111. Pulmonary Embolism (PE)

risk-stratify: low vs intermediate vs high (massive) · anticoagulate most · thrombolysis for hemodynamic instability · RV strain drives disposition · Super Compact

Sx: acute dyspnea (most common), pleuritic chest pain, tachycardia, tachypnea, hypoxemia (often out of proportion to exam/CXR), cough/hemoptysis · unilateral leg swelling/pain (DVT) · high-risk: syncope, hypotension/shock, signs of acute RV failure (elevated JVP, accentuated P2) (the disposition turns on hemodynamics and RV strain — risk-stratify before you treat)

Neg: denies fever + productive cough + lobar consolidation as the primary picture (pneumonia) · denies orthopnea/PND/gradual edema (CHF) · denies positional/reproducible chest wall pain (musculoskeletal) · denies classic tearing pain radiating to back (aortic dissection) · denies wheeze-dominant reversible obstruction (asthma/COPD)

SHx: VTE risk — recent surgery/immobilization/long travel · active malignancy · prior VTE · estrogen (OCP/HRT)/pregnancy/postpartum · thrombophilia · smoking · obesity · indwelling catheters

Etiology: thrombus (usually from lower-extremity/pelvic DVT) embolizing to pulmonary arteries · Virchow's triad — stasis, hypercoagulability, endothelial injury · rarely fat, air, amniotic fluid, tumor emboli · risk categories: low-risk · intermediate-risk (submassive — RV strain without hypotension) · high-risk (massive — hypotension/shock)

RF: immobility/surgery/trauma · malignancy · prior VTE/thrombophilia · estrogen/pregnancy · obesity · age · CHF · nephrotic syndrome · central lines

Data: pretest probability (Wells/Geneva); PERC to exclude in low-risk · D-dimer (high sensitivity — rule out in low/intermediate pretest; age-adjusted threshold) · CT pulmonary angiography (diagnostic test of choice) · V/Q scan (if contrast/renal contraindication) · ECG (sinus tach, S1Q3T3, RV strain/TWI) · troponin + BNP (RV strain/risk-stratify) · echocardiography (RV dilation/dysfunction — risk + thrombolysis decision) · lower-extremity Doppler · ABG, lactate · PESI/sPESI score

DDx: pneumonia (consolidation, fever) · ACS (ECG, troponin pattern) · CHF (BNP, bilateral) · aortic dissection (CT, pulse/BP differential) · pericarditis/tamponade (echo) · pneumothorax (CXR) · musculoskeletal/anxiety

Home Meds: review current anticoagulation/antiplatelets · reconcile bleeding risk meds · hold agents per procedure/thrombolysis · ensure no contraindications to anticoagulation; plan transition to outpatient anticoagulant

Plan

CONSULT: Pulmonary embolism response team (PERT) if available · Pulmonology/Critical care (intermediate-high/high-risk) · Interventional radiology/Cardiology (catheter-directed therapy/embolectomy) · ICU (high-risk/instability) · Hematology (recurrent/unprovoked/thrombophilia)

– First, risk-stratify (this drives everything): assess hemodynamics, RV strain (echo, troponin, BNP), and PESI/sPESI → low-risk vs intermediate-risk (submassive) vs high-risk (massive)
– Anticoagulation (the mainstay for most): start promptly unless contraindicated, even before confirmation if high suspicion + low bleeding risk
  • DOAC — apixaban (10 mg PO BID ×7 days then 5 mg BID) or rivaroxaban (15 mg PO BID ×21 days then 20 mg daily) — preferred for most stable patients
  • LMWH — enoxaparin 1 mg/kg SC q12h (preferred in cancer, pregnancy, or transition); or UFH infusion (preferred if thrombolysis possible, hemodynamic instability, renal failure, or procedures — easily reversible)
– High-risk (massive — hypotension/shock): systemic thrombolysis (e.g. alteplase 100 mg IV over 2 h) unless contraindicated; hemodynamic support (cautious fluids — avoid over-filling the failing RV, norepinephrine, consider inotropy); catheter-directed therapy or surgical embolectomy if thrombolysis contraindicated/failed; ICU
– Intermediate-high risk (RV strain + biomarker positive, but normotensive): anticoagulate + monitor closely in a higher-acuity setting; rescue thrombolysis/catheter-directed therapy if they decompensate (engage PERT)
– Low-risk: anticoagulate; consider outpatient management/early discharge (low sPESI, Hestia criteria) in selected patients with good support
– Supportive care: oxygen to SpO2 ≥92%; analgesia; treat the underlying provoking factor
– IVC filter only if anticoagulation is absolutely contraindicated or recurrent PE despite therapeutic anticoagulation
– Risk stratification, not just the diagnosis, dictates therapy: anticoagulate nearly everyone, reserve thrombolysis for hemodynamic instability (high-risk), and watch the intermediate-high patient like a hawk because they can crash and need rescue. RV dysfunction on echo plus a positive troponin is your warning the "stable" patient isn't low-risk.
– PT/OT: early mobilization once anticoagulated/stable
– Trend: hemodynamics, oxygenation, RV markers (troponin/BNP), bleeding, anticoagulation parameters (anti-Xa/aPTT if UFH), renal function
– Escalation triggers: hypotension/shock or worsening RV strain → thrombolysis/catheter therapy + ICU; decompensation in intermediate-high → rescue reperfusion; major bleeding → reverse/hold, hematology
– Discharge when: hemodynamically stable, oxygenation adequate, established on anticoagulation with a clear plan/duration (≥3 months; longer/indefinite for unprovoked/recurrent/cancer); provocation workup, cancer screening if unprovoked, hematology referral if indicated; anticoagulation education + follow-up; return precautions (chest pain, dyspnea, syncope, bleeding, leg swelling)

111. Pulmonary Embolism (PE)

complete reference · pretest probability and imaging · risk stratification by hemodynamics and RV strain · anticoagulation, thrombolysis, and reperfusion · Full Card

Symptoms / Associated Sx

• Acute dyspnea (the most common symptom), pleuritic chest pain, tachycardia, tachypnea, and hypoxemia that is often out of proportion to the exam and chest film, with cough or hemoptysis

• Unilateral leg swelling or pain suggesting a deep vein thrombosis

• High-risk disease brings syncope, hypotension or shock, and signs of acute RV failure such as an elevated JVP and an accentuated P2

Neg

• Pt denies fever, productive cough, and lobar consolidation as the primary picture — argues against pneumonia

• Pt denies orthopnea, PND, and gradual edema — argues against heart failure

• Pt denies positional or reproducible chest wall pain — argues against a musculoskeletal cause

• Pt denies classic tearing pain radiating to the back — argues against aortic dissection

Social History (SHx)

• VTE risk factors — recent surgery, immobilization, or long-distance travel, and active malignancy

• Prior VTE, estrogen use (oral contraceptives or hormone therapy), pregnancy or the postpartum state, and known thrombophilia

• Smoking, obesity, and indwelling catheters

Main Etiology

• A thrombus, usually arising from a lower-extremity or pelvic deep vein thrombosis, embolizing to the pulmonary arteries

• Driven by Virchow's triad of stasis, hypercoagulability, and endothelial injury; rarely fat, air, amniotic fluid, or tumor emboli

• The clinically critical division is into low-risk, intermediate-risk (submassive, with RV strain but no hypotension), and high-risk (massive, with hypotension or shock) categories

RF

• Modifiable: immobility, estrogen exposure, obesity, and central lines

• Non-modifiable: malignancy, prior VTE or thrombophilia, advanced age, heart failure, and nephrotic syndrome

Data

• A pretest probability assessment (Wells or Geneva), with the PERC rule to exclude PE in low-risk patients

• D-dimer (highly sensitive to rule out PE in low or intermediate pretest probability, using an age-adjusted threshold)

• CT pulmonary angiography (the diagnostic test of choice), or a V/Q scan (when contrast or renal function contraindicates CT)

• ECG (sinus tachycardia, the S1Q3T3 pattern, RV strain with T-wave inversions)

• Troponin and BNP (RV strain and risk stratification) and echocardiography (RV dilation and dysfunction, informing risk and the thrombolysis decision)

• Lower-extremity Doppler, ABG and lactate, and the PESI or simplified PESI score

DDx

Pneumonia (consolidation, fever) · acute coronary syndrome (ECG and troponin pattern) · heart failure (BNP, bilateral findings) · aortic dissection (CT, a pulse or blood-pressure differential) · pericarditis or tamponade (echo) · pneumothorax (CXR) · musculoskeletal pain or anxiety

Home Meds

• Review current anticoagulation and antiplatelet therapy and reconcile bleeding-risk medications

• Hold agents as needed around procedures or thrombolysis

• Confirm there are no contraindications to anticoagulation and plan the transition to an outpatient anticoagulant

Plan

CONSULT: A pulmonary embolism response team (PERT) where available · Pulmonology/Critical care (intermediate-high and high-risk disease) · Interventional radiology or Cardiology (catheter-directed therapy or embolectomy) · ICU (high-risk or instability) · Hematology (recurrent, unprovoked, or thrombophilic disease)

• Risk-stratify first, since it drives everything: assess hemodynamics, RV strain (echo, troponin, BNP), and the PESI or simplified PESI to assign low-risk, intermediate-risk (submassive), or high-risk (massive) categories

• Anticoagulation is the mainstay for most patients, started promptly unless contraindicated, and even before confirmation when suspicion is high and bleeding risk is low: a DOAC such as apixaban (10 mg PO BID for 7 days then 5 mg BID) or rivaroxaban (15 mg PO BID for 21 days then 20 mg daily) for most stable patients; LMWH such as enoxaparin 1 mg/kg SC q12h (preferred in cancer, pregnancy, or as a transition); or a UFH infusion (preferred when thrombolysis is possible, in hemodynamic instability or renal failure, or around procedures, given its easy reversibility)

• High-risk (massive) disease with hypotension or shock: systemic thrombolysis (alteplase 100 mg IV over 2 hours) unless contraindicated, with hemodynamic support (cautious fluids to avoid over-filling the failing RV, norepinephrine, and consideration of inotropy), and catheter-directed therapy or surgical embolectomy if thrombolysis is contraindicated or fails, all in the ICU

• Intermediate-high risk (RV strain with positive biomarkers but normotensive): anticoagulate and monitor closely in a higher-acuity setting, with rescue thrombolysis or catheter-directed therapy if the patient decompensates (engage the PERT)

• Low-risk disease: anticoagulate and consider outpatient management or early discharge (a low simplified PESI, Hestia criteria) in selected patients with good support

• Supportive care: oxygen to keep SpO2 92% or higher, analgesia, and treatment of the underlying provoking factor

• An IVC filter only when anticoagulation is absolutely contraindicated or there is recurrent PE despite therapeutic anticoagulation

• PT/OT: early mobilization once anticoagulated and stable

• Trend: hemodynamics, oxygenation, RV markers, bleeding, anticoagulation parameters (anti-Xa or aPTT for UFH), and renal function

• Escalation triggers: hypotension, shock, or worsening RV strain → thrombolysis or catheter therapy and ICU; decompensation in intermediate-high disease → rescue reperfusion; major bleeding → reverse or hold anticoagulation and involve hematology

• Discharge criteria: hemodynamic stability, adequate oxygenation, and establishment on anticoagulation with a clear plan and duration (at least 3 months, longer or indefinite for unprovoked, recurrent, or cancer-associated disease); pursue a provocation workup, cancer screening if unprovoked, and hematology referral when indicated, with anticoagulation education, follow-up, and return precautions for chest pain, dyspnea, syncope, bleeding, or leg swelling

Red Flags

• Hypotension or shock → high-risk (massive) PE; thrombolysis and ICU

• RV dilation or dysfunction on echo with a positive troponin → intermediate-high risk that can decompensate; monitor closely with a rescue plan

• Syncope as the presenting symptom → a marker of a hemodynamically significant embolism

• Hypoxia out of proportion to a clear chest film → the classic PE signature

• Recurrent PE despite therapeutic anticoagulation → reassess adherence and consider an IVC filter and hematology input

Senior IM Resident Pearls

• Stratify before you treat. The diagnosis is only half the work — hemodynamics and RV strain decide between anticoagulation alone and reperfusion.

• The "stable" intermediate-high patient is the trap. A normal blood pressure with RV strain and a positive troponin can crash; watch them in a monitored bed with a rescue plan.

• Reserve thrombolysis for instability. High-risk disease benefits, but the bleeding risk isn't justified in a normotensive patient without decompensation.

• Don't over-fill the failing RV. Cautious fluids and early norepinephrine support the right heart better than aggressive boluses.

• Start anticoagulation on suspicion. In a high-probability patient with low bleeding risk, don't wait for the scan.

• Unprovoked PE earns a workup. Consider occult malignancy and thrombophilia, and longer anticoagulation duration.

• Common mistake: calling a normotensive PE "stable" and sending it to the floor when RV strain and biomarkers flag an intermediate-high patient who needs closer monitoring.

Pulmonology — Pleural Disease

112. Pleural Effusion

Light's criteria: transudate vs exudate · CHF · malignant · parapneumonic · hepatic hydrothorax · diagnostic ± therapeutic thoracentesis · Super Compact

Sx: dyspnea (especially with large effusions), pleuritic chest pain, dry cough · exam: dullness to percussion, decreased breath sounds + decreased fremitus over the effusion · may be asymptomatic and found on imaging · symptoms of the underlying cause (orthopnea/edema for CHF, fever for parapneumonic, weight loss for malignancy) (the central task is to classify transudate vs exudate, then identify the specific cause)

Neg: denies pleuritic pain + sudden dyspnea + calf swelling (PE with effusion) · denies fever + productive cough as the only explanation (parapneumonic vs malignant) · denies high-volume alcohol/cirrhosis stigmata if hepatic hydrothorax not suspected · denies trauma/instrumentation (hemothorax)

SHx: cardiac/renal/liver disease (transudates) · malignancy history · asbestos exposure (mesothelioma) · recent pneumonia/infection · TB exposure · medications (some cause effusions) · smoking

Etiology: transudates (↑hydrostatic/↓oncotic) — heart failure (most common transudate), cirrhosis/hepatic hydrothorax, nephrotic syndrome, hypoalbuminemia · exudates (↑permeability) — parapneumonic/empyema, malignancy (most common exudate), PE, TB, autoimmune, pancreatitis, chylothorax

RF: heart/liver/kidney failure · pneumonia · malignancy · PE risk · TB exposure · connective tissue disease · recent thoracic/abdominal surgery

Data: CXR (PA + lateral ± decubitus) (blunting, layering, size, loculation) · chest US (quantify, localize, guide tap, detect loculation/septations) · CT (complex/malignancy workup) · diagnostic thoracentesis (unless clearly small/bilateral CHF responding to diuresis) → Light's criteria (exudate if pleural/serum protein >0.5, pleural/serum LDH >0.6, or pleural LDH >2/3 upper-normal serum) · pleural fluid: pH, glucose, cell count/differential, Gram stain/culture, cytology, protein/LDH/albumin (pH<7.2 → drain; cytology + ADA/TB studies as indicated)

DDx: CHF (transudate, bilateral, responds to diuresis) · parapneumonic/empyema (infection, low pH/glucose) · malignant (cytology, exudate) · hepatic hydrothorax (cirrhosis, usually right-sided transudate) · PE (CTA) · TB (lymphocytic exudate, high ADA)

Home Meds: optimize diuretics (CHF/hepatic hydrothorax) · reconcile anticoagulation around thoracentesis (correct coagulopathy as feasible) · treat underlying disease meds · avoid nephrotoxins if renal involvement

Plan

CONSULT: Pulmonology (diagnostic uncertainty, recurrent/complex effusions, pleural procedures) · Interventional pulmonology/Thoracic surgery (loculated, malignant, recurrent — pleurodesis/indwelling catheter) · Cardiology (CHF) · Hepatology (hepatic hydrothorax) · Oncology (malignant)

– First, classify with thoracentesis + Light's criteria (unless a small bilateral effusion clearly from CHF that responds to diuresis): determine transudate vs exudate, then pursue the specific cause
– Diagnostic thoracentesis under ultrasound guidance; send pH, glucose, cell count/differential, protein, LDH, albumin, Gram stain/culture, cytology; add ADA/TB studies, triglycerides (chylothorax), amylase (pancreatic/esophageal) as indicated
– Therapeutic thoracentesis for symptomatic large effusions to relieve dyspnea (limit volume per session to reduce re-expansion pulmonary edema)
– Cause-specific treatment:
  • Transudative (CHF): diurese (furosemide) + treat heart failure — effusion follows; thoracentesis if large/symptomatic
  • Hepatic hydrothorax: sodium restriction + diuretics, manage cirrhosis/ascites; refractory → TIPS evaluation (avoid chest tubes — high complication rate)
  • Parapneumonic: antibiotics for the pneumonia; if complicated (pH <7.2, loculation, frank pus → empyema) → chest tube drainage ± intrapleural therapy (see the empyema card)
  • Malignant: therapeutic drainage for symptoms; recurrent → indwelling pleural catheter or pleurodesis; oncology for systemic therapy
– Treat the underlying disease as the durable solution
– Light's criteria split transudate from exudate, but always send pleural pH and glucose on a parapneumonic effusion: a pH below 7.2 means it needs a chest tube now, not just antibiotics. In hepatic hydrothorax, reach for diuretics and TIPS — a chest tube there courts disaster.
– PT/OT: mobilize; incentive spirometry post-drainage
– Trend: effusion size/recurrence on imaging, dyspnea, fluid studies, response to cause-specific therapy, oxygenation
– Escalation triggers: complicated parapneumonic/empyema → urgent drainage; recurrent symptomatic malignant effusion → IP/thoracic surgery; large effusion with respiratory compromise → therapeutic drainage; refractory hepatic hydrothorax → hepatology/TIPS
– Discharge when: dyspnea controlled, cause identified + management plan in place, drainage strategy defined (catheter teaching if indwelling); subspecialty follow-up (pulmonary/oncology/cardiology/hepatology), repeat imaging plan; return precautions (worsening dyspnea, fever, chest pain, catheter issues)

112. Pleural Effusion

complete reference · Light's criteria classification · transudative and exudative causes · diagnostic and therapeutic thoracentesis · cause-directed management · Full Card

Symptoms / Associated Sx

• Dyspnea, especially with large effusions, along with pleuritic chest pain and a dry cough

• Dullness to percussion with decreased breath sounds and decreased fremitus over the effusion; many effusions are asymptomatic and found on imaging

• Symptoms of the underlying cause — orthopnea and edema for heart failure, fever for a parapneumonic effusion, weight loss for malignancy

Neg

• Pt denies pleuritic pain with sudden dyspnea and calf swelling — argues against a PE-associated effusion

• Pt denies fever and productive cough as the only explanation — helps separate a parapneumonic from a malignant effusion

• Pt denies heavy alcohol use or stigmata of cirrhosis when a hepatic hydrothorax is not suspected

• Pt denies recent trauma or instrumentation — argues against a hemothorax

Social History (SHx)

• Cardiac, renal, or liver disease (transudates), and a malignancy history

• Asbestos exposure (mesothelioma), recent pneumonia, and TB exposure

• Medications that can cause effusions, and smoking

Main Etiology

• Transudates (from increased hydrostatic or decreased oncotic pressure) — heart failure (the most common transudate), cirrhosis with hepatic hydrothorax, nephrotic syndrome, and hypoalbuminemia

• Exudates (from increased capillary permeability) — parapneumonic effusions and empyema, malignancy (the most common exudate), pulmonary embolism, tuberculosis, autoimmune disease, pancreatitis, and chylothorax

RF

• Modifiable: volume status in heart, liver, and kidney failure, and timely pneumonia treatment

• Non-modifiable: malignancy, TB exposure, connective tissue disease, and recent thoracic or abdominal surgery

Data

• Chest radiograph (PA, lateral, and decubitus views) (blunting, layering, size, loculation) and chest ultrasound (to quantify, localize, guide the tap, and detect loculation or septations), with CT for complex effusions or a malignancy workup

• A diagnostic thoracentesis (unless the effusion is clearly small and bilateral from heart failure and responding to diuresis) interpreted with Light's criteria (an exudate if the pleural-to-serum protein ratio exceeds 0.5, the pleural-to-serum LDH ratio exceeds 0.6, or the pleural LDH exceeds two-thirds of the upper limit of normal serum LDH)

• Pleural fluid studies (pH, glucose, cell count and differential, Gram stain and culture, cytology, and protein, LDH, and albumin; a pH below 7.2 prompts drainage, with ADA and TB studies as indicated)

DDx

Heart failure (a transudate, bilateral, responsive to diuresis) · parapneumonic effusion or empyema (infection, low pH and glucose) · malignant effusion (positive cytology, an exudate) · hepatic hydrothorax (cirrhosis, usually a right-sided transudate) · pulmonary embolism (CTA) · tuberculosis (a lymphocytic exudate with a high ADA)

Home Meds

• Optimize diuretics for heart failure and hepatic hydrothorax

• Reconcile anticoagulation around thoracentesis and correct coagulopathy as feasible

• Treat the underlying disease and avoid nephrotoxins when there is renal involvement

Plan

CONSULT: Pulmonology (diagnostic uncertainty, recurrent or complex effusions, pleural procedures) · Interventional pulmonology or Thoracic surgery (loculated, malignant, or recurrent effusions — pleurodesis or an indwelling catheter) · Cardiology (heart failure) · Hepatology (hepatic hydrothorax) · Oncology (malignant effusions)

• Classify with thoracentesis and Light's criteria first (unless a small bilateral effusion is clearly from heart failure and responds to diuresis): establish transudate versus exudate, then pursue the specific cause

• A diagnostic thoracentesis under ultrasound guidance, sending pH, glucose, cell count and differential, protein, LDH, albumin, Gram stain and culture, and cytology, with ADA and TB studies, triglycerides (chylothorax), and amylase (a pancreatic or esophageal source) added as indicated

• A therapeutic thoracentesis for symptomatic large effusions to relieve dyspnea, limiting the volume removed per session to reduce re-expansion pulmonary edema

• Cause-specific treatment: for transudative heart failure, diuresis with furosemide and heart-failure treatment, since the effusion follows, with thoracentesis if it is large or symptomatic; for hepatic hydrothorax, sodium restriction and diuretics with management of the cirrhosis and ascites, and a TIPS evaluation if refractory, avoiding chest tubes given their high complication rate; for a parapneumonic effusion, antibiotics for the pneumonia, with chest tube drainage and possible intrapleural therapy if it is complicated (a pH below 7.2, loculation, or frank pus indicating empyema); and for a malignant effusion, therapeutic drainage for symptoms, with an indwelling pleural catheter or pleurodesis for recurrence and oncology for systemic therapy

• Treat the underlying disease as the durable solution

• PT/OT: mobilization and incentive spirometry after drainage

• Trend: effusion size and recurrence on imaging, dyspnea, the fluid studies, the response to cause-specific therapy, and oxygenation

• Escalation triggers: a complicated parapneumonic effusion or empyema → urgent drainage; a recurrent symptomatic malignant effusion → interventional pulmonology or thoracic surgery; a large effusion with respiratory compromise → therapeutic drainage; refractory hepatic hydrothorax → hepatology and TIPS

• Discharge criteria: controlled dyspnea, an identified cause with a management plan, and a defined drainage strategy (with catheter teaching if indwelling); arrange subspecialty follow-up and a repeat-imaging plan, with return precautions for worsening dyspnea, fever, chest pain, or catheter problems

Red Flags

• A pleural fluid pH below 7.2 in a parapneumonic effusion → a complicated effusion requiring chest tube drainage, not antibiotics alone

• Frank pus or a positive Gram stain → empyema

• A bloody effusion with weight loss → malignancy; send cytology and image further

• A rapidly reaccumulating effusion → a malignant or hepatic source needing a definitive drainage strategy

• Hypoxemia or hypotension after large-volume drainage → re-expansion pulmonary edema; limit the volume removed

Senior IM Resident Pearls

• Always send pH and glucose on a parapneumonic effusion. A pH below 7.2 means it needs a chest tube now — antibiotics alone won't save the lung.

• Light's criteria can mislabel a diuresed CHF effusion as exudative. Check the serum-to-pleural albumin gradient when the clinical picture is clearly transudative.

• Don't put a chest tube in a hepatic hydrothorax. Diuretics and TIPS are the answer; a tube there courts protein loss, infection, and disaster.

• Ultrasound-guide the tap. It improves yield and dramatically reduces pneumothorax and organ injury.

• Limit the volume removed. Large-volume drainage in one sitting risks re-expansion pulmonary edema.

• Recurrent malignant effusions need a durable plan. An indwelling catheter or pleurodesis beats repeated taps.

• Common mistake: treating a complicated parapneumonic effusion with antibiotics alone and watching it organize into an empyema that then needs surgery.

Pulmonology — Pleural Disease

113. Empyema / Complicated Parapneumonic Effusion

pleural-space infection · pH <7.2 / loculation / frank pus → drainage + antibiotics · intrapleural tPA-DNase · surgery for organized · Super Compact

Sx: persistent or recurrent fever, pleuritic chest pain, dyspnea, cough, and failure to improve (or recurrence) during treatment for pneumonia · systemic signs of infection (sweats, weight loss in subacute), dullness + decreased breath sounds over the effusion (suspect it whenever a pneumonia patient isn't improving or has a significant effusion — the pleural space is infected and needs drainage, not just antibiotics)

Neg: denies a clean response to antibiotics alone (an improving simple parapneumonic effusion) · denies a transudative picture from CHF (bilateral, responds to diuresis) · denies malignancy-only effusion without infection · denies hemothorax from trauma/instrumentation

SHx: recent/current pneumonia · aspiration risk · alcohol/substance use · poor dentition (anaerobes) · diabetes/immunosuppression · IV drug use · prior thoracic procedure/trauma · TB exposure

Etiology: progression of a parapneumonic effusion through stages — exudative (free-flowing) → fibrinopurulent (loculation, low pH/glucose, frank pus = empyema) → organizing (thick peel, trapped lung) · organisms: Streptococcus (incl anginosus group), Staph aureus, anaerobes (aspiration/poor dentition), gram-negatives; post-procedure/trauma flora · TB and fungal in selected hosts

RF: pneumonia (esp delayed treatment) · aspiration · alcoholism · diabetes · immunosuppression · poor dentition · IV drug use · prior thoracic surgery/trauma · esophageal rupture

Data: chest US (loculation, septations, complexity — guides drainage) · CT chest with contrast (pleural enhancement/split pleura sign, loculations, lung abscess, underlying cause) · diagnostic thoracentesis → pleural fluid pH, glucose, LDH, cell count, Gram stain/culture (complicated: pH <7.2, glucose low, LDH high; empyema: frank pus or positive Gram stain/culture) · blood cultures · CBC/inflammatory markers · CXR

DDx: simple/uncomplicated parapneumonic effusion (pH >7.2, free-flowing, resolves with antibiotics) · malignant effusion (cytology) · TB pleurisy (lymphocytic, high ADA) · hemothorax (blood, trauma) · lung abscess (parenchymal, air-fluid level)

Home Meds: reconcile antibiotics (often need broader/anaerobic coverage) · review anticoagulation around chest tube/intrapleural therapy · renally dose · ensure VTE prophylaxis; nutrition support (catabolic, often prolonged course)

Plan

CONSULT: Interventional pulmonology/Pulmonology (chest tube, intrapleural therapy) · Thoracic surgery (VATS/decortication for organized/failed drainage) · Infectious Disease (organism-directed + prolonged therapy) · Critical care (sepsis)

– The two pillars: drain the infected pleural space + give antibiotics (antibiotics alone do not cure an empyema)
– Drainage: chest tube (image-guided, often small-bore) for complicated parapneumonic effusion (pH <7.2, loculation) or empyema (frank pus/positive Gram stain or culture) — drain promptly
– Intrapleural therapy: for loculated/incompletely draining collections, intrapleural tPA (alteplase) + DNase (dornase alfa) (the MIST2 combination) improves drainage and reduces surgical referral
– Antibiotics: empiric coverage including anaerobes — e.g. ampicillin-sulbactam 3 g IV q6h, or this institution's cefepime 2 g IV q8h + metronidazole 500 mg IV q8h (community-acquired); broaden for hospital-acquired/MRSA risk (add vancomycin 15–20 mg/kg IV q8–12h); narrow to cultures; prolonged course (often 2–6 weeks) guided by drainage + clinical/radiographic response
– Surgery (thoracic surgery): VATS or decortication for organized empyema with trapped lung, failed tube drainage/intrapleural therapy, or persistent sepsis from an undrained space
– Source/supportive care: treat underlying pneumonia/aspiration, address dental source, nutrition, sepsis management; chest physiotherapy/lung re-expansion
– An empyema is a surgical-space infection: antibiotics never cure pus in the pleural space without drainage. Send pleural fluid pH on every significant parapneumonic effusion — below 7.2 means a chest tube now. Loculated collections often need tPA-DNase, and an organized peel trapping the lung needs the surgeon.
– PT/OT: mobilize; incentive spirometry/lung expansion; prevent deconditioning over a long course
– Trend: fever curve, WBC/inflammatory markers, chest tube output/character, imaging (re-expansion, residual collection), drainage adequacy, organism/sensitivities, response to intrapleural therapy
– Escalation triggers: inadequate drainage/persistent sepsis despite tube + intrapleural therapy → thoracic surgery; septic shock → ICU; undrained loculations → additional drains/IR
– Discharge when: source controlled (space drained, tube removed or plan defined), afebrile/improving, on a defined antibiotic course (frequently completed as OPAT — ID to arrange); imaging shows resolving collection; thoracic surgery/pulmonary/ID follow-up; return precautions (recurrent fever, worsening dyspnea, chest pain, drainage-site issues)

113. Empyema / Complicated Parapneumonic Effusion

complete reference · staging of pleural infection · drainage plus antibiotics · intrapleural tPA-DNase · surgery for organized disease · Full Card

Symptoms / Associated Sx

• Persistent or recurrent fever, pleuritic chest pain, dyspnea, and cough, with a failure to improve or a recurrence during treatment for pneumonia

• Systemic signs of infection including sweats and, in subacute disease, weight loss, with dullness and decreased breath sounds over the effusion

• Suspect it whenever a pneumonia patient is not improving or has a significant effusion — the pleural space is infected and needs drainage, not just antibiotics

Neg

• Pt denies a clean response to antibiotics alone — that would suggest an improving simple parapneumonic effusion

• Pt denies a transudative heart-failure picture (bilateral, responsive to diuresis)

• Pt denies a malignancy-only effusion without infection

• Pt denies recent trauma or instrumentation — argues against a hemothorax

Social History (SHx)

• Recent or current pneumonia and aspiration risk

• Alcohol or substance use, poor dentition (anaerobes), diabetes, and immunosuppression

• IV drug use, a prior thoracic procedure or trauma, and TB exposure

Main Etiology

• Progression of a parapneumonic effusion through stages — an exudative free-flowing stage, a fibrinopurulent stage with loculation, low pH and glucose, and frank pus (empyema), and an organizing stage with a thick peel and trapped lung

• Common organisms include streptococci (including the anginosus group), Staphylococcus aureus, anaerobes (with aspiration or poor dentition), and gram-negatives, with post-procedure or post-traumatic flora

• Tuberculous and fungal empyema occur in selected hosts

RF

• Modifiable: delayed pneumonia treatment, aspiration risk, alcohol use, poor dentition, and IV drug use

• Non-modifiable: diabetes, immunosuppression, prior thoracic surgery or trauma, and esophageal rupture

Data

• Chest ultrasound (loculation, septations, and complexity, which guide drainage)

• Contrast-enhanced CT of the chest (pleural enhancement and the split-pleura sign, loculations, a lung abscess, and the underlying cause)

• A diagnostic thoracentesis sending pleural fluid (pH, glucose, LDH, cell count, and Gram stain and culture — a complicated effusion has a pH below 7.2, low glucose, and high LDH, while an empyema shows frank pus or a positive Gram stain or culture)

• Blood cultures, CBC and inflammatory markers, and a chest radiograph

DDx

A simple uncomplicated parapneumonic effusion (pH above 7.2, free-flowing, resolves with antibiotics) · a malignant effusion (positive cytology) · tuberculous pleurisy (lymphocytic, a high ADA) · a hemothorax (blood, trauma) · a lung abscess (parenchymal, an air-fluid level)

Home Meds

• Reconcile antibiotics, which often need broader and anaerobic coverage

• Review anticoagulation around chest tube placement and intrapleural therapy, and renally dose

• Ensure VTE prophylaxis and nutritional support, given the catabolic and often prolonged course

Plan

CONSULT: Interventional pulmonology or Pulmonology (chest tube, intrapleural therapy) · Thoracic surgery (VATS or decortication for organized disease or failed drainage) · Infectious Disease (organism-directed and prolonged therapy) · Critical care (sepsis)

• The two pillars are draining the infected pleural space and giving antibiotics — antibiotics alone do not cure an empyema

• Drainage: a chest tube (image-guided, often small-bore) for a complicated parapneumonic effusion (a pH below 7.2 or loculation) or an empyema (frank pus or a positive Gram stain or culture), placed promptly

• Intrapleural therapy: for loculated or incompletely draining collections, intrapleural tPA (alteplase) with DNase (dornase alfa) — the MIST2 regimen — improves drainage and reduces the need for surgery

• Antibiotics: empiric coverage including anaerobes, such as ampicillin-sulbactam 3 g IV q6h, or this institution's cefepime 2 g IV q8h with metronidazole 500 mg IV q8h for community-acquired disease, broadened for hospital-acquired or MRSA risk (adding vancomycin 15–20 mg/kg IV q8–12h), narrowed to cultures, and continued as a prolonged course (often 2–6 weeks) guided by drainage and the clinical and radiographic response

• Surgery: VATS or decortication for an organized empyema with trapped lung, failed tube drainage or intrapleural therapy, or persistent sepsis from an undrained space

• Source and supportive care: treat the underlying pneumonia or aspiration, address a dental source, provide nutrition, manage sepsis, and support lung re-expansion with chest physiotherapy

• PT/OT: mobilization, incentive spirometry and lung expansion, and prevention of deconditioning over a long course

• Trend: the fever curve, white count and inflammatory markers, chest tube output and character, imaging for re-expansion and residual collection, drainage adequacy, the organism and sensitivities, and the response to intrapleural therapy

• Escalation triggers: inadequate drainage or persistent sepsis despite a tube and intrapleural therapy → thoracic surgery; septic shock → ICU; undrained loculations → additional drains or interventional radiology

• Discharge criteria: source control (the space drained and the tube removed or a plan defined), afebrile and improving, on a defined antibiotic course (frequently completed as outpatient parenteral therapy arranged by ID), with imaging showing a resolving collection; arrange thoracic surgery, pulmonary, and ID follow-up, with return precautions for recurrent fever, worsening dyspnea, chest pain, or drainage-site problems

Red Flags

• A pleural fluid pH below 7.2, loculation, or frank pus → drain it now; antibiotics alone will fail

• Failure to improve despite a chest tube → loculations needing tPA-DNase or an organized peel needing surgery

• Persistent sepsis from an undrained space → urgent thoracic surgery referral

• A trapped lung that will not re-expand → decortication

• An esophageal or post-procedure source → a distinct, often surgical, problem

Senior IM Resident Pearls

• Pus in the pleural space is a drainage problem. No antibiotic course cures an empyema without evacuating the infected space.

• The pleural pH decides. Below 7.2 in a parapneumonic effusion means a chest tube — this single number changes management.

• Reach for tPA-DNase before the surgeon. The MIST2 combination clears loculated collections and reduces surgical referrals.

• Don't wait too long. An exudative effusion drains easily; an organized empyema with a peel needs decortication — early drainage prevents that.

• Cover the anaerobes. Aspiration and poor dentition make anaerobic coverage essential in community-acquired empyema.

• Plan for a long course. These patients often need weeks of antibiotics and OPAT — set up ID and follow-up early.

• Common mistake: continuing antibiotics for a non-resolving pneumonia while the undrained complicated effusion organizes into a surgical empyema.

Pulmonology — Pleural Disease

114. Pneumothorax

primary vs secondary spontaneous vs traumatic · tension = clinical emergency (decompress now) · size + symptoms + reserve drive management · Super Compact

Sx: sudden ipsilateral pleuritic chest pain and dyspnea · decreased breath sounds + hyperresonance on the affected side, decreased chest expansion · tension pneumothorax (emergency): severe respiratory distress, hypotension, tachycardia, distended neck veins, tracheal deviation away from the affected side, hemodynamic collapse (tension is a clinical diagnosis — decompress immediately, do not wait for imaging)

Neg: denies fever + productive cough/consolidation (pneumonia) · denies orthopnea/PND/edema (CHF) · denies tearing pain to the back (dissection) · denies pleuritic pain + calf swelling (PE) · denies preceding trauma/procedure if spontaneous · denies reproducible chest wall tenderness (musculoskeletal)

SHx: smoking (major risk) · tall thin young male (primary spontaneous) · known lung disease — COPD/emphysema/bullae, asthma, cystic fibrosis, ILD (secondary spontaneous) · recent thoracic procedure/central line/mechanical ventilation (iatrogenic) · trauma · family history · prior pneumothorax

Etiology: primary spontaneous (no underlying lung disease — ruptured subpleural bleb, typically tall thin young smokers) · secondary spontaneous (underlying lung disease — COPD, CF, ILD, infection; more dangerous due to limited reserve) · traumatic/iatrogenic (procedures, ventilation barotrauma, trauma) · tension (one-way valve → progressive air accumulation → mediastinal shift + hemodynamic compromise)

RF: smoking · underlying lung disease · tall thin body habitus/male · prior pneumothorax · mechanical ventilation/positive pressure · invasive thoracic procedures · connective tissue disease (Marfan)

Data: upright CXR (visceral pleural line, absent lung markings peripherally, size estimate) · chest US (POCUS) (absent lung sliding/barcode sign — fast, sensitive) · CT (small/complex, underlying disease, recurrent) · tension is CLINICAL — do not delay decompression for a film · ABG/SpO2 · ECG (exclude cardiac)

DDx: PE (CTA) · pneumonia (consolidation, fever) · ACS (ECG, troponin) · pleuritis (no pleural air) · large bulla (CT — avoid draining a bulla mistaken for pneumothorax) · musculoskeletal chest pain

Home Meds: hold/avoid positive-pressure issues if ventilated · counsel smoking cessation (reduces recurrence) · reconcile anticoagulation around procedures · ensure analgesia · avoid air travel/diving until resolved

Plan

CONSULT: Pulmonology (management, recurrence prevention) · Thoracic surgery (recurrent, persistent air leak, bilateral, high-risk occupation — VATS/pleurodesis) · Interventional/Critical care (tension, unstable)

– Tension pneumothorax (emergency, clinical diagnosis): immediate needle decompression (large-bore angiocatheter, 2nd intercostal space midclavicular line or 4th/5th intercostal space anterior axillary line) followed by chest tube — do not wait for a CXR; this is immediately life-threatening
– Then manage by type, size, symptoms, and physiologic reserve:
  • Primary spontaneous, small + asymptomatic: observation ± supplemental oxygen (speeds reabsorption), serial imaging; many resolve without intervention
  • Primary spontaneous, large or symptomatic: needle aspiration or small-bore chest tube/pigtail catheter
  • Secondary spontaneous (underlying lung disease): generally chest tube drainage + admission (limited reserve, less tolerant, higher failure of conservative management) — even if small, treat more aggressively
  • Traumatic/iatrogenic: chest tube for significant or symptomatic; observe small iatrogenic ones
– Supplemental oxygen accelerates pleural air reabsorption (high-flow when observing)
– Persistent air leak / non-resolution / recurrence: thoracic surgery for VATS with bleb resection + pleurodesis (definitive, reduces recurrence)
– Tension pneumothorax is diagnosed at the bedside and decompressed immediately — a patient in obstructive shock with absent breath sounds and tracheal deviation cannot wait for radiology. For the rest, type and reserve matter: a small primary spontaneous pneumothorax can be watched, but a secondary one in a COPD patient with no reserve usually gets a chest tube even when small.
– PT/OT: mobilize once stable; breathing support
– Trend: respiratory/hemodynamic status, serial CXR (resolution, re-expansion), chest tube air leak (bubbling) + output, oxygenation
– Escalation triggers: tension physiology → immediate decompression + ICU; persistent air leak → thoracic surgery; respiratory failure → escalate support; recurrence → definitive surgical management
– Discharge when: lung re-expanded, tube removed (confirm no recurrence on post-pull CXR), stable on room air; smoking cessation counseling (key to recurrence), avoid air travel/diving until cleared, thoracic/pulmonary follow-up; recurrence-prevention discussion; return precautions (recurrent sudden chest pain/dyspnea)

114. Pneumothorax

complete reference · primary and secondary spontaneous, traumatic, and tension · bedside decompression of tension · size-, symptom-, and reserve-based management · Full Card

Symptoms / Associated Sx

• Sudden ipsilateral pleuritic chest pain and dyspnea, with decreased breath sounds, hyperresonance, and decreased chest expansion on the affected side

• Tension pneumothorax produces severe respiratory distress, hypotension, tachycardia, distended neck veins, tracheal deviation away from the affected side, and hemodynamic collapse

• Tension is a clinical diagnosis to be decompressed immediately, without waiting for imaging

Neg

• Pt denies fever, productive cough, and consolidation — argues against pneumonia

• Pt denies orthopnea, PND, and edema — argues against heart failure

• Pt denies tearing pain radiating to the back — argues against aortic dissection, and denies pleuritic pain with calf swelling, arguing against PE

• Pt denies reproducible chest wall tenderness — argues against a musculoskeletal cause

Social History (SHx)

• Smoking (a major risk) and a tall, thin, young male habitus (primary spontaneous disease)

• Known lung disease — COPD, emphysema and bullae, asthma, cystic fibrosis, or ILD (secondary spontaneous disease)

• A recent thoracic procedure, central line, or mechanical ventilation (iatrogenic), trauma, family history, and prior pneumothorax

Main Etiology

• Primary spontaneous — no underlying lung disease, from a ruptured subpleural bleb, typically in tall thin young smokers

• Secondary spontaneous — underlying lung disease (COPD, cystic fibrosis, ILD, infection), more dangerous because of limited reserve

• Traumatic or iatrogenic — procedures, ventilator barotrauma, and trauma

• Tension — a one-way valve causing progressive air accumulation with mediastinal shift and hemodynamic compromise

RF

• Modifiable: smoking, positive-pressure ventilation, and invasive thoracic procedures

• Non-modifiable: underlying lung disease, a tall thin male habitus, prior pneumothorax, and connective tissue disease such as Marfan syndrome

Data

• An upright chest radiograph (a visceral pleural line with absent peripheral lung markings, and a size estimate)

• Chest ultrasound (POCUS) (absent lung sliding and the barcode sign — fast and sensitive)

• CT (for small or complex pneumothoraces, underlying disease, and recurrence)

• Tension is a clinical diagnosis (do not delay decompression for a film), with ABG, oximetry, and an ECG to exclude a cardiac cause

DDx

Pulmonary embolism (CTA) · pneumonia (consolidation, fever) · acute coronary syndrome (ECG, troponin) · pleuritis (no pleural air) · a large bulla (CT — avoid draining a bulla mistaken for a pneumothorax) · musculoskeletal chest pain

Home Meds

• Address positive-pressure issues if the patient is ventilated and counsel smoking cessation, which reduces recurrence

• Reconcile anticoagulation around procedures and ensure adequate analgesia

• Advise avoiding air travel and diving until the pneumothorax has resolved

Plan

CONSULT: Pulmonology (management and recurrence prevention) · Thoracic surgery (recurrent disease, a persistent air leak, bilateral disease, or a high-risk occupation — VATS and pleurodesis) · Interventional or Critical care (tension or instability)

• Tension pneumothorax is an emergency and a clinical diagnosis: immediate needle decompression (a large-bore angiocatheter in the second intercostal space at the midclavicular line, or the fourth or fifth intercostal space at the anterior axillary line) followed by a chest tube — do not wait for a chest radiograph, as it is immediately life-threatening

• Then manage by type, size, symptoms, and physiologic reserve: a small asymptomatic primary spontaneous pneumothorax with observation and supplemental oxygen (which speeds reabsorption) and serial imaging, since many resolve; a large or symptomatic primary spontaneous pneumothorax with needle aspiration or a small-bore chest tube or pigtail catheter; a secondary spontaneous pneumothorax (underlying lung disease) generally with chest tube drainage and admission, given the limited reserve and higher failure of conservative management, treating even small ones more aggressively; and a traumatic or iatrogenic pneumothorax with a chest tube when significant or symptomatic, observing small iatrogenic ones

• Supplemental oxygen accelerates pleural air reabsorption, used at high flow when observing

• A persistent air leak, non-resolution, or recurrence warrants thoracic surgery for VATS with bleb resection and pleurodesis, which is definitive and reduces recurrence

• PT/OT: mobilization once stable, with breathing support

• Trend: respiratory and hemodynamic status, serial chest radiographs for resolution and re-expansion, the chest tube air leak (bubbling) and output, and oxygenation

• Escalation triggers: tension physiology → immediate decompression and ICU; a persistent air leak → thoracic surgery; respiratory failure → escalation of support; recurrence → definitive surgical management

• Discharge criteria: a re-expanded lung, the tube removed with no recurrence on a post-pull chest radiograph, and stability on room air; provide smoking cessation counseling (key to preventing recurrence), advise avoiding air travel and diving until cleared, arrange thoracic and pulmonary follow-up, discuss recurrence prevention, and give return precautions for recurrent sudden chest pain or dyspnea

Red Flags

• Hypotension, tracheal deviation, and distended neck veins with absent breath sounds → tension pneumothorax; decompress immediately

• A secondary spontaneous pneumothorax in a patient with poor pulmonary reserve → treat aggressively even when small

• A persistent air leak beyond a few days → a bronchopleural communication needing surgery

• A recurrent pneumothorax → definitive surgical pleurodesis or bleb resection

• A large bulla mistaken for a pneumothorax → draining it can be catastrophic; clarify with CT

Senior IM Resident Pearls

• Tension is a bedside diagnosis. A patient in obstructive shock with absent breath sounds and tracheal deviation gets a needle now — radiology comes after.

• Reserve changes the threshold. A small primary spontaneous pneumothorax can be watched; the same size in a COPD patient usually earns a chest tube.

• Oxygen speeds reabsorption. High-flow oxygen during observation accelerates resolution of the pleural air.

• POCUS is fast and sensitive. Absent lung sliding rules a pneumothorax in quickly when imaging is delayed.

• Don't drain a bulla. A large emphysematous bulla can mimic a pneumothorax on a film — confirm with CT before placing a tube.

• Smoking cessation cuts recurrence. It's the single most effective preventive measure after a spontaneous pneumothorax.

• Common mistake: ordering a chest radiograph to "confirm" a tension pneumothorax in a crashing patient instead of decompressing at the bedside.

Pulmonology — Airway / Hemorrhage

115. Hemoptysis Workup

infection · cancer · PE · vasculitis · bronchiectasis · massive hemoptysis = airway emergency (bleeding-side-down, protect airway) · CT + bronchoscopy · Super Compact

Sx: coughing up blood — streaking, frank blood, or clots · associated symptoms point to cause (fever/purulent sputum = infection; weight loss/smoking = cancer; pleuritic pain/dyspnea = PE; hematuria/sinusitis = vasculitis; chronic copious sputum = bronchiectasis) · massive/life-threatening hemoptysis: large volume (variably defined, e.g. >100–600 mL/24h) or any volume causing airway compromise/gas-exchange failure/hemodynamic instability (first confirm it's truly pulmonary — not hematemesis or pseudohemoptysis — then triage by volume because massive hemoptysis kills by asphyxiation, not exsanguination)

Neg: denies vomiting blood/coffee-grounds/nausea (hematemesis — GI source) · denies epistaxis/oropharyngeal/nasopharyngeal bleeding (pseudohemoptysis) · denies the bleeding being preceded by an upper-airway source · helps confirm a true lower-respiratory source

SHx: smoking (cancer, bronchitis) · TB exposure/risk · known bronchiectasis/CF · anticoagulation/antiplatelets/coagulopathy · prior malignancy · connective tissue disease/vasculitis symptoms · recent immobilization/VTE risk (PE) · occupational exposures

Etiology: infection (bronchitis — common/usually mild, pneumonia, TB, lung abscess, aspergilloma) · malignancy (bronchogenic carcinoma, metastases) · PE (with infarction) · vasculitis/alveolar hemorrhage (ANCA-associated, anti-GBM — see DAH card) · bronchiectasis (chronic infection/inflammation) · cardiac (mitral stenosis), coagulopathy, AV malformation, iatrogenic

RF: smoking · TB risk · structural lung disease/bronchiectasis · anticoagulation · malignancy · vasculitis · immunosuppression

Data: CXR (localize, mass, infiltrate, cavity) · CT chest (CT angiography if significant/massive) (source, cause, vascular anatomy — guides embolization) · bronchoscopy (localize + control bleeding, biopsy, lavage) · CBC, coags/INR, type & screen/crossmatch (if significant) · BMP, urinalysis (renal — pulmonary-renal/vasculitis) · ANCA/anti-GBM if vasculitis suspected · sputum studies (AFB, culture, cytology) · D-dimer/CTA if PE

DDx: infection (fever, sputum) · cancer (mass, smoking, weight loss) · PE (CTA) · vasculitis/DAH (renal, serologies, diffuse infiltrates) · bronchiectasis (chronic sputum, CT) · hematemesis/pseudohemoptysis (non-pulmonary source)

Home Meds: hold/reverse anticoagulants + antiplatelets (correct coagulopathy — vitamin K, PCC, platelets, reversal agents as indicated) · reconcile bleeding-risk meds · ensure type & screen; involve hematology if coagulopathic

Plan

CONSULT: Pulmonology/Interventional pulmonology (bronchoscopy, localization, control) · Interventional radiology (bronchial artery embolization) · Thoracic surgery (refractory/surgical lesions) · ICU/Critical care (massive — airway) · cause-specific (ID, Oncology, Rheumatology, Hematology)

– First, assess severity + protect the airway (massive hemoptysis is an airway emergency): ABCs; position the patient bleeding-side-down (protect the good lung from soiling); apply supplemental O2; secure the airway early if compromised (large-bore endotracheal tube to allow bronchoscopy, consider selective intubation/lung isolation); resuscitate + correct coagulopathy
– Stop/reverse anticoagulation and correct any coagulopathy or thrombocytopenia
– Localize + control (massive/significant): CT angiography to map the bleeding source/vascular anatomy → bronchial artery embolization (IR) is the first-line definitive control for most massive hemoptysis; bronchoscopy to localize and apply local measures (iced saline, topical vasoconstrictors, tamponade balloon, endobronchial therapies); surgery for refractory/localized resectable lesions
– Treat the underlying cause: antibiotics/anti-TB for infection; oncology for malignancy; anticoagulation decisions for PE (balance against bleeding); immunosuppression for vasculitis/DAH (steroids ± cyclophosphamide/rituximab ± plasmapheresis — see DAH card); airway clearance/antibiotics for bronchiectasis
– Mild/non-massive hemoptysis (most cases): stabilize, work up the cause (CXR → CT → bronchoscopy as indicated), treat accordingly (often outpatient-appropriate once serious causes excluded)
– Two questions drive everything: is this truly pulmonary (not hematemesis/pseudohemoptysis), and how much is it bleeding? Massive hemoptysis kills by drowning the airway, not by blood loss — so bleeding-side-down positioning, airway protection, and bronchial artery embolization come first, and the diagnostic workup follows once the patient is safe.
– PT/OT: mobilize once stable
– Trend: volume/rate of bleeding, airway/gas exchange, hemodynamics, Hgb, coagulation, response to embolization/bronchoscopy, cause-specific markers
– Escalation triggers: airway compromise/massive bleeding → intubation/lung isolation + IR embolization + ICU; rebleeding after embolization → repeat IR or surgery; pulmonary-renal/vasculitis → urgent immunosuppression + rheumatology/nephrology
– Discharge when: bleeding controlled/resolved, cause identified + treatment plan, anticoagulation decision made; appropriate subspecialty follow-up (pulmonary/oncology/ID/rheumatology), repeat imaging/bronchoscopy plan; return precautions (recurrent or increasing hemoptysis, dyspnea, lightheadedness)

115. Hemoptysis Workup

complete reference · confirm a pulmonary source · triage by volume · airway-first management of massive hemoptysis · cause-directed workup and therapy · Full Card

Symptoms / Associated Sx

• Coughing up blood — streaking, frank blood, or clots — with associated symptoms pointing to the cause (fever and purulent sputum for infection, weight loss and smoking for cancer, pleuritic pain and dyspnea for PE, hematuria and sinusitis for vasculitis, chronic copious sputum for bronchiectasis)

• Massive or life-threatening hemoptysis is a large volume (variably defined, for example more than 100–600 mL in 24 hours) or any volume causing airway compromise, gas-exchange failure, or hemodynamic instability

• First confirm the blood is truly pulmonary rather than hematemesis or pseudohemoptysis, then triage by volume, because massive hemoptysis kills by asphyxiation rather than exsanguination

Neg

• Pt denies vomiting blood, coffee-ground material, or nausea — argues against hematemesis from a GI source

• Pt denies epistaxis or oropharyngeal and nasopharyngeal bleeding — argues against pseudohemoptysis

• Pt denies that the bleeding was preceded by an upper-airway source — helps confirm a true lower-respiratory origin

Social History (SHx)

• Smoking (cancer, bronchitis), TB exposure or risk, and known bronchiectasis or cystic fibrosis

• Anticoagulation, antiplatelet use, or coagulopathy, and prior malignancy

• Connective tissue disease or vasculitis symptoms, recent immobilization or VTE risk (PE), and occupational exposures

Main Etiology

• Infection — bronchitis (common and usually mild), pneumonia, tuberculosis, lung abscess, and aspergilloma

• Malignancy — bronchogenic carcinoma and metastases

• Pulmonary embolism with infarction, and vasculitis or alveolar hemorrhage (ANCA-associated disease, anti-GBM disease — see the DAH card)

• Bronchiectasis from chronic infection and inflammation, with cardiac causes (mitral stenosis), coagulopathy, arteriovenous malformations, and iatrogenic bleeding

RF

• Modifiable: smoking, anticoagulation, and immunosuppression

• Non-modifiable: TB risk, structural lung disease and bronchiectasis, malignancy, and vasculitis

Data

• Chest radiograph (to localize and identify a mass, infiltrate, or cavity)

• CT of the chest, with CT angiography for significant or massive bleeding (to define the source, cause, and vascular anatomy, guiding embolization)

• Bronchoscopy (to localize and control bleeding, biopsy, and lavage)

• CBC, coagulation studies, and a type and screen or crossmatch for significant bleeding, with BMP and urinalysis (renal involvement in a pulmonary-renal vasculitis)

• ANCA and anti-GBM antibodies if vasculitis is suspected, sputum studies (AFB, culture, cytology), and a D-dimer or CTA for PE

DDx

Infection (fever, sputum) · cancer (a mass, smoking, weight loss) · pulmonary embolism (CTA) · vasculitis or diffuse alveolar hemorrhage (renal involvement, serologies, diffuse infiltrates) · bronchiectasis (chronic sputum, CT) · hematemesis or pseudohemoptysis (a non-pulmonary source)

Home Meds

• Hold and reverse anticoagulants and antiplatelets, correcting coagulopathy with vitamin K, prothrombin complex concentrate, platelets, or specific reversal agents as indicated

• Reconcile bleeding-risk medications and ensure a type and screen

• Involve hematology when the patient is coagulopathic

Plan

CONSULT: Pulmonology or Interventional pulmonology (bronchoscopy, localization, control) · Interventional radiology (bronchial artery embolization) · Thoracic surgery (refractory or surgical lesions) · ICU/Critical care (massive hemoptysis — airway) · cause-specific services (Infectious Disease, Oncology, Rheumatology, Hematology)

• Assess severity and protect the airway first, since massive hemoptysis is an airway emergency: address the ABCs, position the patient bleeding-side-down to protect the good lung from soiling, apply supplemental oxygen, secure the airway early if it is compromised (a large-bore endotracheal tube to allow bronchoscopy, with consideration of selective intubation or lung isolation), and resuscitate while correcting coagulopathy

• Stop and reverse anticoagulation and correct any coagulopathy or thrombocytopenia

• Localize and control significant or massive bleeding: CT angiography to map the source and vascular anatomy, leading to bronchial artery embolization by interventional radiology as the first-line definitive control for most massive hemoptysis; bronchoscopy to localize and apply local measures (iced saline, topical vasoconstrictors, a tamponade balloon, or endobronchial therapies); and surgery for refractory or localized resectable lesions

• Treat the underlying cause: antibiotics or anti-tuberculous therapy for infection, oncology for malignancy, anticoagulation decisions for PE (balanced against the bleeding), immunosuppression for vasculitis or diffuse alveolar hemorrhage (steroids with cyclophosphamide or rituximab and plasmapheresis — see the DAH card), and airway clearance with antibiotics for bronchiectasis

• Mild or non-massive hemoptysis, which is most cases: stabilize, work up the cause (chest radiograph, then CT, then bronchoscopy as indicated), and treat accordingly, often as an outpatient once serious causes are excluded

• PT/OT: mobilization once stable

• Trend: the volume and rate of bleeding, airway and gas exchange, hemodynamics, hemoglobin, coagulation, the response to embolization or bronchoscopy, and cause-specific markers

• Escalation triggers: airway compromise or massive bleeding → intubation or lung isolation, IR embolization, and ICU; rebleeding after embolization → repeat IR or surgery; a pulmonary-renal or vasculitic process → urgent immunosuppression with rheumatology and nephrology

• Discharge criteria: controlled or resolved bleeding, an identified cause with a treatment plan, and an anticoagulation decision; arrange appropriate subspecialty follow-up and a repeat-imaging or bronchoscopy plan, with return precautions for recurrent or increasing hemoptysis, dyspnea, or lightheadedness

Red Flags

• Airway compromise or gas-exchange failure from bleeding → massive hemoptysis; protect the airway and embolize

• Bleeding-side-down positioning failing to protect oxygenation → early intubation and lung isolation

• Hemoptysis with hematuria and an active urine sediment → a pulmonary-renal vasculitis needing urgent immunosuppression

• A new mass in a smoker → malignancy until proven otherwise

• Rebleeding after embolization → repeat intervention or surgery

Senior IM Resident Pearls

• Asphyxiation, not exsanguination. Massive hemoptysis kills by drowning the airway — airway protection and bleeding-side-down positioning come before the workup.

• Confirm it's really pulmonary. Hematemesis and pseudohemoptysis masquerade as hemoptysis; sorting the source changes the entire approach.

• Bronchial artery embolization is first-line for massive bleeding. CT angiography maps it and IR controls it before surgery is considered.

• Put the bleeding lung down. Protecting the healthy lung from soiling preserves the gas exchange you have.

• Reverse the anticoagulation. A coagulopathy turns a minor bleed into a life-threatening one — correct it early.

• Don't forget the kidneys. Hemoptysis with hematuria is a pulmonary-renal syndrome until proven otherwise.

• Common mistake: launching into a leisurely diagnostic workup in a patient with massive hemoptysis instead of securing the airway and arranging embolization first.

Pulmonology — Hemorrhage / Immunologic

116. Diffuse Alveolar Hemorrhage (DAH)

bleeding into alveoli · hemoptysis may be ABSENT · dropping Hgb + diffuse infiltrates + sequentially bloodier BAL · ANCA vasculitis / anti-GBM · high-dose steroids ± cyclophosphamide/rituximab ± plasmapheresis · Super Compact

Sx: dyspnea, cough, hypoxemia, diffuse pulmonary infiltrates, and a falling hemoglobin · hemoptysis is often present but can be ABSENT in up to a third (blood stays in the alveoli) · systemic features of the underlying disease — hematuria/renal failure (pulmonary-renal syndrome), sinusitis/saddle nose (GPA), arthralgias, rash (suspect DAH in any patient with new diffuse infiltrates + a dropping Hgb + hypoxemia, even without hemoptysis)

Neg: denies a cardiogenic edema history (orthopnea/PND/known heart failure) · denies a clear infectious prodrome fully explaining it (pneumonia) · denies overt external bleeding accounting for the Hgb drop · denies the infiltrates being chronic/stable (ILD)

SHx: known/suspected autoimmune disease or vasculitis · prior renal disease · drug exposures (e.g. certain agents, cocaine) · anticoagulation · bone marrow transplant/immunosuppression (infection-related DAH) · connective tissue disease symptoms

Etiology: immune/vasculitic (most important to recognize) — ANCA-associated vasculitis (GPA, MPA), anti-GBM disease (Goodpasture), SLE, other connective tissue diseases · non-immune — coagulopathy/anticoagulation, mitral stenosis, infection, drug/toxin (cocaine), bone marrow transplant, idiopathic pulmonary hemosiderosis · pathology: bland hemorrhage, capillaritis, or diffuse alveolar damage

RF: autoimmune/vasculitic disease · anticoagulation/coagulopathy · immunosuppression · certain drugs/toxins · transplant

Data: CXR/CT (bilateral diffuse alveolar/ground-glass infiltrates) · serial CBC (falling hemoglobin) · bronchoscopy with BAL — sequentially bloodier aliquots = diagnostic (also excludes infection) · DLCO elevated (if measurable — increased from intra-alveolar blood) · urinalysis + creatinine (glomerulonephritis — pulmonary-renal) · serologies: ANCA (PR3/MPO), anti-GBM, ANA/dsDNA, complement · coags · consider renal/lung biopsy

DDx: pneumonia/infection (BAL cultures) · cardiogenic pulmonary edema (BNP, echo) · ARDS (precipitant, no progressive bloody BAL) · coagulopathic bleeding (coags) · among DAH causes: ANCA vasculitis vs anti-GBM vs SLE vs drug/infection (serologies, biopsy)

Home Meds: hold/reverse anticoagulation · reconcile immunosuppressants · address contributory drugs/toxins · ensure infection excluded before/alongside immunosuppression · prophylaxis when immunosuppressing (PJP, etc.)

Plan

CONSULT: Pulmonology/Critical care (bronchoscopy, respiratory support) · Rheumatology (vasculitis/autoimmune workup + immunosuppression) · Nephrology (pulmonary-renal, plasmapheresis, biopsy) · ICU (respiratory failure) · Infectious Disease (exclude infection before immunosuppression)

– First, stabilize + secure the diagnosis: supplemental O2 → escalate support (HFNC/NIV/intubation + lung-protective ventilation) for respiratory failure; bronchoscopy with BAL showing progressively bloodier returns confirms DAH and excludes infection
– Reverse anticoagulation/correct coagulopathy
– Send the workup that determines treatment: ANCA (PR3/MPO), anti-GBM, ANA/dsDNA/complement, urinalysis + creatinine; consider renal biopsy (faster/safer than lung) to characterize
– Immunosuppression for immune/vasculitic DAH (start urgently — don't wait for biopsy if the picture is clear):
  • High-dose corticosteroids — IV methylprednisolone "pulse" 500–1000 mg IV daily ×3 days, then taper
  • Plus a steroid-sparing/induction agent — cyclophosphamide or rituximab (RAVE/RITUXVAS for ANCA-associated vasculitis) per rheumatology
  • Plasmapheresis (plasma exchange) — indicated for anti-GBM disease (removes pathogenic antibody) and considered for severe DAH/vasculitis with renal failure (per current evidence)
– Exclude/treat infection (BAL cultures) — critical before and during immunosuppression; add appropriate prophylaxis (e.g. PJP) when immunosuppressing
– Non-immune DAH: treat the cause (correct coagulopathy, manage mitral stenosis, remove offending drug, treat infection)
– DAH is the great mimic: new diffuse infiltrates with a dropping hemoglobin and hypoxemia — and remember hemoptysis can be completely absent because the blood stays in the alveoli. BAL with sequentially bloodier aliquots clinches it. For immune causes don't wait for the biopsy: pulse steroids start now, anti-GBM gets plasmapheresis, and ANCA vasculitis gets cyclophosphamide or rituximab.
– PT/OT: mobilize when stable; rehab after critical illness
– Trend: Hgb, oxygenation/respiratory support, infiltrates on imaging, renal function/urine sediment, serologies, response to immunosuppression, infection surveillance
– Escalation triggers: respiratory failure → intubation/ICU; refractory bleeding → intensify immunosuppression + plasmapheresis; renal failure → nephrology/dialysis; infection on immunosuppression → ID + adjust therapy
– Discharge when: bleeding controlled, oxygenation stable, immunosuppression regimen + monitoring plan established, infection excluded/treated; rheumatology/nephrology/pulmonary follow-up, prophylaxis + steroid taper plan, close monitoring for relapse/infection; return precautions (recurrent hemoptysis, dyspnea, hematuria, fever)

116. Diffuse Alveolar Hemorrhage (DAH)

complete reference · diffuse infiltrates with a falling hemoglobin · BAL diagnosis · ANCA vasculitis and anti-GBM · pulse steroids, cyclophosphamide or rituximab, and plasmapheresis · Full Card

Symptoms / Associated Sx

• Dyspnea, cough, hypoxemia, diffuse pulmonary infiltrates, and a falling hemoglobin

• Hemoptysis is often present but can be absent in up to a third of cases, because the blood remains in the alveoli

• Systemic features of the underlying disease — hematuria and renal failure (a pulmonary-renal syndrome), sinusitis and a saddle-nose deformity (granulomatosis with polyangiitis), arthralgias, and rash

Neg

• Pt denies a cardiogenic edema history (orthopnea, PND, known heart failure)

• Pt denies a clear infectious prodrome that fully explains the picture — argues against simple pneumonia

• Pt denies overt external bleeding accounting for the hemoglobin drop

• Pt denies that the infiltrates are chronic or stable — argues against interstitial lung disease

Social History (SHx)

• Known or suspected autoimmune disease or vasculitis, and prior renal disease

• Drug exposures (certain agents, cocaine) and anticoagulation

• Bone marrow transplant or immunosuppression (infection-related DAH) and connective tissue disease symptoms

Main Etiology

• Immune and vasculitic causes, the most important to recognize — ANCA-associated vasculitis (granulomatosis with polyangiitis, microscopic polyangiitis), anti-GBM disease (Goodpasture syndrome), SLE, and other connective tissue diseases

• Non-immune causes — coagulopathy or anticoagulation, mitral stenosis, infection, drugs and toxins (cocaine), bone marrow transplant, and idiopathic pulmonary hemosiderosis

• The underlying pathology is bland hemorrhage, capillaritis, or diffuse alveolar damage

RF

• Modifiable: anticoagulation, contributory drugs and toxins, and immunosuppression-related infection

• Non-modifiable: autoimmune and vasculitic disease and transplant status

Data

• Chest radiograph and CT (bilateral diffuse alveolar or ground-glass infiltrates) and serial CBC (a falling hemoglobin)

• Bronchoscopy with BAL showing sequentially bloodier aliquots, which is diagnostic (and also excludes infection)

• An elevated DLCO (when measurable, increased from intra-alveolar blood)

• Urinalysis and creatinine (glomerulonephritis in a pulmonary-renal syndrome)

• Serologies — ANCA (PR3 and MPO), anti-GBM, ANA, dsDNA, and complement, along with coagulation studies, and consideration of a renal or lung biopsy

DDx

Pneumonia or infection (BAL cultures) · cardiogenic pulmonary edema (BNP, echo) · ARDS (a precipitant, no progressively bloody BAL) · coagulopathic bleeding (coagulation studies) · among DAH causes, ANCA vasculitis versus anti-GBM versus SLE versus a drug or infection (serologies, biopsy)

Home Meds

• Hold and reverse anticoagulation and reconcile immunosuppressants

• Address contributory drugs and toxins and ensure infection is excluded before and alongside immunosuppression

• Add prophylaxis (such as PJP) when immunosuppressing

Plan

CONSULT: Pulmonology/Critical care (bronchoscopy, respiratory support) · Rheumatology (vasculitis and autoimmune workup and immunosuppression) · Nephrology (pulmonary-renal disease, plasmapheresis, biopsy) · ICU (respiratory failure) · Infectious Disease (exclude infection before immunosuppression)

• Stabilize and secure the diagnosis first: supplemental oxygen escalating to high-flow oxygen, NIV, or intubation with lung-protective ventilation for respiratory failure, with bronchoscopy and BAL showing progressively bloodier returns to confirm DAH and exclude infection

• Reverse anticoagulation and correct coagulopathy

• Send the workup that determines treatment: ANCA (PR3 and MPO), anti-GBM, ANA, dsDNA, and complement, with urinalysis and creatinine, and consideration of a renal biopsy (often faster and safer than a lung biopsy) to characterize the process

• Immunosuppression for immune or vasculitic DAH, started urgently without waiting for biopsy when the picture is clear: high-dose corticosteroids with IV methylprednisolone pulse therapy at 500–1000 mg daily for 3 days then a taper; plus an induction agent — cyclophosphamide or rituximab (the RAVE and RITUXVAS trials for ANCA-associated vasculitis) per rheumatology; and plasmapheresis (plasma exchange), indicated for anti-GBM disease to remove the pathogenic antibody and considered for severe DAH or vasculitis with renal failure per current evidence

• Exclude and treat infection with BAL cultures, which is critical before and during immunosuppression, adding appropriate prophylaxis such as PJP when immunosuppressing

• Non-immune DAH: treat the cause — correct coagulopathy, manage mitral stenosis, remove the offending drug, and treat infection

• PT/OT: mobilize when stable, with rehabilitation after critical illness

• Trend: hemoglobin, oxygenation and respiratory support, infiltrates on imaging, renal function and urine sediment, serologies, the response to immunosuppression, and infection surveillance

• Escalation triggers: respiratory failure → intubation and ICU; refractory bleeding → intensify immunosuppression and add plasmapheresis; renal failure → nephrology and dialysis; infection during immunosuppression → ID involvement and therapy adjustment

• Discharge criteria: controlled bleeding, stable oxygenation, an established immunosuppression regimen with a monitoring plan, and infection excluded or treated; arrange rheumatology, nephrology, and pulmonary follow-up, a prophylaxis and steroid-taper plan, and close monitoring for relapse and infection, with return precautions for recurrent hemoptysis, dyspnea, hematuria, or fever

Red Flags

• New diffuse infiltrates with a falling hemoglobin and hypoxemia → DAH even when hemoptysis is absent

• Hemoptysis or DAH with hematuria and an active sediment → a pulmonary-renal syndrome needing urgent immunosuppression

• A positive anti-GBM antibody → start plasmapheresis without delay

• Rapidly progressive respiratory failure → intubation and lung-protective ventilation

• Fever or new infiltrates during immunosuppression → opportunistic infection; do not assume it is recurrent bleeding

Senior IM Resident Pearls

• Hemoptysis can be absent. Up to a third of DAH presents with no coughed-up blood — a dropping hemoglobin with diffuse infiltrates is the clue.

• The BAL clinches it. Sequentially bloodier aliquots confirm alveolar hemorrhage and simultaneously sample for infection.

• Don't wait for the biopsy. When the picture is clear, pulse steroids start now while the serologies and tissue are pending.

• Anti-GBM gets plasmapheresis. Removing the pathogenic antibody is a defining, time-sensitive part of treatment.

• Always check the kidneys. The pulmonary-renal syndromes link DAH to a glomerulonephritis that drives both prognosis and therapy.

• Exclude infection first. Immunosuppressing an undiagnosed infection masquerading as DAH is dangerous — the BAL protects you.

• Common mistake: dismissing DAH because there's no hemoptysis, and missing the dropping hemoglobin with diffuse infiltrates that needed urgent immunosuppression.

Pulmonology — Parenchymal

117. Interstitial Lung Disease (ILD) Exacerbation

acute worsening on chronic fibrosis · IPF acute exacerbation / CTD-ILD flare · exclude infection, PE, CHF first · high-dose steroids · poor prognosis · Super Compact

Sx: acute or subacute worsening of dyspnea (over days–weeks) on a background of known/suspected ILD, increased cough, hypoxemia, new bilateral ground-glass/consolidation superimposed on fibrosis · fine "velcro" inspiratory crackles, clubbing (IPF), signs of connective tissue disease (CTD-ILD) (an acute exacerbation of ILD is a diagnosis reached by excluding the treatable mimics — infection, PE, heart failure, aspiration — that look identical)

Neg: denies a clear infectious syndrome fully explaining it (though infection must be actively excluded) · denies orthopnea/PND/volume overload as the sole driver (CHF) · denies pleuritic pain + calf swelling pointing to PE · denies a large aspiration event · helps frame it as a true ILD exacerbation rather than a mimic

SHx: known ILD/IPF or connective tissue disease (RA, scleroderma, myositis, etc.) · occupational/environmental/drug exposures (hypersensitivity, drug-induced ILD) · smoking · home oxygen use · antifibrotic therapy (pirfenidone/nintedanib) · immunosuppression

Etiology: acute exacerbation of IPF (idiopathic acceleration of fibrosis — often no identifiable trigger, may be triggered by infection/aspiration/procedure) · CTD-associated ILD flare (RA, systemic sclerosis, myositis/antisynthetase, MCTD, SLE) · drug-induced, hypersensitivity pneumonitis, others · pathology often diffuse alveolar damage superimposed on fibrosis

RF: underlying IPF (especially advanced) · connective tissue disease · recent infection/aspiration/surgery/procedure · drug exposure · environmental triggers

Data: high-resolution CT chest (new bilateral ground-glass/consolidation on background fibrosis — and exclude alternative — PE on CTA, etc.) · infectious workup (respiratory viral PCR, blood/sputum cultures, procalcitonin, consider BAL to exclude infection) · BNP + echo (exclude CHF) · D-dimer/CTA (exclude PE) · ABG/SpO2 · CTD serologies (ANA, RF, anti-CCP, myositis panel) if not established · CBC, BMP

DDx: infection/pneumonia (cultures, BAL, viral PCR) · PE (CTA) · CHF/volume overload (BNP, echo) · aspiration (history, distribution) · drug toxicity (exposure) · DAH (bloody BAL, dropping Hgb) · progression of underlying disease

Home Meds: continue antifibrotics (pirfenidone/nintedanib) unless contraindicated · reconcile/continue immunosuppression for CTD-ILD per rheumatology · careful oxygen · VTE prophylaxis · prophylaxis if heavily immunosuppressed (PJP)

Plan

CONSULT: Pulmonology (ILD management, diagnosis, prognosis) · Rheumatology (CTD-ILD immunosuppression) · ICU/Critical care (respiratory failure) · Infectious Disease (exclude/treat infection) · Palliative care (advanced IPF, goals of care)

– First, exclude the treatable mimics (essential — they look identical and are reversible): rule out infection (cultures, viral PCR, often BAL), PE (CTA), heart failure (BNP/echo), and aspiration before committing to "acute exacerbation of ILD"
– Supportive care: supplemental oxygen to maintain saturations; escalate (HFNC/NIV) for respiratory failure — note mechanical ventilation in advanced IPF exacerbation carries a very poor prognosis; discuss goals of care early
– High-dose corticosteroids — the mainstay for acute exacerbations (e.g. IV methylprednisolone pulse, then taper), per pulmonology; evidence is limited but they are standard of care
– CTD-ILD flare: immunosuppression directed by rheumatology (steroids ± cyclophosphamide, mycophenolate, rituximab depending on the disease)
– Treat any identified trigger (antibiotics if infection found, anticoagulation if PE, etc.) — and empiric antibiotics are often given while infection is being excluded
– Continue antifibrotic therapy (pirfenidone/nintedanib) for IPF as an outpatient disease-modifying treatment (slows progression; not an acute rescue)
– Goals of care: acute exacerbations of IPF have high mortality — have honest prognostic and goals-of-care conversations, involve palliative care, and consider lung transplant evaluation in appropriate candidates
– "Acute exacerbation of ILD" is a diagnosis of exclusion — infection, PE, heart failure, and aspiration mimic it exactly and are treatable, so chase those hard first. High-dose steroids are the mainstay once mimics are excluded, but the prognosis (especially in IPF) is grim, so start the goals-of-care conversation early rather than late.
– PT/OT: as tolerated; pulmonary rehab for survivors
– Trend: oxygenation/respiratory support, imaging, infectious workup results, response to steroids, renal/metabolic, goals-of-care discussions
– Escalation triggers: progressive respiratory failure → ICU + goals-of-care (poor ventilator outcomes in IPF); identified infection → targeted therapy; refractory → transplant evaluation/palliative care
– Discharge when: stabilized/improving, mimics excluded/treated, oxygenation manageable (home O2 plan), steroid taper + antifibrotic/immunosuppression plan defined; pulmonary/rheumatology follow-up, transplant evaluation if candidate, palliative care involvement, advance care planning; return precautions (worsening dyspnea, fever, low saturations)

117. Interstitial Lung Disease (ILD) Exacerbation

complete reference · acute worsening on chronic fibrosis · exclusion of mimics · high-dose corticosteroids · prognosis and goals of care · Full Card

Symptoms / Associated Sx

• Acute or subacute worsening of dyspnea over days to weeks on a background of known or suspected ILD, with increased cough, hypoxemia, and new bilateral ground-glass or consolidation superimposed on fibrosis

• Fine "velcro" inspiratory crackles and clubbing (IPF), with signs of connective tissue disease in CTD-ILD

• An acute exacerbation of ILD is reached by excluding the treatable mimics — infection, PE, heart failure, and aspiration — that look identical

Neg

• Pt denies a clear infectious syndrome that fully explains the presentation, though infection must still be actively excluded

• Pt denies orthopnea, PND, and volume overload as the sole driver — argues against heart failure

• Pt denies pleuritic pain with calf swelling — argues against PE

• Pt denies a large aspiration event — helps frame this as a true ILD exacerbation rather than a mimic

Social History (SHx)

• Known ILD or IPF, or connective tissue disease (rheumatoid arthritis, scleroderma, myositis)

• Occupational, environmental, or drug exposures (hypersensitivity or drug-induced ILD), and smoking

• Home oxygen use, antifibrotic therapy (pirfenidone or nintedanib), and immunosuppression

Main Etiology

• Acute exacerbation of IPF — an idiopathic acceleration of fibrosis, often without an identifiable trigger but sometimes precipitated by infection, aspiration, or a procedure

• A CTD-associated ILD flare — rheumatoid arthritis, systemic sclerosis, myositis or antisynthetase syndrome, mixed connective tissue disease, and SLE

• Drug-induced disease, hypersensitivity pneumonitis, and others, with the pathology often diffuse alveolar damage superimposed on fibrosis

RF

• Modifiable: infection, aspiration, recent surgery or procedures, drug exposure, and environmental triggers

• Non-modifiable: underlying IPF (especially advanced) and connective tissue disease

Data

• High-resolution CT of the chest (new bilateral ground-glass or consolidation on a background of fibrosis, while excluding alternatives such as PE on CTA)

• An infectious workup (respiratory viral PCR, blood and sputum cultures, procalcitonin, and BAL to exclude infection)

• BNP and echocardiography (to exclude heart failure) and a D-dimer or CTA (to exclude PE)

• ABG and oximetry, CTD serologies (ANA, RF, anti-CCP, a myositis panel) if not already established, and CBC and BMP

DDx

Infection or pneumonia (cultures, BAL, viral PCR) · pulmonary embolism (CTA) · heart failure or volume overload (BNP, echo) · aspiration (history, distribution) · drug toxicity (exposure) · diffuse alveolar hemorrhage (a bloody BAL, a falling hemoglobin) · progression of the underlying disease

Home Meds

• Continue antifibrotics (pirfenidone or nintedanib) unless contraindicated

• Reconcile and continue immunosuppression for CTD-ILD per rheumatology, and use careful oxygen

• Ensure VTE prophylaxis and add prophylaxis (such as PJP) if heavily immunosuppressed

Plan

CONSULT: Pulmonology (ILD management, diagnosis, prognosis) · Rheumatology (CTD-ILD immunosuppression) · ICU/Critical care (respiratory failure) · Infectious Disease (exclude and treat infection) · Palliative care (advanced IPF, goals of care)

• Exclude the treatable mimics first, which is essential because they look identical and are reversible: rule out infection (cultures, viral PCR, often BAL), PE (CTA), heart failure (BNP and echo), and aspiration before committing to an acute exacerbation of ILD

• Supportive care: supplemental oxygen to maintain saturations, escalating to high-flow oxygen or NIV for respiratory failure, recognizing that mechanical ventilation in an advanced IPF exacerbation carries a very poor prognosis, so discuss goals of care early

• High-dose corticosteroids are the mainstay for acute exacerbations (such as IV methylprednisolone pulse therapy then a taper) per pulmonology; the evidence is limited but they remain standard of care

• A CTD-ILD flare is treated with immunosuppression directed by rheumatology (steroids with cyclophosphamide, mycophenolate, or rituximab depending on the disease)

• Treat any identified trigger (antibiotics for infection, anticoagulation for PE), and empiric antibiotics are often given while infection is being excluded

• Continue antifibrotic therapy (pirfenidone or nintedanib) for IPF as an outpatient disease-modifying treatment that slows progression but is not an acute rescue

• Goals of care: acute exacerbations of IPF carry high mortality, so have honest prognostic and goals-of-care conversations, involve palliative care, and consider lung transplant evaluation in appropriate candidates

• PT/OT: as tolerated, with pulmonary rehabilitation for survivors

• Trend: oxygenation and respiratory support, imaging, the infectious workup, the response to steroids, renal and metabolic parameters, and goals-of-care discussions

• Escalation triggers: progressive respiratory failure → ICU and goals-of-care discussion, given poor ventilator outcomes in IPF; an identified infection → targeted therapy; refractory disease → transplant evaluation or palliative care

• Discharge criteria: stabilization or improvement, mimics excluded or treated, manageable oxygenation with a home oxygen plan, and a defined steroid taper with an antifibrotic or immunosuppression plan; arrange pulmonary and rheumatology follow-up, transplant evaluation if a candidate, palliative care involvement, and advance care planning, with return precautions for worsening dyspnea, fever, or low saturations

Red Flags

• Progressive respiratory failure in advanced IPF → very poor ventilator outcomes; address goals of care early

• An identified infection, PE, or heart failure → a treatable mimic that changes management entirely

• A bloody BAL with a falling hemoglobin → diffuse alveolar hemorrhage rather than a fibrotic exacerbation

• A new myositis or scleroderma feature → a CTD-ILD requiring directed immunosuppression

• Rapid decline despite steroids → consider transplant evaluation or a transition to comfort-focused care

Senior IM Resident Pearls

• It's a diagnosis of exclusion. Infection, PE, heart failure, and aspiration mimic an ILD exacerbation exactly and are treatable — chase them hard first.

• Steroids are the mainstay, with thin evidence. High-dose corticosteroids are standard once mimics are excluded, but temper expectations.

• The prognosis is grim, especially in IPF. Start goals-of-care conversations early rather than after the patient is on a ventilator with a poor outlook.

• Antifibrotics aren't a rescue. Pirfenidone and nintedanib slow chronic progression; they don't treat the acute exacerbation.

• Sort the CTD. A connective tissue disease flare gets directed immunosuppression, not just steroids — involve rheumatology.

• Consider transplant. In appropriate candidates an exacerbation should prompt or accelerate a transplant evaluation.

• Common mistake: labeling a patient with an "ILD exacerbation" and starting steroids without excluding the infection or PE that was the real, treatable problem.

Pulmonology — Vascular

118. Pulmonary Hypertension Decompensation (RV Failure)

decompensated RV · optimize volume (don't over-fill the failing RV) · maintain systemic pressure · never stop prostacyclin · treat the trigger · avoid intubation if possible · Super Compact

Sx: worsening dyspnea, fatigue, exertional/rest symptoms, presyncope/syncope, chest pain · signs of right heart failure: elevated JVP, hepatomegaly/pulsatile liver, ascites, peripheral edema, accentuated P2/right-sided S3, tricuspid regurgitation murmur · low cardiac output — cool extremities, hypotension, oliguria; can progress to cardiogenic shock from RV failure (the decompensating RV is a fragile, pressure-sensitive pump — the management threads a needle between under- and over-filling while keeping systemic pressure above pulmonary pressure)

Neg: denies a primary left-heart/orthopnea-PND picture as the sole driver (left heart failure — though it can coexist/cause group 2 PH) · denies a clear primary infection alone explaining it (though infection is a common trigger) · denies an acute coronary syndrome presentation · denies a primary pulmonary parenchymal process accounting for all of it

SHx: known pulmonary hypertension + WHO group/class · current PH-specific therapy (prostacyclins — epoprostenol/treprostinil, ERAs, PDE5 inhibitors, riociguat) + adherence · connective tissue disease, congenital heart disease, prior VTE (CTEPH), left heart/lung disease · home oxygen · recent illness/triggers

Etiology (triggers of decompensation): infection/sepsis · arrhythmia (atrial arrhythmias poorly tolerated — loss of atrial kick) · medication noncompliance/interruption of PH therapy (especially abrupt prostacyclin cessation — can be fatal) · volume overload or excessive diuresis/dehydration · PE · pregnancy · surgery/anesthesia · progression of underlying PH

RF: severe/advanced PH · WHO functional class III–IV · prior RV failure/hospitalizations · arrhythmia · nonadherence · intercurrent illness · pregnancy

Data: echocardiography (RV size/function, septal flattening, estimated PA pressure, effusion, exclude tamponade physiology) · ECG (RV strain, arrhythmia) · BNP/NT-proBNP + troponin (RV strain/prognosis) · BMP/LFTs/lactate (end-organ perfusion — congestive hepatopathy, renal) · ABG/SpO2 · infection workup/cultures · D-dimer/CTA if PE suspected · right heart catheterization in selected cases · careful fluid-status assessment

DDx: left heart failure (group 2 PH) (echo, wedge/filling) · acute PE (CTA) · sepsis with RV strain (cultures) · tamponade (echo) · RV infarction (ECG, coronary) · progression of chronic PH

Home Meds: CONTINUE PH-specific therapy — never abruptly stop prostacyclin/prostanoid infusions (epoprostenol/treprostinil); interruption can precipitate rebound PH crisis and death · ensure the infusion line/pump is maintained · reconcile diuretics carefully · avoid drugs that worsen PH/hemodynamics; cautious sedation

Plan

CONSULT: Pulmonary hypertension specialist/Pulmonology (PH-specific therapy — essential, do not adjust alone) · Cardiology (RV failure, arrhythmia, hemodynamics) · ICU/Critical care (shock, RV support) · the patient's PH center (coordinate prostacyclin management)

– Continue PH-specific therapy without interruption: never abruptly stop a prostacyclin/prostanoid infusion (epoprostenol, treprostinil) — abrupt cessation can cause rebound pulmonary hypertensive crisis and death; protect the line/pump, involve the PH center
– Optimize volume carefully (the central challenge): the failing RV tolerates neither over- nor under-filling — avoid aggressive fluid boluses that over-distend and worsen the RV; if volume-overloaded, diurese (IV furosemide) to relieve RV congestion; if truly hypovolemic, give small, cautious fluid challenges with close monitoring
– Maintain systemic blood pressure above pulmonary pressure (preserve RV coronary perfusion): norepinephrine is the preferred vasopressor to support systemic pressure; avoid systemic hypotension which causes RV ischemia and a death spiral
– Support RV contractility: inotropy — dobutamine or milrinone (milrinone also reduces PVR but can cause systemic hypotension — often paired with a vasopressor)
– Reduce RV afterload / pulmonary vasodilation: inhaled pulmonary vasodilators — inhaled nitric oxide or inhaled epoprostenol (selective pulmonary vasodilation without systemic hypotension) in the acute setting
– Optimize oxygenation + avoid hypoxia/hypercarbia/acidosis (all raise pulmonary vascular resistance); careful controlled oxygen
– Identify + treat the trigger: antibiotics for infection, rate/rhythm control for arrhythmia (restore sinus rhythm — atrial kick matters; involve cardiology), anticoagulation for PE, correct nonadherence
– Avoid intubation if at all possible: induction and positive-pressure ventilation can precipitate RV collapse and cardiovascular arrest — if intubation is unavoidable, plan meticulously (experienced operator, hemodynamic support ready, avoid hypotension/hypoxia/high airway pressures); consider ECMO/mechanical support at expert centers for refractory RV failure
– Three rules keep the decompensating RV alive: don't over-fill it (cautious volume, diurese if congested), keep systemic pressure above pulmonary pressure (norepinephrine, never let them get hypotensive), and never abruptly stop the prostacyclin infusion. Intubation is genuinely dangerous here — induction can collapse the RV — so avoid it if you possibly can and plan obsessively if you can't.
– PT/OT: minimal exertion during decompensation; rehab once recovered
– Trend: hemodynamics/MAP, RV function on echo, BNP/troponin, lactate/end-organ perfusion, urine output, oxygenation, response to inotropes/vasopressors, trigger resolution
– Escalation triggers: cardiogenic shock/refractory RV failure → ICU + inotropes/vasopressors/inhaled vasodilators, PH center, ECMO/transplant evaluation; arrhythmia with instability → cardiology; deterioration → expert center transfer
– Discharge when: back to compensated baseline, trigger treated, PH therapy continued/optimized (PH specialist), volume status optimized; PH center + cardiology follow-up, medication adherence + infusion-line plan, oxygen, careful diuretic plan; advance care planning in advanced disease; return precautions (worsening dyspnea/edema, syncope, lightheadedness, infusion pump problems)

118. Pulmonary Hypertension Decompensation (RV Failure)

complete reference · the fragile failing RV · cautious volume, systemic pressure support, pulmonary vasodilation · uninterrupted prostacyclin · avoiding intubation · Full Card

Symptoms / Associated Sx

• Worsening dyspnea, fatigue, exertional and rest symptoms, presyncope or syncope, and chest pain

• Signs of right heart failure — an elevated JVP, hepatomegaly or a pulsatile liver, ascites, peripheral edema, an accentuated P2, a right-sided S3, and a tricuspid regurgitation murmur

• Low cardiac output with cool extremities, hypotension, and oliguria, which can progress to cardiogenic shock from RV failure; the decompensating RV is a fragile, pressure-sensitive pump

Neg

• Pt denies a primary left-heart picture with orthopnea and PND as the sole driver, though left heart disease can coexist and cause group 2 pulmonary hypertension

• Pt denies a clear primary infection alone explaining it, though infection is a common trigger

• Pt denies an acute coronary syndrome presentation

• Pt denies a primary pulmonary parenchymal process accounting for all of it

Social History (SHx)

• Known pulmonary hypertension with its WHO group and functional class, and current PH-specific therapy (prostacyclins such as epoprostenol or treprostinil, endothelin receptor antagonists, PDE5 inhibitors, riociguat) with adherence

• Connective tissue disease, congenital heart disease, prior VTE (chronic thromboembolic PH), and left heart or lung disease

• Home oxygen use and any recent illness or triggers

Main Etiology

• Infection or sepsis and arrhythmia (atrial arrhythmias are poorly tolerated because of the loss of the atrial kick)

• Medication noncompliance or interruption of PH therapy, especially abrupt prostacyclin cessation, which can be fatal

• Volume overload, or excessive diuresis and dehydration, along with pulmonary embolism, pregnancy, surgery and anesthesia, and progression of the underlying PH

RF

• Modifiable: medication nonadherence, intercurrent illness, and volume mismanagement

• Non-modifiable: severe or advanced PH, WHO functional class III–IV, prior RV failure and hospitalizations, and arrhythmia

Data

• Echocardiography (RV size and function, septal flattening, estimated PA pressure, an effusion, and tamponade physiology)

• ECG (RV strain, arrhythmia) and BNP or NT-proBNP with troponin (RV strain and prognosis)

• BMP, LFTs, and lactate (end-organ perfusion — congestive hepatopathy and renal function)

• ABG and oximetry, an infection workup with cultures, a D-dimer or CTA if PE is suspected, right heart catheterization in selected cases, and a careful fluid-status assessment

DDx

Left heart failure (group 2 PH) (echo, wedge and filling pressures) · acute pulmonary embolism (CTA) · sepsis with RV strain (cultures) · tamponade (echo) · RV infarction (ECG, coronary evaluation) · progression of chronic PH

Home Meds

• Continue PH-specific therapy and never abruptly stop a prostacyclin or prostanoid infusion (epoprostenol, treprostinil), since interruption can precipitate a rebound PH crisis and death

• Maintain the infusion line and pump, and reconcile diuretics carefully

• Avoid drugs that worsen PH or hemodynamics and use cautious sedation

Plan

CONSULT: A pulmonary hypertension specialist or Pulmonology (PH-specific therapy — essential, do not adjust alone) · Cardiology (RV failure, arrhythmia, hemodynamics) · ICU/Critical care (shock, RV support) · the patient's PH center (to coordinate prostacyclin management)

• Continue PH-specific therapy without interruption: never abruptly stop a prostacyclin or prostanoid infusion (epoprostenol, treprostinil), since abrupt cessation can cause a rebound pulmonary hypertensive crisis and death; protect the line and pump and involve the PH center

• Optimize volume carefully, the central challenge, since the failing RV tolerates neither over- nor under-filling: avoid aggressive fluid boluses that over-distend and worsen the RV, diurese with IV furosemide when volume-overloaded to relieve RV congestion, and give only small cautious fluid challenges with close monitoring when truly hypovolemic

• Maintain systemic blood pressure above pulmonary pressure to preserve RV coronary perfusion: norepinephrine is the preferred vasopressor, and systemic hypotension that causes RV ischemia and a death spiral must be avoided

• Support RV contractility with inotropy — dobutamine or milrinone, the latter also reducing pulmonary vascular resistance but capable of causing systemic hypotension, so it is often paired with a vasopressor

• Reduce RV afterload with pulmonary vasodilation: inhaled pulmonary vasodilators such as inhaled nitric oxide or inhaled epoprostenol provide selective pulmonary vasodilation without systemic hypotension in the acute setting

• Optimize oxygenation and avoid hypoxia, hypercarbia, and acidosis, all of which raise pulmonary vascular resistance, using careful controlled oxygen

• Identify and treat the trigger: antibiotics for infection, rate or rhythm control for arrhythmia (restoring sinus rhythm, since the atrial kick matters, with cardiology involved), anticoagulation for PE, and correction of nonadherence

• Avoid intubation if at all possible, because induction and positive-pressure ventilation can precipitate RV collapse and cardiovascular arrest; if intubation is unavoidable, plan meticulously (an experienced operator, hemodynamic support ready, and avoidance of hypotension, hypoxia, and high airway pressures), and consider ECMO or mechanical support at expert centers for refractory RV failure

• PT/OT: minimal exertion during decompensation, with rehabilitation once recovered

• Trend: hemodynamics and mean arterial pressure, RV function on echo, BNP and troponin, lactate and end-organ perfusion, urine output, oxygenation, the response to inotropes and vasopressors, and trigger resolution

• Escalation triggers: cardiogenic shock or refractory RV failure → ICU with inotropes, vasopressors, and inhaled vasodilators, the PH center, and ECMO or transplant evaluation; an arrhythmia with instability → cardiology; deterioration → transfer to an expert center

• Discharge criteria: a return to the compensated baseline, a treated trigger, continued and optimized PH therapy (with the PH specialist), and an optimized volume status; arrange PH center and cardiology follow-up, a medication-adherence and infusion-line plan, oxygen, and a careful diuretic plan, with advance care planning in advanced disease and return precautions for worsening dyspnea or edema, syncope, lightheadedness, or infusion-pump problems

Red Flags

• Abrupt interruption of a prostacyclin infusion → a potentially fatal rebound pulmonary hypertensive crisis; restore it urgently

• Systemic hypotension → RV ischemia and a death spiral; support the pressure with norepinephrine immediately

• Aggressive fluid boluses in RV failure → over-distension that worsens the RV; reassess and diurese if congested

• The need for intubation → high risk of RV collapse on induction; avoid if possible and plan obsessively if not

• A new atrial arrhythmia → poorly tolerated loss of the atrial kick; restore rhythm with cardiology

Senior IM Resident Pearls

• Don't over-fill the failing RV. Reflexive fluid boluses distend an already failing ventricle — be cautious, and diurese when it's congested.

• Keep the systemic pressure above the pulmonary pressure. Norepinephrine preserves RV coronary perfusion; letting them get hypotensive starts a death spiral.

• Never stop the prostacyclin. Abrupt cessation of an epoprostenol or treprostinil infusion can be fatal — protect the pump and call the PH center.

• Intubation can kill. Induction and positive pressure can collapse the RV — avoid it if you can, and if you can't, plan every step with support ready.

• Avoid hypoxia, hypercarbia, and acidosis. Each raises pulmonary vascular resistance and worsens the RV's afterload.

• The atrial kick matters. A new atrial arrhythmia is poorly tolerated — restoring sinus rhythm can be hemodynamically decisive.

• Common mistake: treating RV-failure hypotension like septic shock with large fluid boluses, over-distending the RV and accelerating the collapse.

Pulmonology — Airway

119. Bronchiectasis Exacerbation

chronic productive cough/copious sputum · culture-directed antibiotics (Pseudomonas common) · airway clearance is central · treat the underlying cause · Super Compact

Sx: increased cough and sputum volume, increased sputum purulence/change in color, worsening dyspnea, fatigue, sometimes hemoptysis, low-grade fever, pleuritic chest pain · background of chronic daily productive cough with copious sputum, recurrent infections, coarse crackles · exacerbation = sustained worsening of these symptoms (this is a chronically infected, dilated-airway disease — the exacerbation is driven by the airway flora, so culture the sputum and clear the airways, not just antibiotics)

Neg: denies a first-ever acute presentation without chronic sputum history (would suggest simple pneumonia/acute bronchitis) · denies orthopnea/PND/edema (CHF) · denies sudden pleuritic dyspnea + calf swelling (PE) · denies a purely upper-airway source of secretions

SHx: known bronchiectasis + underlying cause (post-infectious, cystic fibrosis, immunodeficiency, ABPA, primary ciliary dyskinesia, prior severe pneumonia/TB, autoimmune) · prior sputum cultures/organisms (esp Pseudomonas) · prior exacerbation frequency · airway clearance regimen · smoking

Etiology: exacerbation of chronic airway infection/inflammation in dilated, poorly clearing airways · organisms: Haemophilus influenzae, Pseudomonas aeruginosa (common, esp advanced/CF), Staph aureus, Moraxella, nontuberculous mycobacteria, fungi (Aspergillus/ABPA) · underlying causes: post-infectious, CF, immunodeficiency, ciliary dyskinesia, ABPA, autoimmune, obstruction

RF: underlying cause (CF, immunodeficiency, etc.) · prior Pseudomonas colonization · frequent prior exacerbations · poor airway clearance · advanced/extensive disease · smoking

Data: sputum Gram stain + culture/sensitivities (incl Pseudomonas; consider AFB/mycobacterial, fungal) (obtain before/with antibiotics — directs therapy) · CXR ± HRCT (bronchiectasis — tram-track/signet-ring/airway dilation; exclude pneumonia, complications) · CBC, BMP, CRP · SpO2/ABG · prior culture history · workup of underlying cause if newly diagnosed (CF testing, immunoglobulins, ABPA workup)

DDx: pneumonia (focal consolidation) · COPD exacerbation (smoking, obstruction, less sputum) · CF exacerbation (known CF) · NTM infection (AFB, indolent) · ABPA (eosinophilia, IgE, central bronchiectasis) · CHF/PE (BNP/CTA)

Home Meds: continue airway clearance + maintenance inhalers/mucolytics · continue chronic suppressive/macrolide therapy if prescribed · reconcile + escalate antibiotics per cultures · ensure adequate hydration · address underlying-cause therapy (e.g. immunoglobulin replacement, ABPA steroids)

Plan

CONSULT: Pulmonology (management, underlying cause, severe/frequent exacerbations) · Infectious Disease (resistant organisms, NTM, complex regimens) · Respiratory therapy (airway clearance) · CF center (if cystic fibrosis) · Immunology (if immunodeficiency)

– Obtain sputum culture before/with starting antibiotics (directs therapy — prior cultures and known colonization guide empiric choice)
– Antibiotics, culture-directed (empiric while awaiting results):
  • No Pseudomonas risk/history: cover Haemophilus/Strep/Moraxella — e.g. amoxicillin-clavulanate, or a respiratory fluoroquinolone, or doxycycline
  • Pseudomonas risk/prior isolation (common in advanced disease): antipseudomonal coverage — ciprofloxacin 750 mg PO BID, or IV antipseudomonal (this institution uses cefepime 2 g IV q8h in place of pip-tazo) — tailor to sensitivities
  • Duration is typically longer than routine pneumonia — usually 7–14 days (guided by severity, organism, response)
– Airway clearance (central to treatment, not an afterthought): chest physiotherapy, oscillatory PEP devices, postural drainage, and mucoactive measures (hypertonic saline nebulization, ensure hydration); intensify the patient's home regimen during the exacerbation
– Bronchodilators if airflow obstruction/reactivity; supplemental O2 as needed
– Treat/address the underlying cause: immunoglobulin replacement for immunodeficiency, steroids ± antifungal for ABPA, NTM-directed multidrug therapy if mycobacterial, CF-specific care (CFTR modulators/CF center) — the durable strategy to reduce future exacerbations
– Manage complications: hemoptysis (see hemoptysis card — can be massive from hypertrophied bronchial arteries → embolization), respiratory failure
– Two things define good bronchiectasis care: culture-directed antibiotics (assume Pseudomonas is on the table in anyone with prior isolation or advanced disease, and treat longer than you would a simple pneumonia) and aggressive airway clearance, which is as important as the antibiotic. And always ask why they have bronchiectasis — treating the underlying cause is what reduces the next exacerbation.
– PT/OT + respiratory therapy: airway clearance training, mobilization, pulmonary rehab referral
– Trend: sputum volume/purulence, fever/CRP, oxygenation, culture/sensitivity results, response to therapy + airway clearance
– Escalation triggers: respiratory failure → escalate support/ICU; resistant organism/treatment failure → ID + adjust; massive hemoptysis → IR embolization; recurrent frequent exacerbations → reassess underlying cause + suppressive therapy
– Discharge when: sputum/symptoms improving toward baseline, stable oxygenation, on a defined (often 7–14 day) culture-directed course, airway clearance regimen reinforced; pulmonary follow-up, underlying-cause management, consider chronic macrolide/suppressive therapy + pulmonary rehab to reduce recurrence, vaccination; return precautions (worsening sputum/dyspnea, fever, hemoptysis)

119. Bronchiectasis Exacerbation

complete reference · chronically infected dilated airways · culture-directed antibiotics with Pseudomonas in mind · airway clearance · underlying-cause management · Full Card

Symptoms / Associated Sx

• Increased cough and sputum volume, increased purulence or a change in sputum color, worsening dyspnea, fatigue, sometimes hemoptysis, low-grade fever, and pleuritic chest pain

• A background of chronic daily productive cough with copious sputum, recurrent infections, and coarse crackles

• An exacerbation is a sustained worsening of these symptoms; the disease is one of chronically infected, dilated, poorly clearing airways

Neg

• Pt denies a first-ever acute presentation without a chronic sputum history — that would suggest a simple pneumonia or acute bronchitis

• Pt denies orthopnea, PND, and edema — argues against heart failure

• Pt denies sudden pleuritic dyspnea with calf swelling — argues against PE

• Pt denies a purely upper-airway source of secretions

Social History (SHx)

• Known bronchiectasis with its underlying cause (post-infectious, cystic fibrosis, immunodeficiency, ABPA, primary ciliary dyskinesia, prior severe pneumonia or TB, autoimmune disease)

• Prior sputum cultures and organisms (especially Pseudomonas) and prior exacerbation frequency

• The home airway clearance regimen and smoking

Main Etiology

• An exacerbation of chronic airway infection and inflammation in dilated, poorly clearing airways

• Common organisms include Haemophilus influenzae, Pseudomonas aeruginosa (common in advanced disease and CF), Staphylococcus aureus, and Moraxella, with nontuberculous mycobacteria and fungi (Aspergillus and ABPA)

• Underlying causes include post-infectious disease, cystic fibrosis, immunodeficiency, ciliary dyskinesia, ABPA, autoimmune disease, and obstruction

RF

• Modifiable: poor airway clearance and smoking

• Non-modifiable: the underlying cause (CF, immunodeficiency), prior Pseudomonas colonization, frequent prior exacerbations, and advanced or extensive disease

Data

• Sputum Gram stain and culture with sensitivities (including Pseudomonas, with mycobacterial and fungal studies considered — obtained before or with antibiotics, since they direct therapy)

• Chest radiograph and HRCT (bronchiectasis with tram-track and signet-ring signs and airway dilation; excluding pneumonia and complications)

• CBC, BMP, and CRP, with oximetry and ABG

• The prior culture history and, in newly diagnosed disease, a workup of the underlying cause (CF testing, immunoglobulins, an ABPA workup)

DDx

Pneumonia (focal consolidation) · COPD exacerbation (smoking, obstruction, less sputum) · a cystic fibrosis exacerbation (known CF) · nontuberculous mycobacterial infection (AFB, an indolent course) · ABPA (eosinophilia, elevated IgE, central bronchiectasis) · heart failure or PE (BNP, CTA)

Home Meds

• Continue airway clearance, maintenance inhalers, and mucolytics, and continue chronic suppressive or macrolide therapy if prescribed

• Reconcile and escalate antibiotics per cultures and ensure adequate hydration

• Address underlying-cause therapy such as immunoglobulin replacement or ABPA steroids

Plan

CONSULT: Pulmonology (management, underlying cause, severe or frequent exacerbations) · Infectious Disease (resistant organisms, NTM, complex regimens) · Respiratory therapy (airway clearance) · a CF center (cystic fibrosis) · Immunology (immunodeficiency)

• Obtain a sputum culture before or with starting antibiotics, since it directs therapy, with prior cultures and known colonization guiding the empiric choice

• Culture-directed antibiotics (empiric while awaiting results): for patients without Pseudomonas risk or history, cover Haemophilus, streptococci, and Moraxella with amoxicillin-clavulanate, a respiratory fluoroquinolone, or doxycycline; for those with Pseudomonas risk or prior isolation (common in advanced disease), use antipseudomonal coverage with ciprofloxacin 750 mg PO BID or an IV antipseudomonal agent (this institution uses cefepime 2 g IV q8h in place of piperacillin-tazobactam), tailored to sensitivities; and treat for a typically longer course than routine pneumonia, usually 7–14 days, guided by severity, organism, and response

• Airway clearance is central to treatment, not an afterthought: chest physiotherapy, oscillatory PEP devices, postural drainage, and mucoactive measures (hypertonic saline nebulization and adequate hydration), intensifying the patient's home regimen during the exacerbation

• Bronchodilators for airflow obstruction or reactivity, with supplemental oxygen as needed

• Treat the underlying cause: immunoglobulin replacement for immunodeficiency, steroids with or without an antifungal for ABPA, NTM-directed multidrug therapy for mycobacterial disease, and CF-specific care (CFTR modulators and a CF center) — the durable strategy to reduce future exacerbations

• Manage complications such as hemoptysis (which can be massive from hypertrophied bronchial arteries and need embolization — see the hemoptysis card) and respiratory failure

• PT/OT and respiratory therapy: airway clearance training, mobilization, and a pulmonary rehabilitation referral

• Trend: sputum volume and purulence, fever and CRP, oxygenation, culture and sensitivity results, and the response to therapy and airway clearance

• Escalation triggers: respiratory failure → escalation of support or ICU; a resistant organism or treatment failure → ID involvement and adjustment; massive hemoptysis → IR embolization; recurrent frequent exacerbations → reassessment of the underlying cause and suppressive therapy

• Discharge criteria: sputum and symptoms improving toward baseline, stable oxygenation, a defined (often 7–14 day) culture-directed course, and a reinforced airway clearance regimen; arrange pulmonary follow-up and underlying-cause management, consider chronic macrolide or suppressive therapy and pulmonary rehabilitation to reduce recurrence, ensure vaccination, and give return precautions for worsening sputum or dyspnea, fever, or hemoptysis

Red Flags

• Prior Pseudomonas isolation or advanced disease → cover Pseudomonas empirically and treat longer

• Massive hemoptysis → hypertrophied bronchial arteries; airway protection and embolization

• An indolent, treatment-refractory course → consider nontuberculous mycobacterial infection

• Eosinophilia with a very high IgE and central bronchiectasis → ABPA needing steroids

• Frequent exacerbations → an undertreated underlying cause; revisit the diagnosis and suppressive therapy

Senior IM Resident Pearls

• Culture every exacerbation. The airway flora drives the disease — prior and current cultures direct therapy far better than empiric guesswork.

• Assume Pseudomonas is in play. In anyone with prior isolation or advanced disease, cover it empirically and tailor down to sensitivities.

• Treat longer than a simple pneumonia. Bronchiectasis exacerbations usually need 7–14 days, not a 5-day course.

• Airway clearance is treatment. Chest physiotherapy, PEP devices, and hypertonic saline matter as much as the antibiotic — intensify them in-hospital.

• Always ask why. Finding and treating the underlying cause — immunodeficiency, ABPA, NTM, CF — is what reduces the next exacerbation.

• Respect the hemoptysis. Hypertrophied bronchial arteries can bleed massively; know the embolization pathway.

• Common mistake: treating an exacerbation like a routine pneumonia — too short a course, no Pseudomonas coverage, and no attention to airway clearance or the underlying cause.

Pulmonology — Oncologic

120. Lung Cancer Complications

malignant effusion · airway obstruction · post-obstructive pneumonia · SVC syndrome · hemoptysis · relieve the obstruction/space + oncology · Super Compact

Sx: depends on the complication — dyspnea + dullness (malignant pleural effusion); stridor/wheeze/dyspnea/post-obstructive collapse (central airway obstruction); fever + consolidation distal to a mass (post-obstructive pneumonia); facial/neck/arm swelling, distended neck/chest veins, headache, dyspnea (SVC syndrome); hemoptysis · constitutional: weight loss, fatigue · known or newly suspected lung cancer/mass (each complication has a mechanical fix layered with oncologic therapy — relieve the obstruction or drain the space, then treat the cancer)

Neg: denies a purely infectious picture without an underlying mass (simple pneumonia) · denies a benign cause of effusion (CHF/transudate) · denies a non-malignant cause of SVC obstruction (thrombus around a line) without imaging confirmation · denies a primary cardiac/PE explanation for the dyspnea

SHx: smoking (major) · known lung cancer + type/stage/treatment · prior radiation/chemo/immunotherapy · indwelling catheters (SVC thrombus) · occupational exposures (asbestos) · performance status + goals of care

Etiology (the complications): malignant pleural effusion (pleural metastases) · central airway obstruction (endobronchial tumor/extrinsic compression) · post-obstructive pneumonia (tumor obstructing a bronchus → distal infection) · SVC syndrome (tumor compressing/invading the SVC — esp right-sided, small cell/squamous) · hemoptysis (tumor erosion into vessels) · also: spinal cord compression, malignant pericardial effusion, paraneoplastic syndromes

RF: smoking · advanced-stage disease · central/large tumors · prior radiation · indwelling central venous catheters (SVC thrombosis)

Data: CT chest (± contrast/CTA) (mass, airway compromise, SVC compression, effusion, post-obstructive changes) · CXR · bronchoscopy (airway obstruction — diagnostic + therapeutic; hemoptysis) · pleural fluid analysis + cytology (malignant effusion) · tissue diagnosis (if new — biopsy, molecular/PD-L1) · CBC, BMP, coags · venous imaging for SVC; cultures if post-obstructive pneumonia

DDx: benign effusion (transudate, cytology negative) · simple pneumonia (no mass) · PE (CTA) · SVC thrombus from catheter (venous imaging) · other mediastinal mass (lymphoma, etc.) · COPD/asthma for wheeze (no fixed obstruction)

Home Meds: reconcile oncologic therapy + steroids · manage anticoagulation (SVC thrombus/hemoptysis tension) · analgesia · VTE prophylaxis (cancer = prothrombotic) vs bleeding risk; coordinate with oncology on systemic therapy timing

Plan

CONSULT: Oncology (systemic therapy, overall plan) · Interventional pulmonology/Pulmonology (airway obstruction — stent/debulking, bronchoscopy) · Radiation oncology (SVC syndrome, airway, hemoptysis, cord compression) · Interventional radiology (embolization, venous stenting) · Thoracic surgery · Palliative care (symptoms, goals of care)

– General principle: relieve the mechanical problem (drain the space / open the airway / decompress the vein) AND treat the cancer (oncology-directed therapy) — and align with the patient's goals of care
– Malignant pleural effusion: therapeutic thoracentesis for symptomatic relief; recurrent → indwelling pleural catheter or pleurodesis; oncology for systemic therapy (see the pleural effusion card)
– Central airway obstruction: bronchoscopic intervention — stent placement, tumor debulking (laser/electrocautery/cryotherapy), and/or radiation to restore airway patency (interventional pulmonology); steroids may reduce edema; urgent if critical obstruction
– Post-obstructive pneumonia: antibiotics (cover the relevant flora) PLUS relieve the obstruction (it will not fully resolve until the bronchus is opened — bronchoscopy/stent/radiation); obtain cultures
– SVC syndrome: elevate head of bed, supplemental O2; radiation and/or chemotherapy directed by tumor type (small cell is chemo-sensitive); endovascular stenting (IR) for severe/refractory symptoms or airway/cerebral edema; steroids/diuretics adjunctively; obtain a tissue diagnosis before treatment when feasible unless life-threatening; anticoagulate if catheter-associated thrombus
– Hemoptysis: airway protection, bronchoscopy, and bronchial artery embolization for significant bleeding (see the hemoptysis card); radiation for tumor-related bleeding
– Always integrate goals of care + palliative care — many complications occur in advanced disease; symptom control and patient priorities guide how aggressively to intervene
– Each lung cancer complication is a "fix the mechanics + treat the cancer" problem: drain the malignant effusion, stent or debulk the obstructed airway, open the bronchus behind a post-obstructive pneumonia (antibiotics alone won't clear it), and decompress the SVC. And because these usually signal advanced disease, the goals-of-care conversation and palliative care belong in the plan from the start, not at the end.
– PT/OT + palliative care: function, symptom management, support
– Trend: the specific complication (effusion recurrence, airway patency, oxygenation, SVC symptoms, bleeding), oncologic response, performance status, symptom burden
– Escalation triggers: critical airway obstruction → urgent IP/radiation; massive hemoptysis → embolization/ICU; severe SVC syndrome with airway/cerebral edema → urgent stenting/radiation; respiratory failure → ICU vs goals-of-care
– Discharge when: the acute complication is controlled (space drained/airway patent/SVC decompressed/infection treated), oxygenation stable, oncology plan + follow-up arranged, goals of care addressed; appropriate subspecialty follow-up (oncology/radiation/IP/palliative), home support; return precautions (worsening dyspnea, facial swelling, hemoptysis, fever)

120. Lung Cancer Complications

complete reference · malignant effusion, airway obstruction, post-obstructive pneumonia, SVC syndrome, hemoptysis · mechanical relief plus oncologic therapy · Full Card

Symptoms / Associated Sx

• Symptoms depend on the complication — dyspnea with dullness (malignant pleural effusion); stridor, wheeze, dyspnea, or lobar collapse (central airway obstruction); fever and consolidation distal to a mass (post-obstructive pneumonia); facial, neck, and arm swelling with distended neck and chest veins, headache, and dyspnea (SVC syndrome); and hemoptysis

• Constitutional symptoms of weight loss and fatigue, in a patient with known or newly suspected lung cancer or a mass

• Each complication layers a mechanical fix with oncologic therapy — relieve the obstruction or drain the space, then treat the cancer

Neg

• Pt denies a purely infectious picture without an underlying mass — argues against a simple pneumonia

• Pt denies a benign cause of the effusion such as heart failure with a transudate

• Pt denies a non-malignant cause of SVC obstruction such as a catheter-associated thrombus, pending imaging confirmation

• Pt denies a primary cardiac or PE explanation for the dyspnea

Social History (SHx)

• Smoking (a major risk) and known lung cancer with its type, stage, and treatment

• Prior radiation, chemotherapy, or immunotherapy, and indwelling catheters (SVC thrombus)

• Occupational exposures such as asbestos, and the performance status and goals of care

Main Etiology

• Malignant pleural effusion from pleural metastases and central airway obstruction from endobronchial tumor or extrinsic compression

• Post-obstructive pneumonia from a tumor obstructing a bronchus with distal infection, and SVC syndrome from tumor compressing or invading the SVC (especially right-sided small cell or squamous tumors)

• Hemoptysis from tumor erosion into vessels, along with spinal cord compression, malignant pericardial effusion, and paraneoplastic syndromes

RF

• Modifiable: smoking and indwelling central venous catheters (SVC thrombosis)

• Non-modifiable: advanced-stage disease, central or large tumors, and prior radiation

Data

• CT of the chest (with contrast or CTA as needed) (the mass, airway compromise, SVC compression, an effusion, and post-obstructive changes) and a chest radiograph

• Bronchoscopy (diagnostic and therapeutic for airway obstruction, and for hemoptysis)

• Pleural fluid analysis with cytology (a malignant effusion) and a tissue diagnosis when new (biopsy with molecular and PD-L1 testing)

• CBC, BMP, and coagulation studies, venous imaging for SVC syndrome, and cultures for a post-obstructive pneumonia

DDx

A benign effusion (a transudate, negative cytology) · a simple pneumonia (no mass) · pulmonary embolism (CTA) · an SVC thrombus from a catheter (venous imaging) · another mediastinal mass (lymphoma) · COPD or asthma for wheeze (no fixed obstruction)

Home Meds

• Reconcile oncologic therapy and steroids and manage anticoagulation (balancing an SVC thrombus against hemoptysis risk)

• Provide analgesia and weigh VTE prophylaxis (cancer is prothrombotic) against bleeding risk

• Coordinate with oncology on the timing of systemic therapy

Plan

CONSULT: Oncology (systemic therapy, overall plan) · Interventional pulmonology or Pulmonology (airway obstruction — stent or debulking, bronchoscopy) · Radiation oncology (SVC syndrome, airway disease, hemoptysis, cord compression) · Interventional radiology (embolization, venous stenting) · Thoracic surgery · Palliative care (symptoms, goals of care)

• The general principle is to relieve the mechanical problem (drain the space, open the airway, or decompress the vein) and treat the cancer with oncology-directed therapy, aligned with the patient's goals of care

• Malignant pleural effusion: therapeutic thoracentesis for symptom relief, with an indwelling pleural catheter or pleurodesis for recurrence, and oncology for systemic therapy (see the pleural effusion card)

• Central airway obstruction: bronchoscopic intervention — stent placement, tumor debulking (laser, electrocautery, or cryotherapy), and radiation — to restore airway patency, with steroids to reduce edema, treated urgently for critical obstruction

• Post-obstructive pneumonia: antibiotics covering the relevant flora plus relief of the obstruction, since it will not fully resolve until the bronchus is opened (bronchoscopy, stent, or radiation), with cultures obtained

• SVC syndrome: head-of-bed elevation and supplemental oxygen, radiation or chemotherapy directed by tumor type (small cell is chemo-sensitive), endovascular stenting for severe or refractory symptoms or airway or cerebral edema, and adjunctive steroids and diuretics, obtaining a tissue diagnosis before treatment when feasible unless the situation is life-threatening, and anticoagulating a catheter-associated thrombus

• Hemoptysis: airway protection, bronchoscopy, and bronchial artery embolization for significant bleeding (see the hemoptysis card), with radiation for tumor-related bleeding

• Always integrate goals of care and palliative care, since many complications occur in advanced disease and symptom control and patient priorities guide how aggressively to intervene

• PT/OT and palliative care: function, symptom management, and support

• Trend: the specific complication (effusion recurrence, airway patency, oxygenation, SVC symptoms, bleeding), the oncologic response, performance status, and symptom burden

• Escalation triggers: critical airway obstruction → urgent interventional pulmonology or radiation; massive hemoptysis → embolization and ICU; severe SVC syndrome with airway or cerebral edema → urgent stenting or radiation; respiratory failure → ICU versus a goals-of-care discussion

• Discharge criteria: the acute complication controlled (space drained, airway patent, SVC decompressed, infection treated), stable oxygenation, an arranged oncology plan and follow-up, and addressed goals of care; arrange appropriate subspecialty follow-up (oncology, radiation, interventional pulmonology, palliative care) and home support, with return precautions for worsening dyspnea, facial swelling, hemoptysis, or fever

Red Flags

• Critical central airway obstruction with stridor → an emergency for interventional pulmonology and radiation

• SVC syndrome with airway compromise or cerebral edema → urgent stenting or radiation

• Massive hemoptysis from tumor erosion → airway protection and embolization

• A post-obstructive pneumonia that won't clear on antibiotics → the bronchus must be opened

• New back pain with neurologic signs → consider malignant spinal cord compression, a separate emergency

Senior IM Resident Pearls

• Fix the mechanics and treat the cancer. Every complication pairs a procedural relief with oncologic therapy — neither alone is enough.

• Antibiotics won't clear a post-obstructive pneumonia. The infection persists until the obstructing bronchus is opened.

• Get tissue before treating SVC syndrome when you safely can. Treatment depends on tumor type, and emergent radiation can obscure the diagnosis — but don't delay in a true airway or cerebral emergency.

• Recurrent malignant effusions need a durable plan. An indwelling catheter or pleurodesis beats repeated taps.

• Small cell is chemo-sensitive. SVC syndrome from small cell often responds rapidly to chemotherapy.

• Goals of care belong at the start. These complications mark advanced disease — involve palliative care early, not as an afterthought.

• Common mistake: treating a post-obstructive pneumonia with antibiotics alone, or rushing emergent radiation for SVC syndrome and losing the chance at a tissue diagnosis when the situation wasn't truly emergent.

Pulmonology — Infectious

121. Tuberculosis (TB)

airborne isolation IMMEDIATELY · AFB smear ×3 + NAAT + culture · RIPE regimen + pyridoxine · public health reporting · HIV testing · Super Compact

Sx: chronic cough (≥2–3 weeks), hemoptysis, fever, drenching night sweats, weight loss, anorexia, fatigue · pulmonary: productive cough, upper-lobe disease ± cavitation; extrapulmonary varies (lymphadenitis, pleural, meningeal, miliary, skeletal, GU) · subacute/chronic course (the first action when TB is suspected is not a test — it's airborne isolation, before the workup, to protect everyone else)

Neg: denies an acute lobar onset typical of bacterial CAP (more chronic course) · denies symptoms fully explained by malignancy alone (overlap — weight loss/hemoptysis) · denies a purely fungal/NTM picture without risk factors · in latent vs active: denies active symptoms/findings (latent = asymptomatic, normal CXR, positive test only)

SHx: TB exposure/contact · birth/travel/residence in endemic area · homelessness, incarceration, congregate living · HIV/immunosuppression (TNF inhibitors, transplant, steroids) · prior TB/treatment · injection drug/alcohol use · healthcare work · diabetes · silicosis

Etiology: Mycobacterium tuberculosis — airborne transmission via respiratory droplet nuclei · latent TB (contained, asymptomatic, non-infectious, positive immune test) vs active TB (replicating, symptomatic, infectious — pulmonary or extrapulmonary) · reactivation (immunosuppression) vs primary progressive · drug-resistant TB (MDR/XDR) — prior treatment, endemic exposure

RF: endemic exposure · HIV/immunosuppression · close contact · congregate settings · injection drug/alcohol use · diabetes · silicosis · prior incomplete treatment (resistance)

Data: AIRBORNE ISOLATION + chest imaging · sputum AFB smear ×3 (serial, often morning) + nucleic acid amplification test (NAAT/GeneXpert — rapid, also detects rifampin resistance) + mycobacterial culture & drug-susceptibility testing (culture is the gold standard; NAAT speeds diagnosis) · CXR/CT (upper-lobe infiltrate/cavitation, miliary pattern, lymphadenopathy, effusion) · HIV test (mandatory) · LFTs/baseline labs (drug monitoring), visual acuity/color (ethambutol), uric acid · IGRA or TST (latent — not for active dx) · extrapulmonary sampling as indicated

DDx: bacterial pneumonia/lung abscess (acute, responds to abx) · lung cancer (mass, cytology) · NTM (culture/speciation) · fungal (histo/cocci/blasto) (endemic, serologies) · sarcoidosis (noncaseating, biopsy) · other cavitary disease

Home Meds: review for drug interactions — rifampin is a potent CYP inducer (reduces levels of many drugs — anticoagulants, antiretrovirals, contraceptives, etc.) · add pyridoxine (vitamin B6) with isoniazid to prevent neuropathy · reconcile hepatotoxic meds (monitor LFTs) · adjust for HIV antiretrovirals (ID/pharmacy)

Plan

CONSULT: Infectious Disease (regimen, resistance, HIV co-infection, extrapulmonary) · Public health/TB control program (MANDATORY reporting, contact tracing, directly observed therapy) · Pulmonology (diagnosis, bronchoscopy if needed) · Pharmacy (interactions, monitoring) · HIV/ID if co-infected

– FIRST, IMMEDIATELY: airborne (respiratory) isolation in a negative-pressure room with appropriate respiratory protection (N95/PAPR) — do this on suspicion, before confirmation, to protect other patients and staff
– Diagnostic workup: sputum AFB smears ×3, NAAT/GeneXpert (rapid + rifampin resistance), mycobacterial culture with drug-susceptibility testing; chest imaging; mandatory HIV testing; baseline LFTs, CBC, creatinine, visual acuity/color vision (for ethambutol), uric acid
– Mandatory public health reporting — notify the local TB control program; they coordinate contact tracing and directly observed therapy (DOT)
– Treatment of active TB — the RIPE regimen (standard, drug-susceptible):
  • Intensive phase ×2 months: Rifampin + Isoniazid + Pyrazinamide + Ethambutol (RIPE)
  • Continuation phase ×4 months: Rifampin + Isoniazid (total ~6 months for drug-susceptible pulmonary TB; longer for some sites/situations)
  • Add pyridoxine (vitamin B6) with isoniazid to prevent peripheral neuropathy
  • Directly observed therapy (DOT) is standard to ensure adherence + prevent resistance
– Drug-resistant TB (MDR/XDR — prior treatment, rifampin resistance on NAAT, endemic exposure): specialized longer multidrug regimens (newer agents — bedaquiline, etc.) directed by ID/TB experts and susceptibility data — do not treat empirically alone
– Monitoring: LFTs (hepatotoxicity — INH/RIF/PZA), visual acuity/color (ethambutol — optic neuritis), uric acid (pyrazinamide), clinical + sputum response (repeat smears/cultures to document conversion)
– De-isolation: per public health/institutional criteria (clinical improvement, reduction in smear positivity on effective therapy, typically serial negative smears) — do not de-isolate prematurely
– Latent TB (asymptomatic, positive test, no active disease): treat to prevent reactivation (e.g. isoniazid + rifapentine weekly ×12 weeks [3HP], or rifampin ×4 months, or isoniazid ×6–9 months) — only after active TB is excluded
– The reflex when TB is on the differential is airborne isolation first, test second — protect the unit before you prove the diagnosis. Then it's a package: AFB smears + NAAT + culture, mandatory HIV test, mandatory public health reporting, the RIPE regimen with pyridoxine, and DOT. Rifampin's CYP induction will wreck half the patient's other medications, so reconcile interactions carefully.
– PT/OT: nutrition support (often malnourished), mobilization as tolerated within isolation
– Trend: sputum smear/culture conversion, symptom + weight response, LFTs + drug toxicity monitoring, adherence (DOT), HIV status/management, drug-susceptibility results
– Escalation triggers: drug resistance → ID/TB expert regimen; hepatotoxicity → hold/adjust + hepatology/ID; respiratory failure/massive hemoptysis → ICU/embolization; extrapulmonary/CNS TB → specialized management
– Discharge when: clinically improving on an effective regimen, de-isolation criteria met (or appropriate home isolation arranged with public health), adherence plan (DOT) + follow-up established, interactions/monitoring plan defined; ID + public health + PCP follow-up, contact tracing underway, education on adherence + infection control; return precautions (worsening symptoms, hemoptysis, drug side effects — jaundice, visual changes, neuropathy)

121. Tuberculosis (TB)

complete reference · immediate airborne isolation · smear, NAAT, and culture · the RIPE regimen with pyridoxine · public health reporting and DOT · Full Card

Symptoms / Associated Sx

• Chronic cough of two to three weeks or more, hemoptysis, fever, drenching night sweats, weight loss, anorexia, and fatigue

• Pulmonary disease with a productive cough and upper-lobe involvement with possible cavitation; extrapulmonary disease varies (lymphadenitis, pleural, meningeal, miliary, skeletal, and genitourinary)

• The course is subacute to chronic; the first action when TB is suspected is not a test but airborne isolation, to protect everyone else

Neg

• Pt denies an acute lobar onset typical of bacterial pneumonia — the course is more chronic

• Pt denies symptoms fully explained by malignancy alone, recognizing the overlap of weight loss and hemoptysis

• Pt denies a purely fungal or nontuberculous mycobacterial picture without risk factors

• In latent disease, the patient denies active symptoms and findings — latent TB is asymptomatic with a normal chest film and only a positive immune test

Social History (SHx)

• TB exposure or contact, and birth, travel, or residence in an endemic area

• Homelessness, incarceration, or congregate living, and HIV or immunosuppression (TNF inhibitors, transplant, steroids)

• Prior TB or treatment, injection drug or alcohol use, healthcare work, diabetes, and silicosis

Main Etiology

• Mycobacterium tuberculosis, transmitted by airborne respiratory droplet nuclei

• Latent TB (contained, asymptomatic, non-infectious, with a positive immune test) versus active TB (replicating, symptomatic, and infectious — pulmonary or extrapulmonary)

• Reactivation (with immunosuppression) versus primary progressive disease, and drug-resistant TB (MDR and XDR) associated with prior treatment and endemic exposure

RF

• Modifiable: congregate-setting exposure, injection drug and alcohol use, and management of diabetes

• Non-modifiable: endemic exposure, HIV and immunosuppression, close contact, silicosis, and prior incomplete treatment (resistance)

Data

• Airborne isolation and chest imaging, with sputum AFB smears times three (serial, often morning), a nucleic acid amplification test (NAAT or GeneXpert, which is rapid and also detects rifampin resistance), and a mycobacterial culture with drug-susceptibility testing (culture is the gold standard while NAAT speeds diagnosis)

• Chest radiograph or CT (an upper-lobe infiltrate or cavitation, a miliary pattern, lymphadenopathy, or an effusion)

• Mandatory HIV testing, with baseline LFTs and labs for drug monitoring, visual acuity and color vision (ethambutol), and uric acid

• An IGRA or tuberculin skin test for latent disease (not for diagnosing active TB), and extrapulmonary sampling as indicated

DDx

Bacterial pneumonia or lung abscess (acute, responsive to antibiotics) · lung cancer (a mass, cytology) · nontuberculous mycobacteria (culture and speciation) · fungal disease such as histoplasmosis, coccidioidomycosis, or blastomycosis (endemic exposure, serologies) · sarcoidosis (noncaseating granulomas on biopsy) · other cavitary disease

Home Meds

• Review for drug interactions, since rifampin is a potent CYP inducer that reduces levels of many drugs (anticoagulants, antiretrovirals, contraceptives)

• Add pyridoxine (vitamin B6) with isoniazid to prevent neuropathy, and reconcile hepatotoxic medications with LFT monitoring

• Adjust for HIV antiretrovirals with ID and pharmacy input

Plan

CONSULT: Infectious Disease (regimen, resistance, HIV co-infection, extrapulmonary disease) · Public health and the TB control program (mandatory reporting, contact tracing, directly observed therapy) · Pulmonology (diagnosis, bronchoscopy if needed) · Pharmacy (interactions, monitoring) · HIV/ID if co-infected

• Immediately institute airborne (respiratory) isolation in a negative-pressure room with appropriate respiratory protection (an N95 or PAPR), done on suspicion before confirmation to protect other patients and staff

• Diagnostic workup: sputum AFB smears times three, a NAAT or GeneXpert (rapid, with rifampin-resistance detection), and a mycobacterial culture with drug-susceptibility testing, along with chest imaging, mandatory HIV testing, and baseline LFTs, CBC, creatinine, visual acuity and color vision (for ethambutol), and uric acid

• Mandatory public health reporting: notify the local TB control program, which coordinates contact tracing and directly observed therapy

• Treatment of active drug-susceptible TB with the RIPE regimen: an intensive phase of two months with rifampin, isoniazid, pyrazinamide, and ethambutol, followed by a continuation phase of four months with rifampin and isoniazid (about six months total for drug-susceptible pulmonary TB, longer for some sites or situations), with pyridoxine added alongside isoniazid to prevent peripheral neuropathy and directly observed therapy as the standard to ensure adherence and prevent resistance

• Drug-resistant TB (MDR or XDR, suggested by prior treatment, rifampin resistance on NAAT, or endemic exposure) requires specialized longer multidrug regimens with newer agents such as bedaquiline, directed by ID and TB experts and susceptibility data rather than treated empirically alone

• Monitoring: LFTs for hepatotoxicity (isoniazid, rifampin, pyrazinamide), visual acuity and color vision for ethambutol-associated optic neuritis, uric acid for pyrazinamide, and the clinical and sputum response with repeat smears and cultures to document conversion

• De-isolation per public health and institutional criteria (clinical improvement and reduced smear positivity on effective therapy, typically serial negative smears), avoiding premature de-isolation

• Latent TB (asymptomatic, a positive test, no active disease) is treated to prevent reactivation (isoniazid with rifapentine weekly for 12 weeks, rifampin for 4 months, or isoniazid for 6–9 months), only after active TB is excluded

• PT/OT: nutritional support, since these patients are often malnourished, and mobilization as tolerated within isolation

• Trend: sputum smear and culture conversion, the symptom and weight response, LFTs and drug-toxicity monitoring, adherence through DOT, HIV status and management, and drug-susceptibility results

• Escalation triggers: drug resistance → an ID or TB expert regimen; hepatotoxicity → hold or adjust with hepatology or ID input; respiratory failure or massive hemoptysis → ICU or embolization; extrapulmonary or CNS TB → specialized management

• Discharge criteria: clinical improvement on an effective regimen, met de-isolation criteria (or appropriate home isolation arranged with public health), an established adherence plan (DOT) and follow-up, and a defined interaction and monitoring plan; arrange ID, public health, and PCP follow-up with contact tracing underway and education on adherence and infection control, and give return precautions for worsening symptoms, hemoptysis, or drug side effects such as jaundice, visual changes, or neuropathy

Red Flags

• Suspected TB without isolation → an exposure risk to the entire unit; isolate immediately on suspicion

• Rifampin resistance on NAAT or prior treatment → possible MDR-TB requiring expert-directed therapy

• A positive HIV test → alters the regimen, the timing of antiretrovirals, and the risk of complications

• Rising transaminases on therapy → drug-induced hepatotoxicity; hold and reassess

• Massive hemoptysis or respiratory failure → an airway emergency requiring escalation

Senior IM Resident Pearls

• Isolate first, test second. The moment TB is on the differential, airborne isolation goes up — protecting the unit can't wait for confirmation.

• NAAT speeds everything. GeneXpert gives a rapid diagnosis and flags rifampin resistance while cultures, the gold standard, mature.

• HIV testing and public health reporting are mandatory. Both are part of the standard package, not optional add-ons.

• Pyridoxine rides with isoniazid. It prevents the peripheral neuropathy that otherwise complicates treatment.

• Respect rifampin's interactions. As a potent CYP inducer it lowers levels of anticoagulants, antiretrovirals, and contraceptives — reconcile carefully.

• DOT prevents resistance. Directly observed therapy is how incomplete treatment and the next MDR case are avoided.

• Common mistake: ordering the TB workup before placing the patient in airborne isolation, exposing staff and other patients while waiting for the smear.