Paediatrics Flashcards
What is the most common cause of croup?
Viral (most commonly parainfluenza virus)
How does croup initially present?
12-48 hours of non-specific cough, rhinorrhoea and fever.
What are the symptoms of mild croup?
Coryza
Fever
Seal-like barking cough
What are the symptoms of moderate croup?
Coryza Fever Seal-like barking cough Stridor Sternal recession
What are the symptoms of severe croup?
Coryza Fever Seal-like barking cough Stridor Sternal and intercostal recession Agitation Lethargy
What are the symptoms of impending respiratory failure in croup?
Increasing upper airway obstruction Sternal/intercostal recession Asynchronous chest wall and abdominal movement Fatigue Pallor/cyanosis Decreased level of consciousness
How is croup treated?
Single dose of oral dexamethasone - 0.15 mg per kg body weight
(If too unwell: inhaled budesonide (2 mg nebulised); or IM dexamethasone (0.6 mg per kg body weight))
Paracetamol/ibuprofen for fever and pain
How is severe upper airway obstruction in croup managed?
Nebulized adrenaline with oxygen via facemask
What are the symptoms of appendicitis in children?
Fever
Vomiting
Anorexia
Abdominal pain (central and colicky, then localises to RIF)
Persistent guarding and tenderness in RIF (often absent)
What is the risk with appendicitis in young children?
Perforation may be rapid as omentum is less well developed and fails to surround appendix
Late presentation or delayed diagnosis due to subtle or atypical signs
How is appendicitis managed in children?
Uncomplicated appendicitis -> appendicectomy
With generalised guarding (perforation) -> fluid resuscitation + IV Abx -> laparotomy
With palpable RIF mass and no signs of pertitonitis -> Abx for several weeks -> appendicectomy
What does the steeple sign on an x-ray indicate?
Croup
What is intussusception?
Invagination of proximal bowel into a distal segment.
Where is the most common location of intussusception?
Ileum passing through ileocaecal valve into caecum.
What is the most common cause of bowel obstruction in infants after the neonatal period?
Intussusception
What are the symptoms of intussusception?
Paroxysmal, severe, colicky pain (episodes of pain cause pallor and drawing up legs) Increasing lethargy Refusing feeds Vomiting ‘Redcurrant jelly’ stool
What are the clinical signs of intussusception?
Palpable sausage-shaped mass
Abdominal distension
Shock
What does ‘redcurrant jelly’ stool indicate?
Intussusception
What is the most serious complication of intussusception?
Stretching and constriction of the mesentery resulting in venous obstruction, causing engorgement and bleeding from the bowel mucosa, fluid loss, and subsequently bowel perforation, peritonitis, and gut necrosis.
What does the target/doughnut sign on an abdominal USS indicate?
Intussusception
What is the characteristic finding of intussusception on an abdominal USS?
Target/doughnut sign
What are the most common pathological lead points in intussusception?
Meckel’s diverticulum
Polyps
?Viral infection leading to enlargement of Peyer’s patches
How is intussusception initially managed?
‘Drip and suck’ - nasogastric tube and IV fluid resuscitation
How should intussusception with no signs of peritonitis be managed? What is the success rate of this intervention?
Reduction by rectal air insufflation, carried out by radiologist.
75% success rate.
What are the indications for laparotomy (reduction/resection) in intussusception?
Peritonitis Perforation High likelihood of pathological lead point Prolonged history (>24hrs) Failed rectal air insufflation
What is mesenteric adenitis?
Inflamed mesenteric lymph nodes in the abdomen.
What is the main cause of mesenteric adenitis in children.
Infection: usually viral; may be bacterial (e.g. Yersinia enterocolitica)
What are the symptoms of mesenteric adenitis?
Abdominal pain (umbilicus, RIF) Sore throat/coryza before onset of pain Fever Nausea Diarrhoea
What is the main differential diagnosis for mesenteric adenitis in children?
Appendicitis
How is mesenteric adenitis diagnosed?
No specific tests; often diagnosed in children with large mesenteric nodes and a normal appendix are seen on laparoscopy.
Define ’constipation’.
The infrequent passage of dry, hardened faeces, often accompanied by straining or pain and bleeding associated with hard stools.
What may cause constipation in children?
Dehydration or reduced fluid intake Anal fissure causing pain Problems with toilet training Anxiety about opening bowels at school or in unfamiliar toilets Underlying pathologies
What is the mechanism of overflow in constipation?
- Longstanding constipation
- Rectum becomes overdistended
- Loss of feeling the need to defecate
- Contractions of the full rectum inhibit the internal sphincter
- Involuntary soiling
After what age is soiling considered abnormal?
4 years old
How should constipation with overflow be managed pharmacologically?
- Evacuate overloaded rectum completely - disimpaction regimen - macrogol laxative, e.g. Movicol Paediatric Plain (+ stimulant laxative, e.g. senna, if not disimpacted after 2 weeks).
- Maintenance treatment to ensure ongoing, pain-free defecation - polyethylene glycol +/- stimulant laxative.
- Reduce dose of maintenance treatment over a period of months in response to improvement.
What conservative management can be used for constipation?
Sufficient fluid
Balanced diet
Sitting on toilet after mealtimes to utilise physiological gastronomic reflex
Behavioural interventions e.g. star chart
Red flag in constipation: Failure to pass meconium in first 24hrs of
Iife
Hirschsprung disease
Red flag in constipation: Faltering growth/growth failure
Hypothyroidism
Coeliac disease
Red flag in constipation: Gross abdominal distension
Hirschsprung disease
Other gastrointestinal dysmotility
Red flag in constipation: Abnormal lower limb neurology or deformity
Lumbosacral pathology
Sacral dimple above natal cleft, over spine - naevus, hairy patch, central pit, discoloured skin
Spina bifida occulta
Red flag in constipation: Abnormal appearance/position/patency of anus
Abnormal anorectal anatomy
Red flag in constipation: Perianal bruising or multiple fissures
Sexual abuse
Red flag in constipation: Perianal fistulae, abscesses, or fissures
Perianal Crohn’s disease
What is the most common pathogen causing UTI in children?
E. coli
What proportion of children with recurrent UTIs have a structural abnormality of the urinary tract?
Up to 50%
What may recurrent UTIs with pseudomonas indicate?
Structural abnormality of the urinary tract
What are the signs of symptoms of UTI in infants?
Fever Lethargy Irritability Poor feeding Vomiting Jaundice Offensive urine Faltering growth Septicaemia Febrile seizures (>6 months)
What are the signs of symptoms of UTI in children?
Fever +/- rigors Lethargy Febrile seizures Anorexia Vomiting Abdominal pain/loin tenderness Diarrhoea Dysuria, frequency and urgency Haematuria Offensive, cloudy urine Recurrence of enuresis
What is dysuria without fever and systemic involvement typically associated with?
Cystitis
Vulvitis in girls
Balanitis in boys
What is fever and systemic involvement in a UTI typically associated with?
Pyelonephritis
What is a differential diagnosis for symptoms associated with a UTI?
Sexual abuse
How should a child with positive leucocyte esterase and positive nitrite on a urine dipstick be managed?
Regard as a UTI and treat with antibiotics
Urine culture
How should a child with positive leucocyte esterase and negative nitrite on a urine dipstick be managed?
Start antibiotic treatment if clinical evidence of UTI
Diagnosis depends on urine culture
How should a child with negative leucocyte esterase and positive nitrite on a urine dipstick be managed?
Start antibiotic treatment if clinical evidence of UTI
Diagnosis depends on urine culture
How should a child with negative leucocyte esterase and negative nitrite on a urine dipstick be managed?
UTI unlikely so consider differential diagnoses
Repeat/send urine for culture if clinical history suggests UTI
How should an infant <3 months with a suspected UTI be managed?
Refer immediately to hospital and give IV antibiotics (e.g. co-amoxiclav) for 5-7 days, followed by oral prophylaxis
How should and infant >3 months with a UTI be managed?
Oral antibiotics (e.g. trimethoprim for 7 days) or IV antibiotics for 2-4 days followed by oral antibiotics for a total of 7-10 days.
How should a child with acute pyelonephritis / upper UTI be managed?
Oral antibiotics (e.g. trimethoprim for 7 days) or IV antibiotics for 2-4 days followed by oral antibiotics for a total of 7-10 days.
How should a child with cystitis / lower UTI be managed?
Oral antibiotics (trimethoprim/nitrofurantoin) for 3 days.
What are the differential diagnoses for acute respiratory distress in an infant?
Bronchiolitis Viral episodic wheeze Pneumonia Heart failure Foreign body Anaphylaxis Pneumothorax/ pleural effusion Metabolic acidosis Severe anaemia
What is the main pathogen causing bronchiolitis?
RSV (80%)
What are the symptoms of bronchiolitis?
Initially coryzal symptoms, followed by a dry cough and increasing breathlessness.
What are the examination findings in bronchiolitis?
Dry wheezy cough Tachycardia Tachypnoea Cyanosis or pallor Hyperinflated chest (sternum prominent, liver displaced downwards) Subcostal and intercostal recession Fine end-inspiratory crackles High-pitched wheeze (expiratory > inspiratory)
What would indicate the need for hospital admission for an infant with bronchiolitis?
Oxygen saturation persistently <90% on room air
Apnoea
Inadequate oral fluid intake (50-75% of usual volume)
Severe respiratory distress (grunting, marked chest recession, RR > 70 breaths per minute)
How is bronchiolitis managed?
Supportive management
- Humidified oxygen via nasal cannulae or head box
- Monitor for apnoea
- Fluids (NG or IV)
- Assisted ventilation (CPAP or mechanical ventilation)
- Infection control
Why are children more susceptible to fluid loss than adults?
Children have a higher surface area to volume ratio and a higher basal metabolic rate, so require a much higher fluid intake per kilogram of body weight than adults, and may therefore become dehydrated if:
- they are unable to take oral fluids
- there are additional fluid losses due to fever, diarrhoea, or increased insensible losses (e.g. due to increased sweating tachypnoea)
- there is loss of normal fluid-retaining mechanisms, e.g. burns, the permeable skin of premature infants, increased urinary losses or capillary leak
What is the mechanism of Hypoxic Ischaemic Encephalopathy (HIE)?
1/ Perinatal asphyxia: compromised gas exchange results in cardiorespiratory depression.
2/ Compromised cardiac output diminishes tissue perfusion, causing hypoxic-ischaemic injury to the brain and other organs.
3/ Results in brain damage, leading to disability or death.
What would you expect to see on the blood gas of a neonate with HIE?
Hypoxia
Hypercapnia
Metabolic acidosis
What events can result in HIE?
Failure of gas exchange across placenta, e.g. excessive/prolonged contractions, placental abruption
Interruption of umbilical blood flow, e.g. cord compression/prolapse
Inadequate maternal placental perfusion
Compromised foetus, e.g. IUGR, anaemia
Failure of cardiorespiratory adaptation at birth
How is moderate/severe HIE managed?
NICU
Mild hypothermia treatment (within 6 hours of birth)
Respiratory support (ventilator, CPAP)
Seizure monitoring and treatment
Treat hypotension - volume and inotrope support
Monitor and treat hypoglycaemia and electrolyte imbalance
What is cerebral palsy?
An umbrella term for a permanent disorder of movement and/or posture and of motor function due to a non-progressive abnormality of the developing brain.
Often accompanied by disturbances of cognition, communication, vision, perception, sensation, behaviour, seizure disorder, and secondary musculoskeletal problems.
What proportion of cases of cerebral palsy are caused by hypoxic ischaemic encephalopathy?
~10%
What proportion of cases of cerebral palsy have an antenatal cause? What are antenatal causes of CP?
~80%
Cerebrovascular haemorrhage/ischaemia
Cortical migration disorders or structural maldevelopment of the brain
What are some postnatal causes of cerebral palsy?
Infection - meningitis, encephalitis Encephalopathy Head trauma Symptomatic hypoglycaemia Hydrocephalus Hyperbilirubinaemia
How might cerebral palsy present clinically?
Feeding difficulties (gagging, vomiting, oromotor incoordination, slow feeding)
Asymmetric head function
Abnormal limb and/or trunk posture and tone
Delayed motor milestones
Poor head control
Abnormal gait (e.g. tiptoes)
Only using one side of body
What are the categories of cerebral palsy?
Spastic (90%) - May be bilateral (diplegic or quadriplegic), unilateral, NOS
Dyskinetic (6%)
Ataxic (4%)
Other
Where is the lesion in spastic cerebral palsy?
Upper motor neurone pathway (pyramidal/corticospinal)
Besides hypertonicity, what features frequently accompany bilateral (quadriplegic) cerebral palsy?
Extensor posturing of trunk Poor head control Seizures Microcephaly Learning disability
What are the typical features of dyskinetic cerebral palsy?
Chorea - irregular, sudden and brief non-repetitive movements
Athetosis - slow writhing movements occurring more dismally
Dystonia - simultaneous contractions of agonist and antagonist muscles of the trunk and proximal muscles giving a twisted appearance
Which area of the brain is damaged in dyskinetic cerebral palsy?
Basal ganglia
Which area of the brain is damaged in ataxic cerebral palsy?
Cerebellum
What are the features of ataxic cerebral palsy?
Incoordinate movements
Intention tremor
Ataxic gait
What is the most common cause of ataxic cerebral palsy?
Genetics
What is the most common cause of dyskinetic cerebral palsy?
Hypoxic ischaemic encephalopathy at term
What is sepsis?
An imbalance in the host response to infection, with release of inflammatory cytokines and activation of endothelial cells leading to multiple organ damage.
What are the most common causative organisms of sepsis in children?
Coagulase-negative Staphylococcus (CoNS), Staphylococcus aureus, non-pyogenic streptococci, Streptococcus pneumonia (pneumococcus).
Although Neisseria meningitidis and Escherichia coli are still prevalent.
What is septic shock?
Sepsis plus hypotension that does not correct with fluids.
How does sepsis present clinically?
Irritability or lethargy Fever Poor feeding Tachypnoea Tachycardia Hypotension Purpuric rash (meningococcal septicaemia) Hx of focal infection (meningitis, osteomyelitis, gastroenteritis, cellulitis)
How should sepsis in a child be managed?
Involve senior clinicians
Gain IV/IO access
-blood cultures
-blood glucose
-arterial/capillary/venous gases
-broad-spectrum antibiotics
ABC approach - secure airway
Give supplementary oxygen
Give IV fluids with central venous pressure monitoring and urinary catheterisation
If normal physiological parameters not achieved after >40ml/kg - give vasoactive inotrope support (e.g. adrenaline)
Correct any clotting derangement with FFP, cryoprecipitate and platelet transfusions
What antibiotics should be given in early onset neonatal sepsis?
Benzylpenicillin and gentamicin
What antibiotics should be given in late onset neonatal sepsis?
Ampicillin or vancomycin plus cefotaxime or gentamicin
+ tazobactam if pseudomonas is suspected
+ metronidazole for necrotising enterocolitis or anaerobes
What is shock?
The circulation is inadequate to meet the metabolic demands of the tissues.
What are the three types of shock?
Hypovolaemic (haemorrhagic or non-haemorrhagic)
Cardiogenic
Distributive
What are the main features of distributive shock?
Leaky blood vessels
Peripheral vasodilation
What type of shock is septic shock?
Distributive shock
How does early, compensated shock present clinically?
Blood pressure maintained:
- Increased HR and RR
- Diversion of blood from non-essential tissues causing cold peripheries
How does late, uncompensated shock present clinically?
Blood pressure falls
Lactic acidosis
What age group are most commonly affected by Kawasaki disease?
6 months to 4 years; peak at end of first year
What ethnic groups is Kawasaki disease most prevalent in?
- Japanese
2. Black Caribbean
What is Kawasaki disease?
A systemic vasculitis of unknown aetiology, affecting the main aortic branch arteries, especially the coronary arteries.
What are the clinical features of Kawasaki disease?
Fever - lasting longer than 5 days; difficult to control Irritability Conjunctivitis Mucous membrane changes - red, dry, cracked lips; strawberry tongue Cervical lymphadenopathy Polymorphous rash Red, oedematous soles and palms Peeling of fingers and toes Inflamed BCG scar
How would you investigate suspected Kawasaki disease?
Rule out other causes of fever (including sepsis)
Blood tests: raised inflammatory markers (CRP, ESR, WCC); raised platelet count in second week
How would infants with Kawasaki disease present differently to older children?
More severely affected
‘Incomplete’ symptoms - not all cardinal features are present
How would you manage Kawasaki disease?
IV immunoglobulin (reduces risk of coronary artery aneurysm if given in first ten days); can repeat if fever recurs Aspirin to reduce risk of thrombosis - initially high dose until fever subsided and inflammatory markers are normal, then low dose until echo Corticosteroid/infliximab/cyclosporin for persistent inflammation/fever
How would you follow up a child with Kawasaki disease?
Echo at six weeks to look for aneurysms
If there are giant coronary artery aneurysms, give long-term warfarin therapy
What is the prognosis for Kawasaki disease?
Most common cause of acquired heart disease in children
Coronary arteries are affected in about one-third of children within the first six weeks of the illness
Subsequent narrowing of vessels from scar formation can result in MI and sudden death
Mortality 1-2%
List causes of prolonged fever in children
Infective
- localised infection
- bacterial infection (e.g. typhoid)
- deep abscesses
- infective endocarditis
- tuberculosis
- non-tuberculous mycobacterial infections
- viral infections (e.g. EBV, CMV, HIV)
- parasitic infections (e.g. malaria, Entamoeba histolytica)
Non-infective
- systemic onset juvenile idiopathic arthritis
- systemic lupus erythematosus
- vasculitis (e.g. Kawasaki disease)
- inflammatory bowel disease
- sarcoidosis
- malignancy (e.g. leukaemia, lymphoma, neuroblastoma, Ewing sarcoma)
- macrophage activation syndromes
- drug fever
- fabricated or induced illness
What are the causes of neonatal jaundice at age >24 hours?
Haemolytic disorders - rhesus incompatibility, ABO incompatibility, G6PD deficiency, spherocytosis
Congenital infection
What are the causes of neonatal jaundice at age 2 days to 2 weeks?
Physiological jaundice Breast milk jaundice Infection e.g. UTI Haemolytic disorders Bruising Polycythaemia Crigler-Najjar syndrome
What are the causes of persistent/prolonged neonatal jaundice? (>2 weeks; or >3 weeks in preterm infants)
Unconjugated:
- physiological/breast milk jaundice
- infection (particularly UTI)
- hypothyroidism
- haemolytic anaemia
- high gastrointestinal obstruction, e.g. pyloric stenosis
Conjugated:
- bile duct obstruction
- neonatal hepatitis
What are the mechanisms causing physiological neonatal jaundice?
- High Hb concentration at birth -> breakdown of RBCs -> large Hb release
- Newborns have a shorter RBC lifespan (70 days) than adults (120 days)
- Hepatic bilirubin metabolism is less efficient in the first few days due to lower enzyme levels
Why is neonatal jaundice important?
- It may be a sign of another disorder.
- High unconjugated bilirubin can cause kernicterus, which may lead to disability or death.
What is kernicterus?
Encephalopathy caused by deposition of unconjugated bilirubin in the brain, particularly in the basal ganglia.
How does kernicterus present clinically?
Jaundiced Lethargy Irritability Poor feeding Seizures Increased muscle tone -> opisthotonos (arched back)
What are the potential complications of kernicterus?
Choroathetoid cerebral palsy
Learning difficulties
Sensorineural deafness
Death
How should neonatal jaundice be investigated?
Serum bilirubin
Blood packed cell volume
Blood group (mother and infant)
Coombs test for ABO incompatibility
Full blood count
Blood G6PD levels (consider ethnic origin)
Blood film for spherocytosis (spherocytes) and G6PD deficiency (Heinz bodies)
Cultures (blood, urine, and/or CSF) if infection is suspected
How should neonatal jaundice be managed?
- Treat underlying cause (infection, dehydration)
- Phototherapy
- Exchange transfusion if potentially dangerous bilirubin levels
What is the defective protein in cystic fibrosis, where is the gene for it found, and what is the most common gene mutation?
CFTR (CF transmembrane conductance regulator)
- cAMP-dependent chloride channel found in cell membrane
- gene found on chromosome 7
- most common mutation: 🔼F508
What is cystic fibrosis?
A life-limiting, autosomal recessive condition where abnormal ion transport across epithelial cells results in a multi system disorder, particularly affecting the lungs and pancreas.
How does cystic fibrosis affect the lungs?
Reduction of the airway surface liquid layer and impaired ciliary function cause retention of mucopurulent secretions. This, combined with dysregulation of inflammation and defence against infection, result in chronic endobronchial infection. Chronic infection can lead to damage to the bronchial walls, bronchiectasis, and abscess formation.
How does cystic fibrosis affect the pancreas?
The pancreatic ducts become blocked by thick secretions, therefore the pancreatic enzymes are not released into the small intestine, resulting in malabsorption. The enzymes remain in the pancreas, and in time attack the pancreas. This can lead to acute and then chronic pancreatitis, and insulin-dependent diabetes mellitus.
How is cystic fibrosis diagnoses?
- Newborn screening (heel-prick test) - measure for raised immunoreactive trypsinogen (IRT); if raised ->
- Screen for common CF mutations; if 2+ mutations ->
- Sweat test to confirm diagnosis - chloride 60-125mmol/L
- Confirm by testing for gene abnormalities in CFTR protein
How might cystic fibrosis present in an infant?
Picked up via heel-prick screening
Meconium ileus (bowel obstruction) due to production of thick viscid meconium
Prolonged neonatal jaundice
Faltering growth due to malabsorption
Frequent respiratory infections
Parents notice salty skin when kissing child
What are the clinical features of cystic fibrosis that might be seen in a child/teenager?
Poor growth
Persistent, ‘wet’ coughs
Recurrent chest infections
Hyperinflation of chest due to air trapping
Coarse inspiratory crepitations and/or expiratory wheeze
Harrison’s sulcus
Finger clubbing
Very salty sweat; may lead to dehydration in hot weather
Symptoms of complications (e.g. diabetes, cirrhosis, bowel obstruction)
Sterility in males (due to absence of vas deferens)
What are possible complications of cystic fibrosis?
Recurrent, persistent bacterial chest infections
Respiratory failure (main cause of death)
Bronchiectasis
Pneumothorax
Recurrent haemoptysis
Allergic bronchopulmonary aspergillosis (ABPA)
Diabetes mellitus (insulin-dependent)
Cirrhosis, portal hypertension and liver failure
Nutritional deficiencies
Distal intestinal obstruction syndrome (DIOS)
Nasal polyps
Sinusitis
Rectal prolapse
Psychological impact, on child and family, of having a chronic and ultimately fatal illness that requires regular physiotherapy and drugs, frequent hospital admissions and considerable absences from school.
What are the main bacteria causing LRTIs in people with cystic fibrosis?
Initially Staphylococcus aureus and Haemophilus influenzae.
Subsequently Pseudomonas aeruginosa and Burkholderia species.
How should cystic fibrosis be managed?
MDT approach; patient’s should be reviewed at a specialist centre at least annually.
Treatment is not curative but aims to prevent progressions of lung disease and maintain adequate nutrition and growth.
Respiratory:
- monitoring - by symptoms (young children) or regular spirometry (older children)
- twice daily physiotherapy
- bronchodilator therapy
- continuous prophylactic oral Abx (usually flucloxacillin)
- additional oral Abx for increased symptoms or decrease lung function
- nebulised antipseudomonal Abx and DNase
- 14 days IV Abx via PIC line for persistent signs of infection - consider Portacath if IVs required regularly
- bilateral sequential lung transplantation for end-stage CF lung disease (not curative)
Nutritional:
- assess dietary status regularly
- oral enteric-coated pancreatic replacement therapy with all meals and snacks
- fat-soluble vitamin supplements
- high calorie diet (150% of normal); consider night-feeding via gastrostomy
Manage complications
What is the prognosis for cystic fibrosis?
Life expectancy is mid-30s; projected life-expectancy for current newborns is into 40s. Most die from respiratory failure. Bilateral lung transplantation has >50% survival at 10 years.
What is the pathophysiology of asthma?
Atopy, genetic predisposition, and/or environmental triggers cause bronchial inflammation, with oedema, excessive mucus production, and infiltration by eosinophils/mast cells/neutrophils/lymphocytes. This leads to bronchial hyperresponsiveness and airway narrowing, resulting in symptoms of wheeze, cough, breathlessness, and chest tightness.
Why is asthma difficult to diagnose in pre-school children?
Around half of children wheeze at some point during the first three years of life. This may be because of asthma, but also may be due to viral episodic wheeze or multiple trigger wheeze.
What is viral episodic wheeze?
Young children may develop a wheeze when they have a viral infection, due to small airways narrowing and obstructing due to inflammation. They typically grow out of it by age 5.
What are the clinical features of asthma?
Wheeze = whistling sound in chest on breathing out
-polyphonic due to many airways of different sizes narrowing
Chest usually normal between exacerbations
In long-standing asthma: generalised polyphonic expiratory wheeze with a prolonged expiratory phase; hyperinflation
Harrison’s sulci if onset was in early childhood
If atopic, may also have signs of allergic rhinitis (check nasal mucosa) and eczema
What would indicate a wheeze being caused by asthma rather than another cause of wheeze?
Symptoms worse at night/early morning
Symptoms have non-viral triggers
Interval symptoms (symptoms between acute exacerbations)
Personal or family history of atopic disease
Positive response to asthma therapy
How would possible asthma be investigated?
Diagnosis is usually made from history and examination, particularly in younger children
In children over ~5yrs, can use peak flow/spirometry if uncertainty in diagnosis or severity needs to be monitored
Skin-prick testing for common allergens
(Chest x-ray if other conditions need to be excluded)
How is asthma managed pharmacologically in <5 year olds?
- Short-acting B2-agonist (salbutamol)
- Add low-dose inhaled corticosteroid (budesonide, beclometasone, fluticasone, mometasone) or leukotriene receptor antagonist (montelukast)
- Increase to medium-dose ICS (stop LTRA)
- Add LTRA in addition to medium-dose ICS
- Increase to high-dose ICS and LTRA; refer to specialist
- Add oral corticosteroid (prednisolone) to high-dose ICS and LTRA or long-acting B2-agonist (salmeterol, formoterol)
How is asthma managed pharmacologically in children aged 5-16 years?
- Short-acting B2-agonist (salbutamol)
- Add low-dose inhaled corticosteroid (budesonide, beclometasone, fluticasone, mometasone) or leukotriene receptor antagonist (montelukast)
- Increase to medium-dose ICS and stop LTRA; or keep low-dose ICS and add LTRA or long-acting B2-agonist (salmeterol, formoterol)
- Add LTRA/LABA in addition to medium-dose ICS
- Increase to high-dose ICS and LTRA/LABA; refer to specialist
- Add oral corticosteroid (prednisolone) to high-dose ICS and LTRA/LABA
What non-pharmacological steps can be taken to manage asthma?
Patient education
Personalised asthma action plan from Asthma UK
Ensure up to date with routine immunisations
Advise about trigger avoidance
Inhaler technique
What clinical features would indicate an asthma attack of moderate severity?
PEFR >50% Normal speech SpO2 >92% HR <140 (age 2-5yrs) or <125 (>5yrs) RR <40 (age 2-5yrs) or <30 (>5yrs)
What clinical features would indicate a severe asthma attack?
PEFR 33-50% Inability to complete sentences in one breath/too breathless to feed/talk SpO2 <92% HR >140 (age 2-5yrs) or >125 (>5yrs) RR >40 (age 2-5yrs) or >30 (>5yrs) Accessory muscle use
What clinical features would indicate a life-threatening asthma attack?
PEFR <33% SpO2 <92% Altered consciousness Exhaustion Cardiac arrhythmia Hypotension Cyanosis Poor respiratory effort Silent chest
How should a moderate exacerbation if asthma be managed?
Salbutamol with large-volume spacer (1 puff every 30-60 seconds up to 10 puffs, take 5 tidal breaths per puff)
Oxygen (keep SpO2>94%)
Consider hospital admission; nebulised ipratropium can reduce hospital admission
Oral prednisolone (3-7 days)
Consider Abx if clinical suspicion of bacterial infection
Once symptoms have subsided, advise to return to using salbutamol as required up to 4x/day (not exceeding 4-hourly)
Advise parents to monitor PEFR; safety net
If not admitted to hospital, follow up within 48hrs of presentation
How should a severe/life-threatening exacerbation if asthma be managed?
Give high-flow oxygen via Venturi mask or nasal cannula
Give nebulised salbutamol (5mg if >5yrs; 2.5mg if 2-5yrs) and ipratropium
Give oral prednisolone
Can give IM adrenaline
Give IV magnesium sulphate
Transfer to ICU
Follow-up within 2nworking days of discharge from hospital
Salmon-pink rash
Juvenile idiopathic arthritis (Stills disease)
Developmental milestones: gross motor at 6 weeks?
Head control begins
Developmental milestones: gross motor at 6 months?
No head lag
Sitting
Developmental milestones: gross motor at 12 months?
Pulls to standing
Cruises, walking
Developmental milestones: gross motor at 18 months?
Walks well
Runs
Developmental milestones: gross motor at 24 months?
Climbs stairs (2 feet/step) Kicks ball
Developmental milestones: gross motor at 36 months?
Stands on one leg
Climbs stairs in adult fashion
Developmental milestones: fine motor and vision at 6 months?
Full hand grip
Hand to hand transfer
Developmental milestones: fine motor and vision at 6 weeks?
Fixes and follows
Developmental milestones: fine motor and vision at 12 months?
Mature pincer grip
Object permanence
Pointing
Developmental milestones: fine motor and vision at 18 months?
Builds tower of 3 blocks
Hand preference
Scribbles
Developmental milestones: fine motor and vision at 24 months?
Builds tower of 7 blocks
Circular scribbles
Developmental milestones: fine motor and vision at 36 months?
Draws circle
Imitates bridge with blocks
Developmental milestones: language and hearing at 6 weeks?
Stills to sounds
Developmental milestones: language and hearing at 6 months?
Turns to sound
Babbles
Developmental milestones: language and hearing at 12 months?
First word
Responds to name
Developmental milestones: language and hearing at 18 months?
6-12 words
Follows simple instructions
Developmental milestones: language and hearing at 24 months?
2 word sentence
Developmental milestones: language and hearing at 36 months?
Speaks in sentences
Developmental milestones: social skills and self-care at 6 weeks?
Smiles
Developmental milestones: social skills and self-care at 6 months?
Laughs
Squeals
Developmental milestones: social skills and self-care at 12 months?
Waves
Peek-a-boo
Drinks from cup
Developmental milestones: social skills and self-care at 18 months?
Spoon feeding
Symbolic play
Developmental milestones: social skills and self-care at 24 months?
Starts toilet training
Removes clothes
Developmental milestones: social skills and self-care at 36 months?
Parallel play
Interacting
Sharing
Developmental warning signs at birth?
Asymmetric Moro reflex
Absent red reflex
Failed neonatal hearing test
Developmental warning signs at 10 weeks?
No head control
No smiles
Developmental warning signs at 6 months?
Primitive reflexes still present
Hand preference
Squint
Minimal response to people, toys or noise
Developmental warning signs at 12 months?
No sitting
No double babble (‘ma-ma’, ‘da-da’)
No pincer grasp
Developmental warning signs at 18 months?
Not walking
<5 words
Mouthing
Drooling
Developmental warning signs at 36 months?
No 2 word phrases
Not interactive
What is meningitis?
Inflammation of the meninges
Specifically, the leptomeninges, i.e. arachnoid and pia mater
What is the most common type of meningitis?
Viral
What is typically the most severe type of meningitis?
Bacterial
What are non-infectious causes of meningitis?
Malignancy
Autoimmune disorders
What viruses most commonly cause meningitis?
Enterovoruses
EBV
Adenoviruses
Mumps
What proportion of cases of bacterial meningitis in the UK are in children?
80%
What is the typical mechanism of meningitis in children?
- Bacteraemia
- Release of inflammatory markers and activated leukocytes; and endothelial damage
- Cerebral oedema, raised ICP, and reduced cerebral blood flow
What are the most common bacteria causing meningitis in neonates?
GBS
E. coli (and other coliforms)
Listeria monocytogenes
What are the most common bacteria causing meningitis in 1-month-olds to 6-year-olds?
Neisseria meningitides
Streptococcus pneumoniae
Haemophilus influenza
What are the most common bacteria causing meningitis in children over the age of 6 years?
Neisseria meningitides
Streptococcus pneumoniae
What is encephalitis?
Inflammation of the brain
Meninges are often affected too -> meningoencephalitis
What are the mechanisms of encephalitis?
- Direct invasion of the brain by a neurotoxic virus e.g. HSV
- Delayed brain swelling following a dysregulated neuroimmunological response to an antigen, usually a virus, such as chickenpox ( = postinfectious encephalopathy)
- A slow virus infection, such as HIV infection, or subacute sclerosing panencephalitis (SSPE) following measles infection
Based on the clinical features, what is a differential diagnosis for encephalitis?
Encephalopathy from a non-infectious cause, e.g. metabolic abnormality
How does meningitis tend to present?
Headache Photophobia Nuchal rigidity (not always in infants) Fever Shock Purpurin rash Positive Brudzinski/Kernig signs
How does encephalitis tend to present?
Fever
Altered/loss of consciousness
Seizures
What investigations should be done for potential meningitis/encephalitis?
Bloods - FBC, glucose and gas (for acidosis), coagulation screen, CRP, U&Es, LFTs
Cultures - blood/urine/throat swab/stool
Viral PCRs
Rapid antigen test for meningitis organsims - blood/CSF/urine
PCR of blood and CSF
Lumbar puncture
What are the contraindications to doing an LP?
Cardiorespiratory instability
Focal neurological signs
Signs of raised ICP (coma, raised BP, bradycardia, papilloedema)
Coagulopathy
Thrombocytopenia
Local infection at LP site
If doing an LP causes undue delay in starting antibiotics
What are the normal values for an LP?
WBCs: 0-5 /mm^3
Protein: 0.15-0.4 g/L
Glucose: >50% of blood
Clear fluid
What would the following lumbar puncture indicate?:
Turbid CSF
High WBCs (polymorphs)
High protein
Low glucose
Bacterial meningitis
What would the following lumbar puncture indicate?:
Clear CSF
Slightly high WBCs (lymphocytes)
Slightly high protein
Slightly low glucose
Viral meningitis or viral encephalitis
What would the following lumbar puncture indicate?:
Viscous CSF
Slightly high WBCs (lymphocytes)
Very high protein
Very low glucose
Tuberculous meningitis
How should meningitis be managed?
START ANTIBIOTIC TREATMENT WITHOUT DELAY
<3mo: IV ampicillin/amoxicillin + cefotaxime
>3mo: IV ceftriaxone
IV aciclovir if suspecting viral encephalitis
Supportive therapy
- Oxygen (reservoir rebreathe mask)
- Anticonvulsant therapy
- IV fluids: NaCl 0.9% and dextrose 5%
- Vasopressors if hypotensive without fluid resuscitation response
Dexamethasone
Notify Health Protection Unit
Follow-up
- By paediatrician 4-6 weeks after discharge
- Formal audiological assessment
Treat anyone who has had close contact with the patient within 7 days before onset with ciprofloxacin
When should dexamethasone be given in meningitis?
> 3mo and CSF analysis shows:
- frankly purulent CSF
- WBC > 1000/uL
- raised WBC + protein concentration > 1g/L
- bacteria on Gram stain
And no meningococcal septicaemia
->May reduce long-term complications such as deafness
How should encephalitis be managed?
Also treat for meningitis if any diagnostic uncertainty
IV aciclovir until cause is determined
- HSV encephalitis: high-dose IV aciclovir for 2-3 weeks
- CMV encephalitis: IV ganciclovir and foscarnet for 2-3 weeks
Supportive care in PICU
- I+V
- IV fluids
- reduce ICP if elevated
After acute phase, rehabilitation for both cognition/behaviour and motor/ambulatory
What are the potential complications of bacterial meningitis?
5-10% mortality
> 10% of survivors have long-term neurological impairment
- hearing impairment (due to inflammatory damage to cochleae hair cells)
- local cerebral infarction (resulting in epilepsy)
- cranial nerve palsies/focal neurological lesions (due to local vasculitis)
Hydrocephalus from impaired resorption of CSF or blockage of cerebral aqueduct/ventricular outlets by fibrin; may require ventricular shunt
Cerebral abscess, requiring drainage (space-occupying lesion)
Subdural effusion, may resolve spontaneously, may require neurosurgical intervention
What are the potential complications of untreated HSV encephalitis?
Mortality >70%
Almost all survivors have severe neurological sequelae
What is Brudzinski sign?
Flexion of the neck with the child supine causes flexion of the knees and hips
What is Kernig sign?
With the child lying supine and with the hips and knees flexed, there is back pain on extension of the knee.
What are differential diagnoses for neck stiffness?
Meningitis
Tonsillitis
Cervical lymphadenopathy
How should meningitis be managed if presenting in primary care?
Single dose of IM/IV benzylpenicillin (check for penicillin allergy - consider moxifloxacin or vancomycin)
Transfer to hospital
