10-16 Pediatric pulmonology Flashcards
- Acute infections of the upper respiratory tract.
- General and the types of infections
- Common cold
- Sore throat (pharyngitis, including tonsillitis)
- Acute otitis media
- Sinusitis
- Acute epiglottitis
- Rhinovirus
- Influenza (parainfluenza)
- Adenovirus
- Enterovirus
- RSV
- Coronavirus
-The common cold
- This is a viral infection of the upper respiratory tract that affects the nose, throat and sinuses.
- The classic feature is that of clear or mucopurulent (indicating possible bacterial secondary infection) nasal discharge
- The most common pathogen is rhinoviruses, coronaviruses and respiratory syncytial virus
- Pain is best treated with paracetamol, cough may persist for weeks after
Pharyngitis and tonsillitis
- Pharyngitis commonly known as sore throat, is an inflammation of the pharynx, resulting in a sore throat. Thus, pharyngitis is a symptom,
- Mostly due to adenovirus, enterovirus and rhinovirus
- In the older children group A beta-hemolytic strep is a common bacterial pathogen, although uncommon under the age of 3
- Tonsillitis is a form of pharyngitis where there is inflammation of the tonsils, this is only possible in children older than 6months as before the children have tiny tonsils that do not become inflamed.
- It is not really possible to distinguish between bacterial and viral inflammation of the tonsils,
- headache, apathy, abdominal pain and white tonsillar exudate are all more common in the bacterial form, however a lack of these features does not exclude a bacterial infection
- Penicillin V or Erythromycin should be given if bacterial infection is suspected. Amoxicillin is best avoided as it may cause widespread maculopapular rash.
- Scarlet fever is occasionally a secondary consequence of group A streptococcal infections, most common in ages 5-12.
A fever appears along with a sandpaper like maculopapular rash with flushed cheeks and a white swollen tounge.
-Group A strep can also cause IgA glomerulonephritis and endocarditis and as such should be treated.
Treatment should be delayed until culture confirms diagnosis (even when fever, swollen lymph nodes and tonsillar exudate there is only a 66% chance of bacterial infection).
If confirmed dosage is:
- Penicillin VK 40mg/kg/day PO for twice daily 10 days
Or second line
- Clindamycin 20mg/kg/day PO three times daily for 10 days
- Or Erythromycin 40mg/kg/day PO three times daily for 10 days
- Acute otitis media
- most common ages 6-12 months, up to 20% will have three or more episodes
- Pain in ear and fever are the most common features, every child with fever should have tympanic membrane examined
- Most common pathogens include RSV and rhinovirus, and bacteria such as pneumococcus
- Serious complications include mastoiditis and meningitis
- Treat with paracetamol or ibuprofen, ABs do not reduce risk of hearing loss
- Consider delayed prescription amoxicillin
- Recurrent infections can lead to otitis media with effusion (glue ear), children may have decreased hearing in some cases
- Gromets can be inserted in recurrent cases
- Antibiotics are rarely indicated for acute otitis media, only consider if under 2 years and bilateral or otorrhea AND has lasted more than 3 days. In which case, can give:
- Amoxicillin
- 1-11 months 125mg 3x daily for 5-7 days
- 2-4 years 250 mg 3x daily for 5-7 days
- 5-17 years 500 mg 3x daily for 5-7 days
- Second line Clarithromycin
-Sinusitis
- Generally rare, swelling and tenderness over the sinus is common, note frontal sinuses do not develop until late in childhood
- Treat with Clindamycin
Stridor
Stridor is not an infection per se, rather it is a symptom precipitated by a number of infectious processes. It is a harsh musical sound due to partial obstruction of the lower portion of the upper airway (trachea and larynx). The most common cause is laryngeal and tracheal infection, where swelling can rapidly occlude the airway.
-Severe obstruction causes cyanosis, tachypnoe, tachycardia and agitation with central cyanosis suggesting severe hypoxia.
The most common cause is viral laryngotracheobronchitis (aka Croup), rarer causes include epiglottitis, bacterial tracheitis, foreign bodies, allergic laryngeal angioedema and a small host of other causes.
There are four grades of stridor:
- I - on inspiration only
- II - inspiration and on passive expiration
- III - inspiration and on active expiration
- IV - as III and recessions, cyanosis and tiredness
Treatment of stridor is with full monitoring of oxygen levels, -dexamethasone, 0.6mg/kg single dose, and in severe cases with race epinephrine in severe cases, 0.25-0.5ml in 2.5ml saline with a nebulizer.
laryngotracheobronchitis (croup)
is the most common cause of stridor. It is commonly caused by parainfluenza, rhinovirus and influenza virus. Typical features include hoarseness, a barking cough (like a cute sea lion), harsh stridor and all of the above symptoms of stridor. The child can usually be managed at home, although those under 1 year should be readily admitted. Inhalation of warm moist air is common but not shown to be beneficial. Oral dexamethasone, prednisolone or budesonide as a nebulizer are first line therapy.
-Symptoms are worse at night due to decreased cortisol levels.
Acute epiglottitis
Acute epiglottitis is a medical emergency with intense swelling of the epiglottis and surrounding tissues. It is caused by H influenzae type b (Hib), there is universal immunization in infancy that has led to more than 99% reduction in incidence. Onset is very acute, with high fever in very ill looking child, intensely painful throat that prevents speech or swallowing of saliva while cough is minimal or absent. Child should have airway secured by senior ENT surgeon, paediatrician and anaesthetist.
- NOTE - IF THEY HAVE ACUTE EPIGLOTTIS DO NOT LOOK IN THROAT, INCREASES RISKS OF SPASM AND AIRWAY COLLAPSE - As a result, you should also not look in throat for STRIDOR
- Children may present with ‘Tripod’ sign, where they hyperextend their neck and put their arm down to support themselves.
Foreign body aspiration
This is when an object is inhaled and becomes lodged in a child’s airway or lungs.
-Diagnosis can be through the observation of child swallowing food or object closely followed by respiratory distress, alternatively Chest X-ray, Inspiratory and expiratory phase x-ray and
bronchoscopy can all help with diagnosis. FB aspiration is most common aged 1-3 as this is the ‘mobile and stupid’ age!
Suspicion of FB aspiration is raised with sudden paroxysms of coughing when not directly supervised or after eating. FBs generally fall directly down into the right bronchus (anatomically straighter), of greater risk is if the FB is too large and blocks the trachea, causing total respiratory failure.
- Management of the obstruction depends on the location. -Laryngeal and subglottic FBs need urgent intervention in the form of tracheostomy or urgent bronchoscopy,
- while FB in the broncohus causes less of a problem.
-Rigid bronchoscopy offers good visualization and is the preferred method for FB removal in neonates and children.
- Acute pneumonia
- General
- clinical features
- Diagnosis
- classification
Acute Pneumonia
Pneumonia is the leading infectious killer of children under the age of 5. The most common etiologies in children vary based on age, lets take a look:
-Newborns - organisms from mothers genital tract, particularly group B strep, but also gram -ve enterococci and bacilli
-Infants and young children - respiratory viruses, such as RSV are most common, but other causes include streptococcus pneumoniae or Haemophilus influenzae. Bordetella pertussis and chlamydia trachomatis are also possible
- Children under 5, one should suspect Mycoplasma pneumoniae, streptococcus pneumoniae and chlamydia pneumoniae.
-Pneumonia is lung inflammation due to infection with alveolar consolidation in the presence of fever and/or acute respiratory systems with evidence of parenchymal infiltrates on chest radiograph.
-Clinical features are as expected, fever, cough, tachypnoea, accessory muscles in breathing.
-A chest x-ray is the first line method for confirming the diagnosis, although this cannot reliably tell the difference between bacterial and viral. Additional tests include nasopharyngeal aspirate, blood tests, full blood count and acute-phase reactants can all be performed.
Full work up:
- CBC
- CRP
- Blood cultures
- Rapid antigen detection test
- Sputum culture (note that mycoplasma pneumonia cannot be detected on sputum as it is intracellular, do PCR/serum culture)
Classifications of pneumonia include:
- Morphological
- Bronchopneumonia
- Lobular pneumonia
- Diffuse pneumonia
- Etiology (bacterial/viral)
- Depending on onset (acute/chronic)
- Depending on site of infection (hospital/community)
- Acute pneumonia
- Management
- Treatment
Management for many children can be at home, however if oxygen saturation drops below 92%, grunting and/or recurrent apnoea occurs, children should be admitted. Supportive care should be oxygen for hypoxia and analgesia if there is pain. IV fluids should also be given to maintain hydration.
In terms of medication, broad spectrum antibiotics can be given in infants, while most older infants can be managed with oral amoxicillin, the broader more potent co-amoxiclav can then be kept for unresponsive pneumonia. Over the age of 5, amoxicillin or oral macrolides such as erythromycin is the choice of treatment. IV or oral are both effective.
- Amoxicillin
- 1-11 months 125mg 3x daily for 5-7 days
- 2-4 years 250 mg 3x daily for 5-7 days
- 5-17 years 500 mg 3x daily for 5-7 days
- Second line Clarithromycin
- 1 month to 11 years:
- Under 8 kg, 7.5 mg/kg twice a day for 5 days
- 8 to 11kg, 62.5 mg twice a day for 5 days
- 12 to 19 kg,125 mg twice a day for 5 days
- 20 to 29 kg, 187.5 mg twice a day for 5 days
- 30 to 40 kg,250 mg twice a day for 5 days
- 12 to 17 years: 250 mg to 500 mg twice a day for 5 days
Is the Pneumonia Viral or Bacterial
Viral
Low grade fever, appears more generalised on Chest X-ray, usually with hyperinflation. WBC<20k, usually increased lymphocytes
bacterial
High grade fever with hacking cough and rigors. Usually consolidates to one lobe. WBC>20k, usually increased granulocytes
Bronchiolitis
- General
- Causes
- Risk factors
Bronchiolitis is the most common serious respiratory infection of infancy, with 3% of all infants admitted to hospital with the disease.
Respiratory syncytial virus is the main causative agent in 80% of cases, other causes include parainfluenza, rhinovirus, adenovirus and influenza virus.
Not all cases require hospitalization, only around 1-2%.
Simply put, if you have a baby (under 2) coming in wheezing, they almost certainly have bronchiolitis, over the age of 2, it is generally bronchitis.
Bronchiolitis is the inflammation, edema and necrosis of smaller airway epithelial cells, with increased mucus production and bronchospasm. The clinical manifestations include cough, wheeze, and laboured breathing along with the general features of respiratory difficulty in more severe cases (cyanosis, accessory muscles for breathing, nasal flaring, grunting, cyanosis and poor feeding).
-Risk factors include being below 12 weeks of age, passive smoking, crowding at home, attendance of daycare, prematurity, concomitant underlying cardiopulmonary disease, immunodeficiency and severe neuromuscular diseases. These risk factors should be searched for in examination, along with the key clinical features by way of diagnosis. Note, fever is generally <40 degrees C.
Bronchiolitis
-Investigations
-Treatment
.-Risk factors
First line investigation is pulse oximetry to ensure the child is maintaining good oxygen saturation. Additional investigations such as CBC, CXR and Viral panels are not actually indicated. CBC does not help distinguish between viral and bacterial infections, CXR has a very high false positive for pneumonia, meaning that ABs are given unnecessarily, and it does not matter which virus is causing the disease, the management is the same.
Treatment where the patient has no history of wheeze:
- Supportive care
- Superficial suctioning with saline drops
- Adjunctive: supplemental oxygen and ribavirin (inhalater)
Treatment with history of wheeze
- Supportive care
- Superficial suctioning with saline drops
- Adjunctive: oral corticosteroid, supplemental oxygen and ribavirin (inhalation)
-Bronchial asthma (below) and bronchiolitis have a great deal of similarities in the clinical picture and it can be hard to distinguish. Take a look below to consider some of the differences:
- Bronchial asthma
- general
- physical examination
- Taking a ‘suspected asthma’ history
Asthma is the reversible constriction and obstruction of the bronchial walls caused by an inflammatory process as an allergic response to house dust mites. The key diagnostic factors are:
- Presence of risk factors (FH, smoking in household etc)
-Wheezing episodes
- Wheezing is typically exhalational, while croup is typically inhalatory
-Increased work of breathing
-Features of atopic disease
-History of response to treatment
Additional indicative features include a dry night-time cough, expiratory wheezing and dyspnoea.
Your physical examination should look for the following:
- Overall appearance and respiratory distress
- Respiratory rate and lung exam
- Heart rate and cardiac exam
- Exam of liver (patients are hyperinflated and as such we expect to palpate the liver border)
- Allergic stigmata (e.g. eczema)
-Where bronchial asthma is suspected, firstlly perform spirometry followed by a dose of bronchodilator and then a repeat of the spirometry. If there is a positive response we can diagnose asthma. Additional tests include peak flow meter, CXR, FBC, sweat test, sputum culture and ABG if the patient is presenting with signs and symptoms
- Taking a ‘suspected asthma’ history
- When did wheezing begin (age)
- Episodic or persistent
- Sudden onset (FB) or gradual
- Associated triggers
- Has it responded to albuterol
- Was this child premature (much higher risk) Signs and symptoms
- Events per week?
- Nighttime awakenings
- Interference with normal activity
- Systemic steroids in the last year?
- Previous hospitalization?
Bronchial asthma
- Treatment
- chronic management
Treatment
-age 0-4
-Step 1 - short acting beta-2 agonist when required
– Step 2 - low dose inhaled corticosteroid + short acting beta-2 agonist when required.
– Step 3 - medium dose-inhaled corticosteroid + short acting beta-2 agonist
when required
- Step 4 high dose corticosteroid + montelukast
- age 4-11
- Step 1 - short acting beta-2 agonist when required
- Step 2 - leukotriene receptor antagonist + short acting beta-2 agonist when required
- Step 3 - Medium dose inhaled corticosteroid + short acting beta-2 agonist when required
– Step 4 - corticosteroid + leukotriene receptor antagonist or short acting beta-2 agonist when required.
-Short acting beta 2 agonist =
Salbutamol 100 micrograms - 200 micrograms (1-2 puffs) 5 mins before exercise or when required
-Corticosteroid =
Budesonide 0.25-1 mg/day inhaled/nebulised or beclometasone inhaler 90-200 micrograms/dose up to 400 micrograms/day (if severe, add prednisolone 0.25-2mg/kg orally and salmeterol 50 micrograms/dose twice daily)
Long acting beta 2 agonist = Salmeterol 0.05mg twice daily
- NOTE - NEVER USE LABA WITHOUT A STEROID
-Leukotriene receptor antagonist = Montelukast 5mg orally once daily
Use step up policy, start with SAB2A, add Corticosteroid, then LAB2A and then Leukotrienes as it gets more severe.
-Chronic management of asthma means we need to categorize patients into one of four categories:
- Intermittent
- Mild persistent
- Moderate persistent - Severe persistent
This category is based on whether the patient wakes up at night, the frequency of their salbutamol use, if their asthma interferes with normal activity, and what use of systemic steroids are being applied.
- Cystic Fibrosis
- general
- pathogenesis
- Treatment
Mucoviscidosis = Cystic fibrosis.
Cystic fibrosis is an autosomal recessive disorder more common in the white population. The error occurs on the long arm of the 7th chromosome, affecting CF transmembrane regulator (CFTR). This gene is responsible for chloride ion conductance in the epithelial cells. It is this defect that gives rise to its clinical manifestations.
CF is a chronic progressive disease, many infants are diagnosed on initial screening using the sweat chloride skin test (>60 mEq/L is positive). Older children will present with poorly controlled asthma and chronic respiratory infections, the respiratory epithelium will show marked impermeability to chloride and excessive reabsorption of sodium causing dehydration of the airway secretions and in return impairment of mucociliary transport. It is this impairment that leads to recurrent infections and wheezing that we see in CF patients. Digital clubbing is common as is chronic sinusitis and nasal polyposis.
The pathogenesis of the disease should be clear, impairment of chloride ion transport means that sodium is retained in the epithelial cells, where sodium goes water follows, as such the epithelial cells are unable to properly secrete, causing highly viscous mucous (hence its old term, mucoviscidosis).
90% of patients also present with exocrine pancreatic insufficiency as a result of the dehydration of the pancreatic ducts. This leads to malabsorption of proteins, sugars and fat, manifesting as steatorrhea(increase in fat excretion in the stools) , vitamin deficiencies and FTT.
-Can present in neonatal period with meconium ileus.
Diagnosis is via the skin sweat chloride test previously mentioned, along with DNA analysis or demonstration of the failed ion transport across the nasal epithelium.
Treatment is multifactorial but primarily geared towards GI and pulmonary complications of the disease. Airway treatment includes airway secretion clearance techniques (chest physio) and antibiotic therapy, while GI treatment is that of enteric coated pancreatic enzyme capsules, including lipase and proteases along with diet change (avoidance of fat).
Bronchiectasis
- General
- types
- diagnostics
- presentation/treatment
- complications
Bronchiectasis is irreversible dilation of the bronchial tree, it may be generalized or restricted to a single lobe.
- The generalised form can be a result of cystic fibrosis, primary ciliary dyskinesia, immunodeficiency or chronic aspiration,
- while the focal form can be the result of severe pneumonia, congenital lung abnormalities or due to obstruction by a foreign body.
- A plain CRX may show gross bronchiectasis however it is often difficult to fully assess by x-ray and CT is preferred, if the cause is unknown in focal cases a bronchoscopy may be required for diagnosis.
- Bronchiectasis can present with infectious flair ups, in such cases sputum cultures should be taken to guide treatment, but first choice is generally Amoxicillin.
- Respiratory insufficiency in childhood
- General
- Early signs
- symptoms
- Adjunctive therapies
- what not to do
Respiratory insufficiency is the failure of the lungs to maintain adequate gas exchange. This may be due to alveolar hypoventilation, diffusion impairment, intrapulmonary shunting or ventilation-perfusion mismatch.
Respiratory failure causes hypoxaemia (PO2 <85mmHg) and/or hypercapnia (PCO2 >45mmHg), the former causing tissue hypoxia and the later leading to carbon dioxide narcosis. Respiratory failure with hypercapnia has a worse prognosis than hypoxaemia alone.
-Early signs of respiratory distress are:
- Accessory muscle use
- Flaring of nose
- Intercostal recessions
- Compelled position
This can progress to respiratory failure which is the failure of compensatory mechanism. The key sign is change in mental status.
Symptoms of respiratory distress in infancy include:
- Tachycardia
- Respiratory rate >50bpm
- Nasal flaring
- Use of accessory muscles
- Intercostal recession
- Head retraction
- Unable to feed
- Cyanosis
- Reduced conscious level
- Low O2 saturation
- High CO2 saturation
In acute cases, patients should be placed on oxygen (via face mask, to non-invasive ventilation and finally endotracheal intubation of PCO2 >50mmHg) and reversible causes identified and treated where possible.
-Where respiratory failure is suspected the following bloods should be performed: - ABGs - CBC - Electrolytes - X-ray
For extrathoracic airway obstruction (e.g. croup):
- Inspired humidity to liquefy secretions
- Heliox (helium + oxygen)
- Racemic epinephrine 2.25%
- Dexamethasone
- Nebulized hypertonic saline (3%)
As lung and respiratory pump support:
- Oxygen therapy
- Humidified high flow nasal cannula therapy, CPAP and NPPV
Adjunctive therapies for severe hypoxemia
- Prone position
- Inhaled NO
- Exogenous surfactant
Note, patients in a chronic hypercapnic state should not be put on oxygen unless their PO2 is very low. The high CO2 levels keep the bran centre stimulated, removing this stimulus will result in the patient decreasing their breathing effort.
- Congenital malformations of respiratory system
- divisions
Congenital malformations of the respiratory system are rare, we can divide them based on the structures that are affected:
- Malformation of the thorax (specifically the diaphragm)
- The lung (lung sequestration, cystic adenomatoid malformation, bronchogenic cyst,
foregut cyst)
- Blood supply (aberrant vasculation, double arch of the aorta)
- Airways (tracheal rings, tracheomalacia, tracheal atresia)
- Larynx and oral cavity
Congenital diaphragmatic hernia
The most common malformation of the respiratory system, with multiple subtypes including the Bochdalek hernia, Morgagni hernia, diaphragm eventration and central tendon type. The malformation allows abdominal organs to push into the chest cavity limiting lung formation. Pulmonary distress will occur within the first 24 hours and can lead to pulmonary hypoplasia and pulmonary hypertension, both of which can lead to death if not properly treated. Treatment is with an orogastric tube and intubation, with extracorporeal membrane oxygenation in some cases. Following securing of the airways, thoracoscopic surgery can be performed.
Tracheoesophageal fistula
-This is an abnormal congenital connection between the trachea and the esophagus. It will present in newborns with copious salivation along with choking, coughing, vomiting and cyanosis. It is the product of the failed fusion of the tracheoesophageal ridges at the fourth week of embryological development.
TEF should be suspected once the baby fails to swallow after his first feed, a diagnosis can be made by a Ryle nasogastric tube, where the tube fails to pass into the stomach then this can indicate loss of communication between the stomach and the esophagus. We classify TEF as type A, B, C (most common), D or H depending on the precise location of the connection. Treatment is surgical resection
- Choanal atresia
- Congenital lobar emphysema
-Choanal atresia
This is the blockage of the nasal passage to the nasopharynx. This blockage can be due to soft tissue or bone and can be unilateral or bilateral (in unilateral cases it is often not picked up until quite late). Bilateral cases are very serious as babies are obligate nasal breathers following birth, as such babies will present as cyanotic, and may require incubation early in life. Presentation often occurs with Coloboma, heart defects, intellectual disability and FTT.
-Congenital lobar emphysema
Also known as congenital lobar overinflation is a disease where air enters the lungs and cannot escape. The lobe (or more) becomes distended and may or may not have an overabundance of alveoli. There are many mechanisms for this, including obstruction, cartilage deficiency, dysplasia and immaturity.
The clinical presentation is that of respiratory distress within the first six months of life, with diagnosis through radiography.
- Pulmonary atresia
- Congenital cystic adenomatoid malformation (congenital pulmonary airway malformation)
-Pulmonary atresia
This is actually a cardiovascular congenital disorder, but it affects the lungs and as such is included in here. The pulmonary valve does not form properly, and blood from the right side of the heart cannot go into the lungs. This most commonly occurs with Tetralogy of Fallot.
-Congenital cystic adenomatoid malformation (congenital pulmonary airway malformation)
This is a congenital disorder where an entire lobe of lung is replaced by a non functioning cstic piece of abnormal tissue. Three quarters of patients are asymptomatic, while 25% develop cyanosis, pneumothorax and tachypnoea, whether the patient is symptomatic or not depends on the size of the congenital cyst. Treatment is surgical removal of the cyst.
- Tuberculosis
- General
- symptoms
- diagnosis
- Treatmnet
- Differences
-Tuberculosis is a bacterial infection caused by the bacterium mycobacterium tuberculosis. Since the development of the BCG vaccine, the incidence of TB has been on the decrease, however, this trend may be reversing as we see the emergence of multidrug-resistant mycobacterium TB (MDR-TB).
-Diagnosis in infants and children can be tricky. 90% of children and 50% of infants are asymptomatic following infection, and the disease will remain latent in their body, with the potential to develop disseminated miliary TB (where the disease can affect a multitude of organs, not just the lungs) at a later date.
The symptomatic form of TB occurs when the host fails to contain the bacteria, allowing spread via the lymphatic system. Lung lesion plus the lymph node constitutes the ‘Ghon complex’.
-Typical symptoms include fever, anorexia and weight loss, cough and chest x-ray changes. The primary complex often c alcifies, and the lesion may cause bronchial obstruction and/or pleural effusion.
Both the symptomatic and asymptomatic forms of the disease can become dormant, and eventually reactivate as secondary TB (Miliary TB).
-Diagnosis of TB in children and infants is a little tricky. Our options are:
- Sputum samples (generally unobtainable from under 8s, specific techniques would
need to be used)
- Gastric washings on three consecutive mornings
- Tuberculin skin test (Mantoux test) however this may be +ve due to vaccine
- Interferon-gamma release assays (IGRAs) are especially useful for dormant TB
-Co-infection with HIV makes it even more of a challenge as X-ray changes may be
due to lymphoid interstitial pneumonitis which looks very similar and affects 20% of HIV children.
-Treatment is triple or quadruple therapy = rifampicin, isoniazid, pyrazinamide, ethambutol. If MDR-TB is suspected, just use rifampicin and isoniazid until antibiotic sensitivities are known. Treatment is for 6 months in ordinary pulmonary TB.
- Differences to adult TB:
1. Harder to diagnose (more often asymptomatic)
2. Increase in percentage of disseminated extrapulmonary TB
3. All latent TB in children should be treated
4. Very young children are not contagious
