Pulmonology Flashcards
Treatment acute asthma exacerbation
BIOMES
Beta-agonists Ipratropium Oxygen Mg sulfate Epinephrine Steroids
Which disease causes a low V/Q ratio?
V/Q mismatch is a ventilation to perfusion mismatch -
A low V:Q ratio could occur with decreased ventilation or a relative increased perfusion
Disease that could cause decreased ventilation:
Pneumonia - consolidation in alveoli
COPD - dec gas coming into alveoli b/c of mucus thickening/build up
Pulm edema - fluid overload in lungs (in alveoli)
What is perfusion with absolutely no ventilation called?
Pulmonary shunt
What is ventilation?
Ventilation is the amount of air/gas traveling into alveoli ready for gas exchange
This is abbreviated V
What is perfusion?
Amount of blood flow to the alveoli that is prepared for gas exchange as well
This is abbreviated Q
How does COPD affect ventilation and perfusion of the lungs?
Decreases ventilation because of mucus plugs in terminal alveoli (chronic bronchitis = mucus & inflammation)
LATE stage COPD also decreases perfusion b/c the capillary beds of the alveoli are destroyed
What is the local response to a low V:Q ratio?
The resultant hypoxemia = local vasoconstriction = pulmonary HTN = RAE/RVH = R-HF = cor pulmonale
What pulmonary diseases cause a HIGH V/Q ratio?
HIGH V/Q ratio = no perfusion! (denominator small)
Pulmonary embolism - clot cuts off blood supply (perfusion) to capillary beds - absolute = called dead space
Also in late stage COPD capillary beds are destroyed = decreased perfusion
Pathophysiology of chronic bronchitis of COPD
Causes inc or decrease V/Q?
What does it lead to terminally if not addressed?
“Blue bloaters”
Pathophys: Chronic inflammation, increased mucus hyper-secretion = chronic productive cough.
= Decreased ventilation (O2/air into lungs) 2/2 mucus plug in terminal alveoli = alveolar hypoxia - O2 not getting thru to alveoli efficiently = hypercapnea (too much CO2 = resp acidosis) and decreased O2 in blood - (body will make more to compensate = inc Hgb = polycythemia)
Dec O2 getting in = dec O2 in blood & inc CO2 in blood = alveolar hypoxia = pulm vessel constriction to shunt blood to healthier alveoli = inc pulm vasc pressure = pulmonary hypertension = backflow of blood to R side of heart = right sided heart failure = cor pulmonale = inc JVD
THIS IS WHY chronic bronchitis of COPD is classically a/w right heart failure 2/2 pulm HTN (cor pulmonale) & why the only medical treatment that reduces mortality is in COPD is oxygen (O2 reduces the hypoxic vasoconstriction)
Low O2 in = CYANOTIC = BLUE BLOATERS
Pathophysiology of emphysema?
Emphysema = “pink puffers”
Prominent thoracic cage, barrel-chested, cachectic (muscle wasting)….but why?
Inflammatory response from cigarette toxins (macro = cytokines = WBC-producing elastase prod) = breakdown of elastic fibers & destruction of alveolar walls = loss of alveolar integrity/recoil = AIR TRAPPING = a ton of gas left in alveoli even after you expire b/c they’re not elastically recoiling like they’re supposed to so you can’t get air out = inc end expiratory volume = BARREL CHEST - usually expiration = passive - use a TON of energy & accessory muscles to try to get more air out & to breathe air in = pink puffer - dyspnea & cachexia
Destruction of wall = decreased ventilation b/c of loss of elastic recoil
Destruction of wall and capillary beds = decreased perfusion
Emphysema = matched V/Q deficit - have dec O2 and inc CO2 in blood - same hypoxemia & hypercapnea that occurs in chronic bronchitis but not as severe
Pathologic description: abnormal permanent enlargement of terminal airspaces
Definition of chronic bronchitis
Productive cough x3 months for two consecutive years
Why are patients with chronic bronchitis from COPD prone to microbial infections?
Because mucus plugging & mucociliary escalator destruction = body can’t get bugs out & perfect environment for bac to grow :(
What is the most common symptom of emphysema?
Dyspnea
Describe a patient with severe emphysema?
PINK PUFFER
DYSPNEIC
Accessory muscle use, tachypnea, prolonged expiration, cachectic, pursed-lip breathing
Describe a patient with chronic bronchitis?
BLUE BLOATER
Chronic productive cough = HALLMARK SYMPTOM
Obese & cyanotic
PE of chronic bronchitis vs emphysema
Emphysema: Hyper-resonance to percussion Decreased breath sounds Decreased tactile fremitus Barrel chested (inc AP diameter) Pursed lip breathig
Chronic bronchitis:
Rales (crackles), wheezing that changes in location w/ cough, signs of cor pulmonale (peripheral edema, cyanosis)
V/Q mismatch in emphysema vs chronic bronchitis
Emphysema: Matched V/Q defects, mild hypoxemia
Chronic bronchitis: Severe V/Q mismatch = severe hypoxemia, hypercapnia
ABG/Labs in chronic bronchitis vs emphysema
Chronic bronchitis: Respiratory acidosis - retention of CO2 and increased Hct/RBC count (polycythemia) 2/2 chronic hypoxia that stimulates EPO)
Emphysema - either
What is the gold standard for diagnosis of COPD?
PFTs/Spirometry
FEV1 < 1 L = inc mortality
FEV1/FVC < 0.7 = obstructive lung dz
More emphysema =
Decreased DLCO
Hyperinflation = increased lung volumes - TLC, RV etc
CXR findings in emphysema
Emphysema: Hyperinflation Flat diaphragm Inc AP diameter Dec vascular markings \+/- bullae/blebs
Chronic bronchitis:
Inc vascular markings
Enlarged right heart border
EKG findings chronic bronchitis
Remember chronic bronchitis = cor pulmonale eventually b/c chronic local hypoxemia = vasoconstriction = pulm HTN = RAE/RVH = R-HF = cor pulmonale
ON EKG:
RAE = p wave amplitude > 2.5 mm)
RVH = RAD, poor r wave progression
Signs R-heart strain etc (s wave in 1, Q in 3, T in 3)
Atrial enlargement = afib/flutter, or multifocal atrial tachycardia
Triggers for COPD exacerbation
Pollutants, beta blockers (non-selective = bronchoconstriction), infections (viral bronchitis, bacterial pna (HCAP)
What is the most important step in the management of COPD?
Smoking cessation
What is the mainstay of COPD treatment?
Besides smoking cessation (= most important management tool), anti-muscarinics to initiate bronchodilation - prevents broncho-constriction - opens up airways, gets more air in
Management of exacerbation of COPD
Keep SaO2 > 90%
Nebulizer (albuterol (SABA or duoneb w/anti-muscarinic)
Add oral or IV corticosteroids
Consider abx therapy
Consider ABG to check for acidosis (CO2 retention) in hospitalized/sick pt
Role of spirometry in COPD
Initial assessment -
diagnosis and prognosis
Follow up assessment -
Rapidly declining lung fxn
Definition of COPD exacerbation
An acute worsening of respiratory sx that results in additional therapy
Mild - SABA/SAMA only
Moderate - SABA, steroids, +/- ABX
Severe - hospitalized
Name the two SABA used in acute COPD exacerbations
Albuterol
Levalbuterol ($$$)
Name the only SAMA
Ipratropium
Comes before T (tiotropium) in the alphabet, acts shorter
Name the only SAMA
Ipratropium
Comes before T (tiotropium) and U (umedlidinium) in the alphabet, acts shorter
Name the 4 LAMA’s used in COPD maintenance
Tiotriopium
Umeclidinium
Aclidinium
Glycopyrrolate
Name the some LABA’s used in COPD maintenance
Anything that ends in “ol” that is not albuterol/levalbuterol (SABS’s)
Salmeterol
Formoterol
Olodaterol
Does regular use of a SABA or SAMA in COPD improve FEV1 and symptoms?
YES
Is combination therapy, or a LABA or LAMA alone superior in improving COPD symptoms and decreasing exacerbation rates?
COMBINATION TREATMENT is superior!!!
Do LAMA’s or LABAs have greater effect on exacerbation reduction?
LAMA’s have greater effect on exacerbation reduction !!!
This is why group C patients (exacerbations prominent w/ less symptoms) a LAMA Is preferred initial treatment, with second treatment being a combo LAMA/LABA if that doesn’t work
Are SAMA’s or SABA’s preferred monotherapy in preventing acute mild exacerbations with moderate/severe COPD?
SAMA’s
Are short-acting or long-acting preparations preferred in COPD maintenance?
Long-acting - for both anti-muscarinics and beta2-agonists
What is the only treatment shown to slow the progression of COPD?
STOP SMOKING
What is the only treatment that reduces mortality in COPD?
OXYGEN
Red flags of COPD management
ICS alone….?! Can increase infections in severe COPD and doesn’t help the airflow obstruction, especially if they have predominantly emphysema-type - need a BRONCHODILATOR = mainstay of COPD therapy
Therapeutic duplicaiton - 2 LABA’s or 2 LAMA’s etc
OTC cough medicine
Poor or erratic adherence
Prevention of exacerbations
Pneumococcal vaccine
Flu vaccine every year
Pulmonary rehab - improves QOL, subjective DOE & exercise tolerance
Indications for abx in COPD exacerbation
Used only for acute bacterial exacerbations of chornic bronchitis IF….
Increased sputum
Change in sputum quality
And/or CXR evidence of infection
Remember azithromycin has anti-inflammatory properties in the lung!
Mild (stage I) COPD definition
Fev1/FEV < 70%
And FEV1 >80%
Therapy: SABA, SAMA
Vaccinations
Moderate (stage II) COPD definition
FEV1/FEV < 70%
And FEV1 50-79%
Therapy:
If FEV1 is not >80%, need a long acting bronchodilator, short not good enough anymore:
LAMA/LABA
Severe (Stage III) COPD definition
FEV1/FEV < 70%
And FEV1 30-50%
Therapy:
Stage II recs: LAMA/LABA
PLUS: Pulmonary rehab & steroids if increased exacerbations
Very severe COPD (Stage IV)
FEV1/FEV < 70%
FEV1 < 30%
Cor pulmonale
Respiratory failure
Stage III recs: LAMA/LABA, pulmonary rehab & steroids if increased exacerbations
PLUS
O2 therapy
What is the signet ring sign? what disease is it seen in?
Signet ring sign is a pulmonary artery coupled with a dilated bronchus seen in bronchiectasis
What are the MC CXR findings in bronchiectasis?
On CT?
“tram-track” markings
Irregular opacities
Crowded bronchial markings
Proximal airway dilation w/ thick walls & lack of airway tapering giving “tram-track appearance
Anything that talks about PROXIMAL (larger airways) that are dilated with thick walls…think bronchiectasis
Pathophys of bronchiectasis?
Permanent abnormal dilation & destruction of BRONCHIAL walls = LARGE airway disease
CF causes >50% of all cases - B. thought to be caused by recurrent inflammation or infection (Rb, fungal, lung abscess, PNA - MYCO!, alpha-1 anti-trypsin def) - lung develops an abnormal defense mechanism that leads to localized airway obstruction = OBSTRUCTIVE physiology
Since infection is the trigger, antibiotics are ALWAYS part of the treatment
Sign & sx of bronchiectasis
VISCID THICK sputum
Chronic daily cough
Rhinosinusitis
Recurrent pleurisy (2/2 lung lining inflam)
Chronic pulmonary crackles
Wheezing
Dx bronchectasis
High resolution CT scan
Will show airway dilation
Lack of tapering of bronchi (BRONCHIAL DILATION!!!)
“Tram-track” (WALL THICKENING)
Mucopurulent plugs consolidations
“Signet ring” sign (= pulmonary artery coupled with a dilated bronchus)
PFTs bronchiectasis
Will show obstructive pattern
Dec FEV1, Dec FVC
FEV1/FVC < 70%
MC pathogen if bronchiectasis is caused by CF
PSEUDOMONAS
3 problematic pathogens a/w bronchiectasis
Pseudomonas (CF)
Mycobacterium avium complex (MAC) - clarithromycin & ethambutol
Aspergillus - thick brown sputum - corticosteroids & itraconazole
Cornerstone of bronchiectasis tx
ANTIBIOTICS
Thick brown sputum
Aspergillus bronchopneumonia
Tx: Itraconazole, corticosteroids
CF etiology, epidemiology
Autosomal recessive mutation in cystic fibrosis transmembrane receptor (CFTR) - defect prevent chloride transport (water movement out of cell) = build up of thick, viscous, mucus in the lungs, pancreas, liver, intestines & reproductive tracts = obstructive lung disease & exocrine gland dysfunction (pancreatic insufficiency)
Indications for bronchoscopy in bronchiectasis?
If have hemoptysis & you’re worried about a tumor
If a therapeutic intervention & you want to removed retained secretions
If you’re worried about obstructive airway lesions (foreign body)
BUT dx = HIGH RES CT!
Someone with recurrent respiratory infections and chronic sinusitis….you’re thinking what?
Cystic fibrosis!!!
Sign is recurrent URI - esp pseud & staph - productive cough, chronic cough, sinusitis
Three most common clinical manifestations of CF
- GI:
- Meconium ileus at birth (DO CF TEST!)
- Pancreatic insufficiency (dec ab fat-soluble vitamins ADEK & steatorrhea, pale stools, weight loss - FTT in kids) - Pulmonary:
- Recurrent URI, chronic sinusitis - Infertility (95%)
What do you do if a full term infant presents with meconium ileus?
DO A CF TEST!!!
Dx of CF
Sweat chloride test
People with CF will have increased chloride levels in their sweat
< 29
30-59 = may have it, additional testing needed
> 60 mmol/L on two occasions after administration of pilocarpine (cholinergic drugs that induces sweating)
Management CF
- Airway clearance tx: bronchodilators, mucolytics, abx, degongestants
- Pancreatic enzyme replacement, supplement fat-soluble vitamins
CXR of CF
Will show bronchiectasis:
Nonspecific findings, tram-track, irregular opacities, crowded bronchial markings (peribronchal fibrosis), signet ring sign etc
Name 4 lung diseases with obstructive physiology & name what their PFTs would likely show
Asthma
COPD
CF
Bronchiectasis
PFTs: FEV1/FVC < .7 Dec FEV1 Dec FVC TLC INCREASED RV increased
What is the definitive test for CF? What is the gold standard test?
Definitive:
DNA analysis
Initial & GOLD standard:
Sweat chloride test
4 restrictive lung diseases and their expected PFTs
Sarcoidosis Pneumoconiosis Idiopathic pulm fibrosis MG (dec effort to expand) Mesothelioma Scoliosis, kyphosis
PFTS:
DECREASED lung volumes
Normal or inc FEV1/FVC
Dec TLC, RV, etc
WHEEZING more indicative of COPD or asthma
Think more asthma in general
Predominant cell in pathophysiology of asthma
Eosinophil - airway hypersensitivity and hyper-reactiveness - to ALLERGENS = mast cell degranulation = histamine, leukotriene, IgE, cytokine release =
Early response: Bronchospasm, edema, airflow obstruction (reversible)
AND
Late response:
Airway inflammation
Airway hyper-responsiveness
Child with recurrent episodes of chest tightness, wheezing and SOB..what to do?
Refer for spirometry
Measure baseline FEV1
Give bronchodilator
FEV1 inc >12% & or FEV1 inc >200 ml = ASTHMA =
REVERSIBLE airway obstruction!!!
If spirometry comes back normal, can order methacholine challenge = cholinergic that asthmatic pt will have an exaggerated response to (>20% decline in FEV1 is diagnostic)
Initial evaluation of asthma
Spirometry w/ bronchodilator test
HX - exzema, allergic rhinitis,
Refer for allergy testing (decreasing triggers = dec need for meds!!! Control sneeze = control the wheeze)
Stage the asthma severity - based on functional impairment (symptom burden) and risk of exacerbations
What is a part of every asthma action plan?
- Daily management - controller medication & environmental control measures (avoid triggers)
- How to manage worsening asthma - how to adjust meds, when to seek medical care
What is the easiest way to assess asthma control?
Peak flow
Make sure pt has personal best peak flow recorded when healthy
Then if they’re at 80-100% of that = green zone = continue w/ regular activities
50-80% = yellow zone - may require med adjustment/intervention - contact health care provider
<50% = emergency - dial 911
Risk factors for death in asthma (4)
Prior severe exacerbation (intubation/ICU)
2+ hospitalizations or 3+ ED visits in the past year
> 2 canisters of SABA per month (call pharm to see)
Poor perceiver of sx, LSES, illicit drug use, psychiatric disease, severe comorbidities
REFER TO PULMONOLOGIST IF PT HAS THESE!!!
Consider pulmonologist if hospitalized, difficulty achieving control & on Step 4 adults or step 3 kids, if immunotherapy is under consideration or if > 2 oral steroid bursts in past year
What is the preferred treatment for long term management of asthma?
INHALED CORTICOSTEROIDS
What monotherapy is contraindicated in asthma?
LABA
NEVER USED ALONE IN ASTHMA MAINTENANCE
CAUSES INCREASED NUMBER OF DEATHS IN TRIAL!!!
YOU MUS HAVE AN ANTI-INFLAMMATORY CONTORLLER AGENT
Why are ICS the TOC for maintenance therapy for asthma?
Because the main pathophys involves inflammation and immune system/ bronchial hypersensitivity to allergens/irritants
To prevent this immune response and resultant inflammation we need an inhaled corticosteroid on board
Bronchodilators can only open up airway so they help but aren’t directed right at main pathophys of diseae
Asthma treatment
CONTROLLER: ICS =
Fluticasone, flunisolide, beclomethasone, mometasone, budesonide etc
RESCUE: SABA =
Albuterol
Stepwise approach to asthma tx
Start on SABA if step 1 (exercise-induced, intermittent - SABA<2x/week, awake < 2/mo, 0-1 exac/year)
Otherwise all need a controller - start w/ low dose ICS, then add LABA (-ol) or increase to med dose ICS If not controlled
5 YO + can try LTRA (zafirlukas, montelukast, zilueton - MONTE = preferred) if > or equal to step 3 as well but not the preferred regimen
When would you consider biologics in asthma management?
LAS LINE therapy - for pt who are step 5/6 who have ALLERGIC asthma with HIGH IgE ab counts who are very poorly controlled on high dose ICS & flaring frequently
Formulations of biologics for asthma
Xolair (omalizumab)
Cinqair (reslizumab)
Nucala (mepoluzumab)
Must have eosinophilic type asthma not controlled on ICS + skin testing for allergies
When do you give oral steroids in asthma?
May be needed to re-establish asthma control if:
Failure of SABA to produce sustained response
Given promptly if pt is deteriorating, if have already tried rescue inhaler before presenting
Continue OCS for 5 days
ACUTE ASTHMA ATTACK managment
- Stacked albuterol nebs
2.
Classic triad asthma sx
- Wheezing
- SOB
- Cough (**esp at night)
Also chest tightness, “lungs feel tight” etc
PE asthma
Prolonged expiration Expiratory wheezing Decreased breath sounds Tachycardia Tachypnea Use of accessory muscles
What is the best & most objective way to assess asthma exacerbation severity & responses to a treatment in the ED?
Peak expiratory flow rate
PEFR> 15% initial value = response to treatment
Normal = 400-600
Admission criteria vs discharge criteria acute asthma attack
Admit: PEFR <50% (red zone), prior ER visit w/in 3 days this exacerbation, status asthmaticus, post-treatment failure, AMS
Discharge:
Admission criteria vs discharge criteria acute asthma attack
Admit: PEFR <50% (red zone), prior ER visit w/in 3 days this exacerbation, status asthmaticus, post-treatment failure, AMS, no air movement (garden hose closed)
Discharge: PEFR > 70%, clear lungs w/ good air movement, adequate follow up w/in 24-72 hrs, response sustained >1 hr post-treatment
What is sarcoidosis?
Chronic, MULTI-systemic, inflammatory, granulomatous d/o or unknown etiolgy
What is sarcoidosis? Pathophys?
Chronic, MULTI-systemic, inflammatory, granulomatous d/o or unknown etiology
Patho: Exaggerated T-cell response to variety of antigens or self-antigens = granuloma formation (mass of immune cells that’s walled off) –> the granulomas (non-caseating) –> the granulomas disrupt normal structure and or function of tissues they form in, resulting in clinical manifestations seen (pulm, LAD< skin, eyes, heart, rheum, neurologic) etc
Typical pt w/ sarcoidosis
20-40 YO AFRICAN AMERICAN or northern european FEMALE
Two most common organ systems involved in sarcoidosis
Lungs - dry nonproductive cough, chest pain, dyspnea
Skin - erythema nodosum, lupus pernio = PATHOGnomonic!!!
Although Eyes = 2nd MC system causing complications - anterior uveitis (blurred vision)
Clinical manifestations of sarcoidosis
SARCO-Not Me!
Skin - erythema nodosum, lupus pernio
Anterior uveitis (inflam of iris/ciliary body = blurred vision, ciliary flush etc - optho exams yearly!)
Rheum - arthralgia, fever, malaise
Cough - dry, nonproductive cough & CP (90%)
O - think of O as a large lymph node - B/L hilar and RIGHT peritracheal LAD = V COMMON but not specific
Not - neurologic - CN VII palsy, DI, pituitary lesions - SARCO-NM = 7, = CN 7 palsy!!
Me - myocardial - infiltrative restrictive cardiomyopathy, arrhythmias!!
Def of interstitial lung disease
Signs of ILD on a CXR
Examples of interstitial lung dz
Definition:
Interstitial lung dz = diseases of lung parenchyma (happening w/in pulm interstitium) = inflam/scarring of the lung tissue = leads to restrictive lung disease
Signs on CXR:
Reticular opacities, +/- fine ground glass appearance
Examples:
- Idiopathic fibrosing interstitial PNA
- Pneumoconiosis (any occupational lung dz inc coal worker’s lung, silicosis, asbestosis etc)
- Sarcoidosis
Stage I sarcoidosis on CXR
Bilateral hilar lymphadenopathy (no sx or mild pulm sx)
Stage II sarcoidosis on CXR
Bilateral hilar LAD & moderate pulm sx
Stage III sarcoidosis on CXR
Interstitial lung disease on CXR
Reticular opacities, +/- fine ground glass appearance
Stage IV sarcoidosis on CXR
Fibrosis (volume loss and full on restrictive lung disease)
What is the most common finding on PFTs in sarcoidosis?
Isolated decreased DLCO (diffusing capacity of CO2 the lung) 2/2 firbrosis
Can also see restrictive patterns w/ advanced dz (dec TLC, RV, normal FEV1FVC etc)
Diagnosis of sarcoidosis
- Compatible clinical and radiologic findings
- Noncaseating granulomas
- Exclusion of other diseases
Lab studies supporting dx of sarcoidosis (3 specific ones related to granulomas/immune rxn)
- 40-80% have increased ACE bc granulomas secrete it
- Hypercalciuria/hypercalcemia - 2/2 granuloma = ince activated vit D prod
- Cutaneous anergy (70%) - aka no skin response to skin allergens b/c peripheral immune system depressed b/c central immune system activated
Also: Inc IgG, eosinophilia, leukopenia, Inc ESR
When would you use a broncheolar lavage in relation to sarcoidosis and what would it show if it was sarcoidosis?
Broncheolar lavage is used to r/o other infectious causes of granulomas
It would show inc CD4 in relation to CD8 if sarcoid (sarcoidosis = 4 syllables = more CD4)
Management of sarcoid
- Observation- most have spontaneous remission w/in 2 years (fibrosis = poor prognosis, but good prognosis overall)
- Oral corticosteroids - TOC when treatment is needed - reduces granuloma formation & fibrosis - ACE levels usu fall after clinical improvement after OCS
Indications for oral corticosteroids in sarcoid
Worsening sx
Deteriorating lung fxn
Progressive radiologic decline
**MUST rule out Tb & infectious etiologies before initiating OCS
When is hydroxychloroquine used in sarcoid?
For chronic disfiguring skin lesions/granulomas
Which two factors are a/w poorer prognosis in sarcoid?
- ILD
(stage III CXR w/ Reticular opacities, +/- fine ground glass appearance, PFTs of restrictive pattern etc) - Lupus pernio
Lupus pernio is pathognomonic for which disease? Describe
for sarcoid
Looks like frost bite - violaceous raised discoloration of nose, ear, cheek & chin
What is the classic sarcoid presentation in clinical practice?
Young female w/ respiratory sx (dry nonproductive cough) & systemic sx (malaise, fever, arthralgias) ….sounds like a bronchitis or PNA maybe BUT will also have BLURRED VISION….weird & doesn’t fit PNA….AND likely have skin involvement (painful nodules)….also weird if just PNA…..
Must recognize this pattern! Cough + Blurred vision + Painful skin nodules = Sarcoidosis
What do sarcoidosis granulomas consist of?
Langerhan’s giant cells w/ star-shaped areas or Schuamann bodies
Epitheloid macrophages
Asteroid bodies
What is the most common interstitial lung disease?
Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis)
What is chronic progressive interstitial fibrosis caused by?
Persistent inflammation (chronic alveolitis) –> loss of pulmonary function with restrictive component
Etiology unknown
Survival < 10 years at time of diagnosis aka POOR prognosis
What would the typical Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis) patient look like?
40-50 YO MALE SMOKER
Dx Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis)
ILD CXR patterns - AKA reticular markings (MC finding), fine ground glass opacities
Specific to pulm fibrosis = HONEYCOMBING, more diffuse patchy FIBROSIS (sarco can have but only in advanced)
“tell your honey to stop smoking b/c he will get pulmonary fibrosis w/ honeycombing”
Also - Persistent inflammation (chronic alveolitis) –> fibrosis is the pathophys - if think of what hardened alvioli would look like, it’s honeycomb
CXR finding descriptions specific to Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis)
HONEYCOMBING
BX also shows HONEYCOMBING!!!
“tell your honey to stop smoking b/c he will get pulmonary fibrosis w/ honeycombing”
Clinical manifestations and PE pulm fibrosis
CP: Similar to other restrictive lung disease - gradual onset dry non-productive cough, DOE, fatigue, tachypnea
PE: Clubbing, inspiratory rales
What sets it apart is patient population it occurs in - OLD MEN w/ exposure risk (smoke, occupational exposures)
Dx of pulm fibrosis
CT Scan w/ characteristic findings (diffuse reticular opacities = synonym for honeycombing) & matching clinical presentation
Tx pulm fibrosis
No effective tx
Stop smoking
Oxygen
Corticosteroid in exac
What is the only cure for pulm fibrosis?
Lung transplant (poor prognosis w/o transplant)
What is pneumoconiosis? Examples?
Environmental or occupational lung dz - chornic fibrotic lung dz 2/2 inhalation of mineral dust = inflam rxn = parenchymal fibrosis = restrictive lung dz & decreased lung compliance
Silicosis Asbestosis Coal-worker's pneumoconiosis Berylliosis Byssinosis
CXR findings coal workers pneumoconiosis
Small, rounded, nodules w/ preference for UPPER lobes
Think of it looking like two little round lumps of coal in upper lung lobes
Later - progressive massive fibrosis
Management Silicosis, asbestosis, coal workers’s pneumoconiosis
No proven treatment! :(
Supportive: bronchodilators, O2, vaccinations (flu, pneumococcal), +/- corticosteroids, rehabilitation
CP pneumoconiosis
All have similar CP - non-productive cough - gradually worsens, DOE, can be ASX, fatigue etc - think about lungs not working (not able to expand and not able to exchange gasses - which sx would you have?)
History of working in manufacturing, working with fluorescent light bulbs …what is the patient at risk for?
May have been exposed to beryllium which can cause berylliosis, a form of pneumoconiosis (group of occupational lung disease causing restrictive ILD)
What are similarities between beryllosis and sarcoidoss, differences?
Both can cause hilar LAD & non-caseating granulomas on CXR, both have CP dry nonproductive cough & other common sx restrictive ILD
Berylliosis wil have exposure hx to beryllium & positive beryllium lymphocyte proliferation test
Tx berylliosis
No treatment - give steroids, O2 + methotrex if steroid unsuccessful
Cotton exposure = risk for ? ILD
Byssinosis - type of pneumoconiosis (occupational restrictive ILD)
AKA “Brown lung disease” or “Monday fever”
Sx worse at beg of week = “monday fever”
Man who worked in ship building, been retire 17 years presents w/ DOE, nonproductive cough
ASBESTOSIS - form of occupational lung dz (pneumoconiosis) 2/2 inhalation of asbestosis - found in ship building, pipe fitters, insulation, destruction & renovation of old buildings
Occurs 15-20 years after exposure
Presents w/ DOE, fatigue dry nonproductive chronic cough etc (all non-specific restrictive ILD sx)
CXR asbestosis
Plaques in LOWER lobes
Think of asbestosis dust settling down & forming a plaque
Asbestosis increases your risk of which cancers?
Bronchogenic carcinoma (MC)!!!
Mesothelioma (RARE but specific)
Silicosis CXR
Small nodular opacities in pper lobes
Nodular densities progress from periphery to hilum
+ EGG SHELL CALCIFICATIONS of hilar & mediastinal nodes
Don’t want sand on your eggs = gross - sand (silicosis) = EGG SHELL calcifications
Think of little eggs in upper lobes of lungs - round small nodules in upper lobes w/ egg shell classifications of hilar nodes- whereas asbestosis dust settles to lower lobes & = plaques
Etiology psitacosis, CP, TX
AKA Parrot fever - think PSIT = PARROS
Etio = chlamydophilia psittaci from infected birds (parrots, ducks)
CP: Atypical PNA - dry cough, FEVER, myalgias, headache
Tx: Tetracyclines FIRST LINE
What is the DLCO? When is it low?
The diffusing capacity of CO
Low in restrictive lung dz, emphysema
What is a pleural effusion?
Abnormally large accumulation of fluid in the pleural cavity - indicator of an underlying pathologic process or underlying illness…
MCC transient pleural effusion
CHF (fluid backup into pulm vasc = inc hydrostatic pressure = fluid leakage)
Dx pleural effusion
CXR - can see effusions >150 ml as blunting of costophrenic angles
Seen in posterior sulcus first (look at lateral film) then lateral sulci
PE pleural effusion
Percussion
Tactile fremitus
Breath sounds
Egophony
Dullness to percussion
Dec tactile fremitus
Inaudible breath sounds
+ Egophony (E–>A)
Light’s criteria (3)
Fluid is EXUDATIVE if >1 criteria are met:
Ratio of pleural fluid LDH : serum LDH > 0.6
Pleural fluid LDH >2/3 ULN reference range of serum LDH
Ratio of pleural fluid protein : serum protein >0.5
Note: Infection = inflammation = inc capillary permeability
When is thoracentesis indicated for pleural effusion?
Done with ALL effusions of unknown causes
C/I systemic anti-coagulation or infected area on skin
MCC exudative effusion
Malignancy
Causes of exudative effusions
Malignancy, inflammation (SLE, RA, granulamatous d/o - sarcoid), or infection
Causes of transudative effusions
Cardiovascular - fluid overload/heart failure
Hypoalbuminemia - liver failure, nephrotic syndrome
Hypothyroidism
Indications for chest tube (indwelling pleural catheters)
RAPIDLY re-accumulating pleural effusions
Failure of lung expansion after thoracentesis
What is a PTX?
Communication through the lung parenchyma into the plural cavity
MCC primary spontaneous PTX
Rupture congenital pulmonary blebs
Typical pt w/ spontaneous primary PTX
YOUNG MALE
14-18YO
SKINNY
TALL
MCC secondary spontaneous PTX
COPD (emphysema)
PTX PE
Decreased breath sounds
Dec tactile fremitus
Hyper-resonant percussion
(air = hyper-resonant)
Gold standard of pleural effusion treatment
Thoracentesis
Treatment for malignant or chronic effusions
Pleurodesis
Talc MCly used
Tx pleural effusion
Tx underlying dx
Gold standard = thoracentesis
Tension PTX
WORST kind - progressive build up of air pushes mediastinum to opposite hemithorax & obstructs venous return to the heart causing cardiac arrest!!!
MC with trauma or iatrogenic cause
CP tension PTX
JVP, pulsus paradoxus, hypotension (b/c no blood getting back to right atria)
Diaphoretic, cyanotic, tachy (HR >135), CP
Treatment tension PTX
Needle decompression - 2nd intercostal space, mid-clavicular line
Foreign body aspiration CP
Sudden onset wheezing,
Stridor, hoarseness, dyspnea,
Severe respiratory distress
80% in children < 3 YO
Marbles = most fatal
Nuts (food)= MC in younger, non-food items in older
60% in right main bronchus
Tx FBA
Rigid/flexible bronchoscopy
Chest pain characteristics if 2/2 PTX
PLEURITIC
UNILATERAL
NON-EXERTIONAL
SUDDEN ONSET
Tx PTX
Chest tube (thoracostomy) placement if large or symptomatic
Observation if small (<15-20%) of diameter of hte hemithorax - O2 increases air resoprtion
Etiology pulmonary nodules
Granulomas - Tb, histo, coccidio
Tumors - benign or malignant
Inflammation - Sarco, RA, wegener’s
Mediastinal tumor - thymoma = MC mediastinal tumor
Characteristics of benign pulmonary nodule
Round Smooth Slow growth \+ Calcifications Cavitary (without thickened walls - thickened walls = malignant)
Characteristics of malignant pulmonary nodule
Irregular border
Speculated
Rapid growth
Cavitary WITH thickened walls
Management of pulmonary nodule
Observation/surveillance if low malignant probability (<50 YO, never smoker, small size, smooth, round, not changing in size)
Often tend to be a Tb granuloma if above is true
Thoracic needle aspiration or bronchoscopy if intermediate probability of malignancy
Resection with biopsy if high probability of malignancy
Bronchial carcinoid tumor
MC site
Clinical manifestations
MC site is GI tract
2nd MC site is lung
Usually well-differentiated, low grade malignancy - rare neuroendocrine tumor from enterochromaffin cell, low risk of mets
Dx bronchial carcinoid tumor
Bronchoscopy
Pathologic description of bronchial carcinoid tumor
Pink to purple well vascularized central tumor
DIARRHEA, FLUSHING & WHEEZING = ?
Bronchial carcinoid tumor secreting serotonin & causing increase in bradykinin & histamine = flushing, wheezing etc
Management bronchial carcinoid tumor
Surgical excision
Often resistant to chemo/radiation
Ocreotide to decrease secretion of active hormones from tumor
Management bronchial carcinoid tumor
Surgical excision
Often resistant to chemo/radiation
Ocreotide to decrease secretion of active hormones from tumor
Lung cancer (bronchogenic carcinoma)
MC form
Most deadly form
Least deadly form
1 cause death
MC form is non-small cell - adenocarcinoma
Most deadly is small cell carcinoma
Least deadly is subtype of Non-small cell adenocarcinoma called broncioalveolar
Squamous cell carcinoma - characteristics?
SQCC = CCCC
Centrally located
Cavitary lesions (central necrosis)
Calcium - high
Coast - Pancoast tumors
Non-small cell carcinomas
Adenocarcinoma
Squamous cell carcinoma
Clinical syndromes caused by small cell lung cancer (para-neoplastic syndromes)
** All can cause it but most common with small cell =
SVC syndrome
SIADH/hypoonatremia
Cushings
Lambert-Eaton syndrome - ab against NMJ - similar to MG but weakness IMPROVES with continued use
Which lung cancer causes gynecomastia?
Adenocarcinoma
Which lung cancer causes cushings syndrome by secreting ACTH?
Small cell
Which type of lung cancer most frequently causes pancoast tumor & which syndrome does a pancoast tumor cause?
Squamous cell carcinoma
Causes pancoast syndrome = tumor at superior sulcus = shoulder pain, horner’s syndrome (miosis, ptosis, anhydrosis), due to cervical cranial sympathetic nerve compression, & atrophy of hand/arm muscles
Pancoast syndrome causes which other syndrome?
Pancoast syndrome = 2/2 tumor at superior sulcus that presses on cervical nerve - compression = HORNER’s syndrome! (miosis, ptosis, anhydrosis)
Pancoast also = shoulder pain, arm/hand atrophy
Characteristics of small cell carcinoma
Mets early - usu found on presentation
Centrally located
Surgery usually NOT treatment b/c already mets on presentation, can’t just resect it
Characteristics of adenocarcinoma of the lung
MC lung cancer - in women, smokers & non-smokers
PERIPHERAL - arises from mucus glands - think of the pleura on periphery as mucousy
Dx of lung cancer
Bronchoscopy used for central lesions (squamous, small cell) or mediastinoscopy used
Transthoracic needle biopsy for peripheral lesions (adenocarcinoma)
Pleural fluid analysis
CT scan used for staging
Non-small cell management
Central lesion so surgical resection preferred
Small cell lung cancer
Chemo = TOC b/c already mets on time of presentation
Done with or without radiation
MC symptom PE
SOB
MC sign PE
tachycardia
PE pulmonary embolism
Often normal
CP PE
Dyspnea
Pleuritic CP
Hemoptysis
Post-op patient w/ sudden tachypnea
Hypoxia
Massive PE CP
Syncope
Hypotension
PEA
Dx PE - gold standard
Pulmonary angiography
Ordered if v high suspicion and CT scan neg
Dx PE - best initial test
Helical CT scan (CT-PA)
CXR signs of PE
Hamptom’s hump - wedge-shaped infiltrate
Westermark’s sign - avascular markings distal to thrombus
ABG of PE
Respiratory alkalosis initially 2/2 hyperventilation
*respiratory acidosis may occur with time
Increased A-a gradient
When to order D-dimer if suspecting PE
Order if LOW suspicion for PE –> only helpful if negative
When to use alteplase (thrombolysis) in PE
MASSIVE hemodynamically unstable PE
Usually preferred over embolectomy
Standard treatment PE
LMWH (not in Cr>2.0) or UFH to prevent potentiation of the clot & as a bridge to therapeutic levels of warfarin - compliant pt may be discahrged on LMWH injections. UFH is an IV drip, must be hospitalized for it
Then need to be on anticoagulant (Warfarin or NOAC) for 3 months - NOAC remember not in CKD
Who gets PE prophylaxis & what do they get?
Low risk clot (<40 YO, minor procedure) - early ambulation
Moderate risk - stockings & pneumatic compression devices
High risk - LMWH - in pt undergoing orthopedic or neurosurgery, trauma patients
PERC PE criteria - what used for? Components?
PERC = PE rule out criteria
Age < 50 YO
Pulse < 100
O2 sat > 95%
No prior PE
No recent trauma/surgery
No hemoptysis
No use of exogenous estrogen
No unilateral leg swelling
MC EKG finding PE
Tachycardia w/ NSSTTWC
Cor Pulmonale 2/2 PE on EKG =
S1Q3T3
Definition of pulmonary HTN
Mean p. aa. pressure > 25 mmHg at rest or > 30 mmHg during exercise
Pathophys - inc p.a. pressure = inc pulm vasc resistance = RVH = R-HF
Describe likely patient w/ primary pulmonary HTN
MC in middle-aged women
- mean age of dx 50 YO
- Idiopathic or BMPR2 gene defect - usually prevents pulm vessel sm muscle growth & vasoconstriction
MCC secondary pulm HTN
COPD - Pulm HTN 2/2 chronic lung dz or hypoxemia is class III
EKG findings pulm HTN
Think = RVH = RAD & poor R -wave progression
Cor pulmonale
Class I pulm HTN
primary pulm HTN
Class II pulm HTN
secondary - pulm HTN 2/2 left heart dz
Class III pulm HTN
secondary pum HTN 2/2 chronic hypoxemia/lung dz (COPD)
Class IV pulm HTN
secondary pulm HTN due to chronic thormoboembolic disease (PE)
PE for pulm HTN
Signs of R sided heart failure (inc JVP, peripheral edema, ascites)
Accentuated S2 (due to prominent P2) first or if worse….a widened or split S2 if worse
Note: Any condition that causes a non-fixed delay in the closure of the pulmonic valve, or early closure of the aortic valve, will result in a wide split S2. Therefore, a persistent split S2 would occur in the setting of a right bundle branch block, pulmonary hypertension or pulmonic stenosis (delayed P2) or severe mitral regurgitation/ventricular septal defect (early A2 closure).
CXR pulm edema
Enlarged pulm arteries
SIgns of heart failure
Cor pulmonale
abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels
Causes of cor pulmonale
Pulm HTN
PE
Restrictive ILD
COPD
Gold standard pulm HTN dx
Right-sided heart catheterization
CBC pulm HTN
Polycytemia w/ increased Hct
Management primary pulm HTN
Do vasoreactivity trial - if vasoreactive then tx w/ CCB
If not reactive or need additional thearpy, tx w/ prostacyclins - epoprostenol, iloprost, PDE-5 inhib (sildenafil, tadalafil)
Oxygen therapy
Long term anticoagulation
Management Type II pulm HTN
Type II is 2/2 left heart disease - treat the underlying disease
Management type III pulm HTN
Type III is 2/2 chronic hypoxiemia or lung dz
Treat underlying cause - OXYGEN decreases mortality
Type IV pulm HTN
TYpe IV is due to chronic thromboembolic dz
Treat w/ long term anticoagulation
Health care-associated or hospital-acquired PNA etiology
S. pneumo MSSA GNR Pseudomonas MRSA
Tx HCAP
COVER FOR MRSA - Vanco IV
PLUS GNR coverage & pseudomonas coverage - cefepime, ceftazadime, carbepenem, zosyn or levo IV
CAP etiology & tx
S pneumo
M pna
C pna
H flu
Tx: healthy - Azithro x 5 d or doxy x 5 d
Looks good but immunosuppressed (DM, ETOH, CA, asplenia) - give them PO respiratory fluoroquinolone
Looks sick - admit - IV fluoroquinolone or IV betalactam (ceftriaxone) + atypical coverage (doxy, macrolide etc)
MCC PNA in kids
VIRAL - RSV, adenovirus
Who does fungal PNA occur in? Examples
IMMUNOCOMPROMISED PT
Histoplasmosis
Cryptococcus
Aspergillus
Pneumocystis jirovecci (PCP)
Which population does mycoplasma pna occur more in?
College students, school-aged, military recruits
Mycoplasma = Myringitis (bullous), URI sx, pharyngitis
CXR atypical PNA
“patchy” infiltrates
Aspiration PNA etiology
AAA
Aspiration = anaerobes = abscess
Also staph & strep
When is staph PNA often seen?
Occurs most frequently after the flu or another viral illness
Usually bilateral w/ multilobar infiltrates or abscesses
Chemical pneumonitis caused by?
Aspiration of gastric acid contents
PCP sx
Pneumocystis jirovecii =
IMMUNOCOMPROMISED HOST
Dry cough
Fatigue
DOE
CLUE ON TEST = DEC O2 SAT ON AMBULATION
MC viral cause of viral pna in adults
Influenza
Histoplasma etiology
MI & OH river valley - from soil contaminated with bat/bird droppings
Klebsiella PNA a/w what kind of infiltrates?
CAVITARY lesions
causes severe illness in ETOH, debilitated, chornic illness
CXR description & PE atypical PNA
Diffuse, patchy, interstitial or reticulonodular infiltrates
Kind of sounds like interstitial lung disease description more than a PNA descrpition - but word PATCHY = key for PNA
PE often normal w/ si consolidation (tactile fremitus, etophony etc) absent
CXR & PE typical PNA
Lobar pna on cxr
PE - signs of a consolidation - local dullness to percussion, bronchial breath sounds, INCREASED tactile fremitus + egophony (E–>A), inspiratory crackles
CP atypical PNA
More of dry cough
Low grade fever
Extrapulmonary sx - myalgias, malaise, sore throat, headache, n/v/d
CP typical PNA
Sudden onset fever
Productive cough - purulent
RIGORS (esp s. pna)
Tachycardia, tachypnea
Rusty sputum - pathogen?
Strep- PNA
Currant jelly sputum
Klebsiella
Green sputum
H. flu, pseudomonas
Foul-smelling sputum
Anaerobes - aspiration
“fetid breath”
Lung disease in which tactile fremitus is increased?
PNA
Decreased in pleural effusion, PTX
Lung disease where breath sounds are bronchial and you have + egophony
PNA
Decreased in pleural effusion, PTX - because more space between the lung tissue and rib cage = decreased sounds
When to give PCV13 vaccine
Given to kids in 4 doses - 2, 4, 6, and 15 months of age
High risk children > 2 should also receive single dose of PPSV23 8 weeks after completed immunization series of PCV13
When to give PPSV23?
Given to all adults > 65
If they’ve received PPSV23 before, wait until they’re > 65 and it’s been > 5 years since they’ve received PPSV23
Age > 2-64 if chornic disease - cardiac, pulmonary, diabetes, ETOH, liver, chronic care facility, immunocompromised (HIV, malignancy, chronic renal disease, chemotherapy, asplenia, sickle cell)
A PNA in which lobe would obscure the R heart border
Right MIDDLE lobe
Which PNA obscures the left heart border
A left LINGULAR PNA would obscure the left heart border
RIGHT UPPER LOBE PNA W/ bulging fissure, CAVITATIONS = ?
Klebsiella PNA
When do pt w/ Tb become PPD positive?
2-4 weeks after infection
Are patients with latent TB infection contagious?
No
Describe location and characteristics of a Tb granuloma - in primary, latent and in secondary reactivation
Primary: Lower lobe consolidation
Latent: Caseating w/ central necrosis
Reactivation: Cavitations in APICES of lungs (Tb likes the apices b/c there’s more O2 concentration up there)
Positive PPD for HIV + OR immunosuppressed (15 mg prednisone/day for example or biologics) person
INDURATION > 5 mm
Positive PPD for person in close contact w/ Tb
INDURATION > 5 mm
Positive PPD for person w/ CXR consistent w/ old/healed Tb (calcified granuloma)
INDURATION > 5 mm
CP Tb
Chronic, productive cough
Pleuritic CP, hemoptysis
Night sweats, fever, chills, fatigue, weight loss, anorexia
High risk populations/ high prefalence population considered + PPD if what size?
> 10 mm
Health care workers, immigrants form high-prevalence areas, homeless
False negative PPD
Cutaneous anergy (sarco, HIV), faulty application (SQ instead of TD)
False positive PPD
Improper reading (erythema is NOT considered positive)
BCG vaccination 2-10 years ago (although usu < 10 mm)
Test used for Tb screening
PPD
Dx studies in suspected cases of active Tb
Acid-fast smear & sputum cultures x 3 days
CXR - indicated to exclude active Tb (ex in newly positive PPD), as yearly screening in pt w/ known positive PPD
Interferon gamma release assay - quantiferon gold - prior BCG vaccination doesn’t affect this!
Tx regimen active Tb
4-drug regimen for SIX months –mnemonic: RIPS, RIPE
Rifampin - orange secretions Isoniazid - hepatitis, peripheral neuropathy - prevented w/ vit B6 (pyridoxine) Pyrazinamide- hepatitis, inc Ca Ethambutol - optic neuritis Streptomycin - oto/nephrotox
**Pt no longer considered infectious after 2 weeks of treatment
Treatment can be stopped 3 mo after negative sputum culture. PZA stopped after 2 months regardless. Can stop ETH, STM if culture comes back as sensitive to INH and RIF.
Treatment latent Tb
Isoniazid & pyridoxine (B6) for NINE months (if INH-sensitive)
Alterative: Rifampin x 4 mo
Latent Tb dx
- Asx
- PPD +
- No evidence of active infection on CXR/CT
**Tx reduces risk of reactivation Tb in the future
MCC acute bronchitis in adults
VIRUSES - adenovirus
Definition of acute bronchitis
Inflammation of the trachea or bronchi (conducting airways)
Often follows a URI
Tx acute bronchitis
Symptomatic - fluids, rest, bronchodilators, antitussives (adults)
CP Pertussis
3 stages jus tlike 3 sylab:
- Catarrheal - uri sx 1-2 wk - most contageous during this phase
- paroxysmal phase - severe parosysmal coughing fits w/ inspiratory whooping sound after coughing fit - +/- post-cough emesis
- Convalescent phase - resolution of the cough - may take weeks/months
Gold standard dx pertussis
PCR nasopharyngeal swab = gold standard - performed in first 3 weeks of sx onset
Other dx - lymphocytosis (60-80% lymphocytes)
Tx pertussis
Supportive tx = MAINSTAY
Abx - macrolide if present in first 7 days b/c shortens course & how contagious you are
Complications of pertusis
PNA
Encephalopathy
otitis media
Sinusitis
Inc mortality in infants due to apnea & cerebral hypoxia a/w coughing fits
Bronchiolitis - what is it? Etiology? Age?
Inflammation of the bronchioles (LRTI of small airways) = proliferation/necrosis of bronchilar epithelium = sloughing of epithelium & increased mucus plugging & edema = peripheral airway narrowing & airway obstruction
Etio: MC RSV, adeno
Age: Kids 2mo = 2 years
RF bronchioligits
2 months old, no breast feeding, exposed to smoke, crowded conditions, premature baby (= lungs not fully developed)
Most common acute complication of bronchiolitis
S. pneumonia PNA w/ otitis media
Dx bronchiolitis
CXR - peribronchial cuffing
Nasal washings - Mab to RSV
PUls ox - single best predictor of disease in children (<96% = admit to hospital)
Treatment bronchiolitis
Humidified O2, IV fluids, APAP/NSAID for fever
Prevention of RSV?
HAND WASHING - transmitted via direct contact w/ secretions & self-innoculation w/ contaminated hands
Also palivizumab prophylaxis in high risk groups
3 D’s of epiglotitis
Dysphagia, DROOLING, distress
Suspect in pt w/ rapidly progressing pharyngitis, muffled voice & otynophagis out of proportion to physical exam findings
Epiglottitis definition
Inflammation of epiglottis that may interfere with breathing (medical emergency) - mortality 2/2 asphyxiation
Xray sign for epiglottitis
Thumbprint sign - engorged epiglottis looks like thumbprint
Definitive dx epiglottitis
Laryngoscopy - shows cherry red epiglottis w/ swelling
Tx epiglottitis
Keep child calm - aka DO NOT attempt to visualize w/ tongue blade if high suspicion = UPSET
Maintain airway - dexamethasone to dec swelilng - intubation if severe
Ceftriaxone, cefoxatime
Typical pt who would have epiglottitis?
Male child 3mo - 6 YO, hx DM, no vaccinations (MCC Hib but rates gone down 2/2 vaccination)
Croup etiology
Parainfluenza
Croup = laryngotracheitis
Virus = inflammation of UPPER airway = subglottic larynx & tracheal swelling
Typical child w/ cropu looks like what?
6mo - 6 years old
FALL/WINTER MONTHS
Common
Cervical radiograph in cropu
Steeple sign (subglottic narrowing of trachea)
Management of croup - mild vs moderate vs severe
Mild = no stridor, no resp distress = cool humidified air mist, hydration, dexamethasone, supplemental O2 if < 92%
Moderate - stridor at rest w/ mild retractions - Dexamethasone PO or IM & supportive treatment +/- nebulized epinephrine
Severe - stridor at rest w/ marked contractions - dexamethasone - nebulized epinephrine & hospitalization
CP flu
Abrupt/SUDDEN ONSET!!! fever, chills, malaise, URI sx, pharyngitis, PNA,
Myalgias in legs & lumbosacral area
When to give Tamiflu
IN pt w/ high risk of complications or if hospitalized - best if initiated win 48 hours of onset of sx
ARDS definition, pathophys, who gets it?
Life-threatening acute hypoxemic respiratory failure
Patho: Inflammatory lung injury due to pro-inflam cytokines = diffuse alveolar damage = inc permieability of alveolar-capillyar barrier = pulmonary edema & alveolar fluid influx, loss of surfactant & vascular endothelial damage = decreased oxygen in blood
Critically ill pt get it - develop while in hospital for another reason - sepsis is MC - also severe trauma, aspiration of gastric contents etc
CP ARDS
Acute dyspnea & hypoxemia
Multi-organ failure if severe
Dx of ARDS
3 Components -
1. Severe refractory hypoxemia = HALLMARK
- B/l pulmonary infiltrates on CXR
- The absence of cardiogenic pulmonary edema/ CHF (PCWP< 18mHg) - ARDS spares the costophernic angles (non-cardiogenic pulmonary edema)
Tx ARDS
Non-invasive or mechanical ventilation:
CPAP w/ full face mask
Attempt to keep O2 sat > 90%
PEEP
Treat underlying cause
RF sleep apnea
Obesity Male 6th-7th decade Large neck Crowded oropharynx Micrognathia
Dx - sleep apnea
In -lab polysomnography
> 15 events/ hr = diagnostic - obstructive or mixed apneas, hypopneas, respiratory effort arousals etc
Labs - polycythemia 2/2 chronic hypoxia
Tx sleep apnea
CPAP
Weight loss, exercise, no alcohol, changes in sleep positioning
Oral appliance if CPAP unsuccessful
