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Belle: Phase 3a > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

When can jaundice in a neonate be aetiologically normal

A

After 24 hours

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2
Q

How does rhesus haemolytic disease occur

A

Mum = rhesus negative
Baby = rhesus positive

Sensitising event eg trauma/abruption (baby’s blood exposed to mothers)
Mother develops antibodies against the baby’s blood = haemolytic anaemia
Unconjugated bilirubin is produced

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3
Q

How is rhesus haemolytic disease prevented

A

With anti-D immunoglobulin:
At 28 weeks
After sensitising events
One dose after birth if the mother is known to be rhesus negative

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4
Q

When does ABO incompatibility occur

A

Mother = type O = can develop anti-B or anti-A antibodies
Baby = type A or B

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5
Q

How is ABO incompatibility diagnosed

A

Coomb’s test

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6
Q

Which infections are included in TORCH

A

Toxoplasmosis
Other (syphilis, parvovirus, varicella zoster)
Rubella
CMV
Herpes; Hepatitis

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7
Q

Genetics of G6PD deficiency

A

X linked recessive

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8
Q

Genetics of hereditary spherocytosis

A

Autosomal dominant

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9
Q

Causes of jaundice under 24 hours

A

Rhesus haemolytic disease
ABO incompatibility
TORCH infections
G6PD deficiency
Hereditary spherocytosis

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10
Q

Causes of jaundice in the first 2-14 days (normal)

A

Physiological jaundice
Breast milk jaundice
Exacerbation by bruising and polycythaemia
Infection

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11
Q

Two main reasons for physiological jaundice

A

Increased bilirubin production as fetal haemoglobin has a lifespan of 70 days (compared to adult 120)

Decreased conjugated bilirubin due to liver immaturity (why premature babies have a higher incidence)

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12
Q

Why can breast milk feeding difficulties or infection cause jaundice in neonates

A

Feeding difficulties and infection cause dehydration which impairs bilirubin elimination

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13
Q

Why can polycythaemia occur in neonates

A

Gestational diabetes

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14
Q

Why can bruising occur in neonates

A

Caput
Cephalohaematoma

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15
Q

What is neonatal biliary atresia

A

Rare condition with failure of the biliary tree to develop

NB: Important to detect early as early surgery improves outcomes

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16
Q

Pathophysiology of kernicterus

A

Acute bilirubin encephalopathy: brain damage due to unconjugated bilirubin deposition in the basal ganglia and brain stem after it exceeds albumin binding capacity

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17
Q

Complications of kernicterus

A

Seizures, hypotonia, opisthotonos
Without treatment: cerebral palsy, learning disabilities, sensorineural deafness

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18
Q

Investigations of neonatal jaundice

A

Transcutaneous bilirubin levels
Bloods: coombs, kleihauer, U&Es (both conjugated and unconjugated bilirubin), FBC + blood film, blood cultures, TFTs
USS if there is a suspicion of biliary atresia

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19
Q

Treatment of neonatal jaundice

A

First line phototherapy: converts unconjugated bilirubin into harmless substances

Exchange transfusion: if bilirubin levels are very high

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20
Q

Clinical features of bronchiolitis

A

LRTI
Coryzal symptoms preceding a dry wheezy cough
Fever + poor feeding
Tachypnoea, tachycardia
Symptoms of RDS e.g. intercostal/subcostal recessions, tracheal tug, grunting, nasal flaring

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21
Q

When should you suspect pneumonia in a differential diagnosis of bronchiolitis

A

High fever
Localised signs (consolidation)

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22
Q

High risk children for bronchiolitis

A

congenital heart disease
BPD (bronchopulmonary dysplasia)
CF
prematurity

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23
Q

Prevention of bronchiolitis in high risk children

A

IM palivizumab (RSV monoclonal antibody)

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24
Q

Most common causal organism of croup/laryngotracheobronchitis

A

Parainfluenza virus

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25
Q

Clinical features of croup

A

URTI
Barking cough
Inspiratory stridor
Hoarse voice
Respiratory distress

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26
Q

Differential diagnosis of croup

A

Bacterial tracheitis – more toxic appearance

Laryngomalacia – no chest signs

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27
Q

Treatment of croup

A

Reassurance

One of dose of oral or nebulised steroids e.g. dexamethasone 150mcg/kg

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28
Q

Treatment of severe croup unresponsive to steroids

A

Hospital for nebulized adrenaline
Careful monitoring

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29
Q

Most common causal organism of epiglottis

A

Haemophilus influenzae

rare now due to the Hib vaccine

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30
Q

Clinical features of epiglottis

A

Toxic looking child - miserable fever

3 Ds: drooling, dysphagia, distress

Tripod position
Muffled voice
Inspiratory stridor

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31
Q

Epiglottis treatment

A

IV cefotaxime

Do not distress the child or examine the airway

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32
Q

Causes of meningitis/encephalitis under 3 months of age

A

Group B strep

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33
Q

Causes of meningitis over 3 months of age

A

Meningococcus, pneumococcus (haemophilus influenza b)

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34
Q

Mumps virus

A

RNA paramyoxovirus

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35
Q

Clinical features of mumps

A

Coryzal symptoms followed by parotid swelling
Ear ache
Trismus – spasm of the muscles of mastication when chewing

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36
Q

Complications of mumps

A

Meningitis
Encephalitis
Orchitis
Pancreatitis

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37
Q

Measles virus

A

RNA paramyxovirus: morbillivirus

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38
Q

Clinical features of measles

A

Catarrhal stage:
- 4 Cs – Cough, Cranky, coryza, conjunctivitis

Exanthematous stage:
- maculopapular rash with cephalocaudal progression

Complications: - most common is otitis media

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39
Q

Diagnosis of measles

A

Clinical diagnosis
Saliva swab for measles IgM to confirm since it is a notifiable disease

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40
Q

Rubella virus

A

RNA paramyxovirus – rubivirus

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41
Q

Clinical features of rubella

A

Coryzal prodrome
Pink maculopapular rash
Lymphadenopathy – sub occipital or posterior auricular
Arthralgia is common

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42
Q

Diagnosis of rubella

A

Clinical
Saliva swab for rubella IgM since it is a notifiable disease

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43
Q

Main risk group for rubella

A

Pregnant women:
<13 weeks: transmission to fetus is 80% (TOP can be offered)
>16 weeks: 25% risk of transmission/unlikely to cause defects

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44
Q

Clinical features of congenital rubella

A

Triad:
sensorineural deafness
cardiac abnormalities
eye abnormalities e.g. cataracts

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45
Q

Clinical features of parvovirus B19/fifth disease

A

Coryzal prodrome, fever
Malar rash
Glove and stocking erythema is also common
Arthropathy is common in older children
Once the rash appears they are no longer infectious

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46
Q

Complications of parvovirus B19

A

Pure red cell aplasia (high risk - sickle cell, thalassaemia)
Transient aplastic crisis (high risk - HIV, organ transplant patients)
Hydrops fetalis (> 70% transmission rate to the fetus if > 16 weeks - may require fetal blood transfusions in utero)

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47
Q

Causal organism of hand, foot and mouth

A

enteroviruses - mostly coxsackie A16

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48
Q

Are most sore throats viral or bacterial

A

viral

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49
Q

Causal organism of bacterial tonsilitis

A

group A beta haemolytic strep (GABHS) – strep. Pyogenes

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50
Q

Tonsilitis ‘Fever PAIN’ score

A

Fever

Purulent tonsils
Attended rapidly (within 3 days)
Inflamed tonsils
No cough or coryza

Score 2/3 = 30 – 40% chance of strep
Score 4/5 = 60% chance of strep

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51
Q

Treatment of tonsilitis

A

Bacterial:
Phenoxymethylpenicillin (pen V) for 7 – 10 days
Clarithromycin if penicillin allergic

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52
Q

Causal organism of scarlet fever

A

GABHS (group A B-haem strep) - release endotoxins that cause scarlet fever

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53
Q

clinical features of scarlet fever

A

Rash 12 – 48 hours after the onset of a sore throat
Red pin prick blanching red
Sandpaper feel to the rash
Strawberry tongue
Circumoral pallor

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54
Q

Treatment of scarlet fever

A

phenoxymethylpenicillin
(same as tonsilitis)

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55
Q

Causal organism of chickenpox

A

varicella zoster virus

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56
Q

Description of chickenpox rash

A

Macular – papular – vesicles (fluid filled)

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57
Q

Treatment of chickenpox

A

Supportive

Signs of infection (staph. Aureus) – flucloxacillin

Immunocompromised – acyclovir

Pregnant women contacts – VZIG or acyclovir if they develop a rash

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58
Q

3 complications of chickenpox

A

bacterial infection
pneumonia
encephalitis

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59
Q

causal organism of impetigo

A

staph aureus

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60
Q

peak ages of impetigo

A

2-5 years old

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61
Q

clinical features of impetigo

A

Pustules + blisters on an erythematous base

Blisters leave a brown ‘honey crust’ when they burst

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62
Q

treatment of impetigo

A

First line – topical hydrogen peroxide 1% or topical fusidic acid (both are just as effective)

If severe/widespread – oral flucloxacillin

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63
Q

school exclusion in impetigo

A

48 hours after antibiotics or until lesions have crusted over

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64
Q

school exclusion in mumps

A

7 days

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65
Q

school exclusion in measles

A

5 days after rash onset

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66
Q

school exclusion in rubella

A

5 days after rash onset

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67
Q

school exclusion in hand, foot and mouth

A

no school exclusion

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68
Q

Transient synovitis/irritable hip clinical features

A

Pain mostly on movement, improves throughout the day - will move it if persuaded!

2-12 years old

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69
Q

aetiology of transient synovitis/irritable hip

A

viral infection

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70
Q

management of any suspicion of septic arthritis or hip pain in a child < 3 years old

A

A&E

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71
Q

Perthe’s disease clinical features

A

Constant pain
Restricted ROM
Leg length discrepancy = late sign

5-10 years old

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72
Q

Dx + Ix Perthe’s disease

A

X ray – joint space widening/irregularity
- crescent sign (late sign)

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73
Q

SCFE clinical features

A

Vague pain
Drehmann’s sign

5-10 years old
overweight
pubertal

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74
Q

Dx + Ix SCFE/SUFE

A

X ray = diagnostic

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75
Q

Tx SCFE

A

Surgical fixation

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76
Q

Septic arthritis causal organism in children (most commonly <2 yrs old)

A

Staph aureus

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77
Q

Clinical features septic arthritis

A

Look for scratches/infected chicken pox
Acutely swollen tender joint
Pseudoparesis

78
Q

Dx + Ix septic arthritis

A

blood cultures, CRP
joint aspiration

79
Q

Tx septic arthritis

A

surgical debridement + IV ABx

80
Q

Oesophageal atresia (OA)

A
81
Q

Clinical features of OA +/- TOF

A

Prenatal:
polyhydramnios (cannot swallow the amniotic fluid)

Postnatal:
- blowing bubbles
- salivation + drooling
- cyanotic episodes on feeding
- respiratory distress + aspiration

82
Q

Dx + Ix OA +/- TOF

A

NG tube > X-ray will show NG coiled in the oesophagus

Abdo X-ray: no bubbles = isolated OA

83
Q

Gastroschisis

A

Paraumbilical defect, always to the right of the cord

84
Q

gastroschisis Ix

A

Typically found on antenatal scans

AFP raised

85
Q

Treatment of gastroschisis

A

Lower segment C section
Staged corrective surgery
TPN slowly introduced

86
Q

Omphalocele

A

Ventral defect in the umbilical ring with herniation of abdominal contents covered by peritoneum

87
Q

Kawasaki crash and burn

A

Conjunctivitis
Rash
Adenopathy
Strawberry tongue
Hand (swelling or erythema)

And burn

88
Q

Kawasaki Tx

A

IgG a
ITP

89
Q

What is caput succedaneum

A

Boggy superficial scalp swelling that can cross the suture line
(CS = Crosses Sutures)

90
Q

What is caput succedaneum commonly caused by

A

pressure against the cervix during birth or ventouse delivery (Chignon)

91
Q

What is cephalohaematoma

A

Subperiosteal haemorrhage
(periosteum is stuck tightly to the skull and so does NOT cross the suture lines)

92
Q

Causes of omphalocele

A

Small defects (ie no liver) are associated with beckwith-Wiedemann syndrome (BWS)

Larger defects are caused by pulmonary hypoplasia

93
Q

Omphalocele Ix

A

Antenatal scans
Raised AFP

94
Q

Omphalocele Tx

A

Protect the herniated contents
Prevent hypothermia
Gastric decompression
Staged surgical repair

95
Q

Signs of congenital diaphragmatic hernia (CDH)

A
  • Resuscitation at birth
  • Displaced apex beat
  • Bowel sounds in hemithorax
  • If small defect – may just have respiratory distress after feeding
  • Scaphoid abdomen
96
Q

Duodenal atresia associated genetic condition

A

Down syndrome

97
Q

Duodenal atresia presentation

A

Small bowel obstruction symptoms with or without bilious vomiting

98
Q

Duodenal atresia X ray finding

A

Double bubble sign

99
Q

volvulus sign on X ray

A

Coffee bean sign

100
Q

Why can small bowel obstruction occur in cystic fibrosis

A

Delayed passage of meconium due to it being thicker - some meconium gets stuck in the distal ileum

101
Q

What treatment can help meconium pass in CF

A

Therapeutic contrast enema (gastrografin)

102
Q

Hirschsprung’s disease pathogenesis

A

Congenital absence of ganglia (both myenteric and submucosal plexus) in a segment of the colon

NB: 75% rectosigmoid

103
Q

Clinical features of Hirschsprung’s disease

A

Functional LBO with failure to pass meconium within 24 – 48 hours

abdominal distention + late bilious vomiting

PR would reveal a contracted distal segment
followed by a rush of liquid stool and temporary relief of symptoms

104
Q

Diagnosis Ix Hirschsprung’s disease

A
105
Q

Undescended testes / cryptorchidism treatment

A

Most will spontaneously descend by 6 months - 1 year

Orchidopexy at 1 year if still undescended

106
Q

Indirect vs direct inguinal hernia

A

NB: ring occlusion test can differentiate between a direct and indirect hernia

107
Q

What are neonatal inguinal hernias due to

A

Patent processus vaginalis (failure to become the tunica vaginalis)

108
Q

Inguinal hernias clinical features

A

Indirect – bulge lateral to the pubic tubercle
more prominent on crying

Look for signs of incarceration e.g. tender
lump, irritable, vomiting

109
Q

6/2 rule in the surgical treatment of Inguinal hernias

A

< 6 weeks operate within 2 days
< 6 months operate within 2 weeks
< 6 years operate within 2 months

Any signs of incarceration = emergency surgery

110
Q

Hypospadias definition

A

Presence of the urethral meatus on the ventral aspect of the penile shaft

(Testosterone is needed for the meatus to move distally during development)

111
Q

Zero to finals

A
112
Q

Which deficiency should you investigate in hypospadias and undescended testes

A

Low testosterone

113
Q

Clinical features of hypospadias

A

Meatus on the ventral surface
Hooded foreskin
Spraying on urination

114
Q

Testicular torsion pathogenesis

A

Twisting of the spermatic cord cutting off blood supply to the testicle

115
Q

Aetiology of testicular torsion

A

Peaks at times of high testosterone – larger
testes = more chance of twisting

Peak times are in neonates and pubertal teenagers

Neonates with undescended testes are at
higher risk because there is less secure attachment within the scrotum

Bell clapper deformity

116
Q

Clinical presentation of testicular torsion

A

Testicle displaced higher, more horizontal
Acutely swollen, tender testicle
Vomiting due to pain
Absent cremasteric reflex
Negative Prehn’s sign

117
Q

Negative prehns sign interpretation

A

differentiates between torsion and epididymitis - lift the testicle – if pain is relieved this is suggestive of epididymitis - if pain is not relieved – torsion

118
Q

Surgical emergency chances of survival for testicular torsion

A

< 6 hours – 90% chance of testicular survival

24 hours – 10% chance of testicular survival

119
Q

Intussusception definition

A

Condition where one section of bowel telescopes into the other, usually the ileum into the caecum

Presents 3 months – 2 years

120
Q

Aetiology intussusception

A

Classically preceded by viral infection
Meckel’s diverticulum
CF
Lymphoma

121
Q

Clinical features of intussusception

A

Episodes of colicky abdominal pain,
legs draw up
May be fine but lethargic in between episodes
Signs of SBO
Sausage shaped mass in the abdomen
Late sign – red current jelly stool due
to bowel ischaemia

122
Q

Diagnosis/Ix intussusception

A

USS – target/donut sign
AXR – dilated proximal bowel loops

123
Q

Treatment intussusception

A

Rectal air insufflation
- 75% success rate
- only perform if there are no signs of peritonism

Surgical correction if air insufflation fails or signs of ischaemia

124
Q

Pyloric stenosis definition

A

Hypertrophy of the pylorus muscle leading to gastric outlet obstruction causing projectile vomiting

Incidence peaks at 2-8 weeks

4 x more common in boys

125
Q

Clinical features of pyloric stenosis

A

Projectile vomiting very shortly after feeds
Non bilious
Hungry after vomiting
Dehydration
Weight loss is a late sign

126
Q

Diagnosis/Ix pyloric stenosis

A

Test feed – feel for an olive size mass in the RUQ
USS – thickened pylorus
Hypochloraemic hypokalaemic metabolic
alkalosis

127
Q

Treatment pyloric stenosis

A

Non urgent outpatient pyloromyotomy

128
Q

Pathogenesis of anaemia

A

Blood loss e.g. acute haemorrhage

Decreased production e.g. nutritional deficiency

Increased consumption e.g. acquired (e.g. immune) or inherited (e.g. enzyme)

129
Q

Blood parameters to check for

A

Hb (always check normal range for age and sex)

Is the abnormality isolated to a single cell line or part of multiple cell
lines (BM failure, infiltration, immune, hypersplenism)

MCV (microcytic, normocytic, macrocytic)

130
Q

Microcytic (MCV low) anaemias

A

Iron deficiency Thalassaemia
Sideroblastic Anaemia Chronic disease
Lead toxicity

131
Q

Macrocytic (MCV high) anaemias

A

Normal newborn
Aplastic anaemia Hypothyroidism Megaloblastic anaemia Early iron deficiency Increased erythropoiesis

132
Q

Normocytic (MCV normal) anaemias

A

Acute blood loss
Infection
Renal failure
Early iron deficiency
Bone marrow infiltration

133
Q

Most common causes of anaemia in childhood

A

Low birth weight
Dietary - excessive cows milk intake
Occult GI bleeding (E.g hookworm)
Cows milk intolerance

134
Q

Presentation of anaemia in childhood

A

pallor, irritability, anorexia
when Hb<50, tachycardia,
cardiac dilatation, murmur,
poss. splenomegaly

135
Q

Treatment of iron deficiency anaemia

A

Oral therapy for 3-6 months

136
Q

Intra corpuscular causes of haemolysis

A

Haemoglobin
Enzyme
Membrane

137
Q

Extra corpuscular causes of anaemia

A

Autoimmune
Fragmentation
Hyper splenism
Plasma factors

138
Q

Presentation of haemolytic anaemia

A

Hydrops fetalis
Neonatal hyperbilirubinaemia (jaundice)
Neonatal ascites
Anaemia/failure to thrive
Splenomegaly
Cholecystitis/gall stones
Hyperbilirubinaemia
Leg ulcers
Aplastic crisis
Thromboembolism

139
Q

Haemolysis screen

A

FBC
Retics
Blood film
LDH
Haptoglobin
Bilirubin
Direct Coombs test

140
Q

Three main presentations of G6PD

A

Neonatal jaundice
Chronic non-spherocytic haemolytic anaemia
Intermittent episodes of intravascular haemolysis

141
Q

Pathophysiology of sickle cell

A

Substitution of valine for
glutamic acid on β chain (HbS)

HbS polymerises when
deoxygenated leading to sickle shape

Occlusion of the microvascular
circulation producing vascular damage, infarcts, pain

Shortened survival of red cells leading to haemolysis

142
Q

Sickle cell genetics

A

Autosomal recessive

NB: most common serious genetic disorder in England

143
Q

Common presentations of sickle cell disease

A

Dactylitis
Acute chest syndrome
Splenomegaly (splenic sequestration)

144
Q

Diagnosis sickle cell

A

Blood film

Screening: sickle solubility test

145
Q

Thalassaemia

A

Reduced rate of one or more of the globin chains

Autosomal recessive

146
Q

A Thalassaemia

A

4 a globin chains per cell (aa/aa)

147
Q

B Thalassaemia

A

2 globin genes per cell

148
Q

Necrotising enterocolitis (NEC) definition

A

Disorder affecting premature neonates where part of the bowel becomes necrotic which can lead to bowel perforation

149
Q

Why is NEC a life threatening emergency

A

Bowel perforation can lead to peritonitis and shock

150
Q

Risk factors for developing NEC

A

Very low BW or very premature
Formula feeds
Respiratory distress and assisted ventilation (hypoxia)
Sepsis
Patient ductus arteriosus / other congenital heart disease

151
Q

Presentation of NEC

A

Intolerance to feeds
Vomiting, particularly with green bile
Generally unwell
Distended, tender abdomen (taught shiny skin)
Absent bowel sounds
PR fresh blood + mucus in stools (due to necrosis)

152
Q

Blood test Ix for NEC

A

Full blood count: thrombocytopenia and neutropenia (low platelets = worse prognosis)
CRP: inflammation
Capillary blood gas: metabolic acidosis
Blood culture for sepsis
Clotting screen (NEC can lead to DIC)

153
Q

Ix of choice for NEC

A

Abdominal X-ray

154
Q

X-ray signs NEC

A

Dilated loops of bowel
Pneumotasis intestinalis (gas in the bowel wall) - PATHOGNOMONIC of NEC
Pneumoperitoneum (free gas in the peritoneal cavity = perforation)

155
Q

NEC Tx

A

NBM with IV fluids + total parenteral nutrition (TPN)
Antibiotics (cefotaxime + vancomycin)
Nasogastric tube can be inserted to drain fluid and gas from the stomach and intestines

Some neonates will require surgery - laparotomy if rapid distention + signs of perforation

156
Q

Why can treatment for patent ductus arteriosus cause NEC

A

Indomethacin (NSAID) causes vasoconstriction of mesenteric arteries

157
Q

🚩 Red flag 🚩

Not keeping down any feed

A

Pyloric stenosis or intestinal obstruction

158
Q

🚩 Red flag 🚩

Projectile or forceful vomiting

A

Pyloric stenosis or intestinal obstruction

159
Q

🚩 Red flag 🚩

Bile stained vomit

A

Intestinal obstruction

160
Q

🚩 Red flag 🚩

Haematemesis or melaena

A

Peptic ulcer, oesophagitis or varices

161
Q

🚩 Red flag 🚩

Abdominal distention

A

Intestinal obstruction

162
Q

🚩 Red flag 🚩

Reduced consciousness, bulging fontanelle or neurological signs

A

Meningitis or raised ICP

163
Q

🚩 Red flag 🚩

Respiratory symptoms

A

Aspiration or infection

164
Q

🚩 Red flag 🚩

Blood in the stools

A

Gastroenteritis or cows milk protein allergy

165
Q

🚩 Red flag 🚩

Signs of infection

A

Pneumonia, UTI, tonsillitis, otitis or meningitis

166
Q

🚩 Red flag 🚩

Rash, angioedema and other signs of allergy

A

Cows milk protein allergy

167
Q

Signs of problematic reflux in GORD

A

Chronic cough
Hoarse cry
Distress, crying or unsettled after feeding
Reluctance to feed
Pneumonia
Poor weight gain/faltering growth
Disturbed sleep
Oesophagitis (can cause anaemia)

168
Q

Why do most babies have gastro oesophageal reflux

A

The lower oesophageal sphincter is immature

(90% of babies stop having reflux by 1 year)

169
Q

GORD Tx

A

Minor: reassurance; smaller and more frequent feds; sit up right after feeding

Severe: PPI e.g. omeprazole

Very severe: unresponsive to treatment and >1 year old: Nissen fundoplication

170
Q

IgE mediated CMPA symptom onset

A

Type 1 hypersensitivity
Immediate symptom onset after only small amounts

171
Q

Non IgE mediated symptom onset

A

Symptoms occur around 72 hours after ingestion

172
Q

Clinical features IgE mediated CMPA

A

Derm: urticaria (hives), pruritus
GI: colicky abdo pain, vomiting, bloody stool
Resp: rhinorrhea (runny nose), itchy nose

173
Q

Clinical features non IgE mediated CMPA

A

Loose frequent stool with blood + mucus
Colicky abdominal pain

174
Q

Diagnosis/Ix CMPA

A

IgE mediated suspicion: skin prick weal = 4mm is positive

Non IgE: temporary removal from diet and then reintroduction to see if symptoms return

175
Q

Tx CMPA

A

Breastfed - mum removes milk from her diet
Bottle fed - extensively hydrolysed formula

176
Q

Sandifer’s syndrome (GORD)

A

Brief episodes of abnormal movements:
Torticollis (twisting of neck)
Dystonia (arching of back)

177
Q

Aetiology acute otitis externa

A

Bacterial - mostly pseudomonas or staph aureus

178
Q

Risk factors acute otitis externa

A

Humidity
Swimming
Scratching from eczema/psoriasis

179
Q

Clinical features acute otitis externa

A

Pain (pulling at the ear)
Scaly skin + discharge
Conductive hearing loss on the affected side

180
Q

Treatment of mild acute otitis externa

A

Topical antibiotics + steroid drops e.g. sofradex (aminoglycoside + steroid

181
Q

Treatment of severe acute otitis externa (occluded ear canal)

A

Send to ENT for ear wicking (impregnated w/ antibiotics)

182
Q

Treatment for spreading erythema around the ear in acute otitis externa

A

Flucloxacillin or ciprofloxacin (good against pseudomonas)

183
Q

Aetiology acute otitis media

A

Mostly viral

184
Q

Clinical feature of acute otitis media

A

Tympanic membrane bulges and becomes erythematous

185
Q

Treatment acute otitis media

A

Watchful waiting - 60% resolve within 24 hours, 80% within 4 days

Indication for antibiotics: amoxicillin 5-7 days or erythromycin if penicillin allergic
— 4 days of symptoms
— Bilateral AOM in a child <2 years old
— Discharger = perforation
— Immunocompromised

186
Q

Complications of acute otitis media

A

Tympanic membrane perforation
Mastoiditis

187
Q

Glue ear definition

A

Otitis media with a collection of fluid behind the TM

188
Q

Aetiology glue ear

A

Eustachian tube dysfunction - children have shorter and more horizontal eustachian tubes
URTI often causes adenoid hypertrophy which blocks the eustachian tubes
Children at increased risk - down syndrome, cleft palate

189
Q

Diagnosis and investigation

A

Otoscopy - opaque + retracted TM, fluid level + bubbles

190
Q

Glue ear treatment

A

Active observation for 3 months/otovent for symptomatic relief to improve conductive hearing loss
3 month: consider ENT referral for grommets

Belle: Phase 3a (7 decks)

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