It’s Only Wheeze – Treatment Is Simple, Isn’t It?: Meredith Borland at DFTB19

Cite this article as:
Team DFTB. It’s Only Wheeze – Treatment Is Simple, Isn’t It?: Meredith Borland at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.20828

Meredith Borland is a paediatric emergency physician and the Director of Emergency Medicine at Perth Children’s Hospital in Perth, Western Australia. She was a founding member of the PREDICT Executive and is the current chair of PREDICT.

Last year at DFTB18, Meredith continued an ongoing discussion about the use of steroids in wheeze. This year, she took us on a journey through an emergency department visit for a number of children who may or may not receive various interventions. This was a fun, interactive and thought-provoking talk that highlighted some common differences in practice.

#doodlemed on this talk by @char_durand below

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

Bronchiolitis: Ed Oakley at DFTB19

Cite this article as:
Team DFTB. Bronchiolitis: Ed Oakley at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22370

When a medical student starts their paediatric ED rotation they need to know three key illnesses and that will cover the majority of patients that they see. To round out the ABC trifecta of asthma and crapping (acute gastroenteritis) we have bronchiolitis. At #DFTB19 Ed Oakley from PREDICT gave us the latest.

 

 

 

DoodleMedicine sketch by @char_durand-done live from Australia via the DFTB19 streaming video link!

 

 

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal. 

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

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Common Rashes Module

Cite this article as:
Aoife Fox. Common Rashes Module, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27731
TopicCommon rashes
AuthorAoife Fox
DurationUp to 2 hours
Equipment requiredNone
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Game
    Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

Definitions/rash description:

  • Macule: a flat area of colour change <1 cm in size (e.g., viral exanthem [such as measles and rubella], morbilliform drug eruption).
  • Patch: a large macule >1 cm in size (e.g., viral exanthem [such as measles and rubella], morbilliform drug eruption).
  • Papule: a raised area <1 cm in size (e.g., wart).
  • Nodule: a larger papule, >1 cm in size (e.g. nodular prurigo). 
  • Plaque: a flat-topped raised area (a cross between a nodule and a patch; e.g., psoriasis).
  • Vesicle: a small fluid-filled lesion (blister) <0.5 cm in size (e.g. varicella, eczema herpeticum).
  • Bulla: a larger vesicle >0.5 cm (e.g. bullous impetigo).
  • Pustule: a pus-filled lesion (e.g. folliculitis).
  • Wheal: a transient raised papule or plaque caused by dermal oedema (e.g. urticaria)
  • Scale: flakes of stratum corneum (e.g. eczema, psoriasis).
  • Crust: dried serum, blood, or purulent exudate on the skin surface (e.g. impetigo).
  • Erosion: loss of epidermis, heals without scarring (e.g. Stevens-Johnson syndrome, toxic epidermal necrolysis).
  • Ulcer: loss of epidermis and dermis, heals with scarring (e.g. venous ulcer, pyoderma gangrenosum).
  • Excoriation: loss of epidermis following trauma such as scratching (e.g. pruritus).
  • Fissure: a split in the skin (e.g. angular cheilitis, palmoplantar keratoderma).
  • Lichenification: thickening of the skin with accentuation of skin markings (e.g. chronic eczema, lichen simplex chronicus).
  • Purpura: an area of colour change (red or purple) due to bleeding into the skin; does not blanch on pressure (e.g. vasculitis, disseminated intravascular coagulation).
  • Petechia: a pin-point purpuric lesion (e.g.,vasculitis, disseminated intravascular coagulation).
  • Ecchymosis: a larger area of purpura (e.g. vasculitis, disseminated intravascular coagulation).
Some important points to note in history:
  • Where did the rash start?
  • Sequence of the rash?
  • Type of rash?
  • Time of onset and duration?
  • Involvement of palms and soles?
  • Involvement of mucous membranes?
  • Involvement of conjunctiva?
  • Desquamating?
  • Systemic involvement?
  • Associated symptoms – fever/cough/conjunctivitis/runny nose/sore throat/strawberry tongue/itchiness/pain/weakness/headache/lymphadenopathy/swollen extremities/nausea/vomiting/diarrhoea? 
  • Exposures – immunizations/pets/foreign travel/bites (insects/ticks)/recent injury to skin/sexual history/sick contacts?

Common childhood rashes

The terminology for all but fifth disease is not used anymore, however, should anyone be curious here they are:

Also known as..What causes it?When?What rash?Where is the rash?FeverAssociated findings
First diseaseMeaslesParamyxovirusWinter – spring Erythematous, confluent, maculopapularBegins at the hairline spreads inferiorlyHigh feverKoplik spots, cough, coryza and conjunctivitis, Forchheimer spots
Second diseaseScarlet feverStreptococcus pyogenesAutumn – spring Generalised erythema with a sandpaper textureBegins on the face and upper part of trunk and spreads inferiorlyHigh feverPastia lines, Forchheimer spots, strawberry tongue, exudative pharyngitis, abdominal pain, rheumatic fever, circumoral pallor
Third diseaseRubellaRubivirusLate winter – spring Rose-pink, maculopapularSpreads inferiorlySlightly high feverLymphadenopathy, arthralgias, Forchheimer spots
Fourth diseaseThe existence of “fourth disease” is controversial. It was described as a generalised maculopapular rash and desquamation. This exanthema may be staphylococcal scalded skin syndrome
Fifth diseaseSlapped cheekParvovirus B19Winter and spring“Slapped cheek” appearance, lacy reticular rashErythematous cheeks, reticular extremities Slightly high feverRash, waxes and wanes over weeks, arthritis, aplastic crisis
Sixth diseaseRoseola Human herpesvirus 6 and 7SpringRose-pink, maculopapularNeck and trunk High feverLymphadenopathy, febrile seizures, Nagayama spots
Others of note..ChickenpoxHerpes zoster virusLater winter and early springVesicles on erythematous base, crustsBegins on face and trunk and spreads centripetallyHigh feverPruritus
Hand-foot-and-mouthCoxsackie A virusLate summer or early winterElliptical vesicles on an erythematous base, oral vesicle, erosionsMouth, hands and feetHigh feverVesicles on the hands, feet and in the mouth

Forchheimer spots: rose coloured spots on the soft palate that may coalesce into a red blush and extend over the fauces

Koplik spots: clustered white lesions on the buccal mucosa. They are pathognomonic for measles.

Pastia lines: where pink or red lines formed of confluent petechiae are found in the skin creases.

Nagayama spots: erythematous papules on the mucosa of the soft palate and the base of the uvula. You may see these present on the fourth day in two thirds of patients with roseola.

(based on case from RCEM Learning RCEM Learning – Common Childhood Exanthems)

Mark is a 3-year-old boy brought to the ED by his mother with a rash, temperatures and decreased oral intake. His older brother has a similar rash and illness and mum reports that there was an outbreak of chickenpox in the older brother’s school. 

On exam you note a quiet child with a diffuse vesicular rash. On palpation he has generalised lymphadenopathy.

What are the differentials of chicken pox in this case?

What is the incubation period of chicken pox? How long will Mark be infective?

What investigations are necessary?

How would you manage this illness? What treatment would you give?

What patients would you give anti-VZV immunoglobulin to?

Mark’s mum tell you that she has a 2-week old baby at home – what will you do?

What complications of chickenpox can occur?

Mum tells you that the children’s childminder is pregnant what advice do you give?

Discussion point – Do you use NSAIDs?

(Diffuse) disseminated gonococcaemia

(Local) hand, foot and mouth (coxsackievirus)

(Local) herpes zoster

Staphylococcal bacteraemia

DFTB – Exclusion period for infections

The incubation period for chicken pox is usually 10-21 days. The infectivity period starts when symptoms first appear and lasts until all the lesions have crusted over. This is usually around 5-6 days after the onset of the illness, with most crusts disappearing by 20 days.

Chicken pox is a very common illness and the vast majority of cases can be managed symptomatically at home. Prolonged fever >4 days should prompt the suspicion of complications of varicella such as secondary bacterial sepsis. Under these circumstances, patients should be examined carefully with appropriate blood test work up and a chest x-ray, depending on their clinical presentation.

Oral acyclovir has been shown to reduce the effects of chicken pox, for example the number of lesions and duration of fever, if used within 24 hours of the onset of rash in immunocompetent children. Oral acyclovir has not been shown to reduce the incidence of varicella zoster virus pneumonia or other complications when compared to placebo. Cochrane results do not support the widespread use of acyclovir in immunocompetent children.

Pediatric EM Morsels – Chicken Pox

It is used for high risk patients including, immunocompromised children, newborns with maternal Varicella that develops 5 days before to 2 days after delivery, premature babies and hospitalized infants.

Paediatrics Open – Management of varicella in neonates and infants

Asymptomatic newborn in contact with VZV from any infected subject

The mother is proved seropositive:
Very low risk of disease in the baby.
No treatment should be provided.

Observance of the baby at home and encourage parents to come back if any clinical sign or symptom appears in the 2 weeks after contact.

The mother is proved seronegative or refuses testing:
Treat the baby with acyclovir PO 80 mg/kg/day divided into four doses to start 7 days after infective contact and administer during 7 days.

Careful surveillance of the baby during the risk period. Indication and duration of hospitalisation (with airborne and contact precautions) should be discussed in each case depending on child clinical status, parental compliance and social setting. If any doubt, hospitalisation with optimal medical surveillance are warranted during the risk period.

Pneumonia

Bacteraemia

Encephalitis

Bacterial superinfection of skin

Problems may arise where there is a failure to recognise the complications of secondary streptococcal or staphylococcal infections or to appropriately manage high-risk groups. A prolonged fever for more than 4 days in a child with chicken pox, for example, should prompt the suspicion of secondary bacterial complications.

A range of complications including pneumonia, bacteraemia and encephalitis are increasingly being recognised. Neurological complications may occur without a preceding rash.

The incidence of congenital varicella syndrome is low if maternal infection occurs before 20 weeks of gestation. Congenital varicella syndrome is associated with shortened limbs, skin scarring, cataracts and growth retardation.

RCOG – Chickenpox in Pregnancy

The childminder should contact her own GP. She should avoid contact with children until establishing her risk of contracting VZV. 

DFTB – Varicella and NSAIDs

There is a long history of anecdotal evidence associating invasive group A Strep (GAS) complications, or severe skin and soft tissue infections (SSTIs) with exposure to NSAIDs. 

There are currently 5 papers, ranging from 1997 to 2008 which try to answer this question. Almost all the studies used a case-control method to try and answer this question. Where they took a group of children who had varicella and the outcome of interest (invasive GAS infection, severe SSTI), and compared them to a group of children who had varicella and did not get these outcomes, seeing which groups were more likely to have had ibuprofen.

The studies are pretty heterogeneous, so unsurprisingly the results varied. These studies all found an association, but they generally all suffer from the same big problem, which is confounding by indication. It might not be that ibuprofen causes complications, but rather bad varicella needs ibuprofen, and is also more likely to get complications anyway. As the famous saying goes, “Correlation does not equal causation”. The absolute risk increase of GAS complications or SSTIs is 0.00016% in the worst case scenario. 

NICE advises against giving ibuprofen due to the uncertainty but you must risk assess the clinical scenario yourself. 

(Based on a case from the American Academy of dermatology – American Academy of Dermatology – Viral exanthems)

Caleb is a 9-year-old boy who presents for evaluation of fever and rash. His mother noted a fever of 40 °C two days ago. He appeared well and was eating and playing normally, so his mother was not alarmed. After the fever resolved, Caleb developed red rash that progressed rapidly over the past 24 hours.

What is the most likely diagnosis?

What are the differentials?

What is the cause of roseola?

Who gets it?

How is it spread?

What are the signs and symptoms of roseola?

How is it diagnosed?

What is the treatment?

What are the complications from roseola?

Roseola

Measles

Rubella

Erythema infectiosum (fifth disease)

It is caused most commonly by human herpesvirus 6 (HHV-6) and less commonly by human herpesvirus 7 (HHV-7).

Children aged 6 months – 4 years are most typically affected. Most children (86%) will have had roseola by the age of 1 year. It is rarely seen in adults and infection is thought to confer lifelong immunity.

It is spread person-to-person via the saliva of asymptomatic family members. The incubation period is 9-10 days.

It results in an acute febrile illness lasting between 3 and 7 days, which is then followed by the characteristic rash of roseola in around 20% of infected children. 

The prodrome to the rash is a high fever (39-40 °C), palpebral oedema, cervical lymphadenopathy and mild upper respiratory symptoms. The child appears well. As the fever subsites the exanthem appear. This consists of a pink macules and papules surrounded by white halos. It begins on the trunk and spreads to the neck and proximal extremities. Nagayama spots may occur on the soft palate and uvula. The rash is non-itchy, painless and does not blister.

Diagnosis is usually based solely on the characteristic history and physical exam. 

Roseola is usually benign and self-limiting. Rest, maintaining fluid intake and paracetamol for fever is all that is usually required. Treatment may be necessary for atypical cases with complications and immunosuppressed patients. 

Complications are rare in most children.  The most common complication is febrile convulsion that occurs in 5-15% of children.

Acute encephalitis, hepatitis, myocarditis, haemophagocytic syndrome and infectious mononucleosis-like illness occur very rarely. 

Reactivation of HHV-6 with drug exposure can lead to drug-induced hypersensitivity syndrome, which results in fever, rash, pneumonia, hepatitis, bone marrow suppression and encephalitis. 

Simple Febrile Convulsions generally occur in children aged from 6 months to 5 years. They are common affecting 1 in every 20 children. The most common causes are viral URTIs, ear infections, bacterial tonsillitis and UTIs. 

They are generalised seizures, which last less than 15 minutes and occur only once during 24 hours. 

The recurrence risk depends on child’s age at presentation: 1 year old: 50% recurrence;

2 year old: 30% recurrence

Where there are no neurodevelopmental problems and no family history of epilepsy, the subsequent risk of epilepsy is 1% (equivalent to the population risk).

A 5-year-old girl, Emma, attends the ED with after being unwell for the last 3 days. It initially started out with fever, headache and a sore throat. She then developed a rash 24 hours ago. Her parents report that the rash started on her abdomen and spread to the neck and arms and legs and it feels rough to touch. 

On exam she has a sandpaper type rash on her trunk and limbs which is more pronounced in flexures. 

What is the most likely diagnosis?

What other symptoms might Emma have?

What is it caused by?

What are the differential diagnoses?

How is the diagnosis confirmed? What investigations will you do?

What is the treatment? Why do you treat?

Discussion point – Evidence for antibiotic therapy 

What are the possible complications? How can you categorise them?

What advice do you give to Emma’s parents in order to prevent transmission of Scarlet fever?

Is there anything else you need to do?

Scarlet fever 

The symptoms of Scarlet fever start with fever (over 38.3°C), sore throat and general fatigue/headache/nausea. 12-48 hours later a rash appears on the abdomen and spreads to neck and extremities. 

Characteristic features of the rash are a rough texture (like sandpaper) and worse in the skin folds e.g. groin, axilla, neck folds (Pastia’s lines). 

Other symptoms include white coating on tongue which then peels and leaves a ‘strawberry tongue’; flushed red face with perioral pallor and cervical lymphadenopathy. Most symptoms resolve within a week. After the symptoms have resolved it is common to get peeling on the fingers and toes. 

In Emma’s case the other symptoms that you would look for are – cervical lymphadenopathy, white tongue or strawberry tongue and a flushed face with peri-oral pallor. 

Scarlet fever is caused by the bacterium Streptococcus pyogenes (also known as group A streptococcus, or GAS). It can be found on the skin or in the throat, where it is usually unproblematic in asymptomatic carriers – 20% of children are colonized. 

However, certain virulent forms of S. pyogenes carry genes that code for streptococcal superantigens, including pyrogenic exotoxins, which can cause non-invasive infections such as scarlet fever. The typical rash is caused by the exotoxin.

They include measles, glandular fever, slapped cheek infections, other viral pathogens, Kawasaki disease, staphylococcal toxic shock syndrome, and allergic reactions.

The diagnosis is clinical. A throat swab is not routinely recommended, although during specific outbreaks Public Health England might advise this.

Streptococcal antibody tests are used to confirm previous group A streptococcal infection. They may be of value in patients with suspected acute renal failure, acute glomerulonephritis or rheumatic fever.  

Antistreptolysin O (ASO) test is the most commonly available streptococcal antibody test. ASO titres peaks 2-4 weeks after an acute infection and returns to normal over the next 6-12 months. Streptolysin O is produced by almost all strains of S. pyogenes (group A streptococci) and many group C and group G beta-haemolytic streptococci. 

Anti-deoxyribonuclease B (anti-DNase B (ADB)) titres rise after both pharyngeal and skin infections. DNase B is produced by group A streptococci and is therefore more specific than the ASO antibody test.

General guidance for patients may include advice on rest, drinking plenty of fluids, good hygiene measures to minimise the risk of cross-infection, and the use of paracetamol to reduce discomfort and high temperature.

Overall, the evidence base for the management of scarlet fever is limited, and there is a need for more evidence of the benefits and harms of antibiotics.

Public Health England, NICE and the Department of Health in Western Australia recommend treating people with scarlet fever with antibiotics regardless of severity of illness to speed recovery, to reduce the length of time the infection is contagious, and to reduce the risk of complications.

Recommended antibiotic therapy is Penicillin V QDS x 10/7 or azithromycin OD x 5/7 if penicillin allergic. 

Complications of Scarlet Fever are much the same as complications of strep tonsillitis. They are divided into suppurative, and nonsuppurative.

Suppurative complications occur due to the infection spreading and include otitis media; mastoiditis; sinusitis; peritonsillar abscess; meningitis; endocarditis; retropharyngeal abscess; and invasive group A strep (IGAS).

Non-suppurative complications occur later and occur mainly in untreated patients. They are rheumatic fever and post-strep glomerulonephritis.

IGAS is not common in children, but those at increased risk are children with co-morbidities, immunocompromised children, and those with co-existing chickenpox.

(DFTB – Exclusion period for infections)

Children should be excluded from school until they have had 24 hours of antibiotics.

Check if you need to contact the public health authorities – scarlet fever is a notifiable disease in many jurisdictions e.g. England, Wales, Northern Ireland and Western Australia. 

(Based on Life in the Fast Lane case – LITFL – Kawasaki Disease)

Alex, a 4 year-old boy has been brought to the emergency department by his worried parents. He has had fevers for the past 6 days. They are concerned because he is not getting better despite repeated visits to a number of doctors. Each time they were told he had a viral illness.

On examination you note the presence of bilateral conjunctivitis, and erythematous rash on his torso and limbs, a 4 cm tender left-sided cervical lymph node and a diffusely red pharynx.

What is the most likely diagnosis?

How is the diagnosis made?

Who gets this condition?

What are the important differential diagnosis?

What investigations should be performed?

What complications may occur?

What specific treatment is required?

Discussion point – Incomplete Kawasaki Disease: Another child, Sarah, attends the ED with 6 days of fever. On exam you find a strawberry tongue and cervical lymphadenopathy >1.5cm. No other signs of Kawasaki disease are present. What might you consider?

Discussion point – Is there a roll for steroids in Kawasaki disease?

Kawasaki disease, also known as Mucocutaneous Lymph Node Syndrome, this vasculitic disorder was first described by Dr. Tomisaku Kawaski in 1967. It is of uncertain etiology, but may be a post-infectious condition.

The diagnosis is made on the basis of the following clinical criteria (A + B):

A.Fever ≥5 days
B.At least 4 of the 5 following physical examination findings:
1.Bilateral, nonexudative bulbar conjunctival injectionbilateral scleral injection with peri-limbic sparing
2.Oropharyngeal mucous membrane changespharyngeal erythema, red/cracked lips, and a strawberry tongue
3.Cervical lymphadenopathywith at least one node >1.5 cm in diameter
4.Peripheral extremity changesacute phase: diffuse erythema and swelling of the hands and feetconvalescent phase: periungual desquamation (weeks 2 to 3)The diffuse palmar erythema seen in KD is in contrast to the discrete macular lesions of various viral illnesses (e.g., measles) that can sometimes be seen on the palms and soles.
5.A polymorphous generalized rashNon-vesicular and non-bullousThere is no specific rash that is pathognomonic for KD

The manifestations may appear sequentially rather than concurrently. Atypical cases may not meet all the criteria but may still have the same risks of cardiac complications. These 

‘incomplete’ cases occur more often in infants less than 6 months-old — further investigations (see Q5) should be performed if fever of 5 days and 2 or 3 of the other criteria are present.

Kawasaki disease may occur in any child of any age, and even adults in some cases. However, it is more common in:

  • children aged < 5 years
  • child of Asian descent
  • males (RR 1.5)

Diagnosis may be difficult as Kawasaki disease may mimic a number of other conditions:

  • Viral exanthemas including measles
  • Streptococcal disease (e.g. scarlet fever, toxic shock syndrome)
  • Staphylococcal disease (e.g. scalded skin syndrome, toxic shock syndrome)
  • Bilateral cervical lymphadenitis
  • Leptospirosis and rickettsial diseases
  • Stevens-Johnson syndrome and Toxic Epidermal Necrolysis
  • Drug reactions including mercury hypersensitivity reaction
  • Juvenile Chronic Arthritis

Echocardiography —
this is the most important investigation to assess for cardiac complications.
If no abnormalities on presentation the study should be repeated in 4-6 weeks.

Laboratory tests
Rule out other causes:
— ASOT, AntiDNAse B, throat swabs, blood cultures
Non-specific findings seen in Kawasaki disease include:
— FBC: normochromic anaemia and leucocytosis; thrombocytosis (in the 2nd week)
— LFT changes and hypoalbuminemia
— increased CRP and ESR
— Sterile pyuria of ≥10 WBCs per high-power field

Cardiac complications:

  • Carditis during the febrile phase
    — myocarditis with ST-T changes (25%), pericardial effusions (20-40%), valvular dysfunction (1-2%) and cardiac failure (~5%)
  • Coronary vessel abnormalities (occur in 20% of cases if untreated and <5% if treated; peaks at 2-4 weeks)
    — aneurysm formation may lead to fatalities from thrombosis, rupture or ischemia-related dysrhythmia (usually within 6 weeks of onset, but may occur many years later.

Kawasaki disease is a vasculitis that can potentially affect almost any organ, it is commonly associated with:

  • arthritis
  • keratitis and uveitis
  • diarrhoea, vomiting and gallbladder disease
  • coryza and cough

IV immunoglobulin and aspirin

IV immunoglobulin

  • 2g/kg IV over 10 hours
  • ideally start within 10 days of the onset of the illness
  • a second dose may be given if fevers persist

Aspirin

  • 3-5 mg/kg PO daily for 6-8 weeks
    (when laboratory parameters have fully normalised)
  • some advise higher doses of aspirin until the patient is afebrile or 48-72 hours, but others argue this offers no benefit in addition to treatment with IV immunoglobulin.

Despite these therapies 2-4% of cases still go on to develop coronary artery abnormalities. Corticosteroids may be considered in refractory cases, although there is little evidence supporting their use.

Another child, Sarah, attends the ED with 6 days of fever. On exam you find a strawberry tongue and cervical lymphadenopathy >1.5cm. No other signs of Kawasaki disease are present. What might you consider?

Incomplete Kawasaki disease

DFTB – Kawasaki Disease

Very easily missed
Makes up 15-20% of all cases
Patients with incomplete KD, particularly those <6 months of age and older children, may experience significant delays in diagnosis and these children are at high risk of developing coronary artery abnormalities.

Consider KD if:

  • Infants <6 months old with prolonged fever and irritability
  • Infants with prolonged fever and unexplained aseptic meningitis
  • Infants or children with prolonged fever and unexplained or culture-negative shock
  • Infants or children with prolonged fever and cervical lymphadenitis unresponsive to antibiotic therapy
  • Infants or children with prolonged fever and retropharyngeal oroparapharyngeal phlegmon unresponsive to antibiotic therapy

Fever and pyuria in an infant or young child may be diagnosed as a urinary tract infection, with subsequent development of rash, red eyes, and red lips attributed to an antibiotic reaction. Irritability and a culture-negative pleocytosis of the cerebrospinal fluid in an infant with prolonged fever suggestive of aseptic meningitis (or if antibiotics have been given, partially treated meningitis) may cause a diagnosis of KD to be overlooked. Cervical lymphadenitis as the primary clinical manifestation can be misdiagnosed as having bacterial adenitis. Gastrointestinal symptoms are considered for surgical causes, other physical findings of KD can be overlooked.

Toxin-mediated illnesses, such as group A streptococcus infections (e.g. toxic shock syndrome and scarlet fever) can also present with fever, rash, mucous membrane involvement and abnormal extremity findings. Desquamation in Kawasaki disease tends to affect the hands and feet as it does in scarlet fever and toxic shock syndrome; however, in Kawasaki disease, it usually begins in the periungual region. In scarlet fever, the desquamation tends to be diffuse and flaking, whereas in Kawasaki disease it tends to be sheet-like.

BMJ – Kawasaki disease

Children with measles and Kawasaki disease tend to be very irritable and inconsolable. It can be difficult securing the diagnosis of Kawasaki disease as the clinical features may appear sequentially rather than at the same time. In Kawasaki disease there may be presence of erythema and induration at the BCG immunisation site as there is cross reactivity between the heat-shock protein and the T-cells of patients with Kawasaki disease. 

The temperature in measles may exceed 40°C but tends to fall after day 5 of the illness. Koplik spots are not seen in Kawasaki disease and the morbilliform rash of measles begins from the ears and hairline and starts to fade by day 4; after day 7 brownish staining may be seen due to capillary haemorrhage. Desquamation in severely affected cases of measles can occur but is not seen in the hands and feet. In measles, clinical improvement typically begins within 2 days of appearance of the rash.

This table can help distinguish between differentials:

(Cochrane – Using steroids to treat Kawasaki disease)

A Cochrane review published January 2017 concluded “steroids appear to reduce the risk of heart problems after Kawasaki disease without causing any important side effects. They also reduce the length of symptoms (fever and rash), length of hospital stay, and blood markers associated with being unwell. Certain groups, including those based in Asia, those with higher risk scores, and those receiving longer steroid treatment, may have greater benefit from steroid use, especially with decreasing rates of heart problems, but more tests are needed to answer these questions”.

What disease is associated with dermatitis herpetiformis?

A: Herpes

B: Coeliac disease

C: Atopic dermatitis

D: Melanoma

The correct answer is B.

In coeliac disease, there are IgA antibodies against gluten that cross-react with reticulin fibres that anchor the basement membrane to the dermis. Thus, IgA is deposited at the tips of dermal papillae, presenting as grouped pruritic vesicles, papules or bullae. Usually found on elbows.

What is the most common causative agent of erythema multiforme?

A: Penicillin and sulphonamides

B: Systemic lupus erythematosus

C: HSV infection

D: Malignancy

The correct answer is C.

HSV is the most common etiologic agent of EM, which presents as a targetoid rash and bullae. All the other options are also associated with the disorder, but less commonly.

What disorder is characterised by an initial ‘herald patch’ which is then followed by scaly erythematous plaques usually in a ‘Christmas tree’ distribution?

A:    Pityriasis rosea

B:    Herpes

C:    Varicella zoster virus

D:   Erysipelas

The correct answer is A.

Pityriasis rosea classically presents with a salmon coloured solitary patch ‘herald patch’ which enlarges over a few days followed by generalised bilateral and symmetric macules with collarette scale. Pruritus is sometimes present. It itself resolves within 6 – 8 weeks.

What is the infective agent implicated in acne? 

A: Staphylococcus aureus

B: Streptococcus pyogenes

C: Staphylococcus epidermidis

D: Propionibacterium acnes

The correct answer is D.

Propionibacterium acnes infection produces lipases resulting in inflammation and breakdown of sebum, leading to pustule formation.

Which of the following statements about the treatment of measles is correct?

A: No specific antiviral therapy is recommend for immunocompetent patients 

B: Prevention of spread of measles depends on prompt immunization of people at risk of exposure or people already exposed who cannot provide documentation of measles immunity

C: Recommend supportive care with antipyretics, fluids and rest

D: All of the above

The correct answer is D.



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Asthma Module

Cite this article as:
Miriam Saey Al-Rifai. Asthma Module, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27232
TopicAsthma
AuthorMiriam Saey Al-Rifai
DurationUp to 2 hours
Equipment requiredNone
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

Joseph, a 10 year old boy comes into the ED. He is a known asthmatic on treatment. He appears breathless with an audible wheeze. He is able to talk in complete sentences. He has a RR of 25, sats of 94%, pulse of 100 and his PEF is 60% of normal.

What is the severity score of this child’s asthma presentation?

What investigations and treatment options should you consider?

How do you decide when it is safe to discharge home?

The boy is 3 years old with the same presentation – his mum asks you if her son has asthma. What is your response?

When seeing a child with an acute asthma attack, the initial assessment is key to establishing the severity of the attack as this influences ongoing management. 

The following clinical signs should be recorded:

Pulse rate – Increasing tachycardia generally denotes worsening asthma; severe airway obstruction can result in pulsus paradoxus and a fall in heart rate in life-threatening asthma is a preterminal event.

Respiratory rate and degree of breathlessness –  Ie too breathless to complete sentences in one breath or to feed.

Use of accessory muscles of respiration – subcostal, intercostal recessions, tracheal tug. You can also assess by palpation of neck muscles. Also consider including a prolonged expiratory phase.

Amount of wheezing – which might become biphasic or less apparent with increasing  airways obstruction. Silent chest is an indicator of life threatening asthma. It is important to auscultate and document any improvement with treatment.

Degree of agitation and conscious level – always give calm reassurance.

Observations

  • Include general observations.

CXR

  • NOT routinely advised. A chest X-ray should be performed if there are persisting unilateral signs suggesting pneumothorax, inhaled foreign body, lobar collapse or consolidation and/or life-threatening asthma not responding to treatment.

Blood Gas

  • Only indicated if not responding to treatment or needing further escalation of care

Oxygen 

  • If any life threatening features or sats <94%. Aim for sats 94-98%

Inhaled β2 agonist 

  • Salbutamol up to 10 puffs via spacer (1 puff = 5 breaths) assess after 15 mins and repeat if necessary. If sats <94% use,or patient refusal/poor inhaler technique use salbutamol nebulisers (2.5 – 5mg).
  • Continuous nebulisation may be better, as intermittent may result in rebound bronchoconstriction. 

Ipratropium Bromide 

  • If symptoms are refractory to initial β2 agonist treatment, add ipratropium bromide (250 micrograms/dose mixed with the nebulised β2 agonist solution) every 20-30 mins for the first two hours in severe asthma attacks. This should then be tapered to 4-6hrly before being discontinued. However, there are no clinical trials supporting ipratropium use beyond the first hour or first 3 doses in children (EMCases).
  • In a systematic review and meta-analysis comparing the use of beta-agonists plus anticholinergics with beta-agonists alone, combination therapy was associated with significantly lower hospitalisation rates and improvements in asthma scores and pulmonary function test results (EMCases).

Oral steroids 

  • Give oral steroids in the management of acute asthma attacks. Dexamethasone is starting to be used more, as a once only dose, but there is no evidence for benefit over Prednisolone, so not recommended yet. 

Nebulised Magnesium 

  • Nebulised magnesium sulphate is not recommended for children with mild to moderate asthma attacks. The RCT entitled MAGNETIC trial in 2013 of about 500 children showed that MgSO4 nebulisers added to the salbutamol and ipratropium bromide nebuliser in the first hour, for kids with acute severe asthma, significantly improved asthma severity scores without any increase in adverse events.

Antibiotics 

  • Insufficient evidence to refute or recommend.

Burst therapy – improves forced expiratory volume with an earlier peak response, and prevents deterioration between doses. Salbutamol 100 mcgs x 10 puffs via inhaler & spacer every 20 mins for 1 hour. Add ipratropium bromide 20 mcgs (x 4 puffs < 5 years, x 8 puffs > 5 years) together with salbutamol as above for severe cases.

BTS/SIGN – Children can be discharged home once requiring no more than 3-4 hourly inhalers (based on a randomised controlled study in 1999), PEF >75% and sats >94% . 

Safe follow up

  • Reducing regime of salbutamol inhaler therapy with a clear plan as to when to come back to hospital (ie. requiring >10 puffs in 4 hours)
  • Ensure good inhaler technique/correct fitting spacer mask. Advise to use the B-agonist BEFORE the inhaled steroid and to wash the mouth out after the steroid inhaler to prevent thrush.
  • If the parent/carer of the child smokes, advise them to stop.
  • Address potentially preventable contributors to the exacerbation, such as exposure to trigger factors
  • Ensure the patient is discharged home with 3-5 days oral steroids. Some trusts are now given single dose Dexamethasone, although prednisolone is still in the national guideline (https://www.stemlynsblog.org/dexamethasone-asthma-children/). 
  • Primary care follow-up in 24-48hrs
  • If second attack in 12 months refer to a secondary care asthma clinic.

Wheeze is a common presentation in the ED and its diagnoses and management differs depending on the age of the child and the detail in the history (Snelson et al, 2019). 

An age based approach to wheeze in children

Bronchiolitis

  • Slow onset of symptoms. 3-4 day period of worsening cough, poor feeding, wheeze and respiratory distress due to inflammation of the airways.

Viral Wheeze

  • Rapid onset of wheeze and respiratory distress over hours due to bronchospasm.

Asthma

  • Described above. 

The age based approach to wheeze can be explained by the changes in a child’s immune system:

  • At birth and in the first few months, immunity is largely provided by maternal antibodies. These antibodies offer protection from most simple viral infections. Acute atopic IgE mediated reactions are very rare. If infections do occur it is likely to be serious bacterial infections. In addition the baby’s own immune system is not yet fully turned on and the response to infection is therefore muted, making the recognition of sepsis difficult in this age group.
  • Preschool age children no longer rely on maternal antibodies. However, their own immune system is still not fully developed. They compensate for this by having heightened and indiscriminate responses to infections. They produce lots of white blood cells, but do not yet have circulating antibodies. You are more likely to see associated problems of viral infections in this age group like transient synovitis. Atopy is becoming more common now. Sepsis is also difficult to recognize in this age group due to the extreme reaction to often uncomplicated viral infections. These children present with viral wheeze. It is worth knowing that there are wheezy presentations in this age group that can look a lot like viral wheeze.  These include bronchomalacia, acute allergy, and cardiac failure due to e.g. acute myocarditis.
  • Older children have a more mature immune system and response to infection is like that of an adult. As the response to infection is less vigorous and indiscriminate than the pre-schoolers, some specific infections like Varicella can cause severe reactions in these children. These children are more likely to have asthma. True asthma is rarely seen under the age of 5 as it requires a fully matured immune system to develop.

Management

  • By looking at the history we can direct our inhaled beta agonist treatment to one that matches a story consistent with bronchospasm. This would include children with likely viral wheeze and asthma.  
  • The best evidence for the use of oral steroids for viral wheeze between the ages of 1 and 5 would suggest that the following group are most likely to have a small benefit (https://gppaedstips.blogspot.com/search/label/Asthma):
  • Children with a diagnosis of asthma
  • Children who have required substantial amounts of inhaled beta-agonist prior to presentation
  • Children whose severity and lack of response to treatment with beta-agonists requires admission to hospital
  • Joseph has presented with features of a moderate asthma attack
  • This can be managed with beta 2 agonist therapy and oral steroids
  • Once Joseph does not need beta 2 agonist bronchodilation for more than 4hrs and obs remain stable he can be safely discharged home with safe follow up.
  • The 3 year old presenting with the same symptoms of sudden onset wheeze and breathlessness, likely has a diagnosis of viral wheeze. They would benefit from beta 2 agonist bronchodilation. They are too young to be diagnosed with asthma, but risk factors for developing asthma could be explored in the history.

Leila, a 13 year old female, known asthmatic on treatment, presented to ED breathless and finding it hard to speak in full sentences. Her oxygen saturations are 92%, HR 130 and RR 35

What is the severity score of this child’s asthma presentation?

What investigations and treatment options should you consider?

When do you need to re-assess response to treatment to decide on discharge vs escalation?

  • In this instance, Leila falls into the acute severe asthma presentation. 
  • As her sats <94% oxygen needs to be given via a facemask. 
  • Beta 2 agonist bronchodilator via a nebuliser (preferably oxygen driven) to be given due to sats <94% and she falls into the severe category. 
  • Oral steroids must be given. This can be given as IV Dexamethasone if too unwell/vomiting.
  • Re-assess response to treatment after 15 minutes. 
  • If no improvement after 15 minutes give a further two beta 2 agonist nebulisers and add Ipratropium Bromide nebuliser. 
  • A consideration of nebulised Mg can be given in acute severe asthma.
  • Plan for admission, escalate and refer to paediatrics for consideration of second line treatment.

Do you know how to use a spacer?

Leila has not improved despite the treatment given in ED as outlined in case 2. Her sats are now 89%, she appears cyanosed and has a poor respiratory effort. On auscultation her chest is quiet. What are the next steps that need to be taken?

How would you rate the severity score of this presentation?

What investigations or treatment needs to be considered?

Which IV medications if any should be used? 

Which important differentials need to be considered?

What escalation plans need to be put in place?

Children with continuing severe asthma despite optimal first-line treatments, frequent nebulised β2 agonists and ipratropium bromide plus oral steroids, and those with life-threatening features, need urgent review by a specialist with a view to management in an appropriate high-dependency area or transfer to a paediatric intensive care unit to receive second-line intravenous therapies. It is important to do a blood gas prior to starting bronchodilators to measure the pCO2 and also to monitor side effects of salbutamol (decreasing potassium and lactic acidosis).

PERUKI (Paediatric Emergency Research in the UK and Ireland network) is a research collaborative of paediatric-specific and mixed adult and paediatric emergency departments (EDs). In 2015 PERUKI carried out a study looking at the variation in practise of the use of IV bronchodilators as a second line treatment in the management of acute asthma in children. There was a large discrepancy between what clinicians felt was the appropriate management and what they actually administered. A survey of 183 clinicians in 30 EDs revealed that when escalating to intravenous bronchodilators, 99 (54%) preferred salbutamol first line, 52 (28%) magnesium sulfate (MgSO4) and 27 (15%) aminophylline. 87 (48%) administered intravenous bronchodilators sequentially and 30 (16%) concurrently, with others basing approach on case severity. 146 (80%) continued inhaled therapy after commencing intravenous bronchodilators. 

Of 170 who used intravenous salbutamol, 146 (86%) gave rapid boluses, 21 (12%) a longer loading dose and 164 (97%) an ongoing infusion, each with a range of doses and durations. Of 173 who used intravenous MgSO4, all used a bolus only. What this demonstrates is the considerable variability in practise and opinion. 

So what is the evidence? (Cochrane review)

IV salbutamol 

  • There have not been enough trials to form a robust evaluation of its benefits.

IV MgSO4 

  • Appears to be safe and beneficial in severe asthma

IV aminophylline 

  • Improves lung function within 6hrs. However, there is no apparent reduction in symptoms, number of nebulised treatments or length of hospital stay. We do not know the impact on oxygenation, PICU admissions or need for NIV. 

IV ketamine 

  • There has only been 1 study conducted, which reveals no known benefit in non intubated children. 

In one RCT comparing IV aminophylline, salbutamol and magnesium in 100 children, a bolus of magnesium sulphate was shown to reduce clinical symptoms faster than the other treatments. There were no significant side effects documented in the magnesium sulphate group. A systematic review of four paediatric trials comparing IV salbutamol with IV aminophylline demonstrated equivalence.

In children who respond poorly to first-line treatments, consider the addition of intravenous magnesium sulphate as first-line intravenous treatment (40 mg/kg/day).

Consider early addition of a single bolus dose of intravenous salbutamol (15 micrograms/kg over 10 minutes) in a severe asthma attack where the child has not responded to initial inhaled therapy. It is not clear whether IV bolus vs infusion is more beneficial. Prior to IV salbutamol administration insure blood potassium is checked and on cardiac monitor. If using an IV infusion monitor lactate to check for toxicity. 

Consider aminophylline for children with severe or life-threatening asthma unresponsive to maximal doses of bronchodilators and steroids. Some of the side effects include abdominal pain, anxiety, headache, nausea, palpitations and seizures. Toxicity can occur with aminophylline. This presents as vomiting (which may be severe and intractable), agitation, restlessness, dilated pupils, sinus tachycardia, and hyperglycaemia. More serious effects are haematemesis, convulsions, and supraventricular and ventricular arrhythmias. Severe hypokalaemia may develop rapidly especially in combination with salbutamol.

Ensuring you have appropriately assessed and optimised their condition

Reassess the patient?

  • Consider revisiting history, respiratory examination and consider adjuncts to assessment such as a capillary or venous blood gas.

Have you exhausted medical management?

  • ? adrenaline ? ketamine ?heliox 

What could be missing? 

  • Consider your confidence of whether you have the right diagnosis or if there is a need to assess for a secondary pathology such as pneumonia, foreign body, anatomic airway anomalies, airway compression by masses/lymph nodes, cardiac disease? Some can be excluded with a good history. Do you need to further investigate with bloods, CXR? Do you need to append your management and provide antibiotic coverage? Do you need to assess for a complication from treatment e.g. pneumothorax.

Escalation options

  • Have you sought a senior review/notified the admitting paediatrician?
  • Do you need an ICU consult, NETS consult or retrieval to a tertiary centre?
  • How long are you comfortable to wait to see if there is a response to IV bronchodilation?

Non invasive ventilation 

  • Is there any evidence in acute asthma attack?
  • What settings/mode would you use?

Does this child need to be intubated?

  • How would you determine this?
  • Who should be involved in the conversation? Who should perform the intubation?
  • What sedation would you use?
  • What equipment would you use?
  • What settings would you use?

Alternative treatment options

Adrenaline

Give for severe or life threatening asthma – if the diagnosis is in doubt. 

Asthma and atopy often co-exist – and in these patients death from anaphylaxis is more likely. So if a patient fails to respond to initial therapy, the diagnosis of anaphylaxis needs to be considered. In addition nebulised Adrenaline causes bronchodilation.  

Heliox 

May improve respiratory score, but it probably won’t reduce the risk of admission. Nor should you use it in routine asthma to stave off intubation (PEMBlog). Can be considered in the ICU setting with maximum oxygen therapy has failed. 

Ketamine

Limited number of trials with mixed outcomes on the benefits of Ketamine. However, it is safe at dissociative dosages, and is a reasonable option when all others measures have failed.

NIV

A few case reports and observational studies of the use of BiPAP in pediatric asthma show some promise. The one RCT of only 20 patients does show a benefit in clinical asthma scores, respiratory rate, and supplemental oxygen need. There is no evidence that it prevents the need for intubation (Basnet S et al, 2012).

Critical care input is the next step for children with severe asthma not responding to treatment or with any life threatening features. There are a number of ongoing trials on the use of ketamine, sevofluorane and NIV, but the evidence is currently lacking so they’re not recommended by BTS/SIGN.

A 15 year old male has been brought into resus with features of life threatening asthma. Pre hospital the paramedics gave continuous salbutamol nebulisers, 500mcg Ipratropium nebulisers and 0.5mg IM Adrenaline. The attending medical team in resus administered 2g IV Mg over 20 mins and a bolus of 250mcg IV Salbutamol. The patient then became unresponsive with no respiratory effort.

What are the next steps that need to be taken?

What is the ‘deadly triad’ in asthma?

What are the key ALS modifications in asthma arrest?

In the pre-hospital setting, paramedics usually give IM Adrenaline to cover for the possibility of a diagnosis of anaphylaxis. 

In this case the patient has arrested. As soon as this has been identified, CPR needs to be initiated as per the ALS guidelines.

The cause of cardiac arrest in asthma is a result of the ‘deadly triad’:

Important modifications and considerations in managing cardio respiratory arrest in asthma (RCEMLearning – https://www.rcemlearning.co.uk/foamed/arrest-asthma/):

  1. Intubate Early

Due to the need for high inflation pressures, an endotracheal tube (ETT) is needed. In addition this protects the airway from the increased risk of regurgitation and aspiration.

  1. Ventilate with caution

The European Resuscitation Council recommends 8-10 breaths per minute with the lowest tidal volume required to see the rise and fall of the chest, to avoid dynamic hyperinflation. Tachypnoea must be avoided as this reducses expiratory time, thus increasing the residual volume in the alveoli. This auto PEEP increases intrathoracic pressure which reduces venous return, impeding CPR. 

  1. Manual chest deflation

If the patient has a hyperinflated chest/poor excursions of the chest wall, disconnect the ETT and apply manual pressure to the patient’s chest to expel the trapped air. 

  1. Consider tension pneumothorax

If ETT disconnection does not improve ventilation, consider performing a bilateral thoracostomy.

  1. Rehydrate

Dehydration and reduced intravascular volume compromises effective CPR. It also causes mucus to be thicker which can plug small airways. So ensure you give IV fluids. 

  1. GIVE ADRENALINE! – Utilise its bronchodilator effect. 

In an acute asthma exacerbation in children, monitoring the oxygen sats is important because:

A: Hypoxaemia is an early sign of clinical deterioration 

B: Sats <95% may suggest the need for prolonged bronchodilator therapy

C: Hypoxaemia occurs in the presence of life threatening asthma. Children may have normal sats for some time before critical desaturation occurs.

D: Sats >96% supports the decision to safely discharge home

The correct answer is C.

In an acute asthma attack hypoxic vasoconstriction occurs. This is coupled with decreased blood flow to the under ventilated lung (matching pulmonary perfusion with alveolar ventilation). 

In the hospital setting SaO2<91% may be a helpful predictor of prolonged frequent bronchodilator therapy more than 4 hours and SaO2 of <89% is associated with a need for bronchodilator therapy over 12 hours.

Hypoxaemia and hypocarbia only occur in the presence of life threatening asthma. Children may have normal sats for some time before critical desaturation occurs. Whilst low oxygen saturations mean that a patient is unwell it should be clinically obvious at this point.  Low oxygen saturations may also represent a degree of mucus plugging that may be helped with repositioning.

Hyperoxia can lead to absorption atelectasis as well as intra-pulmonary shunting with subsequent reduction in cardiac output. In addition concerns have been raised that oxygen administration may lead to potential delay in recognising clinical deterioration.

What is an appropriate length of time to stretch children in the ED prior to discharge?

A: After two sets of 3-4hrly inhaler/nebulisers

B: After they reach the first 3-4 hrs post last inhaler/nebuliser

C: After two sets of 3hrly

D: After 1 hour, if obs are completely normal and has had a consultant review

The correct answer is B.

BUT this is based on a randomised control trial in 1999. The most recent study in 2018 suggests that there is no benefit to 4hours vs 3hrs, and in fact 3 hrs post inhalation resulted in a reduction in length of stay. A recent retrospective analysis study in Australia looked at discharging children after 1 hour. They suggested that children that were clinically ‘well’ at 1 hour were likely to go home and if they were showing any moderate symptoms at one hour would likely need to be admitted. There is no strong evidence or recent studies, which is why there is such variation in practice. 

Under what circumstances would you choose to administer a beta agonist via nebuliser as opposed to a pMDI with a spacer?

A: When the child has become more tachycardic with worsening salbutamol induced tremor

B: In severe or life threatening asthma or when under the age of 1yrs old/learning difficulties

C: If the pMDI is ineffective

D: Some departments prefer nebulisers as it is cheaper than inhaled preparations

The correct answer is B.

Cochrane review 2013 – “Metered-dose inhalers with a spacer can perform at least as well as nebulisation in delivering beta-agonists in children with acute asthma”

Salbutamol has systemic side effects – tremor and increased pulse rate were more common when using nebulisers. SIGN/BTS guidelines state to give nebulisers in severe or life threatening asthma. Nebulisers are also preferential in very young children, or those with learning difficulties, as coordinating breathing with an inhaler can be difficult. Cost savings can be made with inhaled preparations. 

When is intubation indicated in paediatric asthma presentations?

A: When the HR > 160 OR the RR > 60

B: When you have given all first line and second line treatment and trialled NIPPV and the patient has still not improved. 

C: The child looks exhausted with worsening hypercapnia and changes in mental status. 

D: When the child has a history of fast deterioration and need for intubation

The correct answer is C.

Up to 26% of children intubated due to asthma suffer complications including pneumothorax, impaired venous return, and cardiovascular collapse because of increased intrathoracic pressure. Mechanical ventilation during an asthma exacerbation is associated with an increased risk of death and should therefore be a last resort. The decision to intubate should be based on clinical judgement as opposed to any one observation or blood result. Some variables to consider for intubation are worsening hypercapnia, patient exhaustion and changes in mental status (EMCases).

You have a 4 yr old, with two days of wheeze, coryzal symptoms and one day of increased work of breathing symptoms. You suspect that this may be viral induced wheeze. How do you manage this child?

A: Burst therapy with salbutamol. 

B: 6-10 puffs of salbutamol and reassess. If severe symptoms give oral steroids. 

C: Humidified air nebuliser and antipyretics for fever. 

D: 6-10 puffs of salbutamol and Ipratropium bromide nebuliser. If severe symptoms give oral steroids.

The correct answer is B.

At what age would it be appropriate to consider a trial of ventolin for potential viral induced wheeze? 

  • (Note – This is a good opportunity to survey your team and colleagues to see what the practice is at your local department). 
  • Regarding this grey area question, in Australian practice, some clinicians will trial salbutamol for potential viral induced wheeze if the child is 12 months or older. Other doctors may wish to trial if the child is slightly younger (e.g. from 10 months) if they have a strong family history of asthma and atopy or if they have had previous ventolin use reported by their family with good effect. The younger the child is, the less likely that the story and case is to fit viral induced wheeze.

If you are not sure if the child is presenting with asthma or viral induced wheeze, but they are displaying severe symptoms – it is advisable to give steroids. But be cautious in giving too many courses of steroids if presenting frequently to the ED.

M Balfour-Lynn (1996) Why do viruses make infants wheeze?, Archives of Disease in Childhood  74: 251-259

MO Stormon, CM Mellis, PP Van Asperen, HA Kilham (2002) Outcome evaluation of early discharge of asthmatic children from hospital: A randomized control trial, Journal of quality in clinical practise, Vol 19, issue 3, 149-154

Huay-ying Lo, Amanda Messer, Jennifer Loveless, Esther Sampayo, Robert H. Moore, Elizabeth A. Camp, Charles G. Macias and Ricardo Quinonez (2018) Discharging Asthma Patients on 3-Hour β-Agonist Treatments: A Quality Improvement Project, Hospital Pediatrics, 8 (12) 733-739

Basnet S, Mander G, Andoh J, Klaska H, Verhulst S, Koirala J (2012) Safety, efficacy, and tolerability of early initiation of noninvasive positive pressure ventilation in pediatric patients admitted with status asthmaticus: a pilot study. Pediatr Crit Care Med 13(4):393-8.

Snelson, E (2019) A simple model for understanding the causes of paediatric wheeze, Paediatrics and Child Health, Volume 29, Issue 8, Pages 365-368

DFTB – Managing acute asthma, Simon Craig (2017)

DFTB – Asthma for ambos (2016)

DFTB – Are nebulisers or spacers better for managing acute asthma (2013)

DFTB – The curious incident of the wheeze in the night

PEMBLOG – Heliox in the emergency department (2017)

EMCases – Management of acute paediatric exacerbations (2016)

BTS/SIGN British guideline on the management of asthma in children (2019)

PaediatricFOAM – ventilation strategies for the critically ill asthmatic (2019)

RCEMLearning – Arrest in asthma

gppaedstips.blogspot.com – The NYCE guideline for viral induced wheeze – Let’s clear a few things up (2019)



Please download our Facilitator and Learner guides

Bronchiolitis Module

Cite this article as:
Tessa Davis. Bronchiolitis Module, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27061
TopicBronchiolitis
AuthorTessa Davis
DurationUp to 2 hours
Equipment requiredNone
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

A 7 month old infant presents on Day 4 of the illness. He has mild to moderate work of breathing. Sats 95% in air. He is taking around half his normal feeds.

What investigations and treatment options should you consider?

Why doesn’t salbutamol work in this age group?

How do you know when to admit?

See the PREDICT systematic review of all treatments

  • Salbutamol – there is no benefit in using salbutamol in infants with bronchiolitis (and some evidence of adverse effects)
  • Nebulised adrenaline – no clinically useful benefit (there is evidence for temporary effect but not for improvement in outcome)
  • Nebulised hypertonic saline – there is weak evidence of a reduction in length of stay of 0.45 days. However when two studies were removed, both of which used a different discharge criteria than most hospitals, there was no benefit. This is not recommended routinely, although the authors suggest that it should be used only as part of an RCT
  • Glucocorticoids – no benefit
  • Antibiotics – not recommended (The risk of a secondary bacterial infection is very low, and there is potential harm from giving antibiotics)
  • Oxygen – no evidence of benefit in infants with no hypoxia, and low level evidence that maintaining the sats over 91% with oxygen actually prolongs the length of stay. There are no reports of long-term adverse neurodevelopmental outcomes in infants with bronchiolitis, however there is also no data on the safety of targeting sats <92%. Commence oxygen therapy to maintain sats over 91%.
  • Sats monitoring – there is moderate evidence suggesting that continuous sats monitoring increases the length of stay in stable infants
  • High flow – there is low to very-low level evidence of benefit with high flow
  • Chest physiotherapy – not recommended
  • Saline drops – routine saline drops are not recommended but a trial with feeds may help
  • Feeds – both NG and IV are acceptable routes for hydration

See Beta receptor mythbusting (from https://gppaedstips.blogspot.com/)

A 6 month old infant presents on Day 3 of the illness. She has moderate to severe work of breathing. Sats are 91% in air. She is struggling to feed at home.

What management options would you consider?

See the PARIS Paper

This is the biggest and most robust trial yet done to assess the value of high-flow in bronchiolitis. The primary outcome shows that there is a role for high-flow in the non-ICU management of this disease. Importantly PARIS has shown in a large cohort of children that high-flow, when used within the parameters of the trial protocol, does not lead to an increase in adverse events which in-turn suggests the increased patient:nurse ratios for kids on high-flow that are often mandated by hospital policies may not be necessary (depending on the severity of disease of course). Some caution must be used around the potential for erroneous use of the high-flow circuits themselves and the interpretation of early warning scores in the context of high-flow use.

PARIS was supported with significant nursing education resources potentially reducing errors to a level that were below what could be expected with the standard resourcing of mixed EDs and other environments where high-flow use in children may be infrequent. As with many grey areas in medicine protocols as to how we use high-flow vary by institution with little more than opinion to guide them.

Though neither the intention nor the conclusion of this paper in showing the progress of such a large number of children on high-flow, this trial also provides a basis for more robust decision making around how we use high-flow itself.

NICE feeding guidance

  • Give fluids by nasogastric or orogastric tube in children with bronchiolitis if they cannot take enough fluid by mouth.
  • Give intravenous isotonic fluids (see the NICE guideline on intravenous fluids therapy in children) to children who: do not tolerate nasogastric or orogastric fluids; or have impending respiratory failure.

Do you know how to set up high flow? (8 minutes)

How to set up Airvo 2 (Optiflow)  (3.5mins)

How to use Airvo 2 (6 mins)

You have a 12 month old, with two days of coryza and one day of increased work of breathing symptoms.

How do you manage them?

How do you figure out whether they have bronchiolitis or VIW?

Practically speaking, we know that bronchiolitis and viral induced wheeze have two quite different management pathways, but it is not as if a child moves from being 12 months old to 13 months old and therefore cannot have bronchiolitis (or vice versa for viral induced wheeze). These conditions as previously mentioned, exist on a spectrum. 

  • What has been the onset of symptoms? Progressive over days is most consistent with bronchiolitis. Onset of wheeze and respiratory distress over hours is most consistent with bronchospasm (viral induced wheeze).
  • What has been the pattern of their work of breathing? 
  • How significant is the work of breathing? 
  • What are the auscultation findings – is there presence of focal findings? Wheeze? Crackles? 
  • Is this affecting the child functionally with feeding or sleeping difficulties?
  • If auscultation is suggestive of possible viral induced wheeze or at least, a component of wheeze that may be responsive to bronchodilators (If wheeze is present and no crackles or focal findings) and presuming the child has more than just mild work of breathing -then we suggest this may be a possible candidate for viral induced wheeze.  
  • (Note – This is a good opportunity to survey your team and colleagues to see what the practice is at your local department). 
  • Regarding this grey area question, in Australian practice, some clinicians will trial salbutamol for potential viral induced wheeze if the child is 12 months or older. Other doctors may wish to trial if the child is slightly younger (e.g. from 10 months) if they have a strong family history of asthma and atopy or if they have had previous ventolin use reported by their family with good effect. The younger the child is, the less likely that the story and case is to fit viral induced wheeze.

It would be prudent to give 6 puffs (or do you use another number?) and reassess following to see if there is any improvement or change.

You’ve started high flow 2L/kg for a four month old with bronchiolitis, moderate work of breathing and saturations of 88% and titrated FiO2 up to 30% to maintain saturations. However they are still intermittently desaturating so you titrate them up to 40% FiO2.

They have ongoing work of breathing with a respiratory rate of 60-70.

What are your next steps?

Consider revisiting history, respiratory examination and consider adjuncts to assessment such as a capillary or venous blood gas.

  • For example, Do they have an NG tube on free drainage, are they nil by mouth and on IV fluid support at ⅔ maintenance
  • Are their family actually compliant with this or have also been feeding them via a bottle? 
  • Are they working harder to breathe because they are getting “hangry” and might actually tolerate a continuous NG or comfort feed?
  • Consider whether the HFNP has led to no change, improvement and then deterioration or simple worsening of symptoms due to patient distress.
  •  If no improvement was observed on commencement – it may be worth de-escalating them – ie. lower flow rates or low flow nasal prongs

Consider your confidence of whether you have the right diagnosis or if there is need to assess for a secondary pathology such as pneumonia, foreign body, cardiac contribution? Do you need to further investigate with bloods, CXR? Do you need to append your management and provide antibiotic coverage? Do you need to assess for a complication from treatment e.g. pneumothorax.

  • Have you sought a senior review/notified the admitting paediatrician?
  • Do you need an ICU consult, NETS consult or retrieval to a tertiary centre?
  • How long are you comfortable to wait to see if there is a response to high flow?
  • What settings would you start on?
  • Where could you move up to (in terms of peep, FiO2)
  • How soon would you reassess – what are you looking for?

  • How would you determine this?
  • Who should be involved in the conversation? Who should perform the intubation?
  • What sedation would you use?
  • What equipment would you use?
  • What settings would you use?

In bronchiolitis, children do not respond to salbutamol because:

A: They don’t have beta receptors until they are older.

B: The beta receptors are immature and do not begin functioning correctly until the child is older.

C: The large amount of secretions interfere with it and prevent it binding to the receptors

D: There is no bronchospasm for the salbutamol to act on.

The correct answer is D.

All humans have beta receptors. Foetuses develop them from around 15 weeks gestation and are therefore born with them. Developing beta receptors after 1 year of age is a common paediatric myth! In fact, in bronchiolitis, there is no bronchospasm in the same way as there is in viral induced wheeze. Bronchiolitis is a illness developing gradually over 4 days and then slowly improving. Patients have increased mucous rather than bronchospasm, which does not respond to a bronchodilator.

A 3 month old baby presents to ED with coryza, cough, and poor feeding. Breastfeeding is going ok, but the baby is feeding for shorter periods, more frequently than usual. She is having wet nappies as normal. Saturations are 93% on room air, RR is 62, and there is moderate subcostal recession with some nasal flaring. Which of the following is an indication to admit this baby to hospital?

A: The reduced breastfeeding

B: The oxygen sats

C: The work of breathing

D: The age of the baby

The correct answer is C.

The criteria for admission usually are:

  • feeding less than half of usual, or less wet nappies
  • saturations less than 92% on air
  • increased WOB
  • apnoeic episodes

Risk factors such as:

  • Ex-prem
  • Age less than 12 weeks or less than 37 weeks CGA
  • history of lung disease or congenital heart disease or neurological problems
  • smoke exposure

In clinical practice, you would use your judgement to assess if hospitalisation was necessary. Social concerns should always be considered.

In this case, the baby is maintaining good urine output and the feeds, although shorter, are more frequent. The age alone is not an indication for admission. Obviously, an O2 requirement would be an indication for admission but most units would consider sats of 92% or less as reduced. There is significantly increased work of breathing with recession and nasal flaring, however, so this would be the main indication for admission.

You have a 10 month old baby with bronchiolitis who is to be commenced on high flow. Which of the following is false?

A: Nasal prongs size should be estimated based on the width of the patient’s nostrils.

B: Patients can be NG fed immediately once on high flow. 

C: High flow improves the functional residual capacity.

D: The humidified oxygen help clearing mucous secretions.

The correct answer is B.

Patients on high flow will likely need an NG inserted due to abdominal distention, but should usually not be fed for the first couple of hours on high flow. The aim of high flow is to provide humidified, high flow to improve clearance of secretions and to increase the functional residual capacity. Together this should reduce the work of breathing.



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Managing cough: Adam Jaffe at DFTB19

Cite this article as:
Team DFTB. Managing cough: Adam Jaffe at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22157

Adam is a respiratory physician at Sydney Children’s Hospital. He spoke about all things wheezy in Melbourne for DFTB18.  In this talk from our London conference, he deals with that bane of parents’ lives – the coughing child.

 

 

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal. DFTB20 will be held in Brisbane, Australia.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

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Selected references:

Chang AB. Cough, cough receptors, and asthma in children. Pediatric pulmonology. 1999 Jul;28(1):59-70.

The high yield respiratory examination: David Krieser at DFTB19

Cite this article as:
Team DFTB. The high yield respiratory examination: David Krieser at DFTB19, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.21344

One of the challenges of paediatrics is how to distill a life of experience down to something more tangible. When you are asked “How did you know s/he was sick?” you need to be able to give a better answer than “I just know”. In this session from DFTB19  we challenged three clinicians to explain just why they think the way they do.

Wheeze. It’s all in the timing…

Cite this article as:
Patrick Aldridge. Wheeze. It’s all in the timing…, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.21378
You’ve just treated a 5 year old with their second episode of wheeze this year. They’ve had burst therapy,  and are now one hourr post treatment with no work of breathing, scattered wheeze on auscultation and oxygen saturations of 95%. You contemplate giving them steroids and decide against it.

The Medicines Handbook: Simon Craig at DFTB18

Cite this article as:
Team DFTB. The Medicines Handbook: Simon Craig at DFTB18, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.20590

Ask any paediatrician what the hardest, tricksiest procedure that you might ever have to perform and they would all be in agreement – calculating drug doses in the middle of a paediatric resuscitation. In this talk Simon Craig, from Monash, takes us through the how we can do better than scratching out rough calculations on the whiteboard at 6am. He asked the key question…

 

 

 

 

 

This talk was recorded live at DFTB18 in Melbourne, Australia. With the theme of ‘Science and Story‘ we pushed our speakers to step out of their comfort zones and consider why we do what we do. Caring for children is not just about acquiring the scientific knowhow but also about taking a look beyond a diagnosis or clinical conundrum at the patient and their families.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

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*Lori was once one of Andy Tagg’s trainees but he is quick to point out that none of the situations depicted are about him.

 

Exercise induced wheeze: Rob Roseby at DFTB18

Cite this article as:
Team DFTB. Exercise induced wheeze: Rob Roseby at DFTB18, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.20582

Associate Professor Rob Roseby is a respiratory physician. You might see many adults huffing and puffing around the local park every Sunday, bright red in the face, gasping for breath. This shouldn’t be the case for the children in their charge. In this talk Rob reminds the reluctant athletes in the audience that exercise and sport is good for children – both in terms of mental health and physical health. 

 

So, should we prescribe sport for our younger patients? Does it actually make a difference? And if they can’t play the sport that they love how can we get them back to it? Listen to this talk from Rob to find out how we can make that all important difference

 

 

 

This talk was recorded live at DFTB18 in Melbourne, Australia. With the theme of ‘Science and Story‘ we pushed our speakers to step out of their comfort zones and consider why we do what we do. Caring for children is not just about acquiring the scientific knowhow but also about taking a look beyond a diagnosis or clinical conundrum at the patient and their families.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

iTunes Button
 

 

*Lori was once one of Andy Tagg’s trainees but he is quick to point out that none of the situations depicted are about him.

 

Mentoring in Medicine: Melanie Rule at DFTB18

Cite this article as:
Team DFTB. Mentoring in Medicine: Melanie Rule at DFTB18, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.20557

Mel Rule is one of the founding members of the extraordinary WRaPEM group. They are a group of passionate educators and clinicians waim to bring back Wellness, Resilience and Performance coaching for the everyday doctor.