Emergency Medicine EOR: Pulmonology (Smarty PANCE)

What is the most common cause of acute bronchiolitis and the classic demographic affected?

RSV (Respiratory Syncytial Virus) is the most common cause; affects infants < 2 years old, peak incidence in winter months

What are the classic clinical findings in bronchiolitis?

Low-grade fever, rhinorrhea, tachypnea, intercostal retractions, nasal flaring, expiratory wheezing, and fine crackles on auscultation; may progress to hypoxia

What is the gold standard diagnostic test for bronchiolitis?

Clinical diagnosis; nasal swab rapid antigen testing (RSV) can confirm but is not required; CXR shows hyperinflation and peribronchial thickening (nonspecific)

What are the indications for hospitalization in bronchiolitis?

O2 sat < 90-92%, respiratory rate >70, poor feeding/dehydration, age <3 months, prematurity, or significant respiratory distress

What is the first-line treatment for acute bronchiolitis?

Supportive care: supplemental O2 (if SpO2 < 90-92%), suctioning nasal secretions, hydration; bronchodilators and steroids are NOT routinely recommended

What medications are explicitly NOT recommended in bronchiolitis per AAP guidelines?

Antibiotics, corticosteroids, bronchodilators (albuterol/epinephrine), ribavirin, and chest physiotherapy are NOT routinely recommended

What prophylaxis is available for high-risk infants to prevent RSV bronchiolitis?

Nirsevimab (Beyfortus) or clesrovimab (Enflonsia): a single long-acting monoclonal antibody dose for ALL infants

What CXR finding in bronchiolitis can mimic pneumonia?

Patchy atelectasis (especially right upper lobe/right middle lobe) due to mucus plugging can be mistaken for consolidation

What is the most common cause of acute bronchitis?

Viral pathogens in >90% of cases: Influenza A/B, parainfluenza, RSV, rhinovirus, coronavirus; Mycoplasma and Chlamydophila account for most bacterial cases

What is the classic clinical presentation of acute bronchitis?

Cough lasting 1-3 weeks (can persist up to 8 weeks), with or without sputum production, following URI; low-grade fever; normal lung exam or scattered rhonchi

What clinical findings would prompt CXR in a patient with suspected bronchitis (Rale's Criteria)?

Heart rate >100, respiratory rate >24, temperature >100.4°F, focal lung findings on exam — any of these features should prompt CXR to rule out pneumonia

What is the first-line treatment for acute bronchitis?

Supportive care: rest, hydration, honey (adults), antitussives (dextromethorphan); antibiotics are NOT indicated in immunocompetent patients

When are antibiotics indicated for acute bronchitis?

Rarely — consider only if Bordetella pertussis confirmed/suspected, or immunocompromised patient; azithromycin is agent of choice if needed

What distinguishes acute bronchitis from pneumonia clinically?

Bronchitis: normal O2 sat, no focal consolidation on exam, no high fever (usually); Pneumonia: fever >38.5°C, tachycardia, tachypnea, focal crackles/egophony, infiltrate on CXR

What is the expected duration of cough in acute bronchitis and why does this matter?

Cough typically lasts 3 weeks but can persist up to 8 weeks; setting appropriate expectations reduces unnecessary antibiotic prescribing

What organism historically caused epiglottitis in children and what has changed its epidemiology?

Haemophilus influenzae type B (HiB) was the classic pediatric cause; Hib vaccine has shifted epidemiology — now more common in adults; S. aureus, S. pyogenes now predominate

What is the classic clinical triad of acute epiglottitis?

The "3 D's + 1 S": Dysphagia, Drooling, Distress (stridor), + Sitting upright (tripod/sniffing position); high fever and toxic appearance

What is the pathognomonic radiographic finding in epiglottitis?

Lateral neck X-ray showing "thumbprint sign" — enlarged, swollen epiglottis resembling a thumbprint; CXR is normal

What is the MOST IMPORTANT management step in suspected epiglottitis?

DO NOT agitate the patient or examine the oropharynx — emergent airway management; call anesthesia/ENT immediately; maintain patient in position of comfort

How is the airway secured in epiglottitis?

Emergent intubation in OR with surgical backup (anticipated difficult airway); cricothyrotomy may be needed; avoid blind nasotracheal intubation

What is the antibiotic of choice for epiglottitis?

Ceftriaxone (3rd generation cephalosporin) covers HiB, S. pneumoniae, S. pyogenes; add vancomycin if MRSA suspected

How does epiglottitis differ from croup in presentation?

Epiglottitis: abrupt onset, older child/adult, toxic-appearing, NO barky cough, drooling; Croup: gradual onset, < 5 years, barky "seal" cough, steeple sign on X-ray

What is the "sniffing position" in epiglottitis?

Patient sits leaning forward with neck extended and chin forward to maximize airway diameter; a child who prefers to remain upright is a red flag for supraglottic obstruction

What are the Berlin Criteria for diagnosing ARDS?

1) Onset within 1 week of insult or new/worsening symptoms; 2) Bilateral opacities on CXR not fully explained by effusions; 3) Respiratory failure not fully explained by cardiac failure; 4) PaO2/FiO2 < 300

How is ARDS severity classified by Berlin Criteria using P/F ratio?

Mild: PaO2/FiO2 200-300; Moderate: 100-200; Severe: < 100 (all on PEEP ≥5 cmH2O)

What are the most common causes of ARDS? Use mnemonic ARDS

Aspiration/pneumonia, Resuscitation from shock (massive transfusion), Drowning/drugs, Sepsis (most common cause, especially pulmonary sepsis)

What is the pathophysiology of ARDS?

Diffuse alveolar damage → inflammatory cytokines → increased capillary permeability → protein-rich edema floods alveoli → impaired surfactant → atelectasis → intrapulmonary shunt → refractory hypoxemia

What is the lung-protective ventilation strategy for ARDS?

Tidal volume 6 mL/kg ideal body weight, plateau pressure < 30 cmH2O, PEEP titration (high PEEP in moderate-severe), permissive hypercapnia (pH >7.20 acceptable)

What is the mortality benefit intervention in severe ARDS (P/F < 150)?

Prone positioning for ≥16 hours/day reduces mortality in moderate-severe ARDS (PROSEVA trial); reduces shunt by improving V/Q matching in posterior lung zones

What is the role of corticosteroids in ARDS?

Methylprednisolone may be used in early moderate-severe ARDS to reduce inflammation; evidence mixed — used more often in unresolving ARDS

What CXR finding is classic for ARDS and how does it differ from cardiogenic pulmonary edema?

ARDS: diffuse bilateral "whiteout"/ground-glass opacities, normal heart size, no Kerley B lines, no pleural effusions, no cephalization; Cardiogenic edema: enlarged heart, Kerley B lines, cephalization

What is the fluid management strategy in ARDS?

Conservative fluid strategy (net even or slightly negative) preferred once hemodynamically stable — reduces ventilator days; does NOT improve mortality (FACTT trial)

What defines an asthma exacerbation and what are signs of life-threatening status asthmaticus?

Acute worsening of bronchospasm with increased symptoms; life-threatening signs: silent chest (no wheezing = no airflow), pulsus paradoxus >25 mmHg, SpO2

What is the step-wise first-line treatment for an acute asthma exacerbation in the ED?

1) SABA (albuterol) via nebulizer/MDI q20min x3; 2) Ipratropium bromide (anticholinergic) added for moderate-severe; 3) Systemic corticosteroids (prednisone 40-60mg PO or methylprednisolone IV); 4) O2 to keep SpO2 >92%

What is the role of magnesium sulfate in acute asthma?

IV magnesium sulfate 2g over 20 min indicated for severe exacerbations not responding to initial bronchodilators; causes smooth muscle relaxation (blocks calcium)

What are the NAEPP classifications of asthma severity?

Intermittent: symptoms ≤2 days/week; Mild persistent: >2 days/week; Moderate persistent: daily symptoms; Severe persistent: continuous symptoms throughout the day

What is the stepwise pharmacotherapy for persistent asthma?

Step 1 (intermittent): SABA PRN; Step 2 (mild persistent): low-dose ICS; Step 3 (moderate): low-dose ICS + LABA or medium ICS; Step 4: medium ICS + LABA; Steps 5-6: high-dose ICS + LABA ± oral corticosteroids

What is the PEF threshold for admitting vs. discharging an asthma patient?

Peak expiratory flow (PEF) < 40% predicted after treatment → admit; 40-69% → consider discharge with steroids if good response; >70% → discharge appropriate

What triggers classically worsen asthma and are high-yield for boards?

NSAIDs/aspirin (inhibit COX → increased leukotrienes), beta-blockers, exercise (cold/dry air), allergens, occupational exposures, GERD, viral URIs

What is the classic spirometry pattern in asthma and how does it change post-bronchodilator?

Obstructive pattern: decreased FEV1/FVC ratio (< 0.70); FEV1 improves ≥12% AND ≥200 mL after bronchodilator = reversible obstruction (distinguishes asthma from COPD)

What biologic therapies are used for severe allergic asthma?

Omalizumab (anti-IgE): for severe allergic asthma with elevated IgE; Dupilumab (anti-IL-4/13), Mepolizumab (anti-IL-5 for eosinophilic asthma)

What is the most common cause of croup and the classic age group affected?

Parainfluenza virus type 1 (most common); affects children 6 months–3 years; peak in fall; viral URI precedes classic croupy cough

What is the pathognomonic clinical finding of croup?

Barky, "seal-like" cough with inspiratory stridor; preceded by URI; worse at night; symptoms exacerbated by agitation

What is the classic radiographic finding in croup?

AP neck/CXR shows "steeple sign" — subglottic narrowing of the trachea; however, croup is a clinical diagnosis and X-ray is NOT routinely required

What scoring system is used to assess croup severity?

Westley Croup Score: assesses stridor, retractions, air entry, cyanosis, and level of consciousness; mild

What is the first-line treatment for mild croup?

Dexamethasone 0.6 mg/kg PO/IM (single dose) — reduces airway edema and inflammation; effective within 6 hours; reduces return visits

What is the treatment for moderate-to-severe croup?

Dexamethasone 0.6 mg/kg IM/IV + nebulized racemic epinephrine (0.5 mL of 2.25% in 3 mL NS); observe 3-4 hours post-epinephrine for rebound edema before discharge

Why must patients be observed after racemic epinephrine in croup?

Rebound effect — airway edema returns to baseline 2-4 hours after epinephrine wears off; patient must be observed to ensure symptoms do not rebound to severe baseline

How do you distinguish croup from epiglottitis?

Croup: gradual onset, age < 5, barky seal cough, steeple sign, NOT toxic-appearing, NO drooling; Epiglottitis: sudden onset, older child/adult, toxic, drooling, tripod, thumbprint sign

What is the classic demographic and most commonly aspirated objects in foreign body aspiration?

Children ages 1-3 years are highest risk; most common: nuts (especially peanuts), seeds, hard candy, hot dogs, coins, small toy parts

What is the classic triad of foreign body aspiration presentation?

Sudden choking/coughing episode, unilateral decreased breath sounds, and unilateral wheezing (monophonic); may have history of witnessed choking

Where do foreign bodies most commonly lodge in the bronchial tree and why?

Right mainstem bronchus — more vertical, wider, and in more direct line with trachea than left; foreign bodies in esophagus lodge at cricopharyngeus muscle (C6), aortic arch, or LES

What CXR findings suggest foreign body aspiration?

Radiopaque FBs visible on plain film (only 10-15%); hyperinflation of ipsilateral lung (ball-valve obstruction); mediastinal shift AWAY from obstructed side on expiration; atelectasis with complete obstruction

What is the diagnostic gold standard and treatment for suspected FB aspiration?

Rigid bronchoscopy — diagnostic AND therapeutic; allows direct visualization and removal under general anesthesia

What is the immediate management for a witnessed complete airway obstruction (choking) in a conscious adult?

Heimlich maneuver (abdominal thrusts); back blows for infants < 1 year; if unconscious, begin CPR and look in mouth before each breath for foreign body

What is the Café Coronary syndrome?

Sudden death from complete airway obstruction by a large food bolus (typically meat) in adults; often misdiagnosed as MI; occurs in poorly dentated elderly or intoxicated individuals

What defines massive hemoptysis and what is the most common cause of death?

Massive hemoptysis: >200-600 mL/24 hours (various definitions); death occurs from ASPHYXIATION (drowning in blood), not exsanguination

What are the most common causes of hemoptysis in the US? Use mnemonic BATTLE

Bronchiectasis/Bronchitis (most common — chronic), Abscess, TB, Tumor (lung cancer), Lung contusion, Embolism (PE)

What is the most common cause of MASSIVE hemoptysis?

Bronchiectasis (especially from CF or prior TB) — due to hypertrophied bronchial artery erosion; lung cancer is the most common cause of non-massive hemoptysis

What initial diagnostic workup should be ordered for hemoptysis?

CXR first; CT chest with contrast (best to identify source/lesion); CBC, coagulation studies, BMP; bronchoscopy (localize bleeding source); sputum cultures/AFB if TB suspected

What is the most important immediate management step for massive hemoptysis?

Position patient with BLEEDING LUNG DOWN (lateral decubitus with affected side down) to prevent aspiration into good lung; protect airway — intubate with large-bore ETT

What is the definitive treatment for massive hemoptysis not controlled by bronchoscopy?

Bronchial artery embolization (BAE) — interventional radiology; surgical resection reserved for refractory cases

What features of hemoptysis suggest lung cancer?

Age >40, male, smoker, weight loss, chronic cough, clubbing, CXR mass/hilar adenopathy; must biopsy — any smoker >40 with hemoptysis needs CT and bronchoscopy

How do you distinguish hemoptysis from hematemesis?

Hemoptysis: bright red, frothy, alkaline pH, preceded by coughing; Hematemesis: dark red/coffee ground, acidic pH, preceded by nausea

What are the classic presenting symptoms of influenza and how do they differ from the common cold?

Influenza: abrupt onset, high fever (38.5-40°C), myalgias, headache, malaise, dry cough; Cold: gradual onset, low-grade/no fever, rhinorrhea dominant, less systemic symptoms

What is the gold standard diagnostic test for influenza in the clinical setting?

Rapid influenza diagnostic test (RIDT) — rapid antigen detection; low sensitivity (50-70%) but high specificity; RT-PCR is most sensitive/specific but slower

Who is at highest risk for influenza complications and what are the most common complications?

Extremes of age (< 2, >65), pregnancy, immunocompromised, chronic cardiopulmonary disease; complications: primary viral pneumonia, secondary bacterial pneumonia (S. aureus/S. pneumoniae), myocarditis

What is the first-line antiviral treatment for influenza and when should it be started?

Oseltamivir (Tamiflu) 75 mg PO BID x 5 days; most effective if started within 48 hours of symptom onset; use regardless of timing in high-risk patients/hospitalized patients

What are the antiviral options for influenza and their mechanisms?

Oseltamivir/zanamivir/peramivir: neuraminidase inhibitors (prevent viral release from cells); Baloxavir marboxil: PA endonuclease inhibitor (newer, single dose); Amantadine/rimantadine: M2 inhibitors (only influenza A, high resistance)

What medication is contraindicated in children with influenza and why?

Aspirin — associated with Reye syndrome (hepatic encephalopathy); use acetaminophen or ibuprofen instead

What influenza vaccine types are available and who should receive them?

Annual vaccination recommended for ALL persons ≥6 months; trivalent/quadrivalent inactivated (IIV) for most; live attenuated intranasal (LAIV) for healthy non-pregnant individuals 2-49 years; high-dose for ≥65 years

What are the classic CXR findings of influenza pneumonia?

Bilateral interstitial/ground-glass infiltrates (primary viral) vs. lobar consolidation (secondary bacterial superinfection); secondary bacterial pneumonia most commonly S. aureus (cavitary)

What are the four main histologic types of lung cancer and their key distinguishing features?

NSCLC (85%): Adenocarcinoma (peripheral, nonsmoker/female, EGFR mutation), Squamous cell (central, cavitary, smoker, PTHrP → hypercalcemia), Large cell (peripheral, anaplastic); SCLC (15%): central, paraneoplastic syndromes, early mets

What are the classic paraneoplastic syndromes associated with each lung cancer subtype?

SCLC: SIADH (hyponatremia), Cushing syndrome (ACTH), Lambert-Eaton myasthenic syndrome; Squamous cell: hypercalcemia (PTHrP); Adenocarcinoma: hypertrophic pulmonary osteoarthropathy

What is the gold standard diagnostic workup for suspected lung cancer?

CT chest with contrast → PET scan (staging) → tissue biopsy (bronchoscopy for central, CT-guided biopsy for peripheral); sputum cytology for central lesions

What are the USPSTF screening guidelines for lung cancer?

Annual low-dose CT (LDCT) for adults aged 50-80 years who have ≥20 pack-year history AND currently smoke OR quit within past 10 years

What is Pancoast (superior sulcus) tumor syndrome?

Lung cancer at apex of lung (usually squamous cell); causes Horner's syndrome (ptosis, miosis, anhidrosis) from stellate ganglion involvement, shoulder/arm pain, and hand muscle wasting (C8-T2 nerve involvement)

What is Superior Vena Cava (SVC) syndrome and its most common cause?

Obstruction of SVC → facial/arm swelling, venous distension, headache, plethora; most common cause is SCLC (or lymphoma); treated with SVC stenting ± radiation

What distinguishes a solitary pulmonary nodule (SPN) as benign vs. malignant on CT?

Benign: < 6mm, smooth borders, calcification (central, laminated, popcorn), stable ≥2 years; Malignant: >8mm, irregular/spiculated margins, growth on serial imaging, PET avid

What is the staging distinction that determines surgical resectability in NSCLC?

Stage I-II (localized, no mediastinal nodes): surgical resection; Stage III (mediastinal N2/N3): chemo-radiation; Stage IV (distant mets): palliative chemo/targeted therapy

What molecular targets are tested in advanced adenocarcinoma of the lung?

EGFR mutation (erlotinib/osimertinib), ALK rearrangement (crizotinib), ROS1, KRAS G12C, PD-L1 (pembrolizumab); molecular testing mandatory for all stage IV NSCLC

What organism causes pertussis and what is its mechanism of virulence?

Bordetella pertussis — gram-negative coccobacillus; produces pertussis toxin (impairs ciliary function, lymphocytosis), filamentous hemagglutinin (adhesion), and tracheal cytotoxin

What are the three clinical stages of pertussis and their durations?

1) Catarrhal (1-2 weeks): URI-like, most contagious; 2) Paroxysmal (2-6 weeks): paroxysmal cough + inspiratory "whoop," post-tussive emesis, cyanosis; 3) Convalescent (weeks-months): gradual improvement ("100-day cough")

What classic laboratory finding distinguishes pertussis from other respiratory infections?

Marked lymphocytosis (WBC 20,000-50,000 with 60-80% lymphocytes) — pertussis toxin causes demargination of lymphocytes

What is the gold standard diagnostic test for pertussis?

Nasopharyngeal PCR — most sensitive; culture (NP swab on Bordet-Gengou or Regan-Lowe) is gold standard but slow; serology useful later in illness

What is the first-line antibiotic treatment for pertussis?

Azithromycin (preferred, 5-day course) or erythromycin; antibiotics reduce contagiousness if given in catarrhal phase but do NOT significantly shorten paroxysmal stage; all household contacts should receive prophylaxis

What vaccine prevents pertussis and what are the current recommendations?

DTaP (diphtheria, tetanus, acellular pertussis) for children: 2, 4, 6, 15-18 months, 4-6 years; Tdap (booster) at 11-12 years, adults, and EVERY pregnancy (27-36 weeks) to protect newborns

What age group has the highest mortality from pertussis?

Infants < 6 months (too young for full vaccine series); can present with apnea WITHOUT classic whoop; pulmonary hypertension is a deadly complication

What are Light's Criteria and why are they used?

Used to distinguish EXUDATE from TRANSUDATE; EXUDATE if ANY ONE: 1) Pleural protein/serum protein >0.5; 2) Pleural LDH/serum LDH >0.6; 3) Pleural LDH > 2/3 upper limit of normal serum LDH

What are the most common causes of TRANSUDATIVE vs. EXUDATIVE pleural effusions?

Transudative (Starling forces): CHF (most common overall), cirrhosis, nephrotic syndrome, PE; Exudative (pleural/lung pathology): pneumonia (parapneumonic — most common exudate), malignancy, TB, PE, pancreatitis

How much pleural fluid is needed to see blunting on PA CXR vs. lateral decubitus?

>200-300 mL blunts costophrenic angle on PA CXR; >50-75 mL visible on lateral decubitus; >500 mL shifts mediastinum

What is the difference between a simple parapneumonic effusion, complicated parapneumonic effusion, and empyema?

Simple: sterile exudate, pH > 7.2, glucose >60, LDH < 1000 — resolves with antibiotics; Complicated: pH < 7.2, glucose < 60, positive Gram stain — needs drainage; Empyema: frank pus — always drain

What are the indications for thoracentesis in pleural effusion?

New effusion >1cm on lateral decubitus without obvious cause (CHF), or any effusion causing respiratory compromise; bilateral effusions in CHF without fever can be monitored

What pleural fluid findings suggest malignant effusion?

Exudate, bloody, low glucose, high LDH, elevated CEA; cytology positive in 60%; pleural biopsy needed if cytology negative

What is the classic pleural fluid finding in TB pleuritis?

Exudate, lymphocyte-predominant (>90%), elevated ADA (adenosine deaminase) >40 U/L, low glucose; pleural biopsy shows granulomas

What physical exam finding is classic for pleural effusion?

Dullness to percussion, decreased tactile fremitus, absent breath sounds at base; egophony at the upper border of the effusion ("E to A change")

What is the definition and key characteristic of pleuritic chest pain?

Sharp, stabbing chest pain that worsens with inspiration, coughing, or movement; caused by inflammation of parietal pleura (visceral pleura lacks pain fibers)

What is the most dangerous cause of pleuritic chest pain that must be ruled out first?

Pulmonary embolism — use Wells criteria and d-dimer to stratify risk; PE can present with pleuritic pain (from pulmonary infarction, usually peripheral)

What are the common causes of pleuritic chest pain? Use mnemonic CAUSE

Cancer (mesothelioma, lung), Autoimmune (lupus pleuritis, RA), URI/viral (pleurodinia — Coxsackievirus B), Systemic diseases (uremia), Embolism/Everything else (PE, pneumothorax, pericarditis, pneumonia)

What is pleurodinia (Bornholm disease) and its cause?

Coxsackievirus B infection causing epidemic pleuritis; sudden severe pleuritic chest/upper abdominal pain with fever in young adults/children; self-limited