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Resp Exam > Prematurity > Flashcards

Prematurity Flashcards

1
Q

Indications for palivizumab?

A
  • Significant chronic lung disease of prematurity (requiring supplemental oxygen at 36 weeks) + patient is <12 months at start of RSV season and they require ongoing oxygen, diuretic, bronchodilator, steroid
  • Hemodynamically significant congenital heart disease and requiring ongoing diuretic, oxygen + patients is <12 months of age at start of RSV season
  • Preterm <30 +0 weeks who is <6 months at start of RSV season
  • Infant in remote community (where they would need air transport for hospitalization) born at <36+0 weeks and <6 months at start of RSV season
  • Groups that should NOT be routinely offered palivizumab: CF, Down syndrome, immunodeficiency, upper airway obstruction, chronic pulmonary disease unless <24 months of age and requiring home oxygen OR had a prolonged hospitalization or are severely immunocompromised
  • do not continue monthly palivizumab if the child is hospitalized with breakthrough RSV
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2
Q

What is palivizumab and is there risk of transferring infection?

A
  • Monoclonal immunoglobulin directed towards F glycoprotein of RSV
  • It’s made through recombinant DNA technology
  • Not a blood product
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3
Q

Side effects of palivizumab?

A
  • injection site reaction
  • fever
  • rare risk of anaphylaxis
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4
Q

How much does palivizumab decrease hospitalization due to RSV?

A
  • limited effect on hospitalization at a population level, but is effective in certain subgroups
  • Reduction in hospitalizations of 80% in infants with prematurity (<36 weeks and without CLD), 40% in infants with prematurity and CLD, and 45% in children with CHD (but not with cyanotic heart disease)
  • Palivizumab does not decrease severity of illness, icu admission or death
  • It is generally not cost effective
  • Only cost effective in places where high rates of RSV admission and very expensive hospital stays (e.g. Baffin Island)
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5
Q

Patient with suspected empyema versus parapneumonic effusion. What investigations on pleural fluid?

A
  • Cell count
  • gram stain and culture–may also send PCR, mycobacterial culture and gene Xpert
  • chemistry investigations are unlikely to change management

(keep in the back of your mind: could this be a malignant effusion)

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6
Q

When should you insert chest tube in a patient with pneumonia and associated pleural effusion?

A
  • Definitely insert chest tube for large pleural effusion (>1/2 thorax opacified)
  • For medium size effusion (1/4 to 1/2 of thorax): option of either inserting chest tube or trying IV antibiotics
  • For small effusion (10 mm rim to <1/4 of hemithorax): start with IV antibiotics. (May not even need to do an ultrasound right away for a small effusion)
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7
Q

Patient with pneumonia and associated effusion who has chest tube. Do you use fibrinolytic upfront? When should VATS be considered?

A
  • For a simple, non-loculated effusion: IDSA guideline gives the option of either using or not using a fibrinolytic upfront
  • For a complicated, loculated effusion: IDSA gives the option of either trying drainage with fibrinolytic or proceeding straight to VATS
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8
Q

Patient with pneumonia and associated effusion. Treatment?

A
  • Treat for staph aureus and strep pneumo so could use ceftriaxone + vanco. Once cultures are back, you can tailor treatment.

(For a small effusion, it’s probably fine to just cover for strep pneumo with typical pneumonia treatment and not have additional staph coverage)

(This is the same treatment regimen used for other types of complicated pneumonia)

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9
Q

When is chest tube in pneumonia patient with effusion ready for removal?

A

<1 cc/kg/day of drainage

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10
Q

In what scenarios should patient with pneumonia have a follow up CXR after clinical improvement?

A
  • Recurrence of pneumonia in the same location
  • Atelectasis
  • Round pneumonia (Kendig’s actually says follow up imaging for round pneumonia)
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11
Q

Why are children prone to round pneumonia? What age do we typically stop seeing round pneumonia?

A
  • Children do not have well developed collateral ventilation such as pores of kohn (intra-alveolar connections) or canals of lambert (connections between distal bronchi)
  • so an alveolar infection stays localized versus in adults, the infection spreads through an entire lobe
  • less likely to have round pneumonia after 8 years of age
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12
Q

What coverage does vancomycin provide?

A
  • resistant strep pneumo

- MRSA

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13
Q

What are unusual causes of pneumonia that should be considered in children <6 months of age?

A
  • Newborn: think about GBS, E. coli (other enteric gram negatives)
  • 1-6 months:
  • interstitial pattern: Chlamydia trachomatis, B. pertussis, ureaplasma urealyticum –>these pathogens are treated with azithromycin

(Chlamydia pneumonia is an atypical pathogen that can cause pneumonia in children >=1 year of age, similar to mycoplasma)

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14
Q

What is a complicated pneumonia? How is it treated?

A
  • Necrotizing pneumonia
  • Lung abscess
  • Empyema
  • Pneumatocele
  • In general, important to have good staph aureus and strep pneumo coverage–>third generation cephalosporing + clinda or vanco
  • duration of treatment: continue treatment (either IV or oral) for at least 2 weeks after clinically improved. This will often correspond to a total of 4 weeks of treatment. (recall that typical duration of treatment for community acquired pneumonia is 7-10 days).
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15
Q

Two most common bacteria to cause pneumonia after influenza? (secondary bacterial pneumonia)

A
  • Strep pneumonia

- Staph aureus

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16
Q
  1. Chest tube inserted, but not draining adequately. Provide two therapeutic options to assist drainage of effusion
A

External suction

  • Intrapleural fibrinolysis
  • Tube manipulation, ensuring no kinks etc. → tube replacement such as with larger tube or additional tube. Reposition if chest tube appears to be in wrong position on CXR.
  • VATS if not improved with above
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17
Q

Well looking infant <6 months with suspected or confirmed pertussis. Management?

A
  • Admit to hospital for observation given high mortality (ARDS, pulmonary hypertension, seizures, encephalitis)
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18
Q

Child with pertussis. Should this be treated?

A

Yes, you should treat pertussis, regardless of the stage of illness at which it is diagnosed.

  • Early treatment during cattarhal stage will decrease severity, which is especially important for infants<6 months of age
  • Treatment later than cattarahl stage will decrease infectivity
  • All close contacts should be treated regardless of immunization history and history of prior infection. Should give immunization to individuals who are unimmunized or incompletely immunized
  • Treatment and prophylaxis with 5 days of azithro
  • For infants <6 months: azithro 10 mg/kg/day x 5 days
  • For children >6 months: azithro 10 mg/kg/day x 1 day, then 5 mg/kg/day x 4 days
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19
Q

Is surgery usually required for pulmonary abscess?

A
  • No
  • 80-90% of abscesses will resolve by rupturing into the tracheobronchial tree and with appropriate antibiotics
  • Treatment is the same as for any other complicated pneumonia
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20
Q

Child with influenza, uncomplicated illness and no risk factors for severe disease. Is anti-viral recommended?

A

No

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21
Q

Child with influenza, mild or uncomplicated illness, but underlying pulmonary disease (Eg. asthma, CF, obesity, BPD, aspiration), is use of anti-viral recommended?

A
  • If within first 48 hours of illness, then use of antiviral is recommended
  • If beyond the first 48 hours, then assess on case by case basis
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22
Q

Child with moderate, progressive, severe or complicated illness from influenza. Is anti-viral recommended?

A
  • Regardless of time frame from within onset of illness (so even if beyond the first 48 hours), use of antiviral is recommended
  • If the child was already on oseltamivir, then use zanamivir (which is inhaled or IV)
  • if the child wasn’t on an antiviral, then use oseltamivir
  • want to use the antiviral as soon as possible to get maximal benefit
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23
Q

What are the benefits of oseltamivir for influenza?

A
  • In low risk individuals (low risk of complications from influenza), giving tamilu within 48 hours of illness will decrease illness duration by 1 day
  • In individuals at high risk of influenza complications (Basically any respiratory condition), giving tamiflu doesn’t decrease duration of illness, but it decreases illness severity and hospitalization
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24
Q

What are the complications of chronic hypoxemia? (more broadly than just in premature infants?

A
  • pulmonary hypertension
  • cognition
  • growth
  • sleep (hypoxemia may be more likely to predispose to central apnea, arousal in preterms)
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25
Q

Indications for home oxygen therapy in an infant with BPD?

A
  • Chronic hypoxemia as defined for BPD for the purpose of initiating home oxygen:
		* 
Recording of >=5% that is <=93% 
		* 
3 separate findings of saturation <=93% 
		* 
(The problem is that the oximetry does not break it down for <93%)

-This guideline has the same threshold for patients with PH + BPD

With BPD and PH, the target saturation is 92-95%

26
Q

In infants with unrepaired congenital heart disease, is the use of chronic supplemental oxygen recommended?

A

Recommend against supplemental oxygen for unrepaired cyanotic or acyanotic because oxygen will affect hemodynamics and cause more pulmonary blood flow, which could be harmful –>needs to be expert consultation with cardiology or respirology to initiate oxygen

27
Q

Saturation threshold for BPD? BPD with PH?

A

BPD: >=93%
BPD + PH: 92-95%, 93% would be a good number to keep in mind (double check on PH guideline, this is from ATS home oxygen guideline which refers to PH guideline so it’s probably right)

28
Q

What has happened to incidence, prevalence, severity of BPD?

A
  • Incidence has not changed (none of the therapies have changed the incidence)
  • severity has decreased
  • since survival has improved, the prevalence has increased
29
Q

Preterm infant with chronic respiratory complications, who didn’t have BPD. Is this surpising?

A
  • BPD definition is quite poor, it’s not sensitive or specific for predicting pulmonary morbidity, so take the pure definition with a grain of salt
30
Q

Management of PH in BPD patient?

A
  • Key point of PH management in BPD: deal with the underlying lung disease
    • although pulmonary vasodilators are used, there isn’t actually very much evidence for them
    • Underlying lung disease:
		* 
investigate for upper airway abnormalities - subglottic stenosis, tracheomalacia, vocal cord paralysis -->flexible bronchoscopy 
		* 
Reflux/aspiration: upper GI series, pH probe, swallowing study 
		* 
consider G tube, fundo 
	* 
Medical therapy: 
	*  they encourage cardiac cath 
	*  they favor sildenafil, though they also use bosentan 
	*  Sildenafil:
	*  starting dose: 0.5 mg/kg/dose every 8 hours 
	*  increase dose over 2 weeks to 2 mg/kg/dose
31
Q

What is the role of systemic steroids in BPD?

A

Kendig’s:

* late systemic doses can help with earlier extubation (DART study) 
*  inhaled steroids have NOT been shown to improve lung function 
*  early use of steroids and prolonged use impairs head growth and cognitive development 
*  using a short course, high dose (eg. 3-5 days) can help with an acute deterioration 

* DART study: low dose dexamethasone improved extubation rate, no significant complications, but this study was underpowered to look at long-term safety 
*  The approach at many centres (including Edmonton): low dose steroids for short duration (5-7 days) in ventilator dependent infants with severe, persistent lung disease at 1-2 weeks

CPS Statement:
- may consider low dose hydrocortisone in first 48 hours of life x 10 days for infants at high risk of BPD (eg. <28 weeks or exposed to chorioamnionitis), may be an increased risk of late onset sepsis. (no other role for hydrocortisone) –>outcome: increased survival without BPD at 36 weeks, increased survival before discharge without harmful effect on neurodevelopment at 2 years
- dexamethasone: can be used after first week of life for infants who are ventilated with worsening lung disease, increasing O2 requirement, but routine use for evolving BPD is not recommended. It would be a low dose of dexamethasone over 7-10 days –>lower rate of death or BPD
(CPS focuses on the effect of steroid for BPd, as opposed to extubation)

32
Q

What is the typical clinical presentation of RDS?

A

Early onset respiratory distress by 4 hours, worst at 24-36 hours, improved at 36-48 hours
(endogenous surfactant production starts at 24 hours)

33
Q

What are the CXR manifestations of RDS?

A
  • Low lung volumes
  • Diffuse ground glass (reticulonodular)
  • Air bronchograms
34
Q

Pathologic features of new BPD?

A
  • Fewer, larger and simplified alveoli
  • Fewer arteries, but dysmorphic
  • Less regional heterogeneity
  • Rare airway epithelial lesions
  • Mild airway smooth muscle thickening
  • rare fibroproliferative changes
35
Q

Pathologic features of old BPD?

A
  • heterogeneous: alternating atelectasis with hyperinflation
  • severe airway epithelial lesions
  • market airway smooth muscle hyperplasia
  • extensive diffuse fibroproliferation
  • hypertensive remodelling of pulmonary arteries
  • decreased alveolarization and surface area
36
Q

Definition for BPD?

A
  • Need for oxygen >21% for at least 28 days
  • Time point for assessment:
    <32 weeks: assess at 36 weeks or discharge, whichever is sooner
  • > 32 weeks: assess at 56 days or discharge, whichever is sooner
    (need to go with sooner since the patient will be discharge, so need to classify before discharge)
  • Mild: no oxygen
  • Moderate: <30% fiO2
  • Severe: >30% fiO2 +/- PPV/CPAP
37
Q

Why are old and new BPD different?

A

Old BPD: infants were born in late saccular stage. Lung injury was due to hyperoxia, ventilator induced lung injury, inflammation, infection
New BPD: mid to late cannalicular stage, mainly due to aberrant lung development. With antenatal steroids, surfactant and gentl ventilation, less old BPD.

38
Q

Properties of chyle?

A
  • Chylothorax = accumulation of lymphatic fluid in the pleura
  • Lymph generally drains into thoracic duct
  • Sudan IIIn stain positive for fat globules
  • Triglycerides >1.1 mmol/L
  • High lymphocyte content (>80%)
  • sterile
  • fat content higher than plasma
  • electrolytes, BUN, glucose similar to plasma
  • meets the criteria for an exudate
39
Q

Why are old and new BPD different?

A

Old BPD: infants were born in late saccular stage. Lung injury was due to hyperoxia, ventilator induced lung injury, inflammation, infection
New BPD: mid to late cannalicular stage, mainly due to aberrant lung development. With antenatal steroids, surfactant and gentl ventilation, less old BPD.

Old BPD is pre-surfactant
New BPD is post surfactant

40
Q

If neonatal chylothorax is not improving with conservative management, what are next investigations?

A
  • Lymphangiography to localize a site of lymphatic leak
  • CT scan - may see thickened interlobular septa with lymphangiectasia, but can’t visualize lymphatics on CT scn (I’m not sure if this finding is specific to lymphangiectasia)
41
Q

Lymphangioma versus lymphangiomatosis versus lymphangiectasia?

A

Lymphangioma: abnormal proliferation of lymphatic vessels, forming a cyst
Lymphangiomatosis: multiple lymphangiomas, which can be in lung, liver, spleen, mediastinum
Lymphangiectasia: dilated lymphatic channels, which impair drainage. Can be primary or secondary (due to increased venous back pressure such as in heart failure or portal hypertension

42
Q

Infant PFt findings with BPD?

A
  • increased airway resistance
    • flow limitation
    • gas trapping
43
Q

What is the ventilatory strategy in BPD?

A
  • High PEEP
  • Low PIP, low tidal volume
  • Low fiO2
  • Avoid hypocarbia, volutrauma, oxygen toxicity
  • Lung recruitment strategies
  • Permissive hypercapnea

(This is similar to RDS. This is in contrast to established BPD, where you basically just have to ventilate them and the process has already been established–>high PEEP, longer I time, larger tidal volume, lower rate)

44
Q

Why does pulmonary hypertension develop in BPD?

A
  • (Less vessels and surface area): Decreased angiogenesis
  • Smooth muscle proliferation
  • Abnormal vasoreactivity
45
Q

What is the role of inhaled steroids and BPD?

A

The use of inhaled steroids to prevent or treat BPD is not recommended.
although some studies suggest that there is lower BPD rate with ICS, there was also increased mortality.

46
Q

Pulmonary hypertension screening in BPD?

A
  • this should occur at 36 weeks
47
Q

BPA, on home oxygen therapy, what is target oxygen saturation?

A
  • BTS: >=93%
  • ATS:
     Recording of >=5% that is <=93%
     3 separate findings of saturation <=93%
  • They are kind of saying the same thing, just remember 93%
48
Q

what is the effect of antenatal steroids on BPD?

A
  • decrease the incidence of neonatal death
    • decrease RDS by 50%
    • NO change in incidence of BPD (even with surfactant)
49
Q

Incidence of surfactant on BPD?

A

Exogenous surfactant is used in premature babies to decrease the surface tension and increase compliance. It has been shown to decrease mortality from BPD but not the incidence.
Surfactant reduces the combined outcome of death and BPD but not BPD alone

50
Q

Effect of caffeine and nitric oxide on BPD?

A

Nitric oxide: may lower risk of BPD in some preterm infants, but results are conflicting. Routine use is not recommended

• Caffeine:
o actually reduces the risk of BPD***
o Other benefits: decreased need for sugical PDA closure, earlier discontinuation of respiratory support
o ideal to start caffeine on day 1 to get the most benefit from BPD perspective
o more benefit with early initiation (before DOL2) than with late initiation (DOL 3-10)

51
Q

What are epidemiologic risk factors for RDS?

A
  • GA
  • gender (males worse than females)
  • ethnicity (worse for whites than african American)
  • antenatal steroids (which have decreased incidence and severity of RDS)
  • maternal insulin
52
Q

What is the typical clinical presentation of RDS?

A

Early onset respiratory distress by 4 hours, worst at 24-36 hours, improved at 36-48 hours
(endogenous surfactant production starts at 24 hours)

53
Q

What are the CXR manifestations of RDS?

A
  • Low lung volumes
  • Diffuse ground glass (reticulonodular)
  • Air bronchograms
54
Q

Pathologic features of new BPD?

A
  • Fewer, larger and simplified alveoli
  • Fewer arteries, but dysmorphic
  • Less regional heterogeneity
  • Rare airway epithelial lesions
  • Mild airway smooth muscle thickening
  • rare fibroproliferative changes
55
Q

Pathologic features of old BPD?

A
  • heterogeneous: alternating atelectasis with hyperinflation
  • severe airway epithelial lesions
  • market airway smooth muscle hyperplasia
  • extensive diffuse fibroproliferation
  • hypertensive remodelling of pulmonary arteries
  • decreased alveolarization and surface area
56
Q

Definition for BPD?

A
  • Need for oxygen >21% for at least 28 days
  • Time point for assessment:
    <32 weeks: assess at 36 weeks or discharge, whichever is sooner
  • > 32 weeks: assess at 56 days or discharge, whichever is sooner
    (need to go with sooner since the patient will be discharge, so need to classify before discharge)
  • Mild: no oxygen
  • Moderate: <30% fiO2
  • Severe: >30% fiO2 +/- PPV/CPAP
57
Q

Why are old and new BPD different?

A

Old BPD: infants were born in late saccular stage. Lung injury was due to hyperoxia, ventilator induced lung injury, inflammation, infection
New BPD: mid to late cannalicular stage, mainly due to aberrant lung development. With antenatal steroids, surfactant and gentl ventilation, less old BPD.

58
Q

Properties of chyle?

A
  • Chylothorax = accumulation of lymphatic fluid in the pleura
  • Lymph generally drains into thoracic duct
  • Sudan IIIn stain positive for fat globules
  • Triglycerides >1.1 mmol/L
  • High lymphocyte content (>80%)
  • sterile
  • fat content higher than plasma
  • electrolytes, BUN, glucose similar to plasma
  • meets the criteria for an exudate
59
Q

Differential diagnosis of neonatal chylothorax?

A
  • congenital: Down’s, Noonan, Turner
  • Hydrops fetalis
  • Injury to thoracic duct - either congenital (eg. birth trauma), post operative
  • congenital lymphatic abnormality - eg. lymphangiectasis, lymphangioma
  • Increased central venous pressure pressure - eg. post fontan, thrombosis of SVC
  • Chylothorax in general: lymphoma, teratoma, neuroblastoma, TB, histoplasmosis, sarcoid
60
Q

If neonatal chylothorax is not improving with conservative management, what are next investigations?

A
  • Lymphangiography to localize a site of lymphatic leak
  • CT scan - may see thickened interlobular septa with lymphangiectasia, but can’t visualize lymphatics on CT scn (I’m not sure if this finding is specific to lymphangiectasia)
61
Q

Lymphangioma versus lymphangiomatosis versus lymphangiectasia?

A

Lymphangioma: abnormal proliferation of lymphatic vessels, forming a cyst
Lymphangiomatosis: multiple lymphangiomas, which can be in lung, liver, spleen, mediastinum
Lymphangiectasia: dilated lymphatic channels, which impair drainage. Can be primary or secondary (due to increased venous back pressure such as in heart failure or portal hypertension

Resp Exam (16 decks)

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