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*Medicine: Paediatrics > Respiratory (2s + 3s) > Flashcards

Respiratory (2s + 3s) Flashcards

1
Q

Epiglottitis is a cellulitis of the supraglottis with the potential to cause airway compromise, and should be treated as a surgical emergency until the airway is examined and secured.

What organism most commonly causes epiglottitis?

A
  • haemophilus influenza type B
  • therefore a risk factor is non-vaccination with HiB vaccine
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2
Q

What is the clinical presentation of epiglottitis?

A
  • sore throat
  • dysphagia
  • drooling
  • toxic appearance
  • acute distress
  • fever
  • tripod position
  • difficulty breathing
  • muffled voice, stridor, irritability
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3
Q

If you suspect epiglottitis, what should you not do?

A
  • no action should be taken that could stimulate a child w/ suspected epiglottitis
  • do not examine throat, lie pt down, separate from parent or take blood as this may evoke complete airway obstruction
  • it’s a clinical diagnosis
  • lab or other interventions should not preclude or delay timely control of the airway in a suspected case of epiglottitis
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4
Q

What are the relevant investigations for epiglottitis?

A
  • laryngoscopy → key to confirming diagnosis, but also therepeautic as an airway can be established in same setting if a direct laryngoscopy comences, this should be performed in the OR as an emergency surgical airway can be obtained if endotracheal intubation is not possible
  • lateral neck radiograph → only to be obtained w/ HCP capable of securing airway with proper equipment available during the test
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5
Q

What is the management of epiglottitis?

A
  • secure airway + supplemental oxygen
    • if intubation not possible during laryngoscopy then tracheostomy
  • intravenous antibiotics → co-amoxiclav or ceftriaxone
  • adjuncts → corticosteroids, racemic epinephrine, prolonged intubation

The tracheal tube can normally be removed after 24hrs and the child has normally totally recovered in 2-3 days, Abx treatment continues for 3-5 days

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6
Q

Acute otitis media (AOM) is part of a spectrum of inflammatory conditions affecting the middle ear. These range from a single episode of AOM, recurrent episodes of AOM, otitis media with effusion (OME or ‘glue ear’) and chronic suppurative otitis media.

What are the risk factors for AOM?

A
  • day care attendance -> inc exposure to resp viruses
  • older siblings -> inc exposure to resp viruses
  • young age
  • family history
  • absence of breastfeeding
  • immunological deficiency

AOM is generally preceded by a viral URTI that causes congestion of the respiratory mucosa of the nasopharynx + eustachian tube.

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7
Q

80% of children experience at least one episode of AOM before the age of 2 years w/ a peak incidence between 6-11 months.

What are the most common causative organisms for Acute Otitis Media?

A
  • streptococcus pneumonia
  • haemophilus influenzae
  • moraxella catarrhalis
  • streptococcus pyogenes
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8
Q

What are the clinical features of acute otitis media?

A
  • ?preceding viral resp illness
  • acute onset otalgia (ear pain)
  • fever
  • irritability
  • crying
  • sleep disturbance
  • vomiting
  • poor appetite
  • physical examination → bulging, erythematous or opaque tympanic membrane, with impaired mobility, perforation can occur +/- purulent ear discharge
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9
Q

What investigations can be done for AOM?

A
  • rarely required
  • but culture of fluid taken directly from middle ear via tympanocentesis may be useful in immunocompromised children + those <6months, where AOM may be associated w/ an unusual or more invasive pathogen
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10
Q

What is the treatment for acute otitis media?

A
  • natural course of AOM is 3 days but can be up to 1 week
  • use analgesia + antipyretics for symptom control → paracetamol, NSAIDs, calpol
  • IF antibtioics then 5-day course of amoxicillin (*)
    • erythromycin or clarithromycin for penicillin allergies

(*) coming up on next cards

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11
Q

For acute otitis media, the use of antibiotics is more difficult given the self-limiting nature of the condition in most cases. Three separate antibiotic prescribing strategies may be used according to the age + clinical assessment of the child.

When should antibiotics be prescribed immediately?

A
  • if under 2 years w/ bilateral AOM
  • if presenting w/ AOM + ear discharge
  • if initially managed without abx but show no improvement after 4 days
  • if systemically unwell
  • if at high risk of complications due to immunocompromise or other PMHx
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12
Q

For AOM, when should there be no antibiotic prescribed?

A
  • most children + their parents can be reassured that abx are genrally not required in this condition
  • their use may be associated w/ side-effects such as n+v, rashes, diarrhoea + can contribute to antibiotic resistance
  • parents should be advised to re-present if symptoms worsen or if there is no improvement in 4 days
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13
Q

In certain situations it may be more practical to provide a delayed prescription for antibiotics. For AOM, when should there be delayed antibiotic prescibing?

A
  • prescription should be collected if there is no improvement after 4 days
  • significant worsening of symptoms at any stage

Any child w/ suspected acute complications of AOM (mastoiditis, meningitis or facial nerve paralysis) should be urgently referred for ENT assessment

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14
Q

Tonsillitis is inflammation of the palatine tonsils as a result of either bacterial or viral infection. It will often occur in conjunction w/ inflammation of other areas of the mouth, giving rise to terms tonsillopharyngitis (pharynx also involved) and adenotonsillitis (adenoids also involved).

What are the bacterial and viral organisms responsible for tonsillitis?

A
  • Bacterial →
    • group A beta-haemolytic streptococci (GABHS) (strep pyogenes)
    • group C beta-haemolytic streptococci
    • mycoplasma pneumoniae
    • neisseria gonorrhoea
  • Viral →​
    • adenovirus
    • epstein-barr virus
    • rhinovirus
    • coronavirus
    • enterovirus
    • influenza + parainfluenza

It is difficult to differentiate between viral or bacterial aetiology. Blood testing should include an infectious mononucleosis screen.

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15
Q

What are the clinical features of tonsillitis?

A
  • generally lasts 5-7 days
    • if >7 days → consider glandular fever
  • odynophagia + reduced oral intake
  • fever
  • halitosis
  • new onset snoring (or even apnoeic)
  • shortness of breath
  • physical examination → red inflamed tonsils, white exudate (pus) spots on tonsils, cervical lymphadenopathy (most commonly lymph nodes in the region of upper 1/3rd SCM)
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16
Q

Tonsillitis is a clinical diagnosis. Antibiotics will most likely benefit a patient when their sore throat is caused by streptococcal bacteria. Centor criteria will aid in the diagnosis or exclusion of GABHS-tonsillitis and determine whether antibiotics are an option.

What is the Centor criteria?

A

Was developed to try and differentiate between bacterial and viral tonsillitis based on clinical symptoms, there are four key criteria:

  • tonsillar exudate
  • tender anterior cervical lymphadenopathy or lymphadenitis
  • fever or history of fever
  • absence of cough

a score of 3 or more is highly suggestive of bacterial infection (40-60% likelihood) and a score of 2 or less suggests bacterial infection is unlikely (80% likelihood)

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17
Q

The first key decision for tonsillitis is whether the patient requires inpatient admission or not.

What factors suggest severe tonsillitis + an urgent admission and assessment?

A
  • resp compromise (tachypnoea, low sats, use of accessory muscles) or apnoeic episodes -> suggest tonsils are so large that they are affecting the child’s ability to ventilate, alternatively could be epiglottitis
  • pts who are unable to eat or drink are at risk of dehydration - they should be admitted for treatment + monitoring until able to drink again
  • pts who have been treated w/ appropriate antibiotics in community who are still not getting better should also be admitted for IV therapy + further investigation
18
Q

Paracetamol and iboprufen are effective pain relief in tonsillitis + can be alternated in order to give effective pain relief. Topical analgesia such as difflam (benzydramine) spray/mouthwash can be helpful to reduce pain and allow child to swallow oral analgesic agents.

What is the role of antibiotics in treating tonsillitis?

A
  • NICE recommend antibiotics should not be routinely given for tonsillitis
  • in pts fulfulling 3 or more Centor criteria, there is option of antibiotics to cover Group A strep
  • also abx for those systemically unwell, with complications (eg quinsy) or at serious risk of complications due to comorbidity
  • antibiotic of choice → penicillin
  • data suggests cephalosporins may be more effective (?)
  • co-amoxiclav often avoided due to small risk of permanent skin rash if tonsilitis is due to glandular fever
19
Q

Tonsillectomy is reserved for patients with recurrent, troublesome tonsillitis. What are the indications for tonsillectomy?

A
  • sore throats caused by tonsillitis
  • 5 or more episodes of sore throat per year
  • symptoms for at least a year
  • episodes of sore throat that are disabling + prevent normal functioning
20
Q

What is cystic fibrosis?

A
  • autosomal recessive condition
  • caused by mutatipon in CFTR gene
    • this receptor is responsible for the transfer of chloride ions out of the cell + inhibition of the adjacent epithelial sodium channel (ENaC)
    • bc no chloride pumped out of the cell + sodium floods into the cell uninhibited, the cell content becomes v concentrated w/ a high osmolality that draws water in from outside
    • results in thick dehydrated mucus -> builds up in lumens in body
  • more than 1600 known genetic mutations for CF w/ delta F508 mutation accounting for more than 70% of mutations in UK population
  • 1 in 25 caucasians are carriers + disease affects 1 in 2500 live births
21
Q

What is the pathophysiological impact of CF in the respiratory tract?

A
  • CTFR gene encodes CTFR protein - a chloride channel, present in numerous epithelial tissues
  • chloride driven against its concentration gradient using ATP
  • in airway, CTFR present on airway epithelial cells + submucosal glands
  • when defective → results in disruption to chloride ion movement + also affects sodium reabsorption → reduces amount of water in secretions
  • this results in reduced airway surface liquid
  • the airway surface liquid is an important component of the mucociliary escalator + has key immunological functions
  • effects of reduced airway surface liquid serve to impede mucus clearance
  • the altered lung environment provides a niche for bacterial growth
  • main infective agents are S. Aureus, H. Influenzae and P aeruginosa
22
Q

What is the pathophysiological impact of CF in the pancreas?

A
  • pancreatic duct usually occluded in-utero causing permanent damage to exocrine pancreas
  • rendering pts w/ CF ‘pancreatic insufficient’
  • pancreatic insufficiency is closely related to genotype
  • over time, endocrine pancreas affeced
  • 28% of those older than 10yrs requiring treatment for CF-related diabetes mellitus
23
Q

What is the pathophysiological impact of CF in the GI tract?

A
  • small intestine secretes viscous mucus which can cause bowel obstruction in-utero → can cause meconium ileus
  • in the biliary tree in-utero, CF can cause cholestasis → neonatal jaundice
  • later in life, same pathology → distal intestinal obstruction syndrome (DIOS) + CF-related liver disease
24
Q

What is the pathophysiological impact of CF in the reproductive tract?

A
  • 98% of men w/ CF are infertile
  • due to congenital absence of vas deferens
  • in women, nutrition likely to be an important predictor of successful pregnancy
  • it is suggested that timing of pregnancy be carefully planned
  • as pregnancy often associated w/ deterioration in lung health
25
Q

Clinical presentation of CF can differ depending on the age at which patients present.

What is the presentation in neonates?

A

Since the introduction of screening for CF in neonates (part of the Guthrie test) the majority of cases of CF are identified here (however, important to note that it is a screening test + still needs diagnostic testing)

  • meconium ileus - 10% of children present w/ abdominal distension, delayed passage of meconium + bilious vomiting in first few days of life
  • failure to thrive
  • prolonged neonatal jaundice
26
Q

What is the clinical presentation of CF in infancy?

A
  • failure to thrive
  • recurrent chest infections
  • pancreatic insufficiency: steatorrhoea
27
Q

What is the clinical presentation of CF in childhood?

A
  • rectal prolapse
  • nasal polyps (strongly suspect CF in children presenting w/ nasal polyps)
  • sinusitis
28
Q

What is the clinical presentation of CF in adolescence?

A
  • pancreatic insufficiency: diabetes mellitus
  • chronic lung disease
  • DIOS, gallstones, liver cirrhosis
29
Q

Clinical examination may be entirely normal, variably and often related to the severity of lung disease. What are some signs that can be elicted on investigation of a patient w/ cystic fibrosis?

A
  • hands: finger clubbing
  • face: nasal polyps
  • chest: hyperinflated, creps, portacath (indwelling vascular access device)
  • abdo: faecal mass (if constipated/DIOS), may have scar from ileostomy (meconium ileus)
30
Q

A diagnosis of CF can be made if there is a fitting clinical history and a positive chloride sweat test which may be supported by the identification of two identified mutations.

Patients with cystic fibrosis will end up having a large number of investigations, partly directed by their clinical condition and also as standard routine monitoring of the disease.

What should standard investigations include?

A
  • CXR → assess hyperinflation, bronchial thickening, some units undertake CT scanning
  • chloride sweat test → at diagnosis + annually if in receipt of CFTR potentiator/corrector therapy
  • microbiological assessment → eg. cough swab/sputum sample at every clinical encounter
  • glucose tolerance test → at annual assessment at teenage and beyond
  • LFT + coag → at annual assessment
  • bone profile → at annual assessment
  • lung function testing → spirometry/lung clearance index
  • faecal elastase → assess pancreatic fxn
  • chest CT → bronchiectasis
  • genetic analysis → assess for 1 or more of 32 mutations
31
Q

What is the chloride sweat test?

A
  • test measures electrolyte concentration in sweat
  • sweat sample collected by pilocarpine iontophoresis
  • common reason for failure of test is an insufficient sample in a small baby
  • a sweat chloride >60mmol/L is suggestive of CF
  • a sweat chloride of 40-60mmol/L is borderline + should be repeated
  • a single sweat test is not sufficient to diagnose CF
  • a second test or identification of genetic mutation should confirm diagnosis
  • there are number of reasons for false positives/negatives
32
Q

How do you manage CF lung disease?

A
  • monitored in young by observing symptoms + in older children by recording their FEV1
  • physiotherapy 2x / day to clear secretions
    • chest percussion
    • postural drainage
    • breathing exercises for older children
  • prophylactic anti-microbial therapy
    • oral abx eg. flucloxacillin → for S. Aureus prevention
    • nebulised abx eg. colomycin → for pseudomonas prevention
    • oral antifungals → for aspergillus prevention
  • acute infections need to be treated aggressively, typically w/ IV abx + supplementary O2
  • DNase (dornase alpha) + hypertonic saline
  • bronchodilators → airway dilatation, aiding clearance of resp secretions, particularly effective in those w/ concurrent asthma
  • lung transplant for terminal disease
33
Q

How do you manage nutrition in cystic fibrosis?

A
  • high-calorie diet (150% of normal) → needed due to malabsorption + raised metabolism due to chronic infection + resp work
  • pancreatic enzyme supplementation (creon) w/ every meal + snack
  • should encourage children to undertake physical exercise
  • fat-soluble vitamins (ADEK) poorly absorbed in those w/ pancreatic insufficiency, at least vitamins ADE should be supplemented
  • histamine receptor antagonist (eg ranitidine) + PPIs → aids absorption of creon by increasing duodenal pH
  • monitor growth
  • enteral feeding via gastrostomy in extreme cases of malnutrition
34
Q

What is small molecule therapy in CF?

A
  • medication for treating the defective protein itself
  • IVACAFTOR is licensed for individuals w/ gating mutations where CFTR molecule is made + inserted into the cell surface but does not work
  • Ivacaftor can induce a degree of normal function of protein:
    • improves weight gain
    • reduces exacerbation rates
    • returns sweat chlorides to a normal level
  • only suitable for roughly 5% of the CF population
35
Q

What are complications of cystic fibrosis?

A
  • allergic bronchopulmonary aspergiliosis (ABPA)
  • bronchiectasis
  • pneumothorax
  • rectal prolapse
  • distal intestinal obstruction syndrome (DIOS)
  • CF-related: cholestasis, gallstones, liver cirrhosis
  • CF related diabetes (CFRD)
  • delayed puberty
36
Q

What is the prognosis of CF?

A
  • death may be from pneumonia or cor pulmonale
  • 95% die from resp failure
  • most survive to adulthood (median survival >35yrs, >50yrs if born after 2000)
  • psychological morbidity very prevalent
37
Q

How does aspiration cause lung injury?

A
  • infection eg. recurrent pneumonia
  • chemical or physical trauma
  • obstruction leading to collapse
38
Q

What investigations need to be done for aspirational lung injury?

A
  • CXR → metal object will be radio-opaque ie will appear white on film, an object stuck withina bronchus can act as a ball-valve ie let air but not let it out, so lung will expand + the expanded lung will appear hyperlucent on xray and there may also be evidence of mediastinal shift to opposite side of expanded lung
    • a foreign body is more likely to fall into the right bronchus since it is straighter than left one
  • CT or MRI
  • bronchoscopy
39
Q

What is the management of aspirational lung injury?

A
  • removal during bronchoscopy
  • antibiotics if bacterial pneumonia
40
Q

How do you manage a choking child?

A
  • infants → back blows (abdo thrusts may cause intra-abdo injury)
  • older children → Heimlich manoeuvre
    • 1 hand made into fist, placed on abdo between umbilicus + xiphisternum, other hand placed on top of fist, both hands thurst into abdomen several times

*Medicine: Paediatrics (14 decks)

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