Non-infectious disorders (Raf) Flashcards
(135 cards)
1
Q
ECG finding in PH?
A
RVH
(Also: right atrial enlargement, RV strain)
- ECG cannot be used to rule out PH because it will be normal in mild PH
2
Q
Physical exam findings in pulmonary hypertension?
A
Failure to thrive, clubbing RV heave (which is actually in the left parasternal region), loud P2 (pulmonic component of second heart sound), holosystolic murmur of tricuspid regurg Hepatomegaly, high JVP Pedal or sacral edema RV gallop
3
Q
What is the mechanism of injury in drowning?
A
Key point: surfactant dysfunction
- Majority of drownings are wet drowning (with direct aspiration of fluid), in contrast to dry drowning, where there is laryngospasm
- For individuals who are dead on arrival, distinction between salt and freshwater is relevant. Presumably, they have aspirated enough ~15 mL/kg to die and have the mechanism of fluid shifts and electrolyte changes be relevant. (In this context, fresh water drowning is worse than a salt water drowning
- For individuals who are NOT dead on arrival, the distinction is not very important. Both types of aspiration cause:
- Deactivation of surfactant—>decreased lung compliance—>VQ mismatch and shunting—>hypoxemia
- Other mechanisms for lung injury:
- Neurogenic pulmonary edema - due to CNS hypoxemia
- Post obstructive pulmonary edema
- Secondary infection
- Altered pulmonary capillary permeability
- Reactive pulmonary oedema
4
Q
What are the features of failing fontan and why do these complications develop?
A
Two ways a fontan patient can “fail”:
- single ventricle failure
- preserved systolic/diastolic function
Fluid doesn’t drain effectively into the fontan circulation so back up venous pressure
Many of the complications of failing fontan are due to increased lymph production, which can’t be effectively drained due to increased venous pressure.
Increased venous pressure (which I think occurs because passive flow from systemic venous to pulmonary veins is decreased/backing up fluid)–>result in increased production of lymphatic fluid + thoracic duct can’t drain into the vein b/c the venous pressure is high. –>accumulation of lymphatic fluid in various organs and increased back pressure–>chylothorax, plastic bronchitis, lymphangiectasia (secondary cause), protein losing enteropathy.
Retrograde flow from thoracic duct to lung parenchyma–>plastic bronchitis
Hepatic congestion (I’m not sure if lymphatic are related)
5
Q
types of bronchial cases and diseases they are associated with?
A
Cast = obstructive airway plug. Can get big enough to fill branching pattern of tracheobronchial tree
Type 1: cellular, inflammatory, contains fibrin + inflammatory cells (mainly eosinophils). Seen in asthma, CF, acute chest syndrome in sickle cell disease
Type 2: acellular, non-inflammatory, contains mucin, fibrin, no inflammatory cells. this happens in Fontan patient, lymphatic abnormalities
6
Q
Inheritance of PCD?
A
Autosomal recessive
7
Q
Most common genetic defect for PCD?
A
ultrastructural defects are the most common (80% of patients).
Outer dynein arm defect is the most common. –this is a bit of simplified answer. Of the most common defects, 2 are outer dynein arm and 1 has normal ultrasturcutre,
What is the most comment genetic defect for PCD?
• DNAH5 - outer dynein arm
• DNAH11 - normal ultrastructure so TEM could be normal
• DNAI1 - outer dynein arm
8
Q
Diseases due to sensory ciliopathy?
A
Polycystic kidney disease, Baredt-Biedl, Joubert, retinitis pigmentosa.
(It’s important to know these conditions since there isn’t a perfect separation between primary/sensory ciliopathies and PCD (which is a disorder of motile cilia). If seeing patients with these conditions, then keep the diagnosis of PCD at the back of your mind.
Recall that there 3 types of cilia: sensory, motile, nodal (embryonic)
9
Q
Lung function abnormalities in pectus excavatum?
A
2/3 of patients have normal lung function with normal or low normal FVC/TLC
10
Q
CPET and pectus excavatum?
A
- lower maximal stroke volume (O2 pulse)
- decreased VO2 max
- Decreased anaerobic threshold
- higher RR, lower tidal volume (I think they have some ventilatory limitation as well)
11
Q
Effect of surgery for pectus excavatum on lung function and cardiac function?
A
- No clinically significant change in lung function. Studies have either very small improvements in EV1/FVC or no change or decrease
- That being said, there seems to be an improvement in exercise symptoms, which is due to improvements in cardiac function – improvements in stroke volume and VO2 max. Improvements in ECG abnormalities, which shows improvements in preoperative cardiac compression
12
Q
How is severity of pectus excavatum measured?
A
The pectus severity index (PSI), also known as the Haller index → describes the depth of the pectus defect by comparing the ratio of the lateral diameter of the chest to the sternum-to-spine distance, at the point of maximal depression.
- The chest CT scan should be performed at full inspiration to maximize the intrathoracic dimensions and to provide standardization to permit comparison with subsequent scans.
- A normal chest has a PSI of ≤2.5.
- Among patients referred for surgery based on clinical criteria (ie, without consideration of CT scan results), all patients had a PSI of >3.25, whereas patients with PE who were not referred for surgery had PSI <3.25
- PSI>5 is associated with mild restriction
13
Q
Indications for surgery pectus?
A
- exercise limitation
- poor self image
- above is from Kendig’s
- ideally late childhood, early adolescence
- Below if from uptodate, but the indications are not well standardized
As per uptodate, 2 or more of:
- PSI of >3.25 (measured on CT scan)
●Cardiac compression, displacement, mitral valve prolapse, murmurs, or conduction abnormalities
●Pulmonary function testing showing restrictive respiratory disease
●Failed previous repair of PE
(Cosmetic indiction can also be considerd)
14
Q
CT findings of bronchiectasis?
A
- Elevated broncho-arterial ratio of >1-1.5, keeping in mind that normal ratio in children is about 0.8
- Lack of peripheral tapering of bronchi
- Tram track sign
- Signet ring sign
- Ancillary findings:
- Bronchial wall thickening
- Mucoid impaction
- Air trapping
15
Q
CXR findings of bronchiectasis
A
- ring shadows (from appearance of bronchi end on)
- tram track opacities
- increase in bronchovascular markings
- air fluid level with cystic bronchiectasis
16
Q
Advantages and disadvantages of low molecular weight heparin?
A
Advantage:
- long half life so not as frequent dosing, no need for close monitoring
Disadvantage:
- expense
- injection is required
- only partially reversible with vitamin K
- higher half life results in increased risk of bleeding
(I didn’t spend a long time verifying this answer from our study notes)
17
Q
Advantages and disadvantages of warfarin?
A
Advantage:
- oral
- fully reversible with vitamin K
- once daily dosing
- low cost
Disadvantage:
- requires monitoring for INR
- narrow therapeutic window
- may interact with food and medication
- slow onset of action
18
Q
What are the genetics for HHT?
A
Autosomal dominant, with variable penetrance
19
Q
What are the clinical criteria for HHT? Are they reliable in children?
A
Curacoa criteria:
- Spontaneous and recurrent epistaxis
- First degree relative with HHT
- Mucocutaneous telangiectasia
- Visceral organ involvement: telangiectasia in GI tract or AVM in pulmonary, cerebral or hepatic
- 1 criteria: unlikely HHT
- 2 criteria: probable HHT
- 3 criteria: confirmed/definite HHT
These criteria are NOT very reliable in children, since most people don’t achieve a criteria diagnosis till age 40 years.
Criteria are helpful for ruling in, but not ruling out diagnosis.
(Technically you can make a diagnoses based on these criteria OR genetics)
20
Q
What is the approach to genetic testing for first degree relatives with HHT? Eg. asymptomatic child of a parent/sibling with HHT.
A
This child has possible HHT (not based on Curacao, but just generally)
If the familial genetic mutation is known, then first degree relatives should be tested for that mutation. If the genetic mutation is not known, then first degree relative can be managed as if they have HHT with the same screening recommendations.
21
Q
What are the genes implicated in HHT?
A
- ENG gene —>corresponds to HHT1
- ACVRL1 gene—>corresponds to HHT2
- SMAD4—>juvenile polyposis and HHT, so risk of GI malignancy
22
Q
Screening Recommendations for HHT?
A
Seeing a new patient:
- clinical exam -look for orthodeoxia by assessing by supine and upright saturation
- investigate for anemia and iron deficiency (epistaxis)
Cerebral AVM: brain MRI at infancy and adulthood (eg. 18 years). No need to re-screen if these are negative.
Pulmonary AVM: screen with bubble echo at diagnosis and after puberty (makes sense to do before transition to adulthood since there can be growth of pulmonary AVM during teenage yearS). (BTS guideline actually does not recommend rescreening for adults) If echo positive then CT. (Of note, the BTS 2017 guideline prefers CT chest +/- contrast as the preferred screening test. There has to be very good local expertise to rely on bubble echo). (Of note, normal CXR, oxygen saturations and lack of symptoms is NOT enough to exclude a pulmonary AVM)
Hepatic AVM: no routine screening
If a patient has the SMAD4 mutation, then they should be referred to GI for polyposis and GI malignancy screening, with colonoscopy starting at 15-18 years.
23
Q
How do you counsel patients with pulmonary AVM?
A
- Antibiotic prophylaxis for procedures with risk of bacteremia (since many cases of cerebral abscess happen in this context
- Intravenous access—>extra care to avoid intravenous air
- Avoidance of scuba diving
24
Q
Unusual systemic disorders associated with pulmonary hypertension?
A
HHT, in particular hepatic AVM are associated with pulmonary hypertension
Sickle cell
CCHS
25
For an individual with symptoms of HHT, but no family history, could they still have HHT?
Yes, they could have a de novo mutation
26
Long-term Management of epistaxis in patient with HHT?
- Nasal lubricant
- Endonasal coagulation is the first line procedure
- Later procedures: Young's procedure, septal dermoplasty
- In general, you want an ENT with expertise in HHT
27
What is the criteria for embolization of a pulmonary AVM in an asymptomatic patient?
- All patients with PAVM should be referred to interventional for an evaluation.
- embolization should be considered even in asymptomatic patients b/c there are benefits like decreased risk of stroke
- if the shunt is only visible on echo, then there is lower risk with procedure
- if the shunt is radiologically visible, there is no 3 mm rule
- Above is from BTS 2017 pulmonary AVM guideline
2009 guideline: symptomatic, feeding vessel diameter of >=3 mm
28
What are the complications of pulmonary AVM?
```
Cerebral abscess
Embolic Stroke
Ischemic stroke TIA
Pulmonary hemorrhage
Hypoxemia
```
29
Physical exam findings for HHT
- Vitals: saturation, orthodeoxia in supine and upright position
- Epistaxis-->endonasal telangiectasia
- Retinal telangiectasia and hemorrhage
- Telangiectasia on lips, oral mucosa, finger tips. Can use a hand held illuminator to look for vascular anomalies on digits
- Resp: thoracic bruit is heard in ½ of HHT patients with cyanosis (Emedicine), clubbing (association between cyanosis and clubbing with cerebral abscess and stroke)
- CNS: Bruit if cererbrovascular malformation and open fontanelle ?
· GI:
· High-output heart failure
· Hepatomegaly
· Portal hypertension
· Encephalopathy
· Right-upper-quadrant pain and jaundice
30
Definition of PH, PAH and post capillary pulmonary hypertension?
PH = mPAP >20 mmHg, in patient >3 months of age at sea level
Precapillary = pulmonary arterial hypertension:
- mPAP>20 mmHg
- Pulmonary artery wedge pressure or LVEDP <=15 mmg
- PVRi >= 3 WU (woods units)
Post capillary PH:
- mPAP >20 mmHg
- PAWP or LVEDP >15 mmHg
- Isolated post capillary if PVRI<3 woods unit and DPG <7 mmHg
Pre and post capillary: PVRI >=3 WU and DPG >=7
DPG: Diastolic pulmonary gradient (DPG) is a novel hemodynamic marker that is calculated as the difference between pulmonary artery diastolic pressure (PADP), and mean pulmonary capillary wedge pressure (PCWP)
(when assessing patients with left sided cardiac disease for heart transplant, you have to figure out if they just have post capillary PH or if there is also precapillary PH. Longstanding left sided cardiac disease will cause pre-capillary PH. If these patients have significant pulmonary hypertension, then they would need heart lung transplant.
31
Mechanisms of PCD?
Ultrastructural defect:
- dynein arm defect
- radial spoke defect
- microtubular transposition defect
Functional defect - ineffective beat in spite of normal ultrastructure
32
Causes of an elevated D dimer?
- Pulmonary embolus (this is often why the test is sent off, though the test has low specificity)
- D dimer is positive when there is inflammation or coagulation
- DIC
- Inflammation: trauma, surgery, infection: pneumonia, malignancy, inflammatory like kawasaki disease and JIA
33
Risk factors for pulmonary embolism in a teenager?
- Teenage girl: OCP, pregnancy
- Drugs: IV drug use, in particular injection into femoral veins
- Antiphospholipid antibody syndrome
- Inherited thrombophilia: factor V Leidein, Prothrombin gene mutation, protein C or S deficiency, antithrombin deficiency
- Major surgery such as orthopedic
- Malignancy
- Major trauma
- Immobilization due to recent air travel
(on a side note, antiphospholipid syndrome is a hypercoagulable condition, which may or may not be associated with lupus, antibodies: lupus anticoagulant, anticardiolipin, antibeta2glycoprotein)
34
Differential diagnosis for bronchiectasis?
See chapter 26 evernote scheme
Main categories:
- post infectious, post TB, post BO
- immunodeficiency
- CF, PCD
- aspiration
- Obstructive: foreign body. Obstructive airway lesion with TB, lymphadenopathy
- ABPA
- alpha 1 antitrypsin
- ILD such as pulmonary fibrosis
- Congenital: munier kuhn, william campbell
35
Minimum investigations for bronchiectasis?
* CBC
* IgA, M, G, E
* Vaccine response
* Sweat chloride
* Sputum culture for routine and mycobacterial culture
* CXR and CT during clinically stable disease
36
Draw the ultrastructure of a cilia?
(They will likely specify motor cilia (which line the respiratory epithelium), as opposed to primary/sensory cilia (which are non-motile) and nodal cilia (which are present in the embyro). These other cilia have a different structure.
Key points:
- 9+2 arrangement
- 9 doublet of microtubules surrounding a central pair of singlet microtubules
- Within the doublet, there is the A microtubule (left) and the B microtubule (on the right). The outer and inner dynein arms are attached to the A microtubule.
- There is a sheath surrounding the central pair of microtubules
- Radial spoke connects the doublets to the central sheath
- Nexin protein connects the doublets to each other
- Plasma membrane surrounds the whole structure
37
Describe the pathways involved in pulmonary hypertension?
Three pathways:
- Prostacylin pathway:
- Arachidonic acid can undergo two pathways of conversion. One pathway leads to prostacyclin (PGI2). The other pathways leads to production of thromboxane A2. PGI2 causes smooth muscle relaxation and inhibits platelet aggregation. Thromboxane A2 has the opposite effect and causes smooth muscle constriction and platelet aggregation. Treatment for PH: prostacylin derivative. PGI2 mediates it's effects through production of cAMP.
- Eg. epoprostenol is a prostacylin analogue
- Nitric oxide pathway: L-arginine is converted to L-citrulline via eNOS (endogenous NO synthetase). this also produces NO, which stimulates guanylate cyclase to produce cGMP from GTP. cGMP causes vasodilation and anti-proliferation. Phosphodiesterase-5 degrades cGMP. So can use a PDE-5 inhibitor.
- Eg. sildenafil is a phosphodiesterase inhibitor
- Endothelin pathway: endothelin acts on endothelin A and B receptors to cause vasoconstriction. So you want to have an endothelin receptor antagonist.
- Eg. bosentan is an endothelin receptor antagonist
38
Name one genetic mutation involved in PAH and it's inheritance?
BMPR2 = bone morphogenic protein receptor 2. It is autosomal dominant, but has variable penetrance
39
Patient with sickle cell disease who has a vaso-occlusive crisis, but not acute chest syndrome. What would be reasons for hypoxemia?
- Hypoventilation: depression of respiratory rate due to narcotics because of pain; nocturnal hypoventilation due to OSA
- Diffusion barrier: sickle cell chronic lung disease, pulmonary hypertension
- V/Q mismatch due to atelectasis from splinting. Increased frequency of wheezing and obstructive lung disease (which may or may not be asthma) may contribute to VQ mismatch.
40
Patient on BP lower medication who has a cough. Which medication?
Ace inhibitor
- ARB is less likely to cause cough
- ACEi cough starts within 1-2 weeks of starting ACEi
- Cough gets better after stopping ACEi, often within 1-4 days (But can take up to 4 weeks)
41
How is a large pneumothorax defined and why is this definition important?
- Size is defined by measurement of the interpleural distance
Distance from lateral edge to apical dome of lung > 3 cm OR
distance from lateral edge to lung at level of hila >2 cm (BTS) on an upright CXR
If pneumothorax is large, then intervention such as needle aspiration or insertion of chest tube (no consensus on which of these upfront)
For smaller pneumothoraxes that don't meet this threshold-->100% oxygen, but no need for insertion of a drain
If tension pneumo-->needle thoracentesis
42
For a patient with pneuthorax with chest tube inserted, what level of suction should be applied?
NO suction upfront since there can be re-expansion pulmonary edema and persistent air leak. If no improvement at 48 hours, then apply suction at -10 or -20
43
For patient presenting with primary spontaneous pneumothorax, is CT indicated?
No, because even if you find blebs, it's unclear what the next step would be for management.
Since we don’t know which patients are the ones who will have recurrent pneumothoraxes, we have to wait till they recurrently present and identify themselves in order to offer pleurodesis
44
When can patients with pneumothorax fly or dive?
Flight: CXR resolution of pneumothorax + an additional 7 days since there is a risk of re-expansion of the air under lower barometric pressure
Diving: very restrictive guidelines around diving-->definitive surgical management (eg. bilateral pleurectomy) + normal lung function + normal CT. (Pulmonary barotrauma is one of the major causes of death in divers. Lung is compressed on the descent-->pulmonary edema, pulmonary hemorrhage. On the ascent-->alveolar rupture, pneumothorax, pneumomediastinum)
45
In a patient with pneumothorax and chest tube, how is persistent air leak defined? Differential and management?
Persistent air leak: >3-7 days of bubbling.
- Persistent bubbling is either from the patient or the tubing system
1. System leak - chest tube, drainage tube, connections, pleurivac system
2. Bronchopleural fistula
- Clamp the tube close to the patient. If bubbling is still happening, then it's coming from the tubing system. You can identify the location of bubbling by re-clamping and finding out where the bubbling stops
46
Medications for managing oral secretions and their side effects?
- Anticholinergics: transdermal scoplomaine, oral atropine or glycopyrrlate
- Surgical: salivary ligation or removal, botox injection
Anticholinergic side effect:
- They can have significant side effects
- Dry mouth and thickening of oral secretions-->be cautious in patients with small tracheostomy tube and neuromuscular disease (limited ability to cough up secretions)
- Urinary retention, constipation, flushing, behavioural change
- nasal congestion, nausea, vomiting, photophobia
Botulinum toxin:
- pain, difficulty chewing, dysphagia, speech difficulty, dry mouth
47
What is the preferred diagnostic test for pulmonary embolism?
CT-pulmonary angiography. If this is not available or if the results is inconclusive, then do VQ scan
48
What is the role of D-dimer in diagnosing PE in children?
- Role of D dimer in children is not clear
- Diagnostic tools like Wells score and Geneva score have been designed for adults and are not validated in children
- Some studies suggest that in children with low index of suscpicion for PE, negative D dimer can safely exclude PE. If the D dimer is positive, then need to proceed to CT
- Important to note that if there is a high index of suspicion for PE, then don't bother with D dimer and go straight to CTA
49
Why does tension pneumo develop and what are physical exam findings?
- Ball valve phenomenon -->air enters the pleural space (either through defect in lung/visceral pleura or through chest wall/parietal pleura) on inspiration. On expiration-->valve like opening closes and this prevents drainage of pleural air
Physical exam findings: decreased breath sounds on affected side, hyper-resonance, tachycardia, hyopotention, tachypnea, mediastinal shift with tracheal deviation
50
Oncology patient who is receiving chemotherapy. They have fever, diffuse infiltrates, hypoxemia. Differential diagnosis?
Broad differential:
- Vascular: pulmonary hemorrhage - can get DAH as an early complication post HSCT. Thromboembolic (patients with malignancy has higher change of clot)
- Infection: high on the differential since they are immunocompromised.
- Inflammatory/Toxin: drug toxicity, radiation pneumonitis -->watch out for pneumotoxic drugs, especially if there is impaired kidney function. What does of radiation did they receive? (it will be hard to prove drug or radiation as being a cause for their presentation, unless you've rule out other things like infection; as well there is a variety for radiographic and histologic findings, nothing pathognomonic). Factors can work together synergistically so being on pneumotoxic drugs + radiation can cause lung injury.
- Autoimmune - less likely in this context
- Neoplastic - maybe progression of underlying malignancy
Practically:
- probably would do CT and bronch to get a better sense. Are there pathognomonic findings on CT like nodules, which might suggest fungal infection? Bronchoscopy to look for infection, hemorrhage...
51
Older patient (>2 years of age) with ILD symptoms (non-productive cough, dyspnea, poor activity tolerance)
Differential:
- Vascular: diffuse alveolar hemorrhage
- Infection - if immunocompromised-->chronic infection
- Bronchiolitis obliterans - related to post-infectious, rejection or GVHD
- aspiration
- ongoing disorder of infancy - NEHI, surfactant deficiency
- Inflammatory:
- systemic inflammatory disease - eg. lupus, scleroderma, sarcoid
- toxic exposures: pneumotoxic drugs, radiation, inhalational exposures
- autoimmune pulmonary alveolar proteinosis
- other: eosinophilic pneumonia, hypersensitivity pneumonitis, organizing pneumonia
52
complications of radiation therapy?
- acute pneumonitis (within 3 months of radiation)
- chronic radiation fibrosis (within 6-12 months of radiation)
- cryptogenic orgnanizing pneumonia
- impaired chest wall growth
53
risk factors for radiation induced lung injury?
- dose of radiation: >10 Grey units (mean lung dose)
- age of patient
- induction chemotherapy or concurrent chemotherapy - eg. bleomycin
- radiation recall (in a patient who received prior radiation therapy, giving chemotherapy can cause delayed radiation injury)
- younger age at radiation
54
Common organisms in CGD?
- Cadida
- Aspergillus**
- Nocardia
- Pseudomonas, PJP
- Listeria
- Burkholderia cepacia
- E. coli
- Staph aureus**
- Serratia
- H. pylori
(Cats Need PLACES to Belch their Hairballs)
55
Patient presents with primary spontaneous pneumothorax. Risk of recurrence?
60%
| Recurrence risk in patient with CF: 50-90%
56
Causes of secondary pneumothorax?
- Airway disease: asthma, CF
- Infection: necrotic pneumonia, PJP, TB
- Congenital: CPAM, congenital lobar emphysema
- Connective tissue disease: Ehler's Danlos, Marfan's, SLE, rheumatoid arthritis, dermatomyositis
- ILD: sarcoid, LCH
- aspiration
- cattamenial
- Neonates: RDS, meconium aspiration, pulmonary hypoplasia
57
Differential diagnosis for pleural effusion?
Transudative: no pleural pathology, normal capillary permeability, the main issue is because of changes in hydrostatic pressure and oncotic pressure. Eg. CHF, renal (nephrotic syndrome), liver failure, SVC obstruction, hepatic cirrhosis
Exudative: everything else that is not transudative is exudative.
- Hemothorax
- chylothorax:
- infectious - parapneumonia, empyema
- malignancy - leukemia, lymphoma
- inflammatory--RA, Churg strauss, sarcoid
- abdominal pathology - pancreatitis
- endocrine - hypothyroidism
- post op - eg. scoliosis surgery
58
What is Lyte's criteria?
- pleural fluid/serum
- protein >0.5
- LDH >0.6
- pleural fluid LDH>2/3 upper limit of normal serum LDH
59
Threshold for open thoracotomy in patient with hemothorax?
>1 cc/kg/min of blood then open thoracotomy
60
Complication of a retained hemothorax?
empyema
61
5 pulmonary complications of trauma?
- pneumothorax
- rib fracture, flail chest
- hemothorax
- tracheobronchial trauma such as transection
- contusion
- pulmonary compression injury (traumatic asphyxia)--cardiac and hepatic contusion, pneumothorax, interstitial emphysema
- post traumatic atelectasis
62
An example of pulmonary and extrapulmonary cause of ARDS?
pulmonary: pneumonia, aspiration pneumonia, drowning
extrapulmonary: sepsis, pancreatitis
63
COPY cards from other brainscape
To do
64
What are the different lung zones in ARDS?
- non-depenent: normal lung, "baby lung", which is at risk for over distension
- intermediate zone: edema and atelectasis, but recruitable
- most dependent zone: extensive consolidation and atelectasis and will not be recruitable
65
most common cause of death in ARDS?
multi-organ failure (surpisingly, not respiratory failure)
66
what is the role of high frequency ventilation in ARDS?
* earlier application of high frequency-->longer duration of ventilation
*
some studies have shown increased mortality with high frequency, regardless of when it was started
*
other studies have not shown increased mortality
*
basically, HFOV should not be used for all ARDS patients, but rather a select subgroup -->right now, it has a role in rescue, but not upfront
67
Bare bones description of ARDS?
Severe hypoxemic respiratory failure
68
Theoretical mechanism of HFOV in ARDS?
- maintain open lung and recruitment of collapsed alveoli (continuously applied mean pressure)
- minimize barotrauma (avoid high peak pressures and cyclical opening and closing of alveoli with each breath)
69
In which cases is HFOV helpful?
- maintain lung recruitment (since there is a continuously applied mean airway pressure)-->better VQ matching, better lung compliance
- can helpful for pulmonary hypertension, where a higher PCO2 will cause worsening of pulmonary hypertension-->eg. neonate with CDH and pulmonary hypertension
70
Differences between high frequency and conventional ventilation?
- keep the lung open around a high mean airway pressure
- low tidal volume (about the same as dead space volume)--gas exchange does not happen through bulk flow, which is the case with conventional ventilation
- active inspiration and expiration
71
How do you increase CO2 clearance on HFOV?
- Decrease the Hz (rate) so that there is more time to develop a tidal volume
- Increase amplitude
- Increase I:E ratio
(Oxygenation is affected by MAP and fiO2)
72
How does flail chest affect respiration? Management of flail chest?
(three or more ribs fractured in 2 more places, so not connected with chest wall)
paradoxical movement, which can be painful and can cause ineffective ventilation
other complications: atelectasis, pneumonia
Management: oxygen, pain control, non-invasive ventilation, mechanical ventilation
73
which strains of HPV most commonly cause respiratory papillomatosis and are they oncogenic?
6, 11
| non-oncogenic
74
Pathophysiology of ARDS?
- increased permeability at alveolar capillary interface
- leakage of protein rich material
- activation of coagulation
- inactivation of surfactant
- impaired alveolar gas exchange
- decreased lung compliance
- 4 stages (not all patients go through all these stages): exudative, fibroproliferative, fibrotic, recovery
75
PFT abnormalities associated with scoliosis?
- decreased FVC, TLC
- minimal effect on RV and FRC, so increased RV/TLC
- decreased MIP and MEP
start seeing lung function abnormalities at Cobb angle of 50-60 degrees, but very few signs and symptoms at Cobb<70 degrees (for sure at a Cobb angle >70, you would see lung function abnormalities)
76
3 long term complications of marijuana use?
- chronic bronchitis
- bullae, pneumomediastinum
- aspergillosis in immunocompromised patients
77
what are acute and chronic complications of vaping?
Acute:
- E-cigarette or vaping produce use associated lung injury (EVALI)—which has a very broad definition and varies pathologies including diffuse alveolar damage, acute eosinophilic pneumonia, hypersensitivity pneumonitis. Suspected compounds: THC containing products, vitamin E. Other mechanisms of injury: pyrolysis, thermal injury, release of metals
Chronic:
- Chronic bronchitis
- Chronic decline in FEV1
- Chronic airflow obstruction and possible bronchiolitis obliterans –at least 1 case report, which was in a Canadian youth:
78
What is the case definition Ecigarette or vaping product use associated lung injury (EVALI)?
- use of E-cigarette within 90 days of symptoms onset
- pulmonary infiltrate like opacity on CXR or ground glass on CT
- Absence of pulmonary infection, including negative respiratory panel and influenza PCR
- no evidence of alternate diagnosis
79
How does pulmonary hypertension present? (practically, what is the most sensitive time to be screening for symptoms of pulmonary hypertension)
- exercise related symptoms since cardiac output cannot be effectively increased to meet increased oxygen demands during physical activity
- exertional dyspnea, fatigue, chest pain (from right ventricular ishemia), syncope/presyncope (due to limited cerebral blood flow)
- cyanosis if there is shunt such ASD enabling right to left flow
- infants: failure to thrive, irritability, feed intolerance, pedal edema, sacral edema, malabsorption from intestinal edema
- polycythemia
80
Investigations for pulmonary hypertension?
- ECG, Echo, CXR to suspect the diagnosis and see if there are signs of left sided cardiac disease
- pulmonary evaluation: PFT, PSG, CT could be considered
- VQ scan--this is more sensitive for CTEPH, the periphery of the lung can be visualized better
- then cardiac cath with acute vasodilator testing
- look for more unusual causes: liver disease, connective tissue diseaes, HIV, hemoglobinopathy, genetics
- functional testing: 6 minute walk, CPET
81
What are the markers that we use to classify patients with PH as being high risk or low risk?
- WHO class: I and II is lower risk, 3 and 4 is higher risk
- Syncope is considered high risk
- Clinical evidence of RV failure
- Progression of symptoms is high risk
- 6 minute walk (>6 years): <350 m is high risk, >350 m is low risk (from Angela lecture)
- Echo: minimal RV enlargement/dysfunction versus significant enlargement/dysfunction or pericardial effusion
- Hemodynamics: PVRI<10 is low risk, PVRI>20 is high risk
- BNT/NTproBNP mildly elevated versus significantly elevated
- 6 minute walk distance: longer is >500 m, shorter <300 m (was on adult criteria)
- CPET: VO2>25 mL/kg/min or <15 mL/kg/min
- failure to thrive is a bad prognostic factor
- - 6 minute walk test not correlated with survival
- Maintenance of vasoreactivity correlates with survival
82
Treatment for pulmonary hypertension?
- High risk of decompensation during respiratory infections—>hypoxia—>worsening pulmonary hypertension
- Immunizations!!!
- Oxygen-->very important to think about if patient needs oxygen, even mild desaturation during sleep can contribute to worsening pulmonary hypertension. Consider need for supplemental oxygen during sleep, during ambulation. Likely to desaturate with intercurrent illness so patients should have an emergency supply of oxygen at home.
- Anti-coagulation
- Diuretics: but not too aggressive since PH is preload dependent (This is for right heart failure)
- Digoxin: oral inotrope (this is for right heart failure)
- Current recommendation: only anticoagulation if: right heart failure or hyper coagulable
- If they have positive acute vasoreactivity testing, then calcium channel blocker like nifedipine or amlodipine
- - For non-responders:
- Treatment approach depends on risk stratification
- If negative reactivity testing + low risk —>oral mono therapy (PDE5 inhibitor like sildenafil or tadalafil OR endothelia receptor antagonist like bosentan or ambirsentan)
- If negative reactivity testing + high risk—>IV epoprostenol or treprostinil. Surgical considerations: atrial septostomy or Potts shunt (descending aorta to left pulmonary artery shunt), lung transplant
83
Echo showing RV septal flattening. Is there PH?
>1/2 systemic is considered pulmonary hypertension
RV/LV - normal relationship is crescent on top of circle. If abnormal then more than 1/2 systemic.
84
Patient with asthma who has significant exercise dyspnea, chest pain, not improving despite asthma medication. What should you think of?
pulmonary hypertension
85
Side effects of prostacyclins used for PH treatment?
headache, flushing, hypotension, jaw pain with chewing, diarrhea, nausea, blotchy erythematous rash, MSK aches and pains
86
What are some considerations regarding PFTs in patients with pulmonary hypertension?
- DLCO will be decreased with PH, so could be helpful to track
- Ventolin in PH —>tachycardia, increased myocardial oxygen consumptions, try to avoid bronchodilator reactivity testing,
87
Treatment of PH crisis?
* avoid hypoxia, acidosis, agitation
*
induction of alkalosis
*
opiate, sedative, muscle relaxant
*
iNO and/or inhaled PGI2
*
sildenafil to prevent rebound PH in patients with sustained elevation of pulmonary artery pressure after withdrawal of nitric oxide and who have required reinitiation of NO, despite gradual weaning
*
inotropes/pressors to avoid RV ischemia due to systemic hypotension
*
atrial septostomy
88
When do evaluate for pulmonary hypertension in patients with lung disease?
* They make a vague recommendation that patients with chronic diffuse lung disease should be evaluated for PH
*
Severe OSA-->evaluate for PH
*
for exercise limited patient with advanced lung disease-->could do a trial of PAH targeted therapy
- Infant with BPD should be screened at 36 weeks, potentially additional screening sooner if there are other risk factors. If PH is present, then follow up echo in 1 month
89
Target saturation for infant with BPD and PH?
92-95% (aha/ATS 2015 guideline)
90
Recommendations regarding screening and management of PH in sickle cell disease?
* Sickle cell: echo at 8 years of age or earlier if they have frequent cardioresp symptoms
*
In patients with sickle cell who have pulmonary hypertension, contributing mechanisms for pulmonary hypertension: OSA, sickle cell chronic lung disease, thromboembolic disease since they are hypercoagulable
*
Invstigations: PFT, PSG, evaluation for thromboembolic disease, evaluate oxygenation
*
Treatment for PH with sickle cell: optimize sickle cell therapy (eg. blood transfusion, hydroxyurea, iron chelation, oxygen) before starting PAH targeted therapy
91
Side effects of nitric oxide?
methhemoglobinemia
platelet dysfunction
Rebound PH
92
Classification of pulmonary hypertension?
- Group 1: pulmonary arterial hypertension which includes:
- idiopathic
- genetic
- drug and toxin associated
- associated with: connective tissue disease, HIV, portal hypertension, congenital heart disease
- PVOD, pulmonary capillary hemangiomatosis
- PPHN
- Group 2: pulmonary hypertension due to left sided cardiac disease:
- LV systolic dysfunction
- LV diastolic dysfunction
- valvular disease
- congenital cardiomyopathy
```
Group 3: lung disease/hypoxia
- OSA
- alveolar hypoventilation
ILD
- developmental lung diseases
```
Group 4: CTEPH
Group 5: unclear multifactorial mechanisms including:
- hematologic disorders
- systemic disorders like sarcoid
- metabolic disorders
93
symptoms of HHT?
- cerebral: bleed (hemorrhagic stroke)
- pulmonary AVM: hemoptysis, hemothorax, embolic stroke, cerebral abscess, TIA, migraine, cyanosis, exercise intolerance, poor growth, clubbing
- epistaxis
- mucocutaneous telangiectasia
- GI bleed
- Liver: portal hypertension, jaundice, varices, ascites, high output cardiac failure
- cyanosis
- iron deficiency anemia
94
Indications for evacuation of air in a primary spontaneous pneumothorax?
Primary spontaneous:
- Tension pneumothorax: needle thoracentesis to the affected side, followed by intercostal drain
- Not under tension, then use size to help you decide treatment:
- >2 cm between lung margin and chest wall at hila: intercostal drain
- <2 cm: admit to hospital, conservative management with supplemental oxygen (may not consider oxygen for neonate)
Secondary spontaneous:
- insert an intercostal drain (regardless of size) b/c additional impact on respiratory function due to underlying disease
95
Indications for pleurodesis in spontaneous pneumothorax?
A first PSP and an air leak that fails to resolve after approximately five days of thoracostomy drainage.
● Recurrence of PSP (either ipsilateral or contralateral).
Secondary spontaneous pneumothorax--depends more so on the specific case:
Recurrent SSP (either ipsilateral or contralateral).
* Patients with cystic fibrosis and recurrence of a large SSP [47]. Pleurodesis using mechanical abrasion rather than chemical pleurodesis is preferred and does not preclude subsequent lung transplantation. (See "Cystic fibrosis: Overview of the treatment of lung disease", section on 'Spontaneous pneumothorax' and "Treatment of secondary spontaneous pneumothorax in adults".)
* Patients with a first episode of SSP due to other causes, if the underlying lung disease is severe, progressive, persistent, or is known to be associated with recurrent pneumothoraces
96
Management of tension pneumothorax?
large bore needle (14 of 16 Gauge) second intercostal space, mid clavicular line
97
What is an open pneumothorax? Physiological consequences? Treatment?
Open pneumothorax = sucking chest wound, atmostpheric air has direct and unimpended entry into pleural space
- on inspiration, air comes into this space and compresses the ipsilateral lung and drive it's alveolar air onto the opposite side
- on expiration, air will return across the carina
- there is paradoxical breathing and mediastinum swings like a pendulum
- minimal effective gas exchange since there is lots of dead space, more air is being exchanged at this site than at the trachea
- can hear air being sucked in and out of the wound
- Treatment:
- occlude the chest wall with a sterile dressing, put in an intercostal drain (want to prevent this open pneumothorax from becoming a tension pneumothorax)
- After stabilization, go to OR for surgical debridement and closure of chest wound
98
How much blood volume can accumulate in thorax?
40%
99
How does prostacylinc in pulmonary hypertension?
● Pulmonary vasodilator
● Reduce endothelial dysfunction
● Anti-platelet effect (important in thrombogenic milieu that may result from endothelial dysfunction)
● Inhibit SM proliferation
● Possible cardiac inotrope - I'm not sure about this
100
Diagnostic criteria for PARDS?
- Age: exclude patients with perinatal lung disease
- Timing: within 7 days of known clinical insult
- Origin of edema: respiratory failure not fully explained by cardiac failure or fluid overload
- Imaging: new infiltrate on chest imaging, consistent with acute parenchymal lung disease
- Oxygenation: on at least CPAP+5, with PaO2/FIO2 ratio of <=300 or SpO2/FiO2<=264
101
Stratify severity of PARDS?
OI of 8-15 is moderate (101-200)
OI <8 is mild (201-300)
OI >=16 is severe (<=100)
Higher OI is bad
Lower PaO2/FiO2 is bad
so these numbers go in the opposite direction
Oxygenation Index = [mean airway pressure (MAP) x fiO2 x 100]/PaO2
102
Recommendation for ARDS management based on ARDS net?
- tidal volume of 4-8 mL/kg (lower than prior tidal volumes of 10-15 mL/kg)
- low plateau pressure of <=30 cm H2O (lower than previous standard of 50 cm H2)
Other recommendations for management:
- high PEEP
- minimize fiO2
- prone positioning -->this is the lowest priority recommendation, only for patients with refractory hypoxemia
- don't forget to treat the underlying cause, eg. pneumonia
103
Pros/cons of heliox?
- Decreases airway resistance since flow is changed from turbulent flow to laminar flow
- Decreases work of breathing (since helium is less dense so less pressure gradient is required to drive flow)decreased work of breathing and patient is less likely to fatigue
- NOT curative
- NOT routinely recommended for asthma management in ED
- For the patient with respiratory distress who is tiring, it’s a bridge to more definitive management
- Disadvantage: less effective when helium is <70%, so not going to be helpful for patient needing significant amount of oxygen (since can only deliver about 20% oxygen)
- Conditions used for: croup, post-extubation stridor, asthma
104
Post HSCT, what are the different phases you think of to approach complications?
- Pre-engraftment: day 0-30 (early)
- Post-engraftment: day 30-100 (late)
- Late phase: >100
105
Post HSCT patient with respiratory symptoms within first 30 days, what is DDx?
Infectious complications:
- Bacteria: pseudomonas, G-, G+
- Fungi: Candida
- Viral: minimal
Non-infectious complications:
- pulmonary edema
- mucositis
- peri-engraftment respiratory distress syndrome
- diffuse alveolar hemorrhage, which is associated for bone marrow recovery
- idiopathic pneumonia syndrome
- veno-occlusive disease, which can be pulmonary or hepatic
106
What types of infections are seen in late (30-100 days) post transplant?
- Bacteria: staph aureus
- Fungi: PJP, Aspergillus
- Viral/protozoal (quite a few viral infections associated with this stage): EBV, CMV, VZV, adenovirus, Toxoplasma
- this is the phase where you seem to be at risk for most number of bugs
107
What types of infections are seen in the late phase (>100 days) post engraftment?
- Bacteria: H. influenza, Strep pneumo
- No predisposition for fungal infections
- Viral/protozoal: VZV
(don't seem to be at risk for that many unusual bugs)
(It seems like just at risk for non-opportunistic organisms
108
What are late complications (>6 months) post lung
- PTLD
| - Chronic lung allograft dysfunction
109
If suspecting PTLD, what imaging investigation to order?
PET scan
110
What are late non-infectious complications post HSCT?
- these late complications start as early as 2- 3 months post transplant
- Bronchiolitis obliterans, which is often part of chronic GVHD
- ILD - often due to drugs or radiation
- Cryptogenic organizing pneumonia
- PTLD
111
Patient who is 12 months post HSCT, who has SOB and wheeze, top of differential?
- Bronchiolitis obliterans
- Investigations:
- PFT: non-reversible airflow obstruction
- CT: inspiratory and expiratory -->mosaic attenuation
* Treatment:
* Increased immunosuppression: calcineurin inhibitors, azathioprine, steroids
* Azithro + LTRA + ICS/LABA (FAM)
112
Patient who is >3 months post HSCT with dyspnea and PFT showing restriction and decreased DLCO?
- ILD
| - COP
113
Gold standard for diagnosis of PE?
CT chest- pulmonary angiography
114
Risk factors for PE
- Oral contraceptive use
- Pregnancy
- Drugs - heavy cigarette smoking (>=20 packyears, probably difficult to achieve this level for a teenager), IV drug use (in particular injection into femoral veins, which casues direct trauma, irritation, infection), glucocorticoids, antidepressants
- Obesity
- Antiphospholipid antibody syndrome
General risk factors:
- Inherited thrombophilia: factor V Leidein, Prothrombin gene mutation, protein C or S deficiency, antithrombin deficiency
- Acquired:
- Malignancy
- Recent surgery, particularly orthopedic, major vascular, neurosurgery, and cancer surgery
- Major trauma
115
List 5 categories and provide 1 example of each for pulmonary hypertension
1. Pulmonary arterial hypertension:
- idiopathic
- genetic
- drug and toxin
- associated with: HIV, portal hypertension, congenital heart disease, connective tissue disease
- PAH with overt signs of PVOD/PCH (pulmonary capillary hemangiomatosis)
- PPNH
2. PH due to left heart disease - left ventricular systolic dysfunction, diastolic dysfunction, valvular disease, congenital left sided cardiac disease
3. Due to lung disease and/or hypoxia: ILD, COPD, any lung disease with restrictive/obstructive component, hypoxia, sleep disordered breathing, developmental lung disorders
4. Due to pulmonary artery obstruction - CTEPH and other types of obstruction
5. Unclear mechanisms:
- Hematologic - eg. chronic hemolytic anemia
- Systemic disorders - eg. sarcoid
- Metabolic - glycogen storage, gaucher, thyroid
116
Definition of pulmonary hypertension
mPAP >20 mmHg in child >3 months of age at sea level
117
Definition of pulmonary arterial hypertension
mPAP>20 in a child >3 months of age at sea level
pAWP or LVEDP <=15 mmHg
Pvri >= 3 WU
(the other card has more comprehensive definition)
118
categories or drugs and an example for each that are used for treatment of PH
NO pathway - eg. exogenous nitric oxide or phosphodiesterase type 5 inhibitor, like sildnafil
Endothelin pathway - eg. bosentan, endothelin receptor antagonist
Prostacyclin pathway - eg. prostacylin analogue like epoprostenol
119
Medications that can be used for sialorrhea and side effects?
Anticholinergic - glycopyrrlate, scopolamine, atropine. S/E: photophobia (blind as a bad),, behavioural change (mad as a hatter), flushing (red as a beet), full as a flask (urinary retention, constipation), difficulty with temeperature regulation (hot as a hare), thickening of secretions can lead to life threatening obstructions. Need to be very careful with use of these medications in patients with neuromuscular disease or small tracheostomy tube.
Botulinum toxin: pain, dry mouth, speech impairment, difficulty swallowing (basically if the dose is too high, then you get effects on surrounding tissues).
In general, the anticholinergics are NOT well tolerated due to side effects. Botulinum toxin seems to be better tolerated if appropraite do
120
1 example of benign and malignant mediastinal mass in each compartment
- Anterior mediastinum: thyroid goitre for benign, lymphoma for malignant
- Middle: lymph node enlargement from sarcoid (benign), bronchogenic cyst (benign), lymphoma (malignant)
- Posterior: neuroblastoma (malignant), meningocele
121
Light's criteria for pleural effusion
Pleural fluid protein/serum protein >0.5
Pleural fluid LDH/serum LDH >0.6
Pleural fluid LDH >2/3 upper limit of normal
If one of these crtieria is met then the fluid is an exudate
122
What are the 4 clinical features considered in the PCD diagnosis algorithm?
- Year-round daily productive wet cough starting at <6 months
- Year round, daily, non-seasonal rhinosinusitis beginning at <6 months
- Above 2 are often present often immediately after birth
- Neonatal respiratory distress in term infant (needing oxygen or PPV x >24 hours with no clear explanation)
- Organ laterality defect
If 2 out of 4 present, then sensitivity and specifity for diagnosis of PCD is about 75%. (still not the most sensitive criteria)
- Term newborn with unexplained respiratory distress and organ laterality is very likely to have PCD, even if they have not yet developed nasal congestion and cough.
123
How many genes are linked to PCD and how many are included in an extended genetic panel?
39 genes are linked to PCD
| An extended genetic panel should test for >12 genes
124
What is a low nasal nitric oxide?
<77 nL/min
125
What is the first choice diagnostic test for PCD and what are the caveats?
- First choice is nasal nitric oxide since it is reliably low in PCD. If it's normal then you can be pretty sure that PCD is excluded
- In contrast, for genetics-->even if no variant is found, you still go on to do electron microscopy. Even if electron microscopy is normal, PCD is still possible b/c 30% have normal EM.
- In a child >5 years of age, who has had CF excluded (negative sweat chloride), then nasal NO is the preferred first test. Since viral illness and sinusitis can also cause low nNO, the test has to be repeated on 2 separate occasions, at least 2 weeks apart
126
In a patient suspected of PCD, if nasal NO is low x 2, do you do any further investigations?
Genetic investigation as a next step +/- TEM to provide prognostic information
127
If child is <5 years of age, non-cooperative or no access to nNO, how do you proceed with PCD work up?
Extended genetic testing panel, which includes at least 12 genes
128
If PCD genetics are not positive for diagnosis of PCD (eg. 1 pathogenic variant, no pathogenic variants, variants of uncertain clinical significance), do you do any further investigations?
Yes, do TEM
129
Respiratory complications of Hunter syndrome?
Hunter’s syndrome is type II mucopolysaccharidosis, which is a type of lysosomal storage disorder
- Deposition of glycosaminoglycans in throat and trachea-->airway obstruction, OSA (they frequently need CPAP)
- Tracheobronchomalacia from deposition of GAG in tracheal/bronchial cartilage -->this can affect airway clearance and cause recurrent infection infection,
- Restrictive lung disease due abnormal shape of ribs, scoliosis, pectus carinatum, enlargement of abdominal organs which affects diaphragm excursion
- Recurrent pneumonia due to above mechanisms
130
why do lymphatic disorders cause chylothorax and protein losing enteropathy?
Lymphatic fluid leaks into pleural space.
Lymphatic fluid leaks into intestinal lumen-->protein losing enteropathy
(Chyle is lymphatic fluid that contains chylomicrons since it is coming from intestinal lymphatics)
131
In a patient with a lymphatic malformation, when should you suspect a complex lymphatic abnormality?
* Lytic bone lesions
* Presence of nonmalignant chylous effusion (pleural, pericardial, peritoneal)
* Evidence of protein losing enteropathy, with no other proven ethology
132
Examples of complex lymphatic abnormalities and distinguishing features?
Generalized lymphatic abnormality: chylothorax, lytic bone lesion
Gorham stout: lytic bone lesion, chylothorax
Kaposiform lymphangiomatosis: soft tissue mass, consumptive coagulopathy, thrombocytopenia
133
Long term complications of TEF?
- Esophageal stricture and abnormal motility-->reflux and aspiration
- Tracheomalacia
- Recurrent pneumonia
- Recurrent TEF
- Bronchospasm
134
How is chronic cough defined?
>4-8 weeks of cough (Kendig's)
135
Approach to chronic cough
Dry cough:
o Allergic rhinitis and post nasal drip
o Asthma
o GERD
o Tracheobronchomalacia +/ - an associated abnormality like vascular ring
o Habit cough
o Interstitial lung disease – eg. Eosinophilic lung disease
o Post infectious cough: Pertussis and Mycoplasma pneumonia (Kendig’s)
o Drugs like ACEi
- Wet cough:
o Cystic fibrosis
o Primary ciliary dyskinesia
o Retained foreign body – consider in child<5 years, typically wet cough, but could be dry. Associated: wheeze, halitosis.
o Aspiration
o Immunodeficiency
o Chronic endobronchial suppurative disease:
§ Non-CF bronchiectasis- eg. Immunodeficiency
§ Persistent bacterial bronchitis
- Other:
- Chronic infection: TB (cough, monophasic wheeze from hilar lymphadenopathy or tuberculoma), fungal (histoplasmosis, cocciodoides), Chlamydia pneumonia, Mycoplasma pneumonia, non-tuberculous mycobacteria
- In a younger infant-->Chalmydia trachomatis, CMV can cause “afebrile pneumonia of infancy”
- Non-infective bronchitis: from exposure to environmental pollutants - environmental tobacco smoke, biologic pollutants (eg, dust mite, mold, pets), nitrogen dioxide from unvented gas heating, and particulate matter from wood stoves and cooking
- Mediastinal mass
