECHO – visualise abnormalities
• ECG = usually normal
• CXR: ‘egg-on-a-side’ heart outline, pulmonary markings
Management
• Maintain duct patency – prostaglandin analogue
• Balloon atrial septostomy (needed in 20% as emergency procedure)
▶ catheter with balloon passed through umbilical/femoral vein → RA →
foramen ovale → LA
▶ balloon inflated & pulled back to tear hole in atrial septum & allow blood
mixing
• Arterial switch procedure – pulmonary artery & aorta transected above
valves & switched over (must be <4w)
Hypercapnia (resulting from cyanosis)
Signs: persistent crying, irritable, SOB,
pallor
Complications: MI, CVA, death
EISENMENGER SYNDROME
Aetiology
• High pulmonary blood flow due to L→R shunt causes thickening of
pulmonary artery walls = resistance
• L→R flow will gradually decrease due to the resistance until eventually
theshunt reverses
Symptoms
10–15y: become blue as shunt reverses (progressive if untreated)
40–50y: heart failure & death
Management
Prevent condition: early intervention for conditions with pulmonary flow
SUMMARY OF CYANOTIC CONGENITAL HEART DISEASE
Signs/symptoms Management
Tetralogy of Fallot
Transposition of
great arteries
Eisenmenger
syndrome
• Loud murmur ULSE
• Hypercyanotic spells
• Clubbing of fingers/toes
• No murmur
• Severe cyanosis early on
• No murmur
• Right heart failure (later)
• Surgery 6–9m
• Prostaglandin infusion
• Balloon atrial septostomy
• Arterial switch
• Manage causes early
Cardiovascular Chapter 5: Paediatrics 153
https://t.me/med1917
Outflow obstruction in the sick child (shock/collapse)
COARCTATION OF THE AORTA
Aetiology
• Arterial duct tissue surrounds aorta at point of duct insertion
• Duct closure causes constriction of aorta = LV outflow obstruction
Signs/symptoms: present at day 2 when duct closes
• Sick with severe heart failure / renal failure
• Absent femoral pulses
• Severe metabolic acidosis
• Ejection systolic murmur between shoulder blades
Investigations
• ECG – normal unless older (LV hypertrophy)
• CXR – cardiomegaly
HYPOPLASTIC LEFT HEART SYNDROME (HLHS)
Aetiology: underdeveloped left side of the heart (including aorta)
Signs/symptoms: often detected antenatally so Sx prevented
• Profound acidosis & cardiovascular collapse
• Weakness of ALL peripheral pulses
Management: Norwood procedure (3-stage surgery)
Management:
1. Resuscitation
2. Prostaglandin infusion
Outflow obstruction in the well child (asymptomatic)
AORTIC STENOSIS
Aetiology: partial fusion of aortic valve leaflets
Signs
• Ejection systolic murmur at URSE → radiates to neck
• Carotid thrill
• Apical ejection click
• Small volume, slow rising pulses (globally poor perfusion)
Investigations
• ECG – LV hypertrophy (inverted T wave V6)
• CXR – prominent LV & post-stenotic dilation of aorta
PULMONARY STENOSIS
Aetiology: partial fusion of pulmonary valve leaflets
Signs
• Ejection systolic murmur at ULSE
• ± Carotid thrill
• Ejection click at ULSE
• RV heave
Investigations
• ECG – RV hypertrophy (upright T wave V1)
• CXR – post-stenotic dilation of pulm. artery
Management:
Only if symptoms on exercise or resting
high pressure gradient
• Balloon valvotomy (valve dilation)
• Later may need valve replacement
Syndromes associated with congenital
heart defects
Down syndrome – ASDs/AVSDs
Noonan syndrome – pulmonary stenosis,
ASDs, hypertrophic cardiomyopathy
Marfan syndrome – mitral valve prolapse,
aortic aneurysm
Turner syndrome – aortic stenosis,
coarctation of the aorta
DiGeorge syndrome – TOF
Williams syndrome – pulmonary stenosis,
aortic stenosis
Bold = key associations to remember for exams
154 Chapter 5: Paediatrics Cardiovascular
https://t.me/med1917
Other important paediatric cardiac conditions
SUPRAVENTRICULAR TACHYCARDIA SVT = HR 250–300bpm
DDx = SEPSIS
Fig. 5.37 SVT.
Signs/symptoms
• Dizziness, palpitations, chest pains,
SOB → collapse
• Tachyarrhythmia (abnormal, fast HR)
• Heart failure (pulm. oedema, SOB, RR)
• Hydrops fetalis (abnormal fluid accumulation) → intrauterine death
Investigations
• ECG: 250–300bpm & narrow QRS (P waves often hidden)
• ECHO: to r/o structural problem
Management
33
Acute
• Circulatory & respiratory support
– ventilation, correct acidosis
• DIVING REFLEX – dunking infant
in water causes reflexive apnoea &
bradycardia
• Vagal manoeuvres – carotid sinus
massage / ice pack on face / blow into
syringe
NB Sinus arrhythmia = normal in children
• acceleration in inspiration
• slowing on expiration
• IV adenosine – induces AV block
• Electrical cardioversion with
synchronised defib shock – if
adenosine fails
Maintenance
• Flecainide or sotalol
• Radiofrequency
ablation / cryoablation
Common viral causes: parvovirus, influenza,
adenovirus, rubella, HIV
SUSPECT SBE in anyone with: sustained
fever, malaise, ESR, unexplained anaemia or
haematuria
α-haemolytic strep (
common cause of SBE
Strep. viridans
) = most
MYOCARDITIS = inflammation of myocardium (usually due to infection, but
also drug reaction/chemicals/radiation)
Signs/symptoms
• Fever, malaise
• Non-specific Sx of heart failure: SOB, cough, chest pain, oedema, pallor
Management: usually resolves
spontaneously
1. Diuretics
Investigations
• ECHO
• CXR – enlarged heart borders
2. ACEis
3. Beta-blocker – carvedilol
→ Severe cases may need heart transplant
SUBACUTE BACTERIAL ENDOCARDITIS SBE = slowly developing
infection of endocardium
↳ Congenital heart defects =
Symptoms
• Fever, malaise
• New murmur
• Anaemia/pallor
• Arthritis/arthralgia
Investigations
• BLOOD CULTURES – before starting
ABX
• ECHO – visualise vegetations
• Bloods – anaemia, ESR/CRP
• Urine dip – microscopic haematuria
(esp. VSD, PDA, coarctation)
Signs
• Microscopic haematuria
• ± splinter haemorrhages
• ± Osler nodes, Janeway lesions, Roth
spots
Management
• ABX – high dose IV penicillin +
gentamicin for 6w
• May need to remove prosthetic
material
33
Resuscitation Council UK (2021) Paediatric cardiac arrhythmias algorithm
Respiratory
https://t.me/med1917
Respiratory changes at birth
FETAL RESPIRATION
• Fetal lungs are filled with fluid & pulmonary vessels are constricted
• Blood is oxygenated via gas exchange at the placenta
• Most blood bypasses lungs via ductus arteriosus & flows straight into aorta
NB Fetal Hb has higher O2 affinity & better O2 dissociation
NEONATAL RESPIRATION
• During birth, fetal chest is squeezed → some lung fluid drains
• temperature, catecholamines & tactile stimuli initiate breathing*
• Most of remaining fluid is absorbed into lymphatic & pulmonary circulation
• Pulm. resistance falls → LA filling & LA pressure → foramen ovale closes
Respiratory infections
→ Pre-school kids have 6–8 per year
→ 80–90% are viral: rhinovirus, parainfluenza, RSV, adenovirus
→ Bacterial: Strep. pneumoniae, H. influenzae, M. catarrhalis, pertussis,
mycoplasma
Upper respiratory tract infections
Common symptoms: nasal blockage & discharge, fever, sore throat, earache
CORYZA COMMON COLD → most common childhood infection
Cause: rhinovirus, coronavirus, RSV
Symptoms: nasal blockage & discharge (clear or mucopurulent) ± fever, cough
Management: paracetamol/ibuprofen for symptom control → reassure parents it
is self-limiting / ABX of no benefit
PHARYNGITIS (SORE THROAT)
Cause: rhinovirus, adenovirus, enterovirus, group A β-haemolytic strep.
Symptoms: sore throat + cervical lymphadenopathy
TONSILLITIS (FORM OF PHARYNGITIS)
Cause: EBV, group A β-haemolytic strep.
Symptoms
• Very sore throat & difficulty swallowing
• Enlarged tonsils + white exudate
• Cervical lymphadenopathy
• Headache, fever, malaise, apathy
• Abdominal pain
Management
• Analgesia & fluids
• 5 days ABX only if bacterial*
• Tonsillectomy if indicated
Return to school 24h after start ABX
34
: admit if severe dysphagia/dehydration
*CENTOR/ FeverPAIN score to assess likelihood
35
of group A strep
Chapter 5: Paediatrics 155
*6s after birth
RFs for respiratory infections
• Parental smoking
• Poor nutrition
• Overcrowded/damp living
• Chronic lung disease
• Immunodeficiency
• Male
• Premature
• Syndromes
CENTOR score: 1 point each
C: absence of Cough
E: tonsillar Exudates
N: tender cervical Nodes
T: >38°C Temperature
/: no ABX
²/: throat culture/ delayed script
4: ABX (penicillin or erythromycin)
FeverPAIN score: 1 point each
Fever
Pus on tonsils
Attends within 3d
Inflammation of tonsils = severe
No cough
Indications for tonsillectomy
34
NICE (2018) Sore throat (acute) [NG84]
35
ENT UK (2020) Commissioning Guide – Tonsillectomy
• Recurrent tonsillitis
▶ 7× in 1y
▶ 5× in each of 2y
▶ 3× in each of 3y
• Peritonsillar abscess
• Obstructive sleep apnoea
156 Chapter 5: Paediatrics Respiratory
https://t.me/med1917
ACUTE OTITIS MEDIA AOM → most commonly at 6–12m
In any child with fever, must examine tympanic
membranes
Start ABX immediately if: bilateral <2y or
systemically unwell, suspected complication
Cause: RSV, rhinovirus, pneumococcus, H. influenzae, M. catarrhalis
Symptoms: inflammation of middle ear
• Fever & malaise
• Ear pain (tugging at ear)
Complications
• mastoiditis
• meningitis
• Bulging red tympanic membrane & absent
light reflection
Management
36
• Analgesia – regular paracetamol/ibuprofen for pain
• Delayed use of ABX (amoxicillin) → give prescription to start if no improvement
in 2–3d or Sx rapidly worsen
OTITIS MEDIA WITH EFFUSION OME = ‘GLUE EAR’ → most commonly
at 2–7y
Cause: middle ear infection, enlarged adenoids, nasal abnormalities
Complications of OME
• Delay in speech development
• Difficulties at school
Indications for adenoidectomy
• Recurrent OME
• OSA
Symptoms: fluid collection in middle ear without signs of inflammation
• No pain/fever
• Middle ear fluid & dull, retracted TM
• Conductive hearing loss (20–30db)
▶ type B tympanogram (flat line)
▶ air conduction on PTA (if >4y)
Management
37
: 50% resolve spontaneously
If no improvement in 3m / complications: grommets or hearing aids ±
adenoidectomy if indicated
Mx of upper airway obstruction:
contact anaesthetist
• DO NOT EXAMINE THROAT → KEEP CHILD
CALM
• Monitor for hypoxia/deterioration – O2 sat.
• Dexamethasone/prednisolone
• Nebulised adrenaline – if severe
• Urgent tracheal intubation – if respiratory
failure
Laryngeal & tracheal infections
→ mucosal inflammation & swelling can cause life-threatening obstruction
SYMPTOMS
• Stridor (rasping inspiration)
• Hoarseness
• Barking cough
• Variable SOB
If severe: RR & HR, cyanosis, drowsiness
Classifying severity of stridor
Mild: only when active/upset, normal RR, minimal WOB
Moderate: some stridor at rest, RR, WOB
Severe: biphasic stridor at rest, or RR, & HR, WOB, hypoxaemia
DDx upper airway obstruction / stridor
Acute infection
• Croup (very common)
• Epiglottitis
• Bacterial tracheitis
Mechanical obstruction
• Anaphylaxis
• Smoke inhalation
• Inhaled foreign body
Congenital
• Laryngomalacia (floppy
larynx)
• Laryngeal polyps
(congenital HPV)
• Acquired subglottic stenosis
36
NICE (2018, updated 2022) Otitis media (acute) [NG91]
37
NICE (2008) Otitis media with eusion in under 12s [CG60]
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