CCS Integrated Cases

CCS case: severe asthma exacerbation

Clinical Overview and When to Suspect Severe Asthma Exacerbation

— Life-threatening features: silent chest, cyanosis, bradycardia, hypotension, exhaustion, confusion, PEF <33%, "normal" or rising PaCO2

— Near-fatal: elevated PaCO2 with need for mechanical ventilation

— Known asthmatic with progressive dyspnea, wheeze, chest tightness, cough over hours–days

— Failure of home short-acting beta-agonist (SABA) — using albuterol every 1–2 hours without sustained relief

— Recent oral corticosteroid taper, ICS nonadherence, viral URI, allergen exposure, NSAID/beta-blocker trigger

— Prior intubation or ICU admission for asthma

— ≥2 hospitalizations or ≥3 ED visits in past year

— ≥1 canister of SABA per month

— Low socioeconomic status, mental illness, illicit drug use, food allergy with asthma

— Poor perception of airflow obstruction

— Bronchospasm + mucosal edema + mucus plugging → V/Q mismatch → hypoxemia

— Air trapping → dynamic hyperinflation → ↑ work of breathing → respiratory muscle fatigue → hypercapnia

— Initial ABG shows respiratory alkalosis; normalization or rise of PaCO2 = impending respiratory failure

Board pearl: A "normal" PaCO2 (~40) in a tachypneic, severely obstructed asthmatic is not reassuring — it signals fatigue and impending arrest. Prepare for escalation, not discharge.

CCS pearl: On arrival, the first three orders should be continuous pulse oximetry, supplemental O2 titrated to SpO2 92–96%, and nebulized albuterol-ipratropium — order these before completing the history.

Definition: Acute worsening of asthma with one or more of: inability to speak in full sentences, RR >30, HR >120, SpO2 <90% on room air, PEF <50% of personal best/predicted, accessory muscle use, or altered mental status

When to suspect in ED triage:

High-risk history (red flags for fatal asthma):

Pathophysiology highlights driving therapy:

Presentation Patterns and Key History

— Progressive dyspnea, wheeze, chest tightness, nonproductive cough over 6 hours to several days

— Tripod position, diaphoresis, single-word speech

— Patient appears anxious, leaning forward, using pursed-lip breathing

— Type 1 (slow-onset, 80–90%): Days of worsening despite escalating SABA use, often with viral URI; eosinophilic, mucus plugging dominant, slower response to therapy

— Type 2 (sudden asphyxic, 10–20%): Onset over <6 hours, often <2 hours; triggered by allergen, NSAID, stress, food; neutrophilic bronchospasm-predominant, responds rapidly to bronchodilators but can deteriorate fast

— Time of symptom onset and trajectory

— Number of SABA puffs/nebs in last 24 h

— Last dose of oral/inhaled corticosteroid, adherence pattern

— Prior intubations, ICU stays, ED visits, hospitalizations

— Triggers: URI symptoms, allergens, exercise, cold air, smoke, occupational, aspirin/NSAID, beta-blocker, GERD

— Comorbidities: allergic rhinitis, atopic dermatitis, nasal polyps, OSA, pregnancy

— Vaping/tobacco/cannabis, illicit drug use

Key distinction: Cardiac asthma (acute decompensated HF) can mimic — look for orthopnea, PND, JVD, S3, bilateral crackles, leg edema, prior MI; BNP and CXR clarify.

Board pearl: Samter triad = aspirin sensitivity + nasal polyps + asthma. NSAID exposure can precipitate near-fatal exacerbation in these patients — document and counsel avoidance with a MedicAlert bracelet at discharge.

Classic severe exacerbation presentation:

Two phenotypes to recognize:

Key history to obtain (parallel to starting therapy — do not delay treatment):

Step 3 outpatient bridge: Ask about controller regimen — is patient on ICS-LABA? On biologic (omalizumab, mepolizumab, dupilumab, tezepelumab, benralizumab)? Date of last specialist visit?

Physical Exam Findings and Respiratory Assessment

— Mild–moderate: speaks in sentences, alert, can lie flat

— Severe: speaks in phrases or words, anxious, agitated, tripoding, diaphoretic, refuses to lie supine

— Life-threatening: drowsy, confused, cyanotic, exhausted ("quiet patient")

— RR >30, HR >120, SpO2 <90% on RA, PEF <50% predicted/personal best → severe

— Pulsus paradoxus >25 mmHg correlates with severity; absence in fatigued patient is ominous

— Bradycardia or hypotension = peri-arrest

— Prolonged expiratory phase, diffuse polyphonic wheeze

— Accessory muscle use: SCM, scalene, intercostal retractions, abdominal paradox

— Silent chest (no air movement, no wheeze) = critical; minimal airflow, impending arrest

— Decreased breath sounds focally → consider pneumothorax (especially after high-pressure ventilation) or mucus plug atelectasis

— Agitation = hypoxia

— Lethargy/confusion = hypercapnia and CO2 narcosis → prepare to intubate

— Tachycardia (disease and beta-agonist driven)

— JVD, hepatojugular reflux → consider cor pulmonale, tension PTX, or HF mimicker

— Subcutaneous emphysema → pneumomediastinum from barotrauma

— Urticaria, angioedema, stridor → anaphylaxis mimicker — give IM epinephrine

— Reassess RR, HR, SpO2, speech, accessory muscle use, and PEF (if able) every 15–20 minutes during the first hour

— Document response to first three back-to-back nebs

CCS pearl: Order peak expiratory flow (PEF) at arrival, after first hour of treatment, and pre-disposition. PEF <40% predicted after 1 hour of intensive therapy predicts hospitalization.

Board pearl: Disappearance of wheezing in a deteriorating asthmatic is bad — it means no air is moving.

General appearance — single best severity indicator at bedside:

Vital signs and red flags:

Respiratory exam:

Mental status:

Cardiac and other systems:

Reassessment cadence (CCS):

Diagnostic Workup — Initial Labs, Imaging, ECG

— Continuous pulse oximetry, cardiac telemetry, BP cuff q15min

— PEF before and after initial bronchodilator (if patient can cooperate)

— Capnography if available — trending ETCO2 useful

— ABG if SpO2 <92% on supplemental O2, severe distress, drowsy, or not responding to therapy

· Early: respiratory alkalosis with hypoxemia

· Late/severe: normal or rising PaCO2 with acidemia = impending failure

— CBC with diff: leukocytosis common from steroids/stress; eosinophilia supports phenotype

— BMP: baseline K+ (beta-agonists cause hypokalemia), glucose (steroid hyperglycemia), Cr

— Magnesium level (if planning IV magnesium)

— Lactate — elevated from beta-agonist–driven type B lactic acidosis (do not mistake for sepsis)

— Troponin/BNP if cardiac mimicker suspected

— Viral PCR/COVID/influenza swab in season

— Pregnancy test in reproductive-age women (affects therapy choices)

— CXR PA/lateral is not routine but order if: first presentation, fever, focal exam, suspected pneumothorax/pneumonia, failure to respond, age >50, or before intubation

— Findings: hyperinflation, flattened diaphragms; rule out PTX, pneumomediastinum, pneumonia, atelectasis

— Order if HR >130, chest pain, age >50, known CAD, or to evaluate dysrhythmia from beta-agonists

— May show sinus tach, RV strain, P pulmonale, transient RBBB

CCS pearl: Do not order routine spirometry or pulmonary function testing during acute exacerbation — PEF only.

Board pearl: An elevated lactate in an asthmatic on continuous albuterol is usually β2-mediated lactic acidosis, not sepsis — do not chase with broad-spectrum antibiotics if no infectious source.

Diagnosis is clinical — do not delay therapy for tests. Order in parallel.

Immediate bedside (on arrival):

Laboratory orders (CCS order set at 0–30 min):

Imaging:

ECG:

Diagnostic Workup — Advanced and Confirmatory Studies

— Repeat ABG q30–60 min in severe/critical patients

— Watch for: falling pH, rising PaCO2, persistent hypoxemia despite FiO2 escalation

— "Crossover" PaCO2 from <35 to normal-range 38–42 in a tachypneic patient is a pre-intubation finding

— Shark-fin waveform = obstructive expiration

— Useful trend monitor; rising ETCO2 with fatigue confirms hypoventilation

— Suspected PE (pleuritic pain, unilateral leg swelling, hemoptysis, hypoxia out of proportion)

— Suspected complications: pneumomediastinum, occult PTX, ABPA with central bronchiectasis

— Failure to respond and atypical features

— When cardiac asthma or cor pulmonale suspected

— Assess LV function, RV size/strain, IVC, pericardial effusion

— Not routine acutely; consider after stabilization if mucus plugging with persistent lobar collapse, suspected foreign body, or ABPA

— Total IgE, specific IgE/aeroallergen panel, eosinophil count, FeNO

— Aspergillus-specific IgE and precipitins if eosinophilia + bronchiectasis (ABPA workup)

— Alpha-1 antitrypsin if early-onset basilar emphysema overlap

— Sweat chloride if pediatric/young adult with bronchiectasis and recurrent infections (CF)

— Vocal cord visualization (laryngoscopy) if "asthma" unresponsive to therapy with inspiratory stridor → vocal cord dysfunction

Key distinction: Asthma vs VCD — VCD shows inspiratory stridor, normal SpO2, flattened inspiratory loop on flow-volume curve, and laryngoscopy shows paradoxical vocal cord adduction during inspiration. Steroids and bronchodilators won't help; speech therapy will.

Board pearl: Persistent infiltrate + central bronchiectasis + eosinophilia + elevated IgE in an asthmatic → ABPA; treat with oral corticosteroids ± itraconazole.

When initial workup is unrevealing or patient is deteriorating, escalate:

Arterial blood gas trending:

Capnography (continuous ETCO2):

CT chest — reserved for:

Echocardiogram (bedside POCUS or formal):

Bronchoscopy:

Specialist work-up after stabilization (inpatient days 2–3 or outpatient):

Risk Stratification and First-Hour Management Logic

— Mild–moderate: PEF >50%, speaks in sentences, SpO2 >92%

— Severe: PEF 33–50%, speaks in phrases, RR >25, HR >110

— Life-threatening: PEF <33%, SpO2 <92%, silent chest, cyanosis, bradycardia, hypotension, exhaustion, altered mental status, normal/rising PaCO2

— Near-fatal: Hypercapnia or need for mechanical ventilation

— Place on monitor, IV access x2, continuous pulse oximetry

— O2 via nasal cannula or simple mask, titrated to SpO2 92–96% (avoid hyperoxia — worsens V/Q)

— Albuterol 2.5–5 mg + ipratropium 0.5 mg nebulized, repeat q20min x3 (or continuous albuterol 10–15 mg/h for severe)

— Systemic corticosteroid: prednisone 40–60 mg PO OR methylprednisolone 60–125 mg IV if NPO/unable to swallow

— PEF measurement if cooperative

— Begin focused history simultaneously

— Repeat PEF, vitals, work of breathing, speech

— Responding well (PEF >70%, sustained 60 min, no distress) → observe, consider discharge

— Incomplete response (PEF 40–69%, persistent symptoms) → continue nebs q1h, admit to ward/observation

— Poor response (PEF <40%, severe symptoms) → escalate (next chunk)

— Magnesium sulfate 2 g IV over 20 minutes

— Consider heliox, IV beta-agonist (rarely), NIPPV (BiPAP), prepare for intubation

Step 3 management: Every severe exacerbation gets systemic steroids within the first hour — this is the single most important intervention for reducing relapse and admission.

CCS pearl: Move the simulated clock forward in 15–30 min increments during the first hour, reassessing PEF and respiratory status each time; do not jump straight to "6 hours later."

Severity classification (drives disposition):

CCS time-anchored management:

At 0–15 minutes (arrival):

At 30–60 minutes — reassess:

At 1 hour — escalation triggers if not responding:

Pregnancy consideration: Target SpO2 ≥95% to protect fetal oxygenation.

Pharmacotherapy — First-Line Drug Regimen

— Albuterol nebulized 2.5–5 mg every 20 minutes x3, then q1–4h, OR

— Continuous nebulization 10–15 mg/h for severe/life-threatening

— MDI with spacer (4–8 puffs q20min) equivalent in mild–moderate

— Side effects: tachycardia, tremor, hypokalemia, hyperglycemia, lactic acidosis, QT prolongation

— Ipratropium 0.5 mg nebulized q20min x3 added to albuterol in severe exacerbations

— Reduces hospitalization rates when combined in ED

— Not continued after admission to inpatient ward (no added benefit)

— Prednisone 40–60 mg PO daily x 5–7 days (preferred if can swallow — equivalent to IV)

— Methylprednisolone 60–125 mg IV q6h if NPO, vomiting, or intubated

— No taper needed for courses ≤7–10 days

— Onset of action: 4–6 hours — start early

— Dexamethasone 12–16 mg PO/IV x 1–2 doses is an alternative (less mineralocorticoid effect)

— 2 g IV over 20 minutes for severe exacerbations not responding to first hour of therapy

— Smooth muscle relaxant; reduces admissions in severe exacerbations

— Watch for hypotension, flushing, areflexia

— Target SpO2 92–96% (≥95% in pregnancy)

— Avoid hyperoxia — increases V/Q mismatch and CO2 retention

— Heliox (70:30 He:O2): Lower density gas reduces work of breathing; bridge in severe cases

— IV magnesium continuous infusion (controversial)

— Ketamine (1–2 mg/kg IV bolus) — bronchodilator, useful at intubation

— Epinephrine 0.3–0.5 mg IM if anaphylaxis suspected or peri-arrest

— Sedatives in non-intubated patients (mask deterioration)

— Beta-blockers, NSAIDs (if Samter), opioids

— Routine antibiotics — only if pneumonia or purulent sinusitis

Board pearl: Oral prednisone = IV methylprednisolone for efficacy in asthma exacerbation; choose oral if patient tolerates.

Step 3 management: Discharge with 5–7 days of oral prednisone 40–60 mg daily, no taper, plus initiation or step-up of ICS-containing controller before leaving ED.

Short-acting beta-2 agonist (SABA):

Short-acting muscarinic antagonist (SAMA):

Systemic corticosteroids — give within first hour:

Magnesium sulfate IV:

Oxygen:

Adjuncts (second-tier):

Avoid:

Escalation Pharmacology and Airway Management

— Consider in cooperative, awake severe asthmatic with rising PaCO2, fatigue, increased work of breathing

— Settings: IPAP 8–12, EPAP 3–5, titrate up

— Contraindications: altered mental status, vomiting, hemodynamic instability, inability to protect airway

— Reassess in 1–2 hours; if no improvement → intubate

— Cardiac or respiratory arrest

— Coma, severe agitation

— Progressive hypercapnia, exhaustion

— Failure of NIPPV

— Use largest ETT possible (8.0+) to reduce resistance and allow bronchoscopy

— Ketamine 1.5–2 mg/kg IV for induction (bronchodilator, hemodynamically stable)

— Avoid morphine (histamine release); fentanyl preferred

— Anticipate post-intubation hypotension from auto-PEEP, hypovolemia, sedation

— Pre-oxygenate aggressively; consider apneic oxygenation

— Low tidal volume 6–8 mL/kg IBW

— Low RR (8–12) with prolonged expiratory time (I:E 1:4 or 1:5)

— Plateau pressure <30 cmH2O

— Minimal PEEP (0–5)

— Accept pH 7.15–7.20, PaCO2 60–80 to avoid barotrauma

— Sedation + analgesia; avoid paralysis if possible (myopathy risk with steroids)

— If sudden hypotension or rising peak pressures → disconnect ventilator, allow exhalation, then reconnect with lower RR

— Rule out pneumothorax with bedside US/CXR

— Inhaled anesthetics (sevoflurane, isoflurane) in ICU

— VV-ECMO for refractory hypercapnic respiratory failure

— Bronchoscopy for mucus plug removal in lobar collapse

CCS pearl: When you intubate the simulated patient, immediately order continuous albuterol via inline neb, IV methylprednisolone q6h, ICU admission, ventilator settings with low RR/permissive hypercapnia, and arterial line.

Board pearl: Sudden hypotension in a ventilated asthmatic → think DOPES: Displaced tube, Obstruction, Pneumothorax, Equipment failure, Stacking (auto-PEEP). First action: disconnect from vent.

For patients not responding at 1 hour despite SABA + SAMA + systemic steroid + magnesium:

Noninvasive positive-pressure ventilation (NIPPV / BiPAP):

Endotracheal intubation indications:

Intubation technique pearls:

Mechanical ventilation strategy — "permissive hypercapnia":

Auto-PEEP / dynamic hyperinflation management:

Continuous albuterol during ventilation via inline nebulizer

Rescue therapies (limited evidence, refractory only):

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher mortality from asthma exacerbation

— Overlap with COPD (ACOS) common — partial reversibility, smoking history

— Comorbid CAD, HF, atrial fibrillation, OSA complicate management

— Reduced perception of dyspnea → present later, more severe

— Caution with high-dose continuous albuterol: AFib, MAT, MI ischemia, hypokalemia

— Monitor ECG, K+, glucose

— Lower threshold for cardiac biomarker check

— Hyperglycemia → check glucose q6h, especially in diabetics; sliding scale insulin as needed

— Increased risk of delirium, agitation, GI bleeding → consider PPI prophylaxis if other risk factors

— Osteoporosis with repeated/chronic courses → calcium, vit D, DEXA in chronic users

— Adrenal suppression with prior frequent courses — taper if recent prolonged use

— Albuterol: No dose adjustment needed

— Ipratropium: No adjustment; minimal systemic absorption

— Magnesium sulfate: Reduce dose and monitor levels — risk of hypermagnesemia (areflexia, respiratory depression, cardiac arrest); use 1 g IV in moderate–severe CKD, hold in dialysis without close monitoring

— Methylprednisolone/prednisone: No renal adjustment

— Theophylline (rare use): Reduce dose; narrow therapeutic window

— Prednisone activation requires hepatic conversion → use prednisolone in severe liver disease

— Theophylline metabolism reduced → toxicity risk

— Montelukast: caution in hepatic impairment

— Nonselective beta-blockers (propranolol, timolol eye drops) precipitate bronchospasm — switch to cardioselective (metoprolol, bisoprolol) cautiously if needed for cardiac indication

— NSAIDs in Samter patients

— ACEi-induced cough mimics asthma

Step 3 management: Before discharge in elderly, reconcile medications — discontinue offending nonselective beta-blockers and NSAIDs; document conversation about avoidance.

Board pearl: In a dialysis patient with severe asthma, IV magnesium is risky — give a reduced dose (1 g) with continuous cardiac monitoring and check Mg level before redosing.

Elderly asthmatics (>65 years):

Beta-agonist considerations in elderly:

Corticosteroid considerations:

Renal impairment (CKD):

Hepatic impairment:

Polypharmacy red flags:

Special Populations — Pregnancy and Pediatrics

— Asthma course: 1/3 worsen, 1/3 stable, 1/3 improve

— Uncontrolled asthma is more dangerous than asthma medications — preeclampsia, preterm birth, LBW, perinatal mortality risk

— Target SpO2 ≥95% (fetal oxygenation depends on maternal PaO2 >70)

— Albuterol — first-line SABA, well-studied

— Budesonide — preferred ICS (most data)

— Salmeterol, formoterol — LABAs acceptable

— Systemic corticosteroids — use when indicated; benefits outweigh risk

· Slight increase in cleft lip/palate in first trimester (absolute risk small)

· Monitor for gestational diabetes, hypertension

— Ipratropium, magnesium — safe

— Montelukast — generally continued if effective pre-pregnancy

— Omalizumab — continue if already on it; do not initiate in pregnancy unless severe

— Live vaccines, brompheniramine

— Epinephrine SC (causes uterine vasoconstriction) — IV/IM epi only for anaphylaxis

— Severity scoring: PRAM, PASS, or pulmonary score

— Albuterol MDI with spacer = nebulizer for mild–moderate

— Dexamethasone 0.6 mg/kg PO/IV x 1–2 doses = equivalent to 5-day prednisone, better adherence

— IV magnesium 25–50 mg/kg (max 2 g)

— Heliox beneficial in pediatric severe exacerbation

— Watch for paradoxical worsening with high-dose beta-agonists (lactic acidosis, tachycardia)

— Age <2, prior ICU, hypoxia after treatment, inability to feed, social concerns

Key distinction: Adolescent "asthma" unresponsive to therapy with normal SpO2 and inspiratory stridor → vocal cord dysfunction, often in high-performing/athletes. Refer to ENT/SLP.

Board pearl: In pregnant asthmatic in status, give IV methylprednisolone and continuous albuterol — undertreatment harms the fetus more than steroids do.

Pregnancy:

Safe asthma medications in pregnancy:

Avoid in pregnancy:

Labor/delivery: Continue controller; supplemental O2; avoid prostaglandin F2α (carboprost) — bronchoconstrictor. Use oxytocin, PGE1 (misoprostol) safely.

Pediatrics (school-age and adolescents):

Pediatric red flags for admission:

Complications and Adverse Outcomes

— Pneumothorax / pneumomediastinum: From high airway pressures, especially post-intubation; suspect with sudden hypotension, asymmetric breath sounds, subcutaneous emphysema

— Atelectasis from mucus plugging — most common right middle lobe

— Pneumonia — bacterial superinfection; new fever, purulent sputum, focal infiltrate

— Hypoxic respiratory failure progressing to hypercapnic failure

— Hypoxic-ischemic encephalopathy from arrest

— Tachyarrhythmias (AF, MAT, SVT) from beta-agonists and hypoxia

— Demand ischemia, NSTEMI in CAD patients

— Cor pulmonale, RV failure in chronic severe asthma

— Cardiac arrest from hypoxia or tension PTX

— Hypokalemia (beta-agonist driven) → arrhythmia risk

— Hyperglycemia from steroids + beta-agonists

— Lactic acidosis (beta-agonist β2 type B) — mimics sepsis

— Hypomagnesemia

— Hyponatremia (SIADH-like)

— Dynamic hyperinflation / auto-PEEP → hypotension, barotrauma

— Ventilator-associated pneumonia (after >48h)

— Critical illness myopathy (steroid + paralytic combination)

— DVT/PE from immobility

— Steroid psychosis, hyperglycemia, fluid retention, hypertension, peptic ulcer, immunosuppression

— Repeated systemic steroid courses → osteoporosis, cataracts, glaucoma, adrenal suppression, AVN of femoral head

— Beta-agonist tremor, palpitations

— Airway remodeling and progressive loss of FEV1

— Increased risk of subsequent fatal exacerbation — prior intubation is the single strongest predictor

— PTSD/anxiety after ICU stay

CCS pearl: In any intubated asthmatic with sudden deterioration, order stat portable CXR or bedside US and physically disconnect the ventilator for 30 seconds while assessing — this both diagnoses (relieves auto-PEEP) and treats.

Board pearl: Pneumomediastinum + subcutaneous emphysema in a young asthmatic with severe exacerbation = Hamman sign (crunching synchronous with heartbeat); usually self-limited, but rule out PTX and esophageal injury.

Respiratory complications:

Cardiac complications:

Metabolic complications:

Mechanical ventilation–related:

Iatrogenic / medication adverse effects:

Long-term/post-discharge:

When to Escalate Care — Admission, ICU, and Consults

— Sustained PEF ≥70% predicted/personal best for >60 minutes after last bronchodilator

— SpO2 ≥94% on room air

— Minimal symptoms, no accessory muscle use, normal speech

— Reliable follow-up, social support, access to medications, ability to use inhaler

— Adequate response to systemic steroids initiated

— PEF 40–69% with persistent moderate symptoms after initial therapy

— Requires q2–4h nebulizers

— Comorbidities (pregnancy, elderly, cardiac disease)

— Poor social support, repeat ED visits

— PEF <40% despite intensive therapy

— Requires continuous nebulized albuterol

— Hypoxemia not corrected with supplemental O2

— Rising or normal PaCO2 with tachypnea, fatigue

— Altered mental status, exhaustion

— Need for NIPPV or intubation

— Hemodynamic instability, arrhythmia

— Prior intubation for asthma (low threshold)

— Pulmonology: All ICU admissions, first severe exacerbation, refractory asthma, biologic candidates, ABPA workup

— Allergy/Immunology: Suspected allergen triggers, candidate for omalizumab/mepolizumab/dupilumab/tezepelumab

— Critical care: ICU-level care

— Anesthesia/airway team: Difficult airway anticipated for intubation

— OB: Pregnant patients in severe exacerbation

— Psych/social work: Repeated severe exacerbations with nonadherence

— At 1 hour: No improvement → magnesium, NIPPV consideration, ICU consult

— At 2 hours: Worsening or persistent severe → ICU transfer, prepare for intubation

— At 6 hours: Reassess for ward vs ICU; document response

Step 3 management: Any asthmatic with prior ICU admission or intubation presenting with severe exacerbation should be admitted to ICU, not the ward — even if responding initially.

CCS pearl: Always order "Notify physician if RR >30, SpO2 <92%, HR >130, or change in mental status" when admitting an asthmatic to a non-ICU bed.

Discharge from ED criteria (all must be met):

General ward admission:

ICU admission criteria:

Step-down/PCU: Intermediate cases requiring frequent monitoring but not vent support — q1–2h respiratory assessments, telemetry, K+ monitoring

Consult triggers:

CCS time-anchored escalation flow:

Key Differentials — Same Category (Obstructive/Lower Airway)

— Age >40, smoking history, chronic productive cough

— Less reversible obstruction, lower baseline FEV1

— More likely to have purulent sputum, bacterial trigger

— Treatment similar (SABA, SAMA, steroids) but 5-day prednisone 40 mg is standard; antibiotics indicated more often

— Target SpO2 88–92% (avoid CO2 retention)

— Features of both; partial reversibility

— Higher exacerbation frequency

— Treat as severe asthma acutely

— Chronic productive purulent sputum, recurrent infections, clubbing

— CT: dilated bronchi, "signet ring" sign

— Causes: CF, ABPA, post-infectious, immunodeficiency, ciliary dyskinesia

— Treat with airway clearance, antibiotics targeting Pseudomonas/H. influenzae

— Young patient with chronic sinopulmonary disease, pancreatic insufficiency, infertility

— Sweat chloride >60 mmol/L

— Treat with IV antibiotics (anti-pseudomonal), airway clearance, CFTR modulators

— Asthma + central bronchiectasis + eosinophilia + elevated IgE (>1000) + Aspergillus-specific IgE

— Recurrent steroid-dependent asthma exacerbations

— Treat with oral corticosteroids ± itraconazole

— Asthma + eosinophilia + vasculitis (mononeuritis multiplex, sinusitis, cardiomyopathy, renal)

— Often unmasked by leukotriene receptor antagonists or steroid taper

— Treat with high-dose steroids + immunosuppression

— Sudden onset, unilateral wheeze, history of choking (pediatric or altered adult)

— Decreased breath sounds focally

— Inspiratory/expiratory CXR or CT; bronchoscopy diagnostic and therapeutic

— Localized wheeze, hemoptysis, recurrent pneumonia same lobe

— CT chest, bronchoscopy

Key distinction: "Asthma" not responding to standard therapy with eosinophilia and new mononeuritis/rash → think EGPA — order ANCA, eosinophil count, biopsy; this needs urgent rheumatology consult and high-dose steroids.

Board pearl: Unilateral wheeze = think fixed obstruction (foreign body, tumor, mucus plug), not asthma.

COPD exacerbation:

Asthma-COPD overlap (ACOS):

Bronchiectasis exacerbation:

Cystic fibrosis exacerbation:

Allergic bronchopulmonary aspergillosis (ABPA):

Eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss):

Foreign body aspiration:

Endobronchial mass/tumor:

Key Differentials — Other Categories

— Orthopnea, PND, JVD, S3, bilateral basilar crackles, peripheral edema

— BNP >500, CXR with cardiomegaly, pulmonary edema, Kerley B lines

— Treat with diuresis, NIPPV, nitrates — not bronchodilators primarily

— POCUS: B-lines, reduced LVEF

— Pleuritic pain, hemoptysis, unilateral leg swelling, hypoxia out of proportion, sinus tach with S1Q3T3

— D-dimer, CTA chest

— Risk factors: malignancy, OCP, immobilization, pregnancy/postpartum

— Often presents with "asthma-like" wheeze and dyspnea

— Urticaria, angioedema, lip/tongue swelling, GI symptoms, hypotension

— Stridor (upper airway) + wheeze (lower)

— IM epinephrine 0.3–0.5 mg lateral thigh is first-line — before steroids or antihistamines

— Biphasic reaction possible — observe 4–6 hours

— Inspiratory stridor, normal SpO2, flattened inspiratory loop, laryngoscopy with paradoxical adduction

— Often coexists with asthma — confuses diagnosis

— Speech therapy, address triggers (anxiety, GERD)

— Stridor (not wheeze), drooling, tripoding

— Epiglottitis, peritonsillar abscess, angioedema (ACEi-induced), foreign body

— Unilateral absent breath sounds, hyperresonance, tracheal deviation, JVD, hypotension

— Clinical diagnosis — needle decompression first, then tube thoracostomy

— Fever, focal infiltrate, productive cough, leukocytosis

— Can trigger asthma exacerbation; treat both

— Normal SpO2, perioral/finger numbness, carpopedal spasm, no wheeze

— Diagnosis of exclusion

— Smoke, chlorine, ammonia, organophosphate

— Stridor, soot, singed nasal hairs, carboxyhemoglobin

Key distinction: Wheezing + hypotension + urticaria after a med/food/sting = anaphylaxis → IM epinephrine first; don't get tunneled on "asthma" management.

Board pearl: Acute dyspnea with clear lungs and tachycardia in a postpartum or post-op patient → PE until proven otherwise.

Cardiac asthma / acute decompensated heart failure:

Pulmonary embolism:

Anaphylaxis:

Vocal cord dysfunction (paradoxical vocal fold motion):

Upper airway obstruction:

Tension pneumothorax:

Pneumonia / sepsis:

Hyperventilation / panic attack:

Inhalation injury / toxic exposure:

Secondary Prevention and Discharge Plan

— Oral prednisone 40–60 mg daily x 5–7 days, no taper (longer if recent prior course)

— Inhaled corticosteroid (ICS) initiated or stepped up — every exacerbation patient leaves ED on a controller; ICS reduces re-exacerbation by ~50%

· Preferred: ICS-formoterol as single maintenance and reliever therapy (SMART/MART approach) per GINA

· Alternative: ICS-LABA combination (fluticasone-salmeterol, budesonide-formoterol, mometasone-formoterol)

— SABA rescue inhaler (albuterol MDI) with spacer — counsel that ≥2 canisters/year signals poor control

— Continue/start LAMA (tiotropium) in step-up for severe asthma

— Consider leukotriene receptor antagonist (montelukast) — black-box warning for neuropsychiatric effects; counsel

— Step 1–2: ICS-formoterol PRN

— Step 3–4: Low/medium-dose ICS-LABA daily + ICS-formoterol PRN

— Step 5: High-dose ICS-LABA + add-on (tiotropium, biologic)

— Eosinophilic phenotype (eos ≥300): mepolizumab, reslizumab, benralizumab

— High IgE allergic: omalizumab

— Type 2 inflammation/atopic dermatitis: dupilumab

— TSLP-driven: tezepelumab (broad eosinophilic and noneosinophilic)

— Smoking cessation (patient and household) — refer to quit line, prescribe varenicline/bupropion/NRT

— Vaping cessation

— Allergen mitigation: HEPA filter, dust mite encasings, pest control, pet dander

— Influenza vaccine annually, pneumococcal (PCV20 or PCV15+PPSV23), COVID-19 boosters, RSV if eligible, Tdap

— Weight loss if obese, treat GERD, treat OSA (CPAP), treat allergic rhinitis (intranasal steroid)

— Green/Yellow/Red zones based on PEF or symptoms

— Specific actions per zone

— When to call physician, when to go to ED

Step 3 management: No asthma patient should leave the ED or hospital without (1) systemic steroids, (2) an ICS-containing controller, (3) a written Asthma Action Plan, (4) confirmed PCP/pulmonology follow-up within 1–4 weeks.

Board pearl: SABA-only treatment is no longer recommended by GINA — even mild asthma should receive as-needed ICS-formoterol.

Mandatory discharge medication bundle:

GINA step-up logic:

Biologic candidates (specialist referral):

Trigger avoidance and lifestyle:

Avoid: Nonselective beta-blockers, NSAIDs (if aspirin-sensitive), sulfites (in some patients)

Asthma Action Plan (written):

Follow-Up, Monitoring, and Rehabilitation

— Within 1–2 weeks: PCP or pulmonology visit

· Assess symptom control (ACT score, ACQ)

· Inhaler technique observation — single most effective teaching intervention

· Adherence review, side effects of steroids

· Spirometry if not done recently

· Review/update Asthma Action Plan

— At 4–6 weeks: Reassess controller step; consider de-escalation if controlled ≥3 months

— At 3 months: Routine specialist follow-up for moderate–severe persistent

— Annually: Influenza vaccine, spirometry, comorbidity review

— Asthma Control Test (ACT): ≥20 = controlled; <20 = step up

— Daily/weekly symptom frequency, nighttime awakenings, rescue inhaler use

— PEF home monitoring for patients with poor symptom perception

— Spirometry every 1–2 years; FEV1 trajectory is key

— Eosinophil count and FeNO trend (if on biologic or for phenotyping)

— Demonstrate and have patient teach back

— Use spacer with all MDIs — improves drug delivery 2–5x

— Rinse mouth after ICS — prevents oral candidiasis, dysphonia

— Prime device, shake, exhale fully, slow deep inhalation, breath hold 10 sec

— Replace inhalers per dose counter — empty inhalers under-treat

— Consider in severe asthma with deconditioning, especially post-ICU

— Exercise training, breathing techniques, education

— Improves quality of life and exercise tolerance

— Screen for depression and anxiety — high comorbidity, worsens outcomes

— Smoking cessation counseling at every visit

— Discuss occupational triggers; consider workplace modification

— Annual flu, COVID boosters, pneumococcal, RSV (≥60 with chronic lung disease)

— Discharge summary to PCP and pulmonologist within 48 hours

— Direct scheduling of follow-up appointment before discharge (warm handoff)

— Medication reconciliation, pharmacy verification of insurance coverage for ICS-LABA/biologics

— Patient portal access, contact for questions

Step 3 management: Asthma is a chronic disease requiring longitudinal management — every exacerbation is a sentinel event prompting controller intensification, not just rescue. Document the step-up.

CCS pearl: In CCS, before ending the case, order "Schedule follow-up with primary care in 1–2 weeks" and "Asthma education with respiratory therapist before discharge."

Post-discharge follow-up cadence:

Monitoring parameters:

Inhaler technique counseling:

Pulmonary rehabilitation:

Behavioral/psychosocial:

Vaccination tracking:

Outpatient handoff:

Ethical, Legal, and Patient Safety Considerations

— Severe hypoxia or hypercapnia → diminished decision-making capacity

— Emergency exception/implied consent applies for life-saving interventions (intubation) when patient cannot consent and no surrogate available

— Document capacity assessment, attempted surrogate contact, clinical necessity

— When time permits, obtain informed consent from surrogate per state hierarchy

— Ask about code status early, especially in patients with severe persistent asthma, prior ICU/intubation, or comorbidities

— Respect DNR/DNI but clarify: DNI does not preclude NIPPV, steroids, or maximal medical therapy

— Reassess goals of care after stabilization

— ED-to-discharge transition is the highest-risk handoff for asthma readmission

— Common failure points: no controller prescribed, no follow-up scheduled, no inhaler technique taught, no Asthma Action Plan, language barrier

— Use teach-back for medication instructions and AAP

— Provide medications in hand (or e-script to confirmed pharmacy) before discharge

— Address insurance/cost barriers — ICS-LABA can be expensive; use formulary alternatives

— Recurrent severe exacerbations may signal neglect, environmental exposure (secondhand smoke, mold, pests), or medication nonadherence

— Consider social work consult; mandatory reporting if neglect suspected

— Document parent education and environmental counseling

— Ask about workplace triggers (isocyanates, baker's flour, latex, animal dander, cleaning products)

— May require workers' compensation reporting depending on state

— Refer to occupational medicine; document exposure history

— Post-ICU patient may have residual hypoxia, deconditioning — counsel against immediate return to safety-sensitive work (commercial driving, machinery operation) until cleared

— Asthma mortality disproportionately affects Black, Hispanic, low-income patients

— Screen for housing instability, food insecurity (linked to mold, pests, stress)

— Connect to community asthma programs, home visitor services

Board pearl: A child with third ED visit for asthma in 6 months despite "compliance" — screen the home environment (smoking, mold, pests), assess inhaler technique with the parent, and consider social work referral; recurrent exacerbations may reflect modifiable social determinants.

Step 3 management: Always document a written Asthma Action Plan discussion at discharge — failure to provide one is a quality measure miss and a malpractice exposure if the patient subsequently has a fatal exacerbation.

Informed consent in acute exacerbation:

Advance directives:

Patient safety / transitions of care:

Pediatric exacerbation safeguarding:

Occupational asthma:

Driving/work fitness:

Equity considerations:

High-Yield Associations and Rapid-Fire Clinical Facts

— High IgE allergic → omalizumab

— Eosinophilic (≥300) → mepolizumab, benralizumab, reslizumab

— Type 2 + atopic dermatitis → dupilumab

— Broad phenotype → tezepelumab (anti-TSLP)

Board pearl: A young athlete with "exercise-induced asthma" not responsive to albuterol pretreatment, with inspiratory stridor on flow-volume loop → vocal cord dysfunction; refer to speech-language pathology.

Triggers — memorize the big six: Viral URI, allergens (dust mite, cockroach, pet, pollen, mold), exercise, cold air, irritants (smoke, perfume, pollution), drugs (aspirin/NSAIDs, beta-blockers)

Aspirin-exacerbated respiratory disease (Samter triad): Asthma + nasal polyps + aspirin sensitivity → leukotriene overproduction; treat with leukotriene modifier ± aspirin desensitization

Cardinal sign of impending respiratory failure: Normalizing or rising PaCO2 in tachypneic asthmatic

Silent chest = no air movement = peri-arrest

Pulsus paradoxus >25 mmHg = severe obstruction

Best predictor of future fatal asthma: Prior intubation for asthma

Most important ED intervention reducing relapse: Systemic corticosteroids within 1 hour

No-taper rule: ≤7–10 day steroid courses don't need tapering

Continuous albuterol preferred over intermittent in severe exacerbation

Ipratropium adds benefit only in ED, not after admission

Magnesium 2 g IV for severe non-responders at 1 hour

Heliox = lower density, reduces work of breathing

Ketamine = bronchodilator induction agent of choice

Ventilator strategy: Permissive hypercapnia, low TV, low RR, prolonged expiration

DOPES (sudden vent decompensation): Displaced tube, Obstruction, Pneumothorax, Equipment, Stacking (auto-PEEP)

β2-agonist labs: Hypokalemia, hyperglycemia, lactic acidosis (type B), tachycardia, tremor

Pregnancy SpO2 goal: ≥95% (fetus depends on maternal PaO2)

Preferred ICS in pregnancy: Budesonide

Pediatric steroid: Dexamethasone 0.6 mg/kg x1–2 doses = 5-day prednisone

ABPA: Asthma + central bronchiectasis + eos + IgE >1000 + Aspergillus-specific IgE → steroids ± itraconazole

EGPA: Asthma + eosinophilia + vasculitis (mononeuritis, rash, sinusitis) → ANCA, biopsy, high-dose steroids

Biologics by phenotype:

GINA 2024: SABA-only therapy no longer recommended; ICS-formoterol PRN is preferred reliever

Asthma Control Test (ACT) ≥20 = controlled

Board Question Stem Patterns

"A 28-year-old woman with asthma presents with 2 days of worsening dyspnea after a URI. RR 32, HR 124, SpO2 89% RA, speaking in 2-word phrases, diffuse wheeze with prolonged expiration. PEF 35% predicted. After 1 hour of continuous albuterol, ipratropium nebs, and IV methylprednisolone, she remains unchanged. Next best step?"

→ Answer: IV magnesium sulfate 2 g over 20 minutes

"After 90 minutes of intensive therapy, the patient appears drowsy. ABG: pH 7.32, PaCO2 44 (from 28), PaO2 70 on 60% FiO2. Next best step?"

→ Answer: Prepare for intubation — normalizing PaCO2 in a tachypneic asthmatic signals fatigue

"After 6 hours of therapy, patient is comfortable, SpO2 96% RA, PEF 78%. She has had 3 ED visits in the past year and uses albuterol daily. Best discharge regimen?"

→ Answer: Oral prednisone 40 mg x 5 days + initiate ICS-formoterol as maintenance and reliever + asthma action plan + follow-up in 1–2 weeks

"A 26-year-old at 30 weeks gestation presents with severe asthma exacerbation. SpO2 91% on RA. What is the appropriate management?"

→ Answer: Albuterol nebs, ipratropium, IV methylprednisolone, target SpO2 ≥95%, continuous fetal monitoring — undertreatment harms fetus

"Intubated asthmatic suddenly becomes hypotensive with peak pressure 60. First step?"

→ Answer: Disconnect from ventilator and allow passive exhalation (relieves auto-PEEP); evaluate for pneumothorax

"Asthmatic on prednisone taper develops mononeuritis multiplex, eosinophilia 22%, and new rash. Diagnosis?"

→ Answer: EGPA (Churg-Strauss) — order ANCA, biopsy, start high-dose steroids

"Recurrent severe asthma with central bronchiectasis on CT, total IgE 2400, peripheral eosinophilia. Diagnosis and treatment?"

→ Answer: ABPA; oral corticosteroids ± itraconazole

"7-year-old with severe exacerbation, PEF 30%, 3 prior hospitalizations. After nebs and IV methylpred, still distressed. Next step?"

→ Answer: IV magnesium 25–50 mg/kg

"Asthmatic on metoprolol for HFrEF presents with frequent exacerbations. Action?"

→ Continue cardioselective beta-blocker cautiously; avoid nonselective; ensure ICS-LABA optimized

"Severe asthma on high-dose ICS-LABA, eosinophils 480, IgE 220, frequent exacerbations. Best add-on?"

→ Answer: Mepolizumab (anti–IL-5) — eosinophilic phenotype

Board pearl: When the stem mentions "normal PaCO2" during severe exacerbation, the answer involves intubation preparation — never reassurance.

Stem 1 — Classic severe exacerbation:

Stem 2 — Recognizing impending failure:

Stem 3 — Discharge planning:

Stem 4 — Special population:

Stem 5 — Ventilator decompensation:

Stem 6 — Differential:

Stem 7 — Atypical refractory case:

Stem 8 — Pediatric:

Stem 9 — Drug interaction:

Stem 10 — Biologic referral:

One-Line Recap

Severe asthma exacerbation is a clinical diagnosis requiring immediate empirical therapy with oxygen titrated to SpO2 92–96%, continuous or stacked nebulized albuterol-ipratropium, systemic corticosteroids within the first hour, and IV magnesium for non-responders — with escalation to NIPPV or intubation (using permissive hypercapnia ventilation) for impending failure, signaled by a normalizing or rising PaCO2, silent chest, or altered mental status.

Board pearl: The single most powerful intervention in severe asthma — both for the acute event and for preventing the next one — is early systemic corticosteroid administration coupled with ICS-containing controller initiation at discharge. Every exacerbation is a chance to step up chronic therapy, not just resolve the acute event.

High-yield recap bullets:

Severity recognition: Speech fragmentation, accessory muscle use, PEF <50%, SpO2 <92%, RR >30, HR >120 = severe; silent chest, drowsiness, normalizing PaCO2, bradycardia = life-threatening.

First-hour treatment bundle: O2 to SpO2 92–96% (≥95% pregnancy) + albuterol-ipratropium nebs q20min x3 (or continuous) + systemic steroid within 60 minutes + IV magnesium 2 g if no response at 1 hour. Reassess PEF and clinical status every 15–30 minutes.

Escalation triggers: Failure to improve at 1 hour, rising PaCO2, exhaustion, altered mental status → NIPPV or intubation with ketamine induction; ventilate with permissive hypercapnia (low TV, low RR, prolonged expiration, plateau <30). For sudden vent decompensation, disconnect the circuit to relieve auto-PEEP; rule out pneumothorax (DOPES).

Discharge bundle (never omit): Oral prednisone 40–60 mg x 5–7 days no taper, initiate or step-up ICS-formoterol (SMART therapy preferred by GINA), spacer-equipped SABA rescue, written Asthma Action Plan, inhaler technique teach-back, vaccinations updated, smoking cessation, trigger counseling, PCP/pulmonology follow-up within 1–2 weeks, and consider biologic referral for eosinophilic or allergic phenotype with frequent exacerbations.