| Pneumonia — core presentation & workup | - Highest sensitivity (rules out when absent): fever ≥ 38 °C with chills/shivering, pleuritic chest pain, cough productive of mucopurulent sputum, dyspnea, tachypnea (tachypnea especially > age 65)
- highest specificity (rules in when present): asymmetric breath sounds, pleural rubs, egophony, increased tactile fremitus
- also rales ("crackles") over affected area, mental status changes/confusion
- typical = fever, chills, leukocytosis, cough ± sputum, sputum production, increased fremitus
- atypical = fever may be high, leukocytosis may be absent or show a left shift with band forms, cough often dry, headache, sore throat, excessive sweating, chest soreness, more often diffuse on film and may involve multiple segments or both lungs
Highest sensitivity (rules out when absent): fever ≥ 38 °C with chills/shivering, pleuritic chest pain, cough productive of mucopurulent sputum, dyspnea, tachypnea (tachypnea especially > age 65); highest specificity (rules in when present): asymmetric breath sounds, pleural rubs, egophony, increased tactile fremitus; also rales ("crackles") over affected area, mental status changes/confusion; typical = fever, chills, leukocytosis, cough ± sputum, sputum production, increased fremitus; atypical = fever may be high, leukocytosis may be absent or show a left shift with band forms, cough often dry, headache, sore throat, excessive sweating, chest soreness, more often diffuse on film and may involve multiple segments or both lungs | - ⭐ radiographic infiltrate is required for diagnosis
- infiltrate may lag symptoms by 24–48 h → justifies repeat chest X-ray at 24–48 h
- CBC with differential WBC count
- blood cultures
- Gram stain and culture of sputum
- ABGs and/or pulse oximetry
- procalcitonin when available — may aid diagnosing bacterial pneumonia and guide duration of therapy
- CXR searching for a new infiltrate
- both typical and atypical forms show an infiltrate on chest X-ray
⭐ radiographic infiltrate is required for diagnosis; infiltrate may lag symptoms by 24–48 h → justifies repeat chest X-ray at 24–48 h; CBC with differential WBC count; blood cultures; Gram stain and culture of sputum; ABGs and/or pulse oximetry; procalcitonin when available — may aid diagnosing bacterial pneumonia and guide duration of therapy; CXR searching for a new infiltrate; both typical and atypical forms show an infiltrate on chest X-ray | - Start empiric antimicrobial therapy with cultures pending
- revise therapy as culture data returns and as patient improves
- use the narrowest-spectrum agent the known organism is expected to respond to
- cover anaerobes in known or suspected aspiration
- treat coexisting illness simultaneously (COPD, CHF, diabetes, dehydration)
- not everyone needs admission — young adults in particular may be managed as outpatients
- hospitalization decision guided by possibility of rapidly progressive disease, patient's overall status/coexisting problems, and ability to reliably self-administer medication
- if in doubt, observe in hospital during initial therapy and reassess early response
Start empiric antimicrobial therapy with cultures pending; revise therapy as culture data returns and as patient improves; use the narrowest-spectrum agent the known organism is expected to respond to; cover anaerobes in known or suspected aspiration; treat coexisting illness simultaneously (COPD, CHF, diabetes, dehydration); not everyone needs admission — young adults in particular may be managed as outpatients; hospitalization decision guided by possibility of rapidly progressive disease, patient's overall status/coexisting problems, and ability to reliably self-administer medication; if in doubt, observe in hospital during initial therapy and reassess early response | - Antibiotic doses in the elderly — may need to be reduced because of altered renal function or a predisposition to medication side effects
Antibiotic doses in the elderly — may need to be reduced because of altered renal function or a predisposition to medication side effects |
| Pneumonia — risk factors, mortality & vaccines | - Risk: age > 65
- chronic comorbidities
- viral respiratory infection
- impaired airway protection
- smoking
- recent antibiotic use
- immunocompromise — HIV, chemotherapy, transplant
- mortality drivers (comorbidity): congestive heart failure, diabetes mellitus, chronic liver and renal disease, COPD
- the very young and the very old die disproportionately
Risk: age > 65; chronic comorbidities; viral respiratory infection; impaired airway protection; smoking; recent antibiotic use; immunocompromise — HIV, chemotherapy, transplant; mortality drivers (comorbidity): congestive heart failure, diabetes mellitus, chronic liver and renal disease, COPD; the very young and the very old die disproportionately | - Time of year, known epidemics, and comorbid conditions help define which type (typical vs atypical) is being faced
- immunocompromise and recent antibiotic use raise resistant-organism risk and drive regimen selection (see CAP and HAP/VAP rows)
- procalcitonin may aid diagnosis and guide duration
Time of year, known epidemics, and comorbid conditions help define which type (typical vs atypical) is being faced; immunocompromise and recent antibiotic use raise resistant-organism risk and drive regimen selection (see CAP and HAP/VAP rows); procalcitonin may aid diagnosis and guide duration | - Influenza vaccine yearly for everyone 6 months and older
- no preference for vaccine presentation when multiple types are available within an approved age range
- some patients are revaccinated within a season if immunocompromised or if they have severe underlying COPD or heart disease
- PCV13 — conjugate vaccine for infants, children, and adults older than 19 at high risk
- PPSV23 — polysaccharide vaccine for adults older than 65 and those older than 2 at high risk
- ⭐ if giving both, start with PCV13 and give PPSV23 at least 8 weeks later (Chapter 27 says at least 8 weeks; Chapter 32 says at least 1 year — know both)
- if PPSV23 already given, PCV13 comes at least 1 year later
- guidelines change frequently — check the CDC schedule
Influenza vaccine yearly for everyone 6 months and older; no preference for vaccine presentation when multiple types are available within an approved age range; some patients are revaccinated within a season if immunocompromised or if they have severe underlying COPD or heart disease; PCV13 — conjugate vaccine for infants, children, and adults older than 19 at high risk; PPSV23 — polysaccharide vaccine for adults older than 65 and those older than 2 at high risk; ⭐ if giving both, start with PCV13 and give PPSV23 at least 8 weeks later (Chapter 27 says at least 8 weeks; Chapter 32 says at least 1 year — know both); if PPSV23 already given, PCV13 comes at least 1 year later; guidelines change frequently — check the CDC schedule | - If giving both pneumococcal vaccines, do not reverse the order — start with PCV13 and give PPSV23 at least 8 weeks later (Ch 32 says at least 1 year — the source flags this contradiction)
- if PPSV23 was already given, PCV13 comes at least 1 year later
If giving both pneumococcal vaccines, do not reverse the order — start with PCV13 and give PPSV23 at least 8 weeks later (Ch 32 says at least 1 year — the source flags this contradiction); if PPSV23 was already given, PCV13 comes at least 1 year later |
| CAP — outpatient, previously healthy | - Community-acquired — acquired in the community setting or within 48 hours of hospital admission
- ⭐ no MDR S. pneumoniae risk factors
- most common organisms: S. pneumoniae — most common bacterial cause in adults, H. influenzae, M. pneumoniae, C. pneumoniae, respiratory viruses
Community-acquired — acquired in the community setting or within 48 hours of hospital admission; ⭐ no MDR S. pneumoniae risk factors; most common organisms: S. pneumoniae — most common bacterial cause in adults, H. influenzae, M. pneumoniae, C. pneumoniae, respiratory viruses | - Same pneumonia workup: CBC with differential WBC count, blood cultures, Gram stain and sputum culture, ABGs and/or pulse oximetry, procalcitonin when available, chest X-ray for new infiltrate
Same pneumonia workup: CBC with differential WBC count, blood cultures, Gram stain and sputum culture, ABGs and/or pulse oximetry, procalcitonin when available, chest X-ray for new infiltrate | - ⭐ Azithromycin 500 mg initial dose day 1, then 250 mg Q24h days 2–5, or 500 mg Q24h (no renal adjustment needed, but caution if CrCl < 10 mL/min; hepatically eliminated)
- OR doxycycline 100 mg Q12h (no adjustment needed)
⭐ Azithromycin 500 mg initial dose day 1, then 250 mg Q24h days 2–5, or 500 mg Q24h (no renal adjustment needed, but caution if CrCl < 10 mL/min; hepatically eliminated); OR doxycycline 100 mg Q12h (no adjustment needed) | - Azithromycin — no renal adjustment needed, but use with caution if CrCl < 10 mL/min (hepatically eliminated)
Azithromycin — no renal adjustment needed, but use with caution if CrCl < 10 mL/min (hepatically eliminated) |
| CAP — outpatient with comorbidities / MDR risk | - Comorbid conditions or MDR risk: heart disease, lung disease, diabetes, alcoholism, malignancy, immunosuppression, risk of MDR S. pneumoniae, or antibiotics within the past 3 months
Comorbid conditions or MDR risk: heart disease, lung disease, diabetes, alcoholism, malignancy, immunosuppression, risk of MDR S. pneumoniae, or antibiotics within the past 3 months | - Same pneumonia workup — cultures pending empiric start
- the presence of comorbidity/MDR risk (not a lab test) is what selects this regimen tier
Same pneumonia workup — cultures pending empiric start; the presence of comorbidity/MDR risk (not a lab test) is what selects this regimen tier | - Moxifloxacin 400 mg Q24h (no adjustment needed)
- levofloxacin 750 mg Q24h — **CrCl 20–49: 750 mg Q48h
- CrCl 10–19 or ESRD: 750 mg then 500 mg Q48h**
- gemifloxacin 320 mg Q24h — CrCl ≤ 40 or ESRD: 160 mg Q24h, after dialysis on dialysis days
- OR amoxicillin-clavulanate 875 mg Q12h plus azithromycin or doxycycline
Moxifloxacin 400 mg Q24h (no adjustment needed); levofloxacin 750 mg Q24h — CrCl 20–49: 750 mg Q48h; CrCl 10–19 or ESRD: 750 mg then 500 mg Q48h; gemifloxacin 320 mg Q24h — CrCl ≤ 40 or ESRD: 160 mg Q24h, after dialysis on dialysis days; OR amoxicillin-clavulanate 875 mg Q12h plus azithromycin or doxycycline | - **Levofloxacin — renal dose reduction required: CrCl 20–49 → 750 mg Q48h
- CrCl 10–19 or ESRD → 750 mg then 500 mg Q48h**
- gemifloxacin — CrCl ≤ 40 or ESRD → 160 mg Q24h, given after dialysis on dialysis days
Levofloxacin — renal dose reduction required: CrCl 20–49 → 750 mg Q48h; CrCl 10–19 or ESRD → 750 mg then 500 mg Q48h; gemifloxacin — CrCl ≤ 40 or ESRD → 160 mg Q24h, given after dialysis on dialysis days |
| CAP — non-ICU ward | - Hospitalised, not ICU
- same presentation as CAP but requires admission
Hospitalised, not ICU; same presentation as CAP but requires admission | - Same pneumonia workup — chest X-ray for new infiltrate, blood cultures, sputum Gram stain and culture, ABGs/pulse oximetry, procalcitonin when available
Same pneumonia workup — chest X-ray for new infiltrate, blood cultures, sputum Gram stain and culture, ABGs/pulse oximetry, procalcitonin when available | - ⭐ Ceftriaxone 1–2 g IV Q24h or ertapenem 1 g IV Q24h PLUS azithromycin 500 mg IV/PO Q24h or doxycycline 100 mg IV/PO Q12h
- doxycycline can be used as an alternative to a macrolide
⭐ Ceftriaxone 1–2 g IV Q24h or ertapenem 1 g IV Q24h PLUS azithromycin 500 mg IV/PO Q24h or doxycycline 100 mg IV/PO Q12h; doxycycline can be used as an alternative to a macrolide | — |
| CAP — ICU | - ICU-level CAP
- β-lactam backbone required
ICU-level CAP; β-lactam backbone required | - Same pneumonia workup
- obtain blood and sputum cultures before committing to empiric therapy
Same pneumonia workup; obtain blood and sputum cultures before committing to empiric therapy | - β-lactam plus azithromycin or a respiratory fluoroquinolone — options include ampicillin-sulbactam 3 g IV Q6h, ertapenem 1 g IV Q24h, or ceftriaxone 1–2 g IV Q24h
- ⭐ if penicillin or azithromycin allergy: levofloxacin 750 mg IV/PO Q24h or moxifloxacin 400 mg IV/PO Q24h
- if P. aeruginosa is a concern: piperacillin-tazobactam 4.5 g IV Q6h, cefepime 2 g IV Q8h, imipenem 500 mg IV Q6h, or meropenem 1 g IV Q8h
β-lactam plus azithromycin or a respiratory fluoroquinolone — options include ampicillin-sulbactam 3 g IV Q6h, ertapenem 1 g IV Q24h, or ceftriaxone 1–2 g IV Q24h; ⭐ if penicillin or azithromycin allergy: levofloxacin 750 mg IV/PO Q24h or moxifloxacin 400 mg IV/PO Q24h; if P. aeruginosa is a concern: piperacillin-tazobactam 4.5 g IV Q6h, cefepime 2 g IV Q8h, imipenem 500 mg IV Q6h, or meropenem 1 g IV Q8h | - Penicillin or azithromycin allergy — do not use that backbone
- use levofloxacin 750 mg IV/PO Q24h or moxifloxacin 400 mg IV/PO Q24h
Penicillin or azithromycin allergy — do not use that backbone; use levofloxacin 750 mg IV/PO Q24h or moxifloxacin 400 mg IV/PO Q24h |
| HAP | - ⭐ occurs 48 hours or more after admission, not incubating at the time of admission
- includes VAP and healthcare-associated pneumonia
- most common organisms: Staphylococcus aureus, S. pneumoniae, H. influenzae
⭐ occurs 48 hours or more after admission, not incubating at the time of admission; includes VAP and healthcare-associated pneumonia; most common organisms: Staphylococcus aureus, S. pneumoniae, H. influenzae | - Prefer treatment based on respiratory cultures rather than empiric treatment
- use the hospital antibiogram specific to ICU patients
- inflammatory biomarkers such as procalcitonin or CRP should not be used to initiate therapy — clinical criteria guide that decision, but they can help decide when to stop
Prefer treatment based on respiratory cultures rather than empiric treatment; use the hospital antibiogram specific to ICU patients; inflammatory biomarkers such as procalcitonin or CRP should not be used to initiate therapy — clinical criteria guide that decision, but they can help decide when to stop | - ⭐ duration 7 days — extend only if the clinical condition fails to improve or another uncovered organism is identified
- cover S. aureus, P. aeruginosa, and other Gram-negative bacilli
- de-escalate based on susceptibility testing, including MDR organisms and ESBL Gram-negative bacilli
- consult a pharmacist for pharmacokinetic modeling on vancomycin and aminoglycoside orders
- consider MRSA nasal PCR screening to reduce overuse of empiric vancomycin
⭐ duration 7 days — extend only if the clinical condition fails to improve or another uncovered organism is identified; cover S. aureus, P. aeruginosa, and other Gram-negative bacilli; de-escalate based on susceptibility testing, including MDR organisms and ESBL Gram-negative bacilli; consult a pharmacist for pharmacokinetic modeling on vancomycin and aminoglycoside orders; consider MRSA nasal PCR screening to reduce overuse of empiric vancomycin | - Do not use procalcitonin or CRP to initiate therapy — clinical criteria guide that decision
- do not extend beyond 7 days unless the clinical condition fails to improve or another uncovered organism is identified
- prefer treatment based on respiratory cultures rather than empiric treatment
- MRSA nasal PCR screening to reduce overuse of empiric vancomycin
Do not use procalcitonin or CRP to initiate therapy — clinical criteria guide that decision; do not extend beyond 7 days unless the clinical condition fails to improve or another uncovered organism is identified; prefer treatment based on respiratory cultures rather than empiric treatment; MRSA nasal PCR screening to reduce overuse of empiric vancomycin |
| VAP | - ⭐ arises more than 48–72 hours after endotracheal intubation
- ⭐ most common organism: Pseudomonas
- VAP MRSA risk factors: IV antibiotics in the last 90 days, septic shock, ARDS, hospital stay > 5 days, or renal failure
- history of antimicrobial resistance
- or a unit where > 20% of S. aureus isolates are methicillin resistant — or where prevalence is unknown
⭐ arises more than 48–72 hours after endotracheal intubation; ⭐ most common organism: Pseudomonas; VAP MRSA risk factors: IV antibiotics in the last 90 days, septic shock, ARDS, hospital stay > 5 days, or renal failure; history of antimicrobial resistance; or a unit where > 20% of S. aureus isolates are methicillin resistant — or where prevalence is unknown | - ⭐ prefer less-invasive sampling (tracheal suctioning) over more-invasive (bronchial wash)
- consider MRSA nasal PCR screening to reduce overuse of empiric vancomycin
- respiratory cultures preferred over empiric treatment
- ICU-specific hospital antibiogram
⭐ prefer less-invasive sampling (tracheal suctioning) over more-invasive (bronchial wash); consider MRSA nasal PCR screening to reduce overuse of empiric vancomycin; respiratory cultures preferred over empiric treatment; ICU-specific hospital antibiogram | - duration 7 days — extend only if the clinical condition fails to improve or another uncovered organism is identified
- ⭐ double-cover P. aeruginosa in units with > 10% Gram-negative resistance isolates, or if the patient has a history of Gram-negative resistance — otherwise single coverage
- avoid aminoglycosides if adequate Gram-negative coverage is attainable with alternative agents
- de-escalate based on susceptibility testing including MDR and ESBL organisms
duration 7 days — extend only if the clinical condition fails to improve or another uncovered organism is identified; ⭐ double-cover P. aeruginosa in units with > 10% Gram-negative resistance isolates, or if the patient has a history of Gram-negative resistance — otherwise single coverage; avoid aminoglycosides if adequate Gram-negative coverage is attainable with alternative agents; de-escalate based on susceptibility testing including MDR and ESBL organisms | - Avoid aminoglycosides if adequate Gram-negative coverage is attainable with alternative agents
- double-cover P. aeruginosa only in units with > 10% Gram-negative resistance isolates or a history of Gram-negative resistance — otherwise single coverage
- prefer less-invasive sampling (tracheal suctioning) over more-invasive (bronchial wash)
- do not extend beyond 7 days unless the clinical condition fails to improve or another uncovered organism is identified
- MRSA nasal PCR screening to reduce overuse of empiric vancomycin
Avoid aminoglycosides if adequate Gram-negative coverage is attainable with alternative agents; double-cover P. aeruginosa only in units with > 10% Gram-negative resistance isolates or a history of Gram-negative resistance — otherwise single coverage; prefer less-invasive sampling (tracheal suctioning) over more-invasive (bronchial wash); do not extend beyond 7 days unless the clinical condition fails to improve or another uncovered organism is identified; MRSA nasal PCR screening to reduce overuse of empiric vancomycin |
| Aspiration pneumonia | - Mechanism: altered mental status or dysphagia from stroke or neuromuscular disease (e.g., Parkinson disease)
- impaired airway protection
- aspiration of fluid including gastrointestinal contents and near drowning
Mechanism: altered mental status or dysphagia from stroke or neuromuscular disease (e.g., Parkinson disease); impaired airway protection; aspiration of fluid including gastrointestinal contents and near drowning | - Same pneumonia workup — chest X-ray for new infiltrate, sputum Gram stain and culture, blood cultures, ABGs and/or pulse oximetry
Same pneumonia workup — chest X-ray for new infiltrate, sputum Gram stain and culture, blood cultures, ABGs and/or pulse oximetry | - ⭐ cover anaerobes in known or suspected aspiration
- otherwise follow the CAP or HAP/VAP regimen according to where the pneumonia was acquired (see those rows)
- treat coexisting illness simultaneously (COPD, CHF, diabetes, dehydration)
⭐ cover anaerobes in known or suspected aspiration; otherwise follow the CAP or HAP/VAP regimen according to where the pneumonia was acquired (see those rows); treat coexisting illness simultaneously (COPD, CHF, diabetes, dehydration) | — |
| HAP/VAP — empiric regimens, no MRSA risk | - No MRSA risk factors
- treat MSSA empirically with any of the agents listed in Management
No MRSA risk factors; treat MSSA empirically with any of the agents listed in Management | - Base empiric choice on respiratory cultures and the ICU-specific hospital antibiogram
- procalcitonin/CRP can help decide when to stop, not when to start
Base empiric choice on respiratory cultures and the ICU-specific hospital antibiogram; procalcitonin/CRP can help decide when to stop, not when to start | - Piperacillin-tazobactam 4.5 g IV Q6h
- cefepime 2 g IV Q8h
- levofloxacin 750 mg IV/PO Q24h
- imipenem 500 mg IV Q6h
- meropenem 1 g IV Q8h
- ⭐ treat MSSA empirically with piperacillin-tazobactam, cefepime, levofloxacin, imipenem, or meropenem
Piperacillin-tazobactam 4.5 g IV Q6h; cefepime 2 g IV Q8h; levofloxacin 750 mg IV/PO Q24h; imipenem 500 mg IV Q6h; meropenem 1 g IV Q8h; ⭐ treat MSSA empirically with piperacillin-tazobactam, cefepime, levofloxacin, imipenem, or meropenem | - Procalcitonin or CRP should not be used to initiate therapy — clinical criteria guide that decision, though they can help decide when to stop
- MRSA nasal PCR screening to reduce overuse of empiric vancomycin (this row has no MRSA risk factors)
Procalcitonin or CRP should not be used to initiate therapy — clinical criteria guide that decision, though they can help decide when to stop; MRSA nasal PCR screening to reduce overuse of empiric vancomycin (this row has no MRSA risk factors) |
| MRSA pneumonia (CAP & HAP/VAP) | - HAP/VAP high-risk features: **history of MRSA
- recent hospitalisation in a unit where > 20% of S. aureus isolates are methicillin resistant
- IV antibiotics in the last 90 days
- or high mortality risk (multiorgan failure, mechanical ventilation)**
- VAP also adds septic shock, ARDS, hospital stay > 5 days, renal failure
HAP/VAP high-risk features: history of MRSA; recent hospitalisation in a unit where > 20% of S. aureus isolates are methicillin resistant; IV antibiotics in the last 90 days; or high mortality risk (multiorgan failure, mechanical ventilation); VAP also adds septic shock, ARDS, hospital stay > 5 days, renal failure | - Respiratory cultures preferred over empiric treatment
- MRSA nasal PCR screening reduces overuse of empiric vancomycin
Respiratory cultures preferred over empiric treatment; MRSA nasal PCR screening reduces overuse of empiric vancomycin | - ⭐ **CAP: vancomycin load 15–20 mg/kg/dose IV (max 2 g), then 15 mg/kg/dose Q8–12h if renal function > 90 mL/min, to reach target trough 15–20 mcg/mL
- check trough after every 3rd dose**
- CAP: linezolid 600 mg IV or PO Q12h (ESRD: no adjustment, but give after HD on dialysis days)
- ⭐ HAP/VAP: vancomycin load 25 mg/kg/dose IV (max 2 g), then 15 mg/kg/dose Q8–12h if renal function > 90 mL/min, target trough 15–20 mcg/mL
- HAP/VAP: linezolid 600 mg IV or PO Q12h
- consult a pharmacist for pharmacokinetic modeling
⭐ CAP: vancomycin load 15–20 mg/kg/dose IV (max 2 g), then 15 mg/kg/dose Q8–12h if renal function > 90 mL/min, to reach target trough 15–20 mcg/mL; check trough after every 3rd dose; CAP: linezolid 600 mg IV or PO Q12h (ESRD: no adjustment, but give after HD on dialysis days); ⭐ HAP/VAP: vancomycin load 25 mg/kg/dose IV (max 2 g), then 15 mg/kg/dose Q8–12h if renal function > 90 mL/min, target trough 15–20 mcg/mL; HAP/VAP: linezolid 600 mg IV or PO Q12h; consult a pharmacist for pharmacokinetic modeling | - Vancomycin — maintenance dosing of 15 mg/kg/dose Q8–12h only if renal function > 90 mL/min
- check a trough after every 3rd dose (target 15–20 mcg/mL) and consult a pharmacist for pharmacokinetic modeling to reach therapeutic levels and avoid toxicity
- linezolid — no adjustment in ESRD, but give after hemodialysis on dialysis days
Vancomycin — maintenance dosing of 15 mg/kg/dose Q8–12h only if renal function > 90 mL/min; check a trough after every 3rd dose (target 15–20 mcg/mL) and consult a pharmacist for pharmacokinetic modeling to reach therapeutic levels and avoid toxicity; linezolid — no adjustment in ESRD, but give after hemodialysis on dialysis days |
| Pseudomonas pneumonia (CAP & HAP/VAP) | - P. aeruginosa coverage
- HAP/VAP anti-pseudomonal coverage
- risk factors as for VAP
P. aeruginosa coverage; HAP/VAP anti-pseudomonal coverage; risk factors as for VAP | - Respiratory cultures preferred over empiric treatment
- hospital ICU antibiogram guides empiric coverage
Respiratory cultures preferred over empiric treatment; hospital ICU antibiogram guides empiric coverage | - **Piperacillin-tazobactam 4.5 g IV Q6h
- cefepime 2 g IV Q8h
- ceftazidime 2 g IV Q8h**
- **levofloxacin 750 mg IV/PO Q24h
- ciprofloxacin 400 mg IV Q8h**
- **imipenem 500 mg IV Q6h
- meropenem 1 g IV Q8h
- aztreonam 2 g IV Q8h**
- CAP options: piperacillin-tazobactam 4.5 g IV Q6h, cefepime 2 g IV Q8h, imipenem 500 mg IV Q6h, meropenem 1 g IV Q8h
- ⭐ **aminoglycosides — amikacin 15–20 mg/kg IV Q24h
- gentamicin 5–7 mg/kg IV Q24h
- tobramycin 5–7 mg/kg IV Q24h**
- use a second agent for Gram-negative anti-pseudomonal coverage only with history of MDR infection, severe critical illness (ARDS/pneumonia, septic shock), or severe immunocompromise
- ⭐ avoid dual β-lactams
- consult a pharmacist for pharmacokinetic modeling
Piperacillin-tazobactam 4.5 g IV Q6h; cefepime 2 g IV Q8h; ceftazidime 2 g IV Q8h; levofloxacin 750 mg IV/PO Q24h; ciprofloxacin 400 mg IV Q8h; imipenem 500 mg IV Q6h; meropenem 1 g IV Q8h; aztreonam 2 g IV Q8h; CAP options: piperacillin-tazobactam 4.5 g IV Q6h, cefepime 2 g IV Q8h, imipenem 500 mg IV Q6h, meropenem 1 g IV Q8h; ⭐ aminoglycosides — amikacin 15–20 mg/kg IV Q24h; gentamicin 5–7 mg/kg IV Q24h; tobramycin 5–7 mg/kg IV Q24h; use a second agent for Gram-negative anti-pseudomonal coverage only with history of MDR infection, severe critical illness (ARDS/pneumonia, septic shock), or severe immunocompromise; ⭐ avoid dual β-lactams; consult a pharmacist for pharmacokinetic modeling | - Avoid dual β-lactams
- use a second agent for Gram-negative anti-pseudomonal coverage only with a history of MDR infection, severe critical illness (ARDS/pneumonia, septic shock), or severe immunocompromise
- aminoglycosides — consult a pharmacist for pharmacokinetic modeling to reach therapeutic levels and avoid toxicity
Avoid dual β-lactams; use a second agent for Gram-negative anti-pseudomonal coverage only with a history of MDR infection, severe critical illness (ARDS/pneumonia, septic shock), or severe immunocompromise; aminoglycosides — consult a pharmacist for pharmacokinetic modeling to reach therapeutic levels and avoid toxicity |
| Influenza — antivirals | - Epidemic timing and viral respiratory infection are pneumonia risk factors
- severe disease may progress to pneumonia or ARDS
Epidemic timing and viral respiratory infection are pneumonia risk factors; severe disease may progress to pneumonia or ARDS | - ⭐ RT-PCR on a nasopharyngeal specimen has the highest sensitivity and specificity in the shortest time
⭐ RT-PCR on a nasopharyngeal specimen has the highest sensitivity and specificity in the shortest time | - ⭐ start within 48 hours
- oseltamivir 75 mg PO BID × 5 days
- zanamivir inhaled 10 mg BID × 5 days
- baloxavir 80 mg PO single dose if > 80 kg (40 mg if 40–79 kg)
- peramivir 600 mg IV × 1 dose
- consider longer treatment for immunocompromised patients or severe respiratory disease (ARDS, pneumonia)
- treat empirically for bacterial coinfection in severe disease
⭐ start within 48 hours; oseltamivir 75 mg PO BID × 5 days; zanamivir inhaled 10 mg BID × 5 days; baloxavir 80 mg PO single dose if > 80 kg (40 mg if 40–79 kg); peramivir 600 mg IV × 1 dose; consider longer treatment for immunocompromised patients or severe respiratory disease (ARDS, pneumonia); treat empirically for bacterial coinfection in severe disease | — |
| COPD exacerbation — antibiotics & steroids | - ⭐ give antibiotics only if exacerbation and/or acute infection is suspected — increased dyspnea, sputum production, sputum purulence, and increased coughing
- most common organisms: H. influenzae ≈ 45%, S. pneumoniae ≈ 30%, M. catarrhalis ≈ 20%, and E. coli/Klebsiella/Enterobacter/P. aeruginosa ≈ 5%
⭐ give antibiotics only if exacerbation and/or acute infection is suspected — increased dyspnea, sputum production, sputum purulence, and increased coughing; most common organisms: H. influenzae ≈ 45%, S. pneumoniae ≈ 30%, M. catarrhalis ≈ 20%, and E. coli/Klebsiella/Enterobacter/P. aeruginosa ≈ 5% | - Clinical criteria, not a laboratory test, drive the decision: increased dyspnea, sputum production, sputum purulence, increased coughing
Clinical criteria, not a laboratory test, drive the decision: increased dyspnea, sputum production, sputum purulence, increased coughing | - ⭐ first choice: amoxicillin-clavulanate or azithromycin
- hypersensitivity or resistance, including pseudomonas risk: a macrolide (azithromycin) or a respiratory fluoroquinolone (levofloxacin)
- ⭐ add concomitant oral corticosteroids (source states no steroid dose)
⭐ first choice: amoxicillin-clavulanate or azithromycin; hypersensitivity or resistance, including pseudomonas risk: a macrolide (azithromycin) or a respiratory fluoroquinolone (levofloxacin); ⭐ add concomitant oral corticosteroids (source states no steroid dose) | - Antibiotics only if exacerbation and/or acute infection is suspected (increased dyspnea, sputum production, sputum purulence, increased coughing) — otherwise not indicated
- hypersensitivity or resistance, including pseudomonas risk — do not use the first-choice agents
- use a macrolide (azithromycin) or a respiratory fluoroquinolone (levofloxacin)
Antibiotics only if exacerbation and/or acute infection is suspected (increased dyspnea, sputum production, sputum purulence, increased coughing) — otherwise not indicated; hypersensitivity or resistance, including pseudomonas risk — do not use the first-choice agents; use a macrolide (azithromycin) or a respiratory fluoroquinolone (levofloxacin) |
| TB — transmission, primary infection/LTBI & reactivation | - ⭐ **infectious droplet nuclei are inhaled through the respiratory tract
- bacteria are dispersed through coughing, sneezing, speaking, and singing**
- humans are the only known reservoir
- ⭐ **primary TB/LTBI — organisms enter the alveoli, become engulfed by macrophages, and spread via regional lymph nodes to the bloodstream
- patients are usually asymptomatic, but it may be progressive/fatal in immunocompromised hosts
- it may progress to active TB (5–10%)**
- ⭐ reactivation TB — LTBI becomes active TB, with systemic (15%) and pulmonary (85%) symptoms
- etiologic organism — Mycobacterium tuberculosis, a slow-growing, aerobic, acid-fast bacillus
- recent TB epidemics — HIV-infected patients, multidrug-resistant TB, and extensively drug-resistant TB (high mortality, few effective drugs)
⭐ infectious droplet nuclei are inhaled through the respiratory tract; bacteria are dispersed through coughing, sneezing, speaking, and singing; humans are the only known reservoir; ⭐ primary TB/LTBI — organisms enter the alveoli, become engulfed by macrophages, and spread via regional lymph nodes to the bloodstream; patients are usually asymptomatic, but it may be progressive/fatal in immunocompromised hosts; it may progress to active TB (5–10%); ⭐ reactivation TB — LTBI becomes active TB, with systemic (15%) and pulmonary (85%) symptoms; etiologic organism — Mycobacterium tuberculosis, a slow-growing, aerobic, acid-fast bacillus; recent TB epidemics — HIV-infected patients, multidrug-resistant TB, and extensively drug-resistant TB (high mortality, few effective drugs) | - ⭐ **a positive reaction to purified protein derivative (PPD) indicates past exposure or infection
- a negative PPD does not rule out active TB**
- **chest radiography is the most valuable test for active pulmonary TB, plus TB skin testing (PPD)
- diagnosis is difficult due to the variety of clinical presentations**
- **TB affects about one-third of the world's population
- an estimated 10–15 million people are infected in the US alone, with an increase in US foreign-born cases**
⭐ a positive reaction to purified protein derivative (PPD) indicates past exposure or infection; a negative PPD does not rule out active TB; chest radiography is the most valuable test for active pulmonary TB, plus TB skin testing (PPD); diagnosis is difficult due to the variety of clinical presentations; TB affects about one-third of the world's population; an estimated 10–15 million people are infected in the US alone, with an increase in US foreign-born cases | - **Isolate in negative pressure rooms with at least 6 air exchanges per hour
- place a mask on the patient to prevent respiratory spread
- providers should wear submicron particulate filter masks (N-95 designation)
- inform close contacts**
- ⭐ predisposing factors to elicit — HIV infection and other immunocompromised states (organ transplant, renal failure, diabetes), drug and alcohol abuse, poverty and homelessness (living in shelters), institutionalization (nursing homes, prisons), immigration from an endemic area, and a positive PPD test/previous infection
Isolate in negative pressure rooms with at least 6 air exchanges per hour; place a mask on the patient to prevent respiratory spread; providers should wear submicron particulate filter masks (N-95 designation); inform close contacts; ⭐ predisposing factors to elicit — HIV infection and other immunocompromised states (organ transplant, renal failure, diabetes), drug and alcohol abuse, poverty and homelessness (living in shelters), institutionalization (nursing homes, prisons), immigration from an endemic area, and a positive PPD test/previous infection | - Isolation is mandatory — patient isolation during initial evaluation and treatment, per OSHA standards, is not a judgment call
- isolate in negative pressure rooms with at least 6 air exchanges per hour
- place a mask on the patient to prevent respiratory spread and providers must wear submicron particulate filter masks (N-95 designation)
- inform close contacts
Isolation is mandatory — patient isolation during initial evaluation and treatment, per OSHA standards, is not a judgment call; isolate in negative pressure rooms with at least 6 air exchanges per hour; place a mask on the patient to prevent respiratory spread and providers must wear submicron particulate filter masks (N-95 designation); inform close contacts |
| TB — active disease: findings & isolation | - ⭐ most patients are asymptomatic
- fever
- cough generally productive of purulent sputum that may contain blood
- weight loss
- night sweats that may require changing the bed linen
- ⭐ pulmonary TB — cough, fever, night sweats, malaise, weight loss, hemoptysis, pleuritic chest pain, shortness of breath
- ⭐ **extrapulmonary TB — CNS infection (meningismus, cranial nerve defects, diplopia, headache, fever, malaise, confusion, acute ischemic stroke)
- pericarditis (pleuritic chest pain increased with recumbency)
- renal infection (fever, flank pain)
- spinal TB/Pott disease (back pain/stiffness, point tenderness, fever, decreased range of motion)
- cervical lymphadenitis/scrofula (unilateral, painless, may form draining sinus tracts)
- miliary TB (multiorgan system involvement, diffuse adenopathy, hepatomegaly)**
- exam: body temperature elevation, cachexia, tachycardia, hypoxia, abnormal breath sounds, cervical lymphadenopathy, rales over affected areas — apical posttussive rales for apical disease
⭐ most patients are asymptomatic; fever; cough generally productive of purulent sputum that may contain blood; weight loss; night sweats that may require changing the bed linen; ⭐ pulmonary TB — cough, fever, night sweats, malaise, weight loss, hemoptysis, pleuritic chest pain, shortness of breath; ⭐ extrapulmonary TB — CNS infection (meningismus, cranial nerve defects, diplopia, headache, fever, malaise, confusion, acute ischemic stroke); pericarditis (pleuritic chest pain increased with recumbency); renal infection (fever, flank pain); spinal TB/Pott disease (back pain/stiffness, point tenderness, fever, decreased range of motion); cervical lymphadenitis/scrofula (unilateral, painless, may form draining sinus tracts); miliary TB (multiorgan system involvement, diffuse adenopathy, hepatomegaly); exam: body temperature elevation, cachexia, tachycardia, hypoxia, abnormal breath sounds, cervical lymphadenopathy, rales over affected areas — apical posttussive rales for apical disease | - Normal CBC
- low serum cortisol if disseminated disease has destroyed the adrenal cortices
- acid-fast smears often positive — but treat empirically if findings suggest TB without a positive smear
- ⭐ culture usually positive within 6 weeks
- ⭐ **chest radiograph is the most valuable test for active pulmonary TB and may be normal — primary disease: parenchymal infiltrates with unilateral hilar adenopathy are the classic findings
- reactivation TB typically appears as cavitary lesions with or without calcification, usually in upper lung segments
- miliary TB shows bilateral disseminated 2-mm nodules throughout the lungs
- the chest radiograph may be nondefinitive in AIDS/immunocompromised patients
- unilateral pleural effusion in both primary and reactivation TB
- tracheal deviation with scarring or atelectasis
- Ghon focus (calcified scar/healed primary focus of infection)
- Ghon complex (primary infiltrate with associated unilateral hilar adenopathy)
- spine radiographs for Pott disease may be normal or show anterior wedging of 2 involved vertebral bodies and destruction of the disk
- CT chest better defines the extent of disease**
- chest X-ray: infiltrate especially in the upper lobes or the superior segments of the lower lobes (can appear anywhere) and cavity within the lungs
- ⭐ multidrug-resistant TB = resistance to isoniazid and rifampin
Normal CBC; low serum cortisol if disseminated disease has destroyed the adrenal cortices; acid-fast smears often positive — but treat empirically if findings suggest TB without a positive smear; ⭐ culture usually positive within 6 weeks; ⭐ chest radiograph is the most valuable test for active pulmonary TB and may be normal — primary disease: parenchymal infiltrates with unilateral hilar adenopathy are the classic findings; reactivation TB typically appears as cavitary lesions with or without calcification, usually in upper lung segments; miliary TB shows bilateral disseminated 2-mm nodules throughout the lungs; the chest radiograph may be nondefinitive in AIDS/immunocompromised patients; unilateral pleural effusion in both primary and reactivation TB; tracheal deviation with scarring or atelectasis; Ghon focus (calcified scar/healed primary focus of infection); Ghon complex (primary infiltrate with associated unilateral hilar adenopathy); spine radiographs for Pott disease may be normal or show anterior wedging of 2 involved vertebral bodies and destruction of the disk; CT chest better defines the extent of disease; chest X-ray: infiltrate especially in the upper lobes or the superior segments of the lower lobes (can appear anywhere) and cavity within the lungs; ⭐ multidrug-resistant TB = resistance to isoniazid and rifampin | - ⭐ **patient isolation during initial evaluation and treatment, according to OSHA standards, is mandatory — not a judgment call
- the lecture adds: isolate in negative pressure rooms with at least 6 air exchanges per hour
- place a mask on the patient to prevent respiratory spread
- providers should wear submicron particulate filter masks (N-95 designation)
- inform close contacts**
- rates of new infection are increasing especially among the homeless and those in crowded conditions (nursing homes, prisons), coinciding with more patients living with HIV and AIDS
- endotracheal intubation may be required in patients with severe hemoptysis or respiratory compromise
- differential diagnosis to consider — bacterial pneumonia, bronchiectasis, coccidiomycosis, histoplasmosis, lung abscess, lung carcinoma, lymphoma, Pneumocystis carinii pneumonia, pulmonary embolism, sarcoidosis
⭐ patient isolation during initial evaluation and treatment, according to OSHA standards, is mandatory — not a judgment call; the lecture adds: isolate in negative pressure rooms with at least 6 air exchanges per hour; place a mask on the patient to prevent respiratory spread; providers should wear submicron particulate filter masks (N-95 designation); inform close contacts; rates of new infection are increasing especially among the homeless and those in crowded conditions (nursing homes, prisons), coinciding with more patients living with HIV and AIDS; endotracheal intubation may be required in patients with severe hemoptysis or respiratory compromise; differential diagnosis to consider — bacterial pneumonia, bronchiectasis, coccidiomycosis, histoplasmosis, lung abscess, lung carcinoma, lymphoma, Pneumocystis carinii pneumonia, pulmonary embolism, sarcoidosis | - Isolation and strict respiratory precautions are mandatory
- do not wait for a positive smear — treat empirically if findings suggest TB without a positive smear
- the chest radiograph may be normal, and may be nondefinitive in AIDS/immunocompromised patients
- a negative PPD does not rule out active TB
Isolation and strict respiratory precautions are mandatory; do not wait for a positive smear — treat empirically if findings suggest TB without a positive smear; the chest radiograph may be normal, and may be nondefinitive in AIDS/immunocompromised patients; a negative PPD does not rule out active TB |
| TB — four-drug therapy: doses & toxicities | - Four-drug therapy is the backbone for suspected or active disease, or smear-positive disease pending culture return
- toxicities: isoniazid → peripheral neuropathy (prevented by pyridoxine, vitamin B6)
- **ethambutol → red/green color blindness and changes in visual acuity
- the lecture adds optic neuritis, so give a lower dose if renal function is impaired**
- rifampin — the lecture adds: warn patients that rifampin causes red coloration of body secretions, which is nothing to be alarmed about
- pyrazinamide — no toxicity stated in this source
Four-drug therapy is the backbone for suspected or active disease, or smear-positive disease pending culture return; toxicities: isoniazid → peripheral neuropathy (prevented by pyridoxine, vitamin B6); ethambutol → red/green color blindness and changes in visual acuity; the lecture adds optic neuritis, so give a lower dose if renal function is impaired; rifampin — the lecture adds: warn patients that rifampin causes red coloration of body secretions, which is nothing to be alarmed about; pyrazinamide — no toxicity stated in this source | - ⭐ precede ethambutol with screening of color vision
- modify the regimen if susceptibility studies show resistance to first-line drugs
- ⭐ if the isolate proves to be fully susceptible to INH and RIF, then ethambutol may be dropped
- ⭐ **toxicity monitoring and follow-up — sputum analysis periodically to document clearance
- INH, RIF and PZA: monitor liver function tests for hepatitis
- PZA: check uric acid levels
- ethambutol: eye testing for color blindness**
⭐ precede ethambutol with screening of color vision; modify the regimen if susceptibility studies show resistance to first-line drugs; ⭐ if the isolate proves to be fully susceptible to INH and RIF, then ethambutol may be dropped; ⭐ toxicity monitoring and follow-up — sputum analysis periodically to document clearance; INH, RIF and PZA: monitor liver function tests for hepatitis; PZA: check uric acid levels; ethambutol: eye testing for color blindness | - ⭐ isoniazid (INH) 300 mg PO daily — or 5 mg/kg, maximum 300 mg/day — given with pyridoxine 25–50 mg PO daily
- rifampin 600 mg PO each day — or 10 mg/kg daily, maximum 600 mg/dose
- ethambutol generally 15–25 mg/kg PO daily, maximum 2.5 g/dose (weight-based alternative per the drug-susceptible TB guidelines: 40–55 kg → 800 mg; 56–75 kg → 1200 mg; 76–90 kg → 1600 mg, all PO daily)
- pyrazinamide 15–30 mg/kg in 3 divided doses daily, maximum 2 g/dose (the lecture deck prints a maximum of 25 g/dose — inconsistent with the reading's 2 g/dose)
- ⭐ give steroids to decrease the risk of constrictive pericarditis
- ⭐ duration usually 6–9 months — 6 months for most patients, 9 months for HIV-positive patients and pregnant women
⭐ isoniazid (INH) 300 mg PO daily — or 5 mg/kg, maximum 300 mg/day — given with pyridoxine 25–50 mg PO daily; rifampin 600 mg PO each day — or 10 mg/kg daily, maximum 600 mg/dose; ethambutol generally 15–25 mg/kg PO daily, maximum 2.5 g/dose (weight-based alternative per the drug-susceptible TB guidelines: 40–55 kg → 800 mg; 56–75 kg → 1200 mg; 76–90 kg → 1600 mg, all PO daily); pyrazinamide 15–30 mg/kg in 3 divided doses daily, maximum 2 g/dose (the lecture deck prints a maximum of 25 g/dose — inconsistent with the reading's 2 g/dose); ⭐ give steroids to decrease the risk of constrictive pericarditis; ⭐ duration usually 6–9 months — 6 months for most patients, 9 months for HIV-positive patients and pregnant women | - Isoniazid (INH) — peripheral neuropathy, prevented by pyridoxine (vitamin B6)
- **ethambutol — red/green color blindness and changes in visual acuity
- precede with screening of color vision, and the lecture adds optic neuritis — give a lower dose if renal function is impaired**
- rifampin — warn patients that red coloration of body secretions occurs and is nothing to be alarmed about
- **monitor liver function tests for hepatitis on INH, RIF and PZA
- check uric acid on PZA
- eye testing for color blindness on ethambutol**
- modify the regimen if susceptibility studies show resistance to first-line drugs
- the pyrazinamide maximum dose is inconsistent between the sources (reading 2 g/dose vs lecture 25 g/dose) — the discrepancy is already flagged in this rundown
Isoniazid (INH) — peripheral neuropathy, prevented by pyridoxine (vitamin B6); ethambutol — red/green color blindness and changes in visual acuity; precede with screening of color vision, and the lecture adds optic neuritis — give a lower dose if renal function is impaired; rifampin — warn patients that red coloration of body secretions occurs and is nothing to be alarmed about; monitor liver function tests for hepatitis on INH, RIF and PZA; check uric acid on PZA; eye testing for color blindness on ethambutol; modify the regimen if susceptibility studies show resistance to first-line drugs; the pyrazinamide maximum dose is inconsistent between the sources (reading 2 g/dose vs lecture 25 g/dose) — the discrepancy is already flagged in this rundown |
| TB — regimen timeline & intermittent/DOT | - Intensive phase, then continuation
- ⭐ the standard course is 26 weeks
- HIV-positive patients and pregnant women extend the continuation phase
- ⭐ **therapy is continued usually for 6–9 months (6 months for most patients, 9 months for HIV-positive and/or immunocompromised patients)
- extend the treatment to a total of 9 months if miliary TB**
Intensive phase, then continuation; ⭐ the standard course is 26 weeks; HIV-positive patients and pregnant women extend the continuation phase; ⭐ therapy is continued usually for 6–9 months (6 months for most patients, 9 months for HIV-positive and/or immunocompromised patients); extend the treatment to a total of 9 months if miliary TB | - ⭐ advanced HIV (CD4 < 100/mcL) — treat with daily or three-times-weekly therapy in both the initial and continuation phases
⭐ advanced HIV (CD4 < 100/mcL) — treat with daily or three-times-weekly therapy in both the initial and continuation phases | - ⭐ standard: INH + RIF + PZA + EMB daily for 56 doses (8 weeks), then INH + RIF for 126 doses (18 weeks)
- HIV-positive/pregnant: intensive phase 8 weeks daily or three times weekly, continuation phase extended to 9 months total
- also acceptable: 3-times-weekly dosing — 24 doses (8 wk) then 54 doses (18 wk)
- other accepted intermittent regimens: INH + RIF + PZA + EMB daily 8 weeks then INH + RIF 3 times weekly for 16 weeks (especially if susceptibility to INH/rifampin is noted)
- INH + RIF + PZA + EMB daily 2 weeks then the same agents 2 times weekly for 6 weeks then INH + RIF 2 times weekly for 16 weeks (if susceptible)
- thrice-weekly INH + RIF + PZA + EMB for 24 doses (8 weeks) then thrice-weekly INH + RIF for 54 doses (18 weeks)
- for nonadherent patients, directly observed treatment may be initiated at 3 times per week, usually after 2 weeks of observed therapy — often in hospital
⭐ standard: INH + RIF + PZA + EMB daily for 56 doses (8 weeks), then INH + RIF for 126 doses (18 weeks); HIV-positive/pregnant: intensive phase 8 weeks daily or three times weekly, continuation phase extended to 9 months total; also acceptable: 3-times-weekly dosing — 24 doses (8 wk) then 54 doses (18 wk); other accepted intermittent regimens: INH + RIF + PZA + EMB daily 8 weeks then INH + RIF 3 times weekly for 16 weeks (especially if susceptibility to INH/rifampin is noted); INH + RIF + PZA + EMB daily 2 weeks then the same agents 2 times weekly for 6 weeks then INH + RIF 2 times weekly for 16 weeks (if susceptible); thrice-weekly INH + RIF + PZA + EMB for 24 doses (8 weeks) then thrice-weekly INH + RIF for 54 doses (18 weeks); for nonadherent patients, directly observed treatment may be initiated at 3 times per week, usually after 2 weeks of observed therapy — often in hospital | - Any regimen must contain at least 2 drugs to which the TB bacillus is susceptible — the CDC recommends initial therapy that includes 4 first-line drugs
- consult infectious disease specialists when treating HIV patients on antiretroviral therapies
- do not shorten therapy in HIV-positive, immunocompromised or pregnant patients — extend the continuation phase to 9 months total (extend to a total of 9 months if miliary TB)
- advanced HIV (CD4 < 100/mcL) — treat with daily or three-times-weekly therapy in both the initial and continuation phases
- nonadherent patients — directly observed treatment may be necessary (nonadherent active TB patients are considered a public health hazard, with specific state laws)
Any regimen must contain at least 2 drugs to which the TB bacillus is susceptible — the CDC recommends initial therapy that includes 4 first-line drugs; consult infectious disease specialists when treating HIV patients on antiretroviral therapies; do not shorten therapy in HIV-positive, immunocompromised or pregnant patients — extend the continuation phase to 9 months total (extend to a total of 9 months if miliary TB); advanced HIV (CD4 < 100/mcL) — treat with daily or three-times-weekly therapy in both the initial and continuation phases; nonadherent patients — directly observed treatment may be necessary (nonadherent active TB patients are considered a public health hazard, with specific state laws) |
| Latent TB infection — prophylaxis | - ⭐ consider for asymptomatic, positive PPD, normal chest X-ray
- exposed to active TB with a negative PPD
- undergoing immunosuppressive therapy for other reasons
- HIV infected
⭐ consider for asymptomatic, positive PPD, normal chest X-ray; exposed to active TB with a negative PPD; undergoing immunosuppressive therapy for other reasons; HIV infected | - Positive PPD with a normal chest X-ray
- ⭐ a positive PPD indicates exposure, not necessarily active infection
- QuantiFERON TB Gold may be used instead of the PPD
Positive PPD with a normal chest X-ray; ⭐ a positive PPD indicates exposure, not necessarily active infection; QuantiFERON TB Gold may be used instead of the PPD | - ⭐ isoniazid 300 mg PO daily
- controversy exists over 6 months versus up to 1 year, but the standard regimen is 9 months — also the preferred duration for HIV-positive patients and pregnant women
- ⭐ the lecture's alternative — LTBI with a normal chest radiograph may be given isoniazid for 9 months OR a weekly combination of INH and rifapentine (RPT) for 12 weeks
- pyridoxine 25–50 mg PO daily (the lecture prints 50 mg PO daily) may be given during INH therapy to prevent neuropathy
⭐ isoniazid 300 mg PO daily; controversy exists over 6 months versus up to 1 year, but the standard regimen is 9 months — also the preferred duration for HIV-positive patients and pregnant women; ⭐ the lecture's alternative — LTBI with a normal chest radiograph may be given isoniazid for 9 months OR a weekly combination of INH and rifapentine (RPT) for 12 weeks; pyridoxine 25–50 mg PO daily (the lecture prints 50 mg PO daily) may be given during INH therapy to prevent neuropathy | - Latent TB prophylaxis is not for active disease — consider it only for the asymptomatic patient with a positive PPD and a normal chest X-ray, exposure to active TB with a negative PPD, immunosuppressive therapy for other reasons, or HIV infection
- a positive PPD indicates exposure, not necessarily active infection
- INH is always given with pyridoxine (B6) to prevent peripheral neuropathy
Latent TB prophylaxis is not for active disease — consider it only for the asymptomatic patient with a positive PPD and a normal chest X-ray, exposure to active TB with a negative PPD, immunosuppressive therapy for other reasons, or HIV infection; a positive PPD indicates exposure, not necessarily active infection; INH is always given with pyridoxine (B6) to prevent peripheral neuropathy |
| PPD interpretation thresholds & QuantiFERON | - Read 48 hours after intradermal injection of 0.1 mL purified protein derivative (the lecture: inject 0.1 mL of PPD intradermally in the forearm; results are read between 48 and 72 hr after administration)
- ⭐ measure the indurated area — the largest diameter, not including flat erythema
- ⭐ a positive PPD indicates prior or current infection with M. tuberculosis (past exposure, not necessarily active infection), and a negative PPD does not rule out active TB
Read 48 hours after intradermal injection of 0.1 mL purified protein derivative (the lecture: inject 0.1 mL of PPD intradermally in the forearm; results are read between 48 and 72 hr after administration); ⭐ measure the indurated area — the largest diameter, not including flat erythema; ⭐ a positive PPD indicates prior or current infection with M. tuberculosis (past exposure, not necessarily active infection), and a negative PPD does not rule out active TB | - ⭐ ≥ 5 mm — positive in HIV-infected patients, recent TB exposure, immunocompromised patients, or a chest film typical for TB
- ⭐ ≥ 10 mm — positive in health care workers, HIV-negative injection drug users, residents of nursing homes or homeless shelters, recent immigrants
- ⭐ ≥ 15 mm — positive in any person
- anything under 5 mm is a negative test
- ⭐ **lecture's > 5 mm group — close contacts with TB patients
- positive chest radiographs for TB
- HIV-positive
- organ transplant or other immunosuppression**
- ⭐ **lecture's > 10 mm group — IV drug users
- immigrants from high-prevalence countries (within 5 yr)
- underlying disease (diabetes, renal failure, malignancies)
- healthcare workers
- prison inmates
- institutionalized (nursing home, homeless shelters)**
- ⭐ lecture's > 15 mm group — low-risk individuals
- **QuantiFERON TB Gold — a serum test used for diagnosis of TB, either latent or active, instead of the PPD
- its advantage is that it is not affected by prior bacille Calmette-Guérin vaccination**
⭐ ≥ 5 mm — positive in HIV-infected patients, recent TB exposure, immunocompromised patients, or a chest film typical for TB; ⭐ ≥ 10 mm — positive in health care workers, HIV-negative injection drug users, residents of nursing homes or homeless shelters, recent immigrants; ⭐ ≥ 15 mm — positive in any person; anything under 5 mm is a negative test; ⭐ lecture's > 5 mm group — close contacts with TB patients; positive chest radiographs for TB; HIV-positive; organ transplant or other immunosuppression; ⭐ lecture's > 10 mm group — IV drug users; immigrants from high-prevalence countries (within 5 yr); underlying disease (diabetes, renal failure, malignancies); healthcare workers; prison inmates; institutionalized (nursing home, homeless shelters); ⭐ lecture's > 15 mm group — low-risk individuals; QuantiFERON TB Gold — a serum test used for diagnosis of TB, either latent or active, instead of the PPD; its advantage is that it is not affected by prior bacille Calmette-Guérin vaccination | - ⭐ the cut-off that counts as positive drops as the patient's risk rises (5 / 10 / 15 mm)
- the test is read at 48 hours
⭐ the cut-off that counts as positive drops as the patient's risk rises (5 / 10 / 15 mm); the test is read at 48 hours | - Measure the indurated area — the largest diameter, not flat erythema
- anything under 5 mm is a negative test
- a negative PPD does not rule out active TB
- a positive PPD indicates exposure, not necessarily active infection
Measure the indurated area — the largest diameter, not flat erythema; anything under 5 mm is a negative test; a negative PPD does not rule out active TB; a positive PPD indicates exposure, not necessarily active infection |
| ARDS / acute lung injury — thresholds & etiologies | - ⭐ refractory hypoxemia is the classic finding
- ⭐ the two most common precipitants are pneumonia and sepsis
- also massive trauma or injury (including burns and smoke inhalation), increased intracranial pressure especially after trauma or intracranial bleeding, pancreatitis, shock of any cause, cardiopulmonary bypass, aspiration of fluid (gastrointestinal contents, near drowning), bacteremia and other severe systemic infections
- overall mortality remains nearly 40%
- severe respiratory distress occurring during the course of one of the inciting events
- breathlessness, agitation, confusion, obtundation
- other organ failure — kidneys, liver, bone marrow (reduced platelets), multisystem organ failure
- ⭐ lungs often sound clearer than the chest X-ray would suggest
⭐ refractory hypoxemia is the classic finding; ⭐ the two most common precipitants are pneumonia and sepsis; also massive trauma or injury (including burns and smoke inhalation), increased intracranial pressure especially after trauma or intracranial bleeding, pancreatitis, shock of any cause, cardiopulmonary bypass, aspiration of fluid (gastrointestinal contents, near drowning), bacteremia and other severe systemic infections; overall mortality remains nearly 40%; severe respiratory distress occurring during the course of one of the inciting events; breathlessness, agitation, confusion, obtundation; other organ failure — kidneys, liver, bone marrow (reduced platelets), multisystem organ failure; ⭐ lungs often sound clearer than the chest X-ray would suggest | - ⭐ **PaO₂/FiO₂ greater than 300 — does not meet criteria for ALI or ARDS
- less than 300 — acute lung injury (ALI)
- less than 200 — ARDS**
- chest X-ray often shows evolving bilateral infiltrates ("whited out")
- CT chest shows the heterogeneous nature of the opacities
- ABG with PaO₂/FiO₂ ratio
- CBC with differential and platelet count
- coagulation studies — PT, PTT, fibrinogen, fibrin degradation products
- renal and liver function
- urinalysis
- blood and urine cultures, sputum culture and Gram stain
⭐ PaO₂/FiO₂ greater than 300 — does not meet criteria for ALI or ARDS; less than 300 — acute lung injury (ALI); less than 200 — ARDS; chest X-ray often shows evolving bilateral infiltrates ("whited out"); CT chest shows the heterogeneous nature of the opacities; ABG with PaO₂/FiO₂ ratio; CBC with differential and platelet count; coagulation studies — PT, PTT, fibrinogen, fibrin degradation products; renal and liver function; urinalysis; blood and urine cultures, sputum culture and Gram stain | - ⭐ first priority: identification and prompt treatment of the underlying cause
- in sepsis-associated ARDS, good outcomes require early resuscitation, appropriate antibiotics, and source control
- intubate if ventilation is significantly compromised — especially with altered mentation
- mechanical ventilation if work of breathing not met (patient fatigue, elevated PaCO₂) or if hypoxemia is not correctable with an FiO₂ of 0.5
- vigorous fluid resuscitation if hypotension is present, regulated by hemodynamic parameters especially left ventricular ejection fraction
⭐ first priority: identification and prompt treatment of the underlying cause; in sepsis-associated ARDS, good outcomes require early resuscitation, appropriate antibiotics, and source control; intubate if ventilation is significantly compromised — especially with altered mentation; mechanical ventilation if work of breathing not met (patient fatigue, elevated PaCO₂) or if hypoxemia is not correctable with an FiO₂ of 0.5; vigorous fluid resuscitation if hypotension is present, regulated by hemodynamic parameters especially left ventricular ejection fraction | - PaO₂/FiO₂ greater than 300 does not meet criteria for ALI or ARDS — do not label it ALI/ARDS
PaO₂/FiO₂ greater than 300 does not meet criteria for ALI or ARDS — do not label it ALI/ARDS |
| ARDS — ventilation, barotrauma & support | - ⭐ barotrauma is the trap — the risk of pneumothorax or pneumomediastinum is high with ARDS
- ⭐ sudden increases in ventilating pressure with desaturation indicate the need for an immediate repeat chest X-ray and possible chest tube insertion
- repeated physical and radiographic assessment may be needed to rule out barotrauma
⭐ barotrauma is the trap — the risk of pneumothorax or pneumomediastinum is high with ARDS; ⭐ sudden increases in ventilating pressure with desaturation indicate the need for an immediate repeat chest X-ray and possible chest tube insertion; repeated physical and radiographic assessment may be needed to rule out barotrauma | - Monitor peak and plateau pressures to prevent barotrauma
- ⭐ persistent breath-to-breath peak pressures greater than 45 cm H₂O are a risk factor
- immediate repeat chest X-ray if pressure rises with desaturation
Monitor peak and plateau pressures to prevent barotrauma; ⭐ persistent breath-to-breath peak pressures greater than 45 cm H₂O are a risk factor; immediate repeat chest X-ray if pressure rises with desaturation | - Mechanical ventilation often requires positive end-expiratory pressure (PEEP)
- to prevent barotrauma: ⭐ reduced tidal volumes — typically 6 mL/kg, pressure-cycled ventilation, and in severe ARDS high-frequency oscillatory ventilation may be the only way to oxygenate and ventilate
- permissive hypercapnia, with bicarbonate repletion to avoid excessive acidosis
- the patient should be sedated for comfort
- ⭐ **nutritional support started early — use the enteral route (TPN with caution if enteral is unavailable)
- most patients require nearly twice their usual daily caloric requirements**
Mechanical ventilation often requires positive end-expiratory pressure (PEEP); to prevent barotrauma: ⭐ reduced tidal volumes — typically 6 mL/kg, pressure-cycled ventilation, and in severe ARDS high-frequency oscillatory ventilation may be the only way to oxygenate and ventilate; permissive hypercapnia, with bicarbonate repletion to avoid excessive acidosis; the patient should be sedated for comfort; ⭐ nutritional support started early — use the enteral route (TPN with caution if enteral is unavailable); most patients require nearly twice their usual daily caloric requirements | - Avoid high ventilating pressures — persistent breath-to-breath peak pressures greater than 45 cm H₂O are a risk factor for barotrauma
- reduce tidal volumes — typically 6 mL/kg to prevent barotrauma
- TPN with caution if the enteral route is unavailable
- permissive hypercapnia with bicarbonate repletion to avoid excessive acidosis
Avoid high ventilating pressures — persistent breath-to-breath peak pressures greater than 45 cm H₂O are a risk factor for barotrauma; reduce tidal volumes — typically 6 mL/kg to prevent barotrauma; TPN with caution if the enteral route is unavailable; permissive hypercapnia with bicarbonate repletion to avoid excessive acidosis |
| Idiopathic pulmonary fibrosis (IPF) | - ⭐ **etiology unknown
- strongly linked to cigarette smoking**
- the most common cause of interstitial lung disease among elderly patients, and more common in men
- symptoms: progressive dyspnea (slow or rapid) and nonproductive cough
- ⭐ "Velcro crackles" on auscultation (shared interstitial signature with restrictive defect and reduced diffusing capacity)
⭐ etiology unknown; strongly linked to cigarette smoking; the most common cause of interstitial lung disease among elderly patients, and more common in men; symptoms: progressive dyspnea (slow or rapid) and nonproductive cough; ⭐ "Velcro crackles" on auscultation (shared interstitial signature with restrictive defect and reduced diffusing capacity) | - CXR and high-resolution CT — interstitial infiltrates, nodules, cystic ("honeycombing") changes, especially in the lower lobes
- PFTs — **restrictive ventilatory defect
- DLCO commonly reduced**
- ABG and pulse oximetry — hypoxemia as disease progresses
- CO₂ retention indicates severe disease
- tissue — **fiber-optic bronchoscopy with transbronchial biopsy first
- bronchoalveolar lavage at the same time
- thoracoscopic lung biopsy if more assurance is needed**
- PPD testing should be done
- complement fixation serology for deep fungi (histoplasmosis, coccidioidomycosis, blastomycosis)
- rule out before treating — inhalation exposure (inorganic dusts silica/asbestos; organic dusts from silos = hypersensitivity pneumonia; fumes chlorine/sulfur dioxide), drugs (chemotherapeutic agents bleomycin; antibiotics nitrofurantoin, sulfa; gold salts; amiodarone), autoimmune disorders, chronic lung infection (tuberculosis, deep fungal infection), radiation to lung parenchyma, and in prior malignancy exclude lymphangitic spread of tumor
CXR and high-resolution CT — interstitial infiltrates, nodules, cystic ("honeycombing") changes, especially in the lower lobes; PFTs — restrictive ventilatory defect; DLCO commonly reduced; ABG and pulse oximetry — hypoxemia as disease progresses; CO₂ retention indicates severe disease; tissue — fiber-optic bronchoscopy with transbronchial biopsy first; bronchoalveolar lavage at the same time; thoracoscopic lung biopsy if more assurance is needed; PPD testing should be done; complement fixation serology for deep fungi (histoplasmosis, coccidioidomycosis, blastomycosis); rule out before treating — inhalation exposure (inorganic dusts silica/asbestos; organic dusts from silos = hypersensitivity pneumonia; fumes chlorine/sulfur dioxide), drugs (chemotherapeutic agents bleomycin; antibiotics nitrofurantoin, sulfa; gold salts; amiodarone), autoimmune disorders, chronic lung infection (tuberculosis, deep fungal infection), radiation to lung parenchyma, and in prior malignancy exclude lymphangitic spread of tumor | - ⭐ IPF has no cure — no procedure or medication can remove the scarring
- pirfenidone (Esbriet) and nintedanib (Ofev) slow progression
- oxygen support to maximise blood oxygen levels
- lung rehabilitation to help exercise with less dyspnea
- noninvasive positive airway pressure by mask may benefit selected patients
- lung transplant for advanced disease
- prognosis is often poor — counsel on palliative care and end-of-life issues
- ⭐ vaccinate IPF patients against influenza and pneumococcus — these infections are poorly tolerated
⭐ IPF has no cure — no procedure or medication can remove the scarring; pirfenidone (Esbriet) and nintedanib (Ofev) slow progression; oxygen support to maximise blood oxygen levels; lung rehabilitation to help exercise with less dyspnea; noninvasive positive airway pressure by mask may benefit selected patients; lung transplant for advanced disease; prognosis is often poor — counsel on palliative care and end-of-life issues; ⭐ vaccinate IPF patients against influenza and pneumococcus — these infections are poorly tolerated | - Rule these out before treating — inhalation exposure (inorganic dusts silica/asbestos; organic silo dusts; fumes chlorine/sulfur dioxide), drugs (bleomycin; nitrofurantoin, sulfa; gold salts; amiodarone), autoimmune disorders, chronic lung infection (tuberculosis, deep fungal infection), radiation to lung parenchyma, and lymphangitic spread of tumor in prior malignancy
- IPF has no cure — no procedure or medication can remove the scarring
- PPD testing should be done to exclude TB
Rule these out before treating — inhalation exposure (inorganic dusts silica/asbestos; organic silo dusts; fumes chlorine/sulfur dioxide), drugs (bleomycin; nitrofurantoin, sulfa; gold salts; amiodarone), autoimmune disorders, chronic lung infection (tuberculosis, deep fungal infection), radiation to lung parenchyma, and lymphangitic spread of tumor in prior malignancy; IPF has no cure — no procedure or medication can remove the scarring; PPD testing should be done to exclude TB |
| Sarcoidosis — features, the 5 stages & treatment | - ⭐ characterised pathologically by noncaseating granulomas and interstitial lung disease, with systemic manifestations: lymphadenopathy, cardiac involvement, iritis, cutaneous lesions, arthritis, GI involvement
- more common among females, North Americans, African Americans, and northern European Caucasians
- typical onset ages 20–40
- "Velcro crackles" and a restrictive defect with reduced DLCO
⭐ characterised pathologically by noncaseating granulomas and interstitial lung disease, with systemic manifestations: lymphadenopathy, cardiac involvement, iritis, cutaneous lesions, arthritis, GI involvement; more common among females, North Americans, African Americans, and northern European Caucasians; typical onset ages 20–40; "Velcro crackles" and a restrictive defect with reduced DLCO | - ⭐ **Stage 0 — normal chest X-ray
- Stage I — bilateral hilar lymphadenopathy (BHL)
- Stage II — BHL plus pulmonary infiltrates
- Stage III — pulmonary infiltrates without BHL
- Stage IV — pulmonary fibrosis**
- interstitial infiltrates, nodules, cystic ("honeycombing") changes on CXR and HRCT, especially lower lobes
- PFTs restrictive with reduced DLCO
- sarcoidosis is associated with hypercalcemia — check calcium
- ⭐ **blood panel: CBC, calcium, LFTs, BUN, creatinine
- plus EKG, urinalysis, PPD, ophthalmologic exam**
⭐ Stage 0 — normal chest X-ray; Stage I — bilateral hilar lymphadenopathy (BHL); Stage II — BHL plus pulmonary infiltrates; Stage III — pulmonary infiltrates without BHL; Stage IV — pulmonary fibrosis; interstitial infiltrates, nodules, cystic ("honeycombing") changes on CXR and HRCT, especially lower lobes; PFTs restrictive with reduced DLCO; sarcoidosis is associated with hypercalcemia — check calcium; ⭐ blood panel: CBC, calcium, LFTs, BUN, creatinine; plus EKG, urinalysis, PPD, ophthalmologic exam | - ⭐ **no cure
- treatment based on symptoms and severity of organ involvement**
- refer to specialists for the organs involved
- ⭐ alternatives are indicated only when sarcoidosis does not respond to oral corticosteroids, when there is intolerance or contraindication, or when the steroid dose must be reduced
- options: methotrexate, hydroxychloroquine, azathioprine, cyclophosphamide, infliximab, adalimumab, leflunomide
⭐ no cure; treatment based on symptoms and severity of organ involvement; refer to specialists for the organs involved; ⭐ alternatives are indicated only when sarcoidosis does not respond to oral corticosteroids, when there is intolerance or contraindication, or when the steroid dose must be reduced; options: methotrexate, hydroxychloroquine, azathioprine, cyclophosphamide, infliximab, adalimumab, leflunomide | - Rule these out before treating — inhalation exposure, drugs (bleomycin; nitrofurantoin, sulfa; gold salts; amiodarone), autoimmune disorders, chronic lung infection (TB, deep fungal infection), radiation to lung parenchyma, and lymphangitic spread of tumor in prior malignancy
- no cure
- alternatives are indicated only when sarcoidosis does not respond to oral corticosteroids, when there is intolerance or contraindication, or when the steroid dose must be reduced — methotrexate, hydroxychloroquine, azathioprine, cyclophosphamide, infliximab, adalimumab and leflunomide are not first-line
Rule these out before treating — inhalation exposure, drugs (bleomycin; nitrofurantoin, sulfa; gold salts; amiodarone), autoimmune disorders, chronic lung infection (TB, deep fungal infection), radiation to lung parenchyma, and lymphangitic spread of tumor in prior malignancy; no cure; alternatives are indicated only when sarcoidosis does not respond to oral corticosteroids, when there is intolerance or contraindication, or when the steroid dose must be reduced — methotrexate, hydroxychloroquine, azathioprine, cyclophosphamide, infliximab, adalimumab and leflunomide are not first-line |
| Cardiogenic pulmonary edema — presentation & workup | - ⭐ most common driver is ischemia — coronary artery disease with myocardial ischemia and infarction, aggravated by obesity, limited exercise, dyslipidemia, and cigarette smoking
- also arrhythmias (tachycardia especially, and bradycardia), hypertension, valvular dysfunction, thyroid dysfunction (hyper- or hypothyroidism), diabetes mellitus, viral myocarditis, idiopathic cardiomyopathy, renal failure, drug therapy (especially certain chemotherapeutic agents)
- progression: ⭐ exertional dyspnea → orthopnea → paroxysmal nocturnal dyspnea
- frank respiratory failure may follow
- a dry cough is common
- exam: edema and jugular venous distention, rales, tachycardia or bradycardia, inability to tolerate lying flat (orthopnea), tachypnea, pleural effusions, ascites when CHF is advanced
- **NYHA 1 — no limitations from ordinary activities
- NYHA 2 — slight limitations with moderate exertion
- NYHA 3 — marked limitation with activity, comfortable only at rest
- NYHA 4 — symptoms with any activity and occasionally at rest, patient should be on complete rest**
⭐ most common driver is ischemia — coronary artery disease with myocardial ischemia and infarction, aggravated by obesity, limited exercise, dyslipidemia, and cigarette smoking; also arrhythmias (tachycardia especially, and bradycardia), hypertension, valvular dysfunction, thyroid dysfunction (hyper- or hypothyroidism), diabetes mellitus, viral myocarditis, idiopathic cardiomyopathy, renal failure, drug therapy (especially certain chemotherapeutic agents); progression: ⭐ exertional dyspnea → orthopnea → paroxysmal nocturnal dyspnea; frank respiratory failure may follow; a dry cough is common; exam: edema and jugular venous distention, rales, tachycardia or bradycardia, inability to tolerate lying flat (orthopnea), tachypnea, pleural effusions, ascites when CHF is advanced; NYHA 1 — no limitations from ordinary activities; NYHA 2 — slight limitations with moderate exertion; NYHA 3 — marked limitation with activity, comfortable only at rest; NYHA 4 — symptoms with any activity and occasionally at rest, patient should be on complete rest | - CXR: ⭐ vascular redistribution to upper lung fields, interstitial edema, Kerley B lines, pleural effusions (usually bilateral or on the right), cardiomegaly
- EKG to assess ischemia/infarction and determine rhythm
- ABG and pulse oximetry to ensure adequate oxygenation and assess CO₂ retention
- CBC to rule out anemia
- TSH (if abnormal, check free T3/T4 to separate true disease from euthyroid sick state), BUN, creatinine, liver function, electrolytes including magnesium
- cardiac enzymes especially if recent MI or unstable angina suspected
- echocardiography — systolic function (rate of demise matters more than the actual ejection fraction), valvular function, global and segmental dyskinesia, diastology, right heart pressures to detect pulmonary hypertension
- pulmonary function studies — not useful during acute pulmonary edema, but when stable they demonstrate a restrictive defect (reduced vital capacity) and evaluate coexisting COPD
- ⭐ **PA catheterization — occasionally needed to document severity, especially with hypotension
- in general, insertion is not necessary in treating CHF**
- the PA catheter caveat: **when hypotension is present, aggressive fluid therapy could further aggravate CHF
- catheterization can determine cardiac output, cardiac index, systemic vascular resistance, and pulmonary capillary wedge pressure — but it is not routine**
- guide fluid administration with bedside ultrasound measurement of the inferior vena cava (IVC) plus clinical indicators of volume status
CXR: ⭐ vascular redistribution to upper lung fields, interstitial edema, Kerley B lines, pleural effusions (usually bilateral or on the right), cardiomegaly; EKG to assess ischemia/infarction and determine rhythm; ABG and pulse oximetry to ensure adequate oxygenation and assess CO₂ retention; CBC to rule out anemia; TSH (if abnormal, check free T3/T4 to separate true disease from euthyroid sick state), BUN, creatinine, liver function, electrolytes including magnesium; cardiac enzymes especially if recent MI or unstable angina suspected; echocardiography — systolic function (rate of demise matters more than the actual ejection fraction), valvular function, global and segmental dyskinesia, diastology, right heart pressures to detect pulmonary hypertension; pulmonary function studies — not useful during acute pulmonary edema, but when stable they demonstrate a restrictive defect (reduced vital capacity) and evaluate coexisting COPD; ⭐ PA catheterization — occasionally needed to document severity, especially with hypotension; in general, insertion is not necessary in treating CHF; the PA catheter caveat: when hypotension is present, aggressive fluid therapy could further aggravate CHF; catheterization can determine cardiac output, cardiac index, systemic vascular resistance, and pulmonary capillary wedge pressure — but it is not routine; guide fluid administration with bedside ultrasound measurement of the inferior vena cava (IVC) plus clinical indicators of volume status | - Correct the cause of the CHF if known, especially ischemia
- oxygen usually via nasal cannula at low flow rates (e.g., 2 L/min)
- in frank pulmonary edema give oxygen in higher amounts — use mask delivery PRN
Correct the cause of the CHF if known, especially ischemia; oxygen usually via nasal cannula at low flow rates (e.g., 2 L/min); in frank pulmonary edema give oxygen in higher amounts — use mask delivery PRN | - Pulmonary function studies are not useful during acute pulmonary edema (only when stable)
- pulmonary artery catheterization — insertion is not necessary in treating CHF and is not routine
- when hypotension is present, aggressive fluid therapy could further aggravate CHF
Pulmonary function studies are not useful during acute pulmonary edema (only when stable); pulmonary artery catheterization — insertion is not necessary in treating CHF and is not routine; when hypotension is present, aggressive fluid therapy could further aggravate CHF |
| Cardiogenic pulmonary edema — treatment | - Nitrates may be indicated — but may or may not be appropriate depending on the cause (e.g., arrhythmia, valvular heart disease)
- if the patient has chest pain, morphine may be used as well
Nitrates may be indicated — but may or may not be appropriate depending on the cause (e.g., arrhythmia, valvular heart disease); if the patient has chest pain, morphine may be used as well | - Correct the cause of the CHF if known, especially ischemia
- guide fluid administration with bedside ultrasound IVC measurement and clinical indicators of volume status
Correct the cause of the CHF if known, especially ischemia; guide fluid administration with bedside ultrasound IVC measurement and clinical indicators of volume status | - Sublingual or intravenous nitroglycerin
- nitroglycerin patches such as Nitro-Dur 0.4 mg, applied daily
- oral, long-acting nitrates such as isosorbide
- ⭐ if the patient cannot sustain the work of breathing during an acute episode, attempt noninvasive positive pressure ventilation via CPAP, followed by intubation and mechanical ventilation if necessary — this redistributes edema out of the lungs and back into the vascular space and offloads the work of breathing
- eliminate cardiac depressants — nondihydropyridine calcium channel blockers (diltiazem, verapamil)
- remove β-blockers for acute decompensation and resume when clinically stable
- ⭐ **inotropic support in acute decompensation — dobutamine and milrinone
- inotropes should only be started when there is hypotension AND evidence of reduced organ perfusion, and in those cases dobutamine is usually first-line**
- decrease afterload with an ACE inhibitor or angiotensin II receptor blocker (ARB) as blood pressure tolerates
- decrease preload with appropriate diuretics
- β-adrenergic antagonists to help regulate catecholamines if blood pressure and heart rate will tolerate
- aggressiveness must be proportionate to the severity of interstitial edema and respiratory distress
Sublingual or intravenous nitroglycerin; nitroglycerin patches such as Nitro-Dur 0.4 mg, applied daily; oral, long-acting nitrates such as isosorbide; ⭐ if the patient cannot sustain the work of breathing during an acute episode, attempt noninvasive positive pressure ventilation via CPAP, followed by intubation and mechanical ventilation if necessary — this redistributes edema out of the lungs and back into the vascular space and offloads the work of breathing; eliminate cardiac depressants — nondihydropyridine calcium channel blockers (diltiazem, verapamil); remove β-blockers for acute decompensation and resume when clinically stable; ⭐ inotropic support in acute decompensation — dobutamine and milrinone; inotropes should only be started when there is hypotension AND evidence of reduced organ perfusion, and in those cases dobutamine is usually first-line; decrease afterload with an ACE inhibitor or angiotensin II receptor blocker (ARB) as blood pressure tolerates; decrease preload with appropriate diuretics; β-adrenergic antagonists to help regulate catecholamines if blood pressure and heart rate will tolerate; aggressiveness must be proportionate to the severity of interstitial edema and respiratory distress | - Eliminate cardiac depressants — nondihydropyridine calcium channel blockers (diltiazem, verapamil)
- remove β-blockers for acute decompensation and resume only when clinically stable
- nitrates may or may not be appropriate depending on the cause (e.g., arrhythmia, valvular heart disease)
- inotropes only when there is hypotension AND evidence of reduced organ perfusion
- ACE inhibitor or ARB only as blood pressure tolerates
- β-adrenergic antagonists only if blood pressure and heart rate will tolerate
- aggressiveness must be proportionate to the severity of interstitial edema and respiratory distress
Eliminate cardiac depressants — nondihydropyridine calcium channel blockers (diltiazem, verapamil); remove β-blockers for acute decompensation and resume only when clinically stable; nitrates may or may not be appropriate depending on the cause (e.g., arrhythmia, valvular heart disease); inotropes only when there is hypotension AND evidence of reduced organ perfusion; ACE inhibitor or ARB only as blood pressure tolerates; β-adrenergic antagonists only if blood pressure and heart rate will tolerate; aggressiveness must be proportionate to the severity of interstitial edema and respiratory distress |
| Pulmonary hypertension — mechanisms & WHO groups | - ⭐ PH is not the same as pulmonary arterial hypertension (PAH) — PAH is a specific subgroup of PH
- three mechanisms: 1) increased vascular resistance — vasoconstriction (hypoxemia and acidosis), loss of vasculature (emphysema, lung resection), occlusion (pulmonary embolism), relative stenosis (vasculitis)
- 2) increased venous pressure — left ventricular failure or hypertrophy, right ventricular hypertrophy (e.g., due to PE), valvular disease (mitral stenosis, aortic stenosis), constrictive pericarditis
- 3) increased blood flow — left-to-right shunt, polycythemia (primary or secondary, e.g. from hypoxemia)
- PH develops without a known cause (primary/idiopathic) or as the result of other diseases (secondary)
⭐ PH is not the same as pulmonary arterial hypertension (PAH) — PAH is a specific subgroup of PH; three mechanisms: 1) increased vascular resistance — vasoconstriction (hypoxemia and acidosis), loss of vasculature (emphysema, lung resection), occlusion (pulmonary embolism), relative stenosis (vasculitis); 2) increased venous pressure — left ventricular failure or hypertrophy, right ventricular hypertrophy (e.g., due to PE), valvular disease (mitral stenosis, aortic stenosis), constrictive pericarditis; 3) increased blood flow — left-to-right shunt, polycythemia (primary or secondary, e.g. from hypoxemia); PH develops without a known cause (primary/idiopathic) or as the result of other diseases (secondary) | - ⭐ Group I — PAH (or primary): idiopathic PAH (seen most often in young women), familial or heritable PAH, associated PAH (collagen vascular disease such as scleroderma, congenital shunts between systemic and pulmonary circulation, portal hypertension, HIV infection, drugs, toxins)
- ⭐ Group II — associated with left heart disease: left ventricular systolic or diastolic dysfunction, valvular disease (e.g., mitral stenosis), congenital/acquired left heart inflow/outflow tract obstruction, congenital cardiomyopathies
- ⭐ Group III — lung disease and/or hypoxemia: COPD, interstitial lung disease, sleep-disordered breathing, alveolar hypoventilation, chronic exposure to high altitude, developmental lung abnormalities
- ⭐ **Group IV — CTEPH: PE in the proximal or distal pulmonary arteries
- embolization of other matter such as tumor cells or parasites**
- ⭐ Group V — miscellaneous, hematologic, systemic: myeloproliferative disorders, sarcoidosis, sickle cell disease
⭐ Group I — PAH (or primary): idiopathic PAH (seen most often in young women), familial or heritable PAH, associated PAH (collagen vascular disease such as scleroderma, congenital shunts between systemic and pulmonary circulation, portal hypertension, HIV infection, drugs, toxins); ⭐ Group II — associated with left heart disease: left ventricular systolic or diastolic dysfunction, valvular disease (e.g., mitral stenosis), congenital/acquired left heart inflow/outflow tract obstruction, congenital cardiomyopathies; ⭐ Group III — lung disease and/or hypoxemia: COPD, interstitial lung disease, sleep-disordered breathing, alveolar hypoventilation, chronic exposure to high altitude, developmental lung abnormalities; ⭐ Group IV — CTEPH: PE in the proximal or distal pulmonary arteries; embolization of other matter such as tumor cells or parasites; ⭐ Group V — miscellaneous, hematologic, systemic: myeloproliferative disorders, sarcoidosis, sickle cell disease | - Treatment depends on the WHO group and its driver — see the PH general-treatment row and the Table 28.1 targeted-therapy row
- treat the underlying disorders contributing to hypoxemia (COPD, CHF, obstructive sleep apnea)
Treatment depends on the WHO group and its driver — see the PH general-treatment row and the Table 28.1 targeted-therapy row; treat the underlying disorders contributing to hypoxemia (COPD, CHF, obstructive sleep apnea) | — |
| PH — symptoms, signs, diagnostics & general treatment | - Symptoms: dyspnea on exertion, those related to the cause of the PH, substernal discomfort, fatigue, ⭐ dizziness, near or true syncope, palpitations
- exam: ⭐ splitting of the second heart sound with an increased pulmonic component (P₂), peripheral edema from RV failure, ascites, RV heave, holosystolic murmur, elevated JVP
Symptoms: dyspnea on exertion, those related to the cause of the PH, substernal discomfort, fatigue, ⭐ dizziness, near or true syncope, palpitations; exam: ⭐ splitting of the second heart sound with an increased pulmonic component (P₂), peripheral edema from RV failure, ascites, RV heave, holosystolic murmur, elevated JVP | - ⭐ right-heart catheterization is the gold standard — pulmonary artery pressure > 25 mmHg and left atrial pressure < 18 mmHg suggests WHO group 1
- vasodilator study (acute vasodilator challenge)
- BNP/proBNP to assess cardiac strain and monitor therapy
- D-dimer if PE suspected
- echocardiography with bubble study
- EKG shows RV hypertrophy, right axis deviation, ± right bundle branch block
- CXR — enlarged proximal pulmonary arteries, narrowing in the medial third
- lower-extremity Doppler, V/Q scan, CT angiography
- ⭐ **geriatric caution: heart failure with preserved ejection fraction is a commonly under-recognized cause of PH in the elderly
- older patients are very unlikely to have PAH and more likely have pulmonary venous hypertension from left ventricular systolic or diastolic failure, aortic or mitral valve disease, or left atrial noncompliance**
⭐ right-heart catheterization is the gold standard — pulmonary artery pressure > 25 mmHg and left atrial pressure < 18 mmHg suggests WHO group 1; vasodilator study (acute vasodilator challenge); BNP/proBNP to assess cardiac strain and monitor therapy; D-dimer if PE suspected; echocardiography with bubble study; EKG shows RV hypertrophy, right axis deviation, ± right bundle branch block; CXR — enlarged proximal pulmonary arteries, narrowing in the medial third; lower-extremity Doppler, V/Q scan, CT angiography; ⭐ geriatric caution: heart failure with preserved ejection fraction is a commonly under-recognized cause of PH in the elderly; older patients are very unlikely to have PAH and more likely have pulmonary venous hypertension from left ventricular systolic or diastolic failure, aortic or mitral valve disease, or left atrial noncompliance | - ⭐ **oxygen — shown to reduce peripheral vascular resistance, but long-term therapy has not been shown beneficial
- may be recommended with COPD, low arterial oxygen pressure, symptomatic benefit, and correctable desaturation on exercise**
- ⭐ exercise is recommended for all — cardiopulmonary rehabilitation improves functional status, exercise capacity, and quality of life
- loop diuretics for decompensated right-heart failure with fluid retention, ascites, and peripheral edema
- anticoagulation recommended for PAH
- digoxin may improve cardiac output in idiopathic PAH and slow ventricular rate in arterial tachyarrhythmias — evidence for chronic use is lacking
- supplemental oxygen during the night
- ⭐ if polycythemia is severe with hematocrit above 60%, consider therapeutic phlebotomy to yield a hematocrit of approximately 55%
- maintain immunization against influenza and pneumococcal pneumonia
⭐ oxygen — shown to reduce peripheral vascular resistance, but long-term therapy has not been shown beneficial; may be recommended with COPD, low arterial oxygen pressure, symptomatic benefit, and correctable desaturation on exercise; ⭐ exercise is recommended for all — cardiopulmonary rehabilitation improves functional status, exercise capacity, and quality of life; loop diuretics for decompensated right-heart failure with fluid retention, ascites, and peripheral edema; anticoagulation recommended for PAH; digoxin may improve cardiac output in idiopathic PAH and slow ventricular rate in arterial tachyarrhythmias — evidence for chronic use is lacking; supplemental oxygen during the night; ⭐ if polycythemia is severe with hematocrit above 60%, consider therapeutic phlebotomy to yield a hematocrit of approximately 55%; maintain immunization against influenza and pneumococcal pneumonia | - Geriatric caution — older patients are very unlikely to have PAH
- they more likely have pulmonary venous hypertension from left ventricular systolic or diastolic failure, aortic or mitral valve disease, or left atrial noncompliance, and heart failure with preserved ejection fraction is a commonly under-recognized cause of PH in the elderly
- oxygen — long-term therapy has not been shown beneficial
- digoxin — evidence for chronic use is lacking
- therapeutic phlebotomy only if polycythemia is severe with hematocrit above 60% (target approximately 55%)
Geriatric caution — older patients are very unlikely to have PAH; they more likely have pulmonary venous hypertension from left ventricular systolic or diastolic failure, aortic or mitral valve disease, or left atrial noncompliance, and heart failure with preserved ejection fraction is a commonly under-recognized cause of PH in the elderly; oxygen — long-term therapy has not been shown beneficial; digoxin — evidence for chronic use is lacking; therapeutic phlebotomy only if polycythemia is severe with hematocrit above 60% (target approximately 55%) |
| PAH — Table 28.1 targeted drugs & doses | - ⭐ **a trial of CCBs is only recommended for patients with a positive response to vasoreactivity testing
- CCB therapy can lose effectiveness over time**
- ERAs are **teratogenic — limited distribution through REMS programs and only available through specialty pharmacies
- not recommended with moderate-to-severe liver disease**
- prostacyclins may cause bleeding due to platelet aggregation inhibition — all prostacyclin-related drugs are only available through specialty pharmacies
- selexipag — bleeding risk, specialty pharmacy only, many drug–drug interactions
- ⭐ avoid PDE-5 inhibitors with nitrates
- **riociguat is contraindicated with nitrates or PDE-5 inhibitors
- smokers may require higher dosages
- teratogenic — REMS-restricted, specialty pharmacy only**
⭐ a trial of CCBs is only recommended for patients with a positive response to vasoreactivity testing; CCB therapy can lose effectiveness over time; ERAs are teratogenic — limited distribution through REMS programs and only available through specialty pharmacies; not recommended with moderate-to-severe liver disease; prostacyclins may cause bleeding due to platelet aggregation inhibition — all prostacyclin-related drugs are only available through specialty pharmacies; selexipag — bleeding risk, specialty pharmacy only, many drug–drug interactions; ⭐ avoid PDE-5 inhibitors with nitrates; riociguat is contraindicated with nitrates or PDE-5 inhibitors; smokers may require higher dosages; teratogenic — REMS-restricted, specialty pharmacy only | - Treatment depends on underlying etiology, WHO functional class, and severity of symptoms
- ⭐ none of the targeted therapies has been shown to slow pathological progression
- depending on severity, two or more drugs from different classes are usually needed
- **oral drugs, as monotherapy or in combination, are recommended for less severe disease
- parenteral prostacyclins are usually used as combination therapy for more severe disease**
- sequential therapy — start with monotherapy and add a second or third drug based on inadequate response or deterioration
- initial or upfront combination therapy is used when there are increased mortality risks or concurrent severe medical illness based on WHO functional class
Treatment depends on underlying etiology, WHO functional class, and severity of symptoms; ⭐ none of the targeted therapies has been shown to slow pathological progression; depending on severity, two or more drugs from different classes are usually needed; oral drugs, as monotherapy or in combination, are recommended for less severe disease; parenteral prostacyclins are usually used as combination therapy for more severe disease; sequential therapy — start with monotherapy and add a second or third drug based on inadequate response or deterioration; initial or upfront combination therapy is used when there are increased mortality risks or concurrent severe medical illness based on WHO functional class | - ⭐ **calcium channel blockers (WHO-FC II, III) — amlodipine (Norvasc) PO 20–30 mg/day
- nifedipine ER (Procardia XL) PO 120–240 mg/day
- diltiazem ER (Cardizem LA) PO 240–960 mg/day**
- ⭐ **endothelin receptor antagonists (WHO-FC II, III) — ambrisentan (Letairis) PO 5–10 mg/day
- bosentan (Tracleer) PO < 40 kg max 125 mg/day, > 40 kg max 250 mg/day
- macitentan (Opsumit) PO 10 mg/day**
- ⭐ **prostacyclin analogues (WHO-FC III, IV) — epoprostenol (Flolan, Veletri) IV start 1–2 ng/kg/min, titrate every 15 min to target 25–40 ng/kg/min
- iloprost (Ventavis) INH 2.5–5 mcg inhaled 6–9 times/day (≥ 2 h apart), max 45 mcg/day
- treprostinil (Remodulin, Tyvaso, Orenitram) IV/SC start 1.25 ng/kg/min, titrate by 1.25 ng/kg/min weekly for 4 weeks, then 2.5 ng/kg/min per week up to 40 ng/kg/min**
- prostacyclin receptor agonist (WHO-FC II, III) — selexipag (Uptravi) PO max 3,200 mcg/day
- **PDE-5 inhibitors (WHO-FC II, III) — sildenafil (Revatio) PO max 60 mg/day
- tadalafil (Adcirca) PO max 40 mg/day**
- guanylate cyclase inhibitor (WHO-FC II, III) — riociguat (Adempas) PO max 2.5 mg TID
⭐ calcium channel blockers (WHO-FC II, III) — amlodipine (Norvasc) PO 20–30 mg/day; nifedipine ER (Procardia XL) PO 120–240 mg/day; diltiazem ER (Cardizem LA) PO 240–960 mg/day; ⭐ endothelin receptor antagonists (WHO-FC II, III) — ambrisentan (Letairis) PO 5–10 mg/day; bosentan (Tracleer) PO < 40 kg max 125 mg/day, > 40 kg max 250 mg/day; macitentan (Opsumit) PO 10 mg/day; ⭐ prostacyclin analogues (WHO-FC III, IV) — epoprostenol (Flolan, Veletri) IV start 1–2 ng/kg/min, titrate every 15 min to target 25–40 ng/kg/min; iloprost (Ventavis) INH 2.5–5 mcg inhaled 6–9 times/day (≥ 2 h apart), max 45 mcg/day; treprostinil (Remodulin, Tyvaso, Orenitram) IV/SC start 1.25 ng/kg/min, titrate by 1.25 ng/kg/min weekly for 4 weeks, then 2.5 ng/kg/min per week up to 40 ng/kg/min; prostacyclin receptor agonist (WHO-FC II, III) — selexipag (Uptravi) PO max 3,200 mcg/day; PDE-5 inhibitors (WHO-FC II, III) — sildenafil (Revatio) PO max 60 mg/day; tadalafil (Adcirca) PO max 40 mg/day; guanylate cyclase inhibitor (WHO-FC II, III) — riociguat (Adempas) PO max 2.5 mg TID | - A trial of CCBs is only recommended for patients with a positive response to vasoreactivity testing, and CCB therapy can lose effectiveness over time
- ERAs are teratogenic — REMS-restricted, specialty pharmacy only, not recommended with moderate-to-severe liver disease, monitor LFTs
- prostacyclins may cause bleeding due to platelet aggregation inhibition — specialty pharmacy only
- selexipag — bleeding risk, specialty pharmacy only, many drug–drug interactions
- avoid PDE-5 inhibitors with nitrates
- riociguat is contraindicated with nitrates or PDE-5 inhibitors, is teratogenic (REMS-restricted, specialty pharmacy only) and smokers may require higher dosages
- none of the targeted therapies has been shown to slow pathological progression
A trial of CCBs is only recommended for patients with a positive response to vasoreactivity testing, and CCB therapy can lose effectiveness over time; ERAs are teratogenic — REMS-restricted, specialty pharmacy only, not recommended with moderate-to-severe liver disease, monitor LFTs; prostacyclins may cause bleeding due to platelet aggregation inhibition — specialty pharmacy only; selexipag — bleeding risk, specialty pharmacy only, many drug–drug interactions; avoid PDE-5 inhibitors with nitrates; riociguat is contraindicated with nitrates or PDE-5 inhibitors, is teratogenic (REMS-restricted, specialty pharmacy only) and smokers may require higher dosages; none of the targeted therapies has been shown to slow pathological progression |
| Pulmonary embolism — Virchow triad, findings & workup | - A clot (or other undissolved solid, liquid, or gaseous material) travels to the lung via the venous system and lodges in the pulmonary arterial circulation, interrupting blood flow
- ⭐ death occurs as a result of right ventricular failure
- ⭐ considered massive if more than 50% of flow is obstructed
- ⭐ Virchow triad — venous stasis (DVT of the lower extremities and pelvis leads to 70% of pulmonary emboli; prolonged immobility, surgery under general anesthesia > 30 min, CHF, dehydration, obesity, advanced age), vessel wall injury (surgery, fractured hip or pelvis), hypercoagulability (estrogen, malignancy), plus genetic predisposition
- other emboli — fat (orthopedic trauma, especially marrow-containing bone, and surgery), air (e.g., from a central line), tumor fragments, amniotic fluid, septic debris (indwelling venous access device)
- subjective: ⭐ dyspnea — insidious or sudden — the most common symptom
- apprehension, anxiety, and a perception of "impending doom"
- substernal discomfort
- pleuritic pain with PE with infarction
- hemoptysis with pulmonary infarction
- syncope
- objective: **tachycardia
- tachypnea and dyspnea**
- initially elevated blood pressure
- diaphoresis
- chest pain (dull, central, pleuritic with infarction)
- **decreased cardiac output
- hypotension and shock**
- signs of RV overload — jugular venous distention, increased intensity of the second heart sound
- peripheral phlebitis
A clot (or other undissolved solid, liquid, or gaseous material) travels to the lung via the venous system and lodges in the pulmonary arterial circulation, interrupting blood flow; ⭐ death occurs as a result of right ventricular failure; ⭐ considered massive if more than 50% of flow is obstructed; ⭐ Virchow triad — venous stasis (DVT of the lower extremities and pelvis leads to 70% of pulmonary emboli; prolonged immobility, surgery under general anesthesia > 30 min, CHF, dehydration, obesity, advanced age), vessel wall injury (surgery, fractured hip or pelvis), hypercoagulability (estrogen, malignancy), plus genetic predisposition; other emboli — fat (orthopedic trauma, especially marrow-containing bone, and surgery), air (e.g., from a central line), tumor fragments, amniotic fluid, septic debris (indwelling venous access device); subjective: ⭐ dyspnea — insidious or sudden — the most common symptom; apprehension, anxiety, and a perception of "impending doom"; substernal discomfort; pleuritic pain with PE with infarction; hemoptysis with pulmonary infarction; syncope; objective: tachycardia; tachypnea and dyspnea; initially elevated blood pressure; diaphoresis; chest pain (dull, central, pleuritic with infarction); decreased cardiac output; hypotension and shock; signs of RV overload — jugular venous distention, increased intensity of the second heart sound; peripheral phlebitis | - ABG — ⭐ acute respiratory alkalosis and variable degrees of hypoxemia
- EKG — nonspecific changes, **most common is sinus tachycardia
- atrial fibrillation also common**
- chest X-ray — normal, or with small infiltrates and/or effusion
- ⭐ **ventilation/perfusion lung scan — high probability → treat with anticoagulants
- indeterminate or low probability with high clinical suspicion → consider pulmonary angiography**
- if the chest X-ray is abnormal or COPD is present, lung scanning may be misinterpreted — consider CTA
- ⭐ pulmonary angiography remains the accepted gold standard for detecting pulmonary emboli
- venous Doppler of the lower extremities may reveal DVT, which requires anticoagulation in part obviating evaluation of PE
- spiral-cut, high-resolution CT of the chest reliably shows central PE
ABG — ⭐ acute respiratory alkalosis and variable degrees of hypoxemia; EKG — nonspecific changes, most common is sinus tachycardia; atrial fibrillation also common; chest X-ray — normal, or with small infiltrates and/or effusion; ⭐ ventilation/perfusion lung scan — high probability → treat with anticoagulants; indeterminate or low probability with high clinical suspicion → consider pulmonary angiography; if the chest X-ray is abnormal or COPD is present, lung scanning may be misinterpreted — consider CTA; ⭐ pulmonary angiography remains the accepted gold standard for detecting pulmonary emboli; venous Doppler of the lower extremities may reveal DVT, which requires anticoagulation in part obviating evaluation of PE; spiral-cut, high-resolution CT of the chest reliably shows central PE | - ⭐ accurate diagnosis is the key to reducing associated mortality
- if the V/Q scan is high probability, treat with anticoagulants
- otherwise see the parenteral anticoagulant, oral anticoagulant, and fibrinolytic/filter rows
⭐ accurate diagnosis is the key to reducing associated mortality; if the V/Q scan is high probability, treat with anticoagulants; otherwise see the parenteral anticoagulant, oral anticoagulant, and fibrinolytic/filter rows | - If the chest X-ray is abnormal or COPD is present, lung scanning may be misinterpreted — consider CTA
- indeterminate or low-probability V/Q scan with high clinical suspicion — consider pulmonary angiography
If the chest X-ray is abnormal or COPD is present, lung scanning may be misinterpreted — consider CTA; indeterminate or low-probability V/Q scan with high clinical suspicion — consider pulmonary angiography |
| Fat embolism syndrome | - ⭐ sudden, marked dyspnea in a susceptible patient
- ⭐ altered consciousness
- ⭐ body temperature elevation > 102 °F
- ⭐ petechiae over the thorax, shoulders, and axillae
- susceptible patients — orthopedic trauma, especially marrow-containing bone, and surgery
⭐ sudden, marked dyspnea in a susceptible patient; ⭐ altered consciousness; ⭐ body temperature elevation > 102 °F; ⭐ petechiae over the thorax, shoulders, and axillae; susceptible patients — orthopedic trauma, especially marrow-containing bone, and surgery | - ABG — acute respiratory alkalosis and variable degrees of hypoxemia
- chest X-ray — normal, or with small infiltrates and/or effusion
- EKG — nonspecific, most commonly sinus tachycardia
ABG — acute respiratory alkalosis and variable degrees of hypoxemia; chest X-ray — normal, or with small infiltrates and/or effusion; EKG — nonspecific, most commonly sinus tachycardia | - No fat-embolism-specific management is stated in this source — see the PE parenteral anticoagulant, fibrinolytic, and supplemental-oxygen rows
No fat-embolism-specific management is stated in this source — see the PE parenteral anticoagulant, fibrinolytic, and supplemental-oxygen rows | — |
| PE — parenteral anticoagulants | - Monitoring findings: anti-factor Xa requires monitoring in pregnancy, obesity (BMI > 30 kg/m² or 98 kg), renal failure, and bleeding/high bleeding risk
- enoxaparin carries a lower risk of bleeding and of heparin-induced thrombocytopenia than unfractionated heparin
- vancomycin and the aminoglycosides require pharmacist pharmacokinetic modeling
Monitoring findings: anti-factor Xa requires monitoring in pregnancy, obesity (BMI > 30 kg/m² or 98 kg), renal failure, and bleeding/high bleeding risk; enoxaparin carries a lower risk of bleeding and of heparin-induced thrombocytopenia than unfractionated heparin; vancomycin and the aminoglycosides require pharmacist pharmacokinetic modeling | - **Unfractionated heparin — goal anti-factor Xa activity of 0.3–0.7 international units/mL
- PTT goal is institution-specific and instrument/reagent dependent
- some hospitals draw PTT or anti-factor Xa every 6 hr**
- argatroban — goal PTT of 1.5–3 times the patient's baseline PTT
- enoxaparin — anti-factor Xa monitoring in pregnancy, obesity, renal failure, and bleeding/high bleeding risk
Unfractionated heparin — goal anti-factor Xa activity of 0.3–0.7 international units/mL; PTT goal is institution-specific and instrument/reagent dependent; some hospitals draw PTT or anti-factor Xa every 6 hr; argatroban — goal PTT of 1.5–3 times the patient's baseline PTT; enoxaparin — anti-factor Xa monitoring in pregnancy, obesity, renal failure, and bleeding/high bleeding risk | - ⭐ unfractionated heparin — initial bolus 80 units/kg, then continuous infusion of 18 units/kg/hr
- enoxaparin (Lovenox) 1 mg/kg subQ every 12 hr — acceptable alternative to heparin
- ⭐ **argatroban — non-ICU: 2 mcg/kg/min continuous IV infusion
- ICU/critically ill with organ dysfunction: 0.2–0.5 mcg/kg/min**
- ⭐ **fondaparinux (Arixtra) — < 50 kg: 5 mg subQ once daily
- 50–100 kg: 7.5 mg subQ once daily
- > 100 kg: 10 mg subQ once daily** (weight-banded dosing)
- consult a pharmacist for pharmacokinetic modeling
⭐ unfractionated heparin — initial bolus 80 units/kg, then continuous infusion of 18 units/kg/hr; enoxaparin (Lovenox) 1 mg/kg subQ every 12 hr — acceptable alternative to heparin; ⭐ argatroban — non-ICU: 2 mcg/kg/min continuous IV infusion; ICU/critically ill with organ dysfunction: 0.2–0.5 mcg/kg/min; ⭐ fondaparinux (Arixtra) — < 50 kg: 5 mg subQ once daily; 50–100 kg: 7.5 mg subQ once daily; > 100 kg: 10 mg subQ once daily (weight-banded dosing); consult a pharmacist for pharmacokinetic modeling | - Anti-factor Xa monitoring is required in pregnancy, obesity (BMI > 30 kg/m² or 98 kg), renal failure, and bleeding/high bleeding risk
- argatroban — use the reduced ICU dose of 0.2–0.5 mcg/kg/min in critically ill patients with organ dysfunction
- vancomycin and the aminoglycosides require pharmacist pharmacokinetic modeling
Anti-factor Xa monitoring is required in pregnancy, obesity (BMI > 30 kg/m² or 98 kg), renal failure, and bleeding/high bleeding risk; argatroban — use the reduced ICU dose of 0.2–0.5 mcg/kg/min in critically ill patients with organ dysfunction; vancomycin and the aminoglycosides require pharmacist pharmacokinetic modeling |
| PE — oral anticoagulants & reversal agents | - ⭐ factor Xa inhibitors reach therapeutic effect rapidly — bridging with heparin is unnecessary
- renal function, liver function, age, and weight must be considered and monitored every 3–6 months, with dosages adjusted accordingly
⭐ factor Xa inhibitors reach therapeutic effect rapidly — bridging with heparin is unnecessary; renal function, liver function, age, and weight must be considered and monitored every 3–6 months, with dosages adjusted accordingly | - ⭐ **warfarin — adequate effect when INR is 2–2.5 for at least 2–3 days
- monitor INR after the initial daily dose
- continue heparin until therapeutic**
- rivaroxaban — avoid if CrCl < 30 mL/min
⭐ warfarin — adequate effect when INR is 2–2.5 for at least 2–3 days; monitor INR after the initial daily dose; continue heparin until therapeutic; rivaroxaban — avoid if CrCl < 30 mL/min | - Dabigatran (Pradaxa) 150 mg PO BID — reversal idarucizumab (Praxbind) for life-threatening conditions such as intracranial hemorrhage, GI bleeding, and trauma
- rivaroxaban (Xarelto) 15 mg PO BID with food for 21 days, then 20 mg PO once daily with food — reversal andexanet alfa (Andexxa)
- apixaban (Eliquis) 10 mg PO BID for the first 7 days, then 5 mg PO BID — reversal andexanet alfa
- edoxaban (Savaysa) 60 mg PO per day — 30 mg PO per day if CrCl 15–50 mL/min, weight < 60 kg, or on certain P-gp inhibitors
- warfarin (Coumadin) usual first dose 5 mg PO per day
Dabigatran (Pradaxa) 150 mg PO BID — reversal idarucizumab (Praxbind) for life-threatening conditions such as intracranial hemorrhage, GI bleeding, and trauma; rivaroxaban (Xarelto) 15 mg PO BID with food for 21 days, then 20 mg PO once daily with food — reversal andexanet alfa (Andexxa); apixaban (Eliquis) 10 mg PO BID for the first 7 days, then 5 mg PO BID — reversal andexanet alfa; edoxaban (Savaysa) 60 mg PO per day — 30 mg PO per day if CrCl 15–50 mL/min, weight < 60 kg, or on certain P-gp inhibitors; warfarin (Coumadin) usual first dose 5 mg PO per day | - Rivaroxaban — avoid if CrCl < 30 mL/min
- edoxaban — 30 mg PO daily if CrCl 15–50 mL/min, weight < 60 kg, or on certain P-gp inhibitors
- renal function, liver function, age and weight must be considered and monitored every 3–6 months, with dosages adjusted accordingly
- warfarin — continue heparin until therapeutic (do not stop heparin early)
- factor Xa inhibitors — bridging with heparin is unnecessary
Rivaroxaban — avoid if CrCl < 30 mL/min; edoxaban — 30 mg PO daily if CrCl 15–50 mL/min, weight < 60 kg, or on certain P-gp inhibitors; renal function, liver function, age and weight must be considered and monitored every 3–6 months, with dosages adjusted accordingly; warfarin — continue heparin until therapeutic (do not stop heparin early); factor Xa inhibitors — bridging with heparin is unnecessary |
| PE — fibrinolytics, embolectomy, filters & duration | - ⭐ fibrinolytic therapy — note contraindications before instituting
- may be appropriate for massive proximal PE with persistent systemic hypotension and signs of right heart strain, and in patients with very little cardiopulmonary reserve
⭐ fibrinolytic therapy — note contraindications before instituting; may be appropriate for massive proximal PE with persistent systemic hypotension and signs of right heart strain, and in patients with very little cardiopulmonary reserve | - After fibrinolytic therapy is completed, begin heparin or enoxaparin when the PTT is < 2 times control
- hemodynamic support may be needed for massive emboli with hypotension
After fibrinolytic therapy is completed, begin heparin or enoxaparin when the PTT is < 2 times control; hemodynamic support may be needed for massive emboli with hypotension | - ⭐ alteplase (recombinant tPA) 100 mg IV infused over 2 hours
- surgical embolectomy — reserved for massive emboli in central pulmonary arteries where the clot is creating hypotension and shock
- inferior vena cava interruption ("umbrella" device, Greenfield filter) — indicated when the risk of further emboli is perceived to be high, or when there is an absolute risk to anticoagulation
- supplemental oxygen to keep oxygen saturation above 90%
- ⭐ **length of treatment: 3–6 months for the initial episode of PE
- for recurrent or unprovoked PE, treat 6–12 months or longer, or consider an indwelling vena cava filter to protect against massive embolization in patients with ongoing risk factors**
⭐ alteplase (recombinant tPA) 100 mg IV infused over 2 hours; surgical embolectomy — reserved for massive emboli in central pulmonary arteries where the clot is creating hypotension and shock; inferior vena cava interruption ("umbrella" device, Greenfield filter) — indicated when the risk of further emboli is perceived to be high, or when there is an absolute risk to anticoagulation; supplemental oxygen to keep oxygen saturation above 90%; ⭐ length of treatment: 3–6 months for the initial episode of PE; for recurrent or unprovoked PE, treat 6–12 months or longer, or consider an indwelling vena cava filter to protect against massive embolization in patients with ongoing risk factors | - Fibrinolytic therapy — note the contraindications before instituting (this source does not list them)
- use only for massive proximal PE with persistent systemic hypotension and signs of right heart strain, or in patients with very little cardiopulmonary reserve
- after fibrinolysis, do not begin heparin or enoxaparin until the PTT is < 2 times control
- surgical embolectomy is reserved for massive emboli in central pulmonary arteries creating hypotension and shock
- inferior vena cava interruption (Greenfield filter) — indicated when the risk of further emboli is perceived to be high, or when there is an absolute risk to anticoagulation
Fibrinolytic therapy — note the contraindications before instituting (this source does not list them); use only for massive proximal PE with persistent systemic hypotension and signs of right heart strain, or in patients with very little cardiopulmonary reserve; after fibrinolysis, do not begin heparin or enoxaparin until the PTT is < 2 times control; surgical embolectomy is reserved for massive emboli in central pulmonary arteries creating hypotension and shock; inferior vena cava interruption (Greenfield filter) — indicated when the risk of further emboli is perceived to be high, or when there is an absolute risk to anticoagulation |
| Pulmonary vasculitis — Wegener granulomatosis | - ⭐ triad you must recognize: necrotizing granulomas of the respiratory tract (upper and lower), pulmonary microangiitis, and glomerulonephritis
- associated with hemoptysis, dyspnea, cough, pulmonary infiltrates
⭐ triad you must recognize: necrotizing granulomas of the respiratory tract (upper and lower), pulmonary microangiitis, and glomerulonephritis; associated with hemoptysis, dyspnea, cough, pulmonary infiltrates | - ⭐ antineutrophilic cytoplasmic antibodies (ANCA) are often positive
- recognition of the triad is the diagnostic key
- treatment has two components — induction of remission, then maintenance to prevent relapse
⭐ antineutrophilic cytoplasmic antibodies (ANCA) are often positive; recognition of the triad is the diagnostic key; treatment has two components — induction of remission, then maintenance to prevent relapse | - prednisone 1 mg/kg/day or cyclophosphamide 2 mg/kg/day, with a reasonable chance of remission within 1 year
- ⭐ **induction options — prednisone 1 mg/kg/day (max 60–80 mg/day)
- oral cyclophosphamide 1.5–2 mg/kg/day
- IV cyclophosphamide 0.5 g/m² every 2 weeks for 3–6 months
- rituximab 375 mg/m² weekly for 4 weeks
- methotrexate 20–25 mg PO weekly**
- maintenance — methotrexate or azathioprine 2 mg/kg/day
- prophylaxis against PCP/PJP during induction may be necessary
prednisone 1 mg/kg/day or cyclophosphamide 2 mg/kg/day, with a reasonable chance of remission within 1 year; ⭐ induction options — prednisone 1 mg/kg/day (max 60–80 mg/day); oral cyclophosphamide 1.5–2 mg/kg/day; IV cyclophosphamide 0.5 g/m² every 2 weeks for 3–6 months; rituximab 375 mg/m² weekly for 4 weeks; methotrexate 20–25 mg PO weekly; maintenance — methotrexate or azathioprine 2 mg/kg/day; prophylaxis against PCP/PJP during induction may be necessary | — |
| Pneumothorax — spontaneous | - ⭐ disruption of the visceral pleura — air enters the pleural space from the lung
- occurs in individuals with or without underlying lung disease
- look for it with COPD, tuberculosis, sarcoidosis, pulmonary fibrosis, bronchogenic carcinoma, or rupture of a subpleural bleb
⭐ disruption of the visceral pleura — air enters the pleural space from the lung; occurs in individuals with or without underlying lung disease; look for it with COPD, tuberculosis, sarcoidosis, pulmonary fibrosis, bronchogenic carcinoma, or rupture of a subpleural bleb | - ⭐ **established by demonstrating a white visceral pleural line — the interface between lung and pleural air
- increased translucency confirms the degree of collapse**
- ABGs typically show mild to moderate hypoxemia and hypercapnia
- recognizing small pneumothoraces, particularly in mechanically ventilated patients, is crucial to preventing tension pneumothorax
⭐ established by demonstrating a white visceral pleural line — the interface between lung and pleural air; increased translucency confirms the degree of collapse; ABGs typically show mild to moderate hypoxemia and hypercapnia; recognizing small pneumothoraces, particularly in mechanically ventilated patients, is crucial to preventing tension pneumothorax | - ⭐ depends on size and underlying lung disease
- if small — supplemental oxygen with a 100% non-rebreather mask and observe, and repeat chest X-ray frequently
- ⭐ nontraumatic pneumothorax estimated at <15% collapse and no cardiovascular or respiratory compromise — observe with 100% oxygen support for 4–6 hr, repeat chest radiograph, and discharge if unchanged
- ⭐ if collapse is greater than 20% — insert a chest tube at the fourth or fifth intercostal space, midaxillary line, to water-seal drainage
⭐ depends on size and underlying lung disease; if small — supplemental oxygen with a 100% non-rebreather mask and observe, and repeat chest X-ray frequently; ⭐ nontraumatic pneumothorax estimated at <15% collapse and no cardiovascular or respiratory compromise — observe with 100% oxygen support for 4–6 hr, repeat chest radiograph, and discharge if unchanged; ⭐ if collapse is greater than 20% — insert a chest tube at the fourth or fifth intercostal space, midaxillary line, to water-seal drainage | — |
| Pneumothorax — traumatic, open | - ⭐ penetrating chest trauma — the parietal pleura is disrupted
- air enters from the atmosphere during inspiration and exits during expiration — which decreases the likelihood of mediastinal tension and shift
⭐ penetrating chest trauma — the parietal pleura is disrupted; air enters from the atmosphere during inspiration and exits during expiration — which decreases the likelihood of mediastinal tension and shift | - Chest X-ray — white visceral pleural line with increased translucency confirming the degree of collapse
- ABGs may show mild to moderate hypoxemia and hypercapnia
Chest X-ray — white visceral pleural line with increased translucency confirming the degree of collapse; ABGs may show mild to moderate hypoxemia and hypercapnia | - ⭐ prompt chest tube insertion at the fourth or fifth intercostal space, midaxillary line, with closed chest drainage
- ⭐ negative pressure (suction to the drainage apparatus) — use when the water seal fails to re-expand the lung after 24–48 hours, or when persistent pneumothorax perpetuates hypoxemia and/or hypercapnia
⭐ prompt chest tube insertion at the fourth or fifth intercostal space, midaxillary line, with closed chest drainage; ⭐ negative pressure (suction to the drainage apparatus) — use when the water seal fails to re-expand the lung after 24–48 hours, or when persistent pneumothorax perpetuates hypoxemia and/or hypercapnia | — |
| Pneumothorax — traumatic, closed | - ⭐ **blunt chest trauma — usually due to rib fractures
- the visceral pleura is disrupted and air enters the pleural space from the lung**
⭐ blunt chest trauma — usually due to rib fractures; the visceral pleura is disrupted and air enters the pleural space from the lung | - Chest X-ray — white visceral pleural line with increased translucency confirming the degree of collapse
- ABGs may show mild to moderate hypoxemia and hypercapnia
Chest X-ray — white visceral pleural line with increased translucency confirming the degree of collapse; ABGs may show mild to moderate hypoxemia and hypercapnia | - ⭐ prompt chest tube insertion at the fourth or fifth intercostal space, midaxillary line, with closed chest drainage
- negative pressure (suction) when the water seal fails to re-expand the lung after 24–48 hours, or when persistent pneumothorax perpetuates hypoxemia and/or hypercapnia
⭐ prompt chest tube insertion at the fourth or fifth intercostal space, midaxillary line, with closed chest drainage; negative pressure (suction) when the water seal fails to re-expand the lung after 24–48 hours, or when persistent pneumothorax perpetuates hypoxemia and/or hypercapnia | — |
| Pneumothorax — iatrogenic | - ⭐ disruption of the visceral pleura as a complication of an invasive thoracic procedure — and also after procedures involving the neck or abdomen
- includes IV access device insertion, needle biopsy of liver or lung, and thoracentesis
⭐ disruption of the visceral pleura as a complication of an invasive thoracic procedure — and also after procedures involving the neck or abdomen; includes IV access device insertion, needle biopsy of liver or lung, and thoracentesis | - Chest X-ray — white visceral pleural line with increased translucency confirming the degree of collapse
- recognizing small pneumothoraces, particularly in mechanically ventilated patients, is crucial to preventing tension pneumothorax
Chest X-ray — white visceral pleural line with increased translucency confirming the degree of collapse; recognizing small pneumothoraces, particularly in mechanically ventilated patients, is crucial to preventing tension pneumothorax | - Follow the spontaneous/traumatic size rules: if small — supplemental oxygen with a 100% non-rebreather mask and observation with frequent repeat chest X-ray
- if collapse is greater than 20% — chest tube at the fourth or fifth intercostal space, midaxillary line, to water-seal drainage
- suction if the water seal fails to re-expand the lung after 24–48 hours
Follow the spontaneous/traumatic size rules: if small — supplemental oxygen with a 100% non-rebreather mask and observation with frequent repeat chest X-ray; if collapse is greater than 20% — chest tube at the fourth or fifth intercostal space, midaxillary line, to water-seal drainage; suction if the water seal fails to re-expand the lung after 24–48 hours | — |
| Pneumothorax — tension | - ⭐ **air in, no air out — air enters the pleural space but is unable to exit
- as pressure rises, the lung collapses, the mediastinum shifts to the opposite side, and venous return to the right heart is impaired — decreasing cardiac output and causing hypotension**
- ⭐ a medical emergency
- sudden onset dyspnea and shortness of breath (air hunger), pleuritic chest pain that may be sharp and severe, apprehension and agitation
- **other tension-specific findings — hypotension, tachycardia with heart rate >120 bpm, diaphoresis, cyanosis, and cardiovascular collapse
- jugular venous distention and tracheal deviation to the contralateral side may be evident in tension pneumothorax**
- exam: **splinting and decreased inspiratory expansion of the involved hemithorax
- bulging of the intercostal spaces on the affected side during exhalation
- decreased breath sounds and fremitus with hyperresonant percussion
- tracheal deviation toward the unaffected side (a late sign)
- subcutaneous emphysema
- possible Hamman sign (mediastinal crepitus on auscultation)
- on the ventilator — high peak inspiratory pressure with decreased compliance**
⭐ air in, no air out — air enters the pleural space but is unable to exit; as pressure rises, the lung collapses, the mediastinum shifts to the opposite side, and venous return to the right heart is impaired — decreasing cardiac output and causing hypotension; ⭐ a medical emergency; sudden onset dyspnea and shortness of breath (air hunger), pleuritic chest pain that may be sharp and severe, apprehension and agitation; other tension-specific findings — hypotension, tachycardia with heart rate >120 bpm, diaphoresis, cyanosis, and cardiovascular collapse; jugular venous distention and tracheal deviation to the contralateral side may be evident in tension pneumothorax; exam: splinting and decreased inspiratory expansion of the involved hemithorax; bulging of the intercostal spaces on the affected side during exhalation; decreased breath sounds and fremitus with hyperresonant percussion; tracheal deviation toward the unaffected side (a late sign); subcutaneous emphysema; possible Hamman sign (mediastinal crepitus on auscultation); on the ventilator — high peak inspiratory pressure with decreased compliance | - ⭐ never wait for the film
- chest X-ray shows a white visceral pleural line with increased translucency confirming the degree of collapse
- ABGs may show mild to moderate hypoxemia and hypercapnia
⭐ never wait for the film; chest X-ray shows a white visceral pleural line with increased translucency confirming the degree of collapse; ABGs may show mild to moderate hypoxemia and hypercapnia | - ⭐ FIRST ACTION — immediate decompression with a 14- to 16-gauge needle into the second intercostal space, midclavicular line of the affected side
- ⭐ **the lecture's needle thoracostomy — 14G–18G angiocatheter in the 2nd intercostal space at the midclavicular line, or the 4th or 5th intercostal space at the anterior axillary line
- the length of most standard angiocatheters is too short to penetrate the pleural cavity in moderate to large framed patients, so longer, purpose-specific catheters may be required**
- ⭐ must follow with chest tube insertion at the fourth or fifth intercostal space, midaxillary line, to closed water-seal drainage
- **suspected tension pneumothorax requires either immediate needle thoracostomy or tube thoracostomy
- unstable patients with a suspected tension pneumothorax require immediate needle thoracostomy**
⭐ FIRST ACTION — immediate decompression with a 14- to 16-gauge needle into the second intercostal space, midclavicular line of the affected side; ⭐ the lecture's needle thoracostomy — 14G–18G angiocatheter in the 2nd intercostal space at the midclavicular line, or the 4th or 5th intercostal space at the anterior axillary line; the length of most standard angiocatheters is too short to penetrate the pleural cavity in moderate to large framed patients, so longer, purpose-specific catheters may be required; ⭐ must follow with chest tube insertion at the fourth or fifth intercostal space, midaxillary line, to closed water-seal drainage; suspected tension pneumothorax requires either immediate needle thoracostomy or tube thoracostomy; unstable patients with a suspected tension pneumothorax require immediate needle thoracostomy | - Do not wait for imaging — immediate needle decompression comes first (never wait for the film)
- needle thoracostomy must be followed by chest tube insertion
- the length of most standard angiocatheters is too short to penetrate the pleural cavity in moderate-to-large framed patients — longer, purpose-specific catheters may be required
Do not wait for imaging — immediate needle decompression comes first (never wait for the film); needle thoracostomy must be followed by chest tube insertion; the length of most standard angiocatheters is too short to penetrate the pleural cavity in moderate-to-large framed patients — longer, purpose-specific catheters may be required |
| Pneumothorax — assessment, imaging & workup | - ⭐ severity of symptoms is generally proportional to the size of the pneumothorax
- chest pain on the ipsilateral side — sharp, pleuritic, sudden onset (dull ache in delayed presentations)
- shortness of breath
- rarely cough, asymptomatic, or generalized malaise
- tachypnea
- ⭐ heart rate <120 bpm is generally seen in simple spontaneous pneumothoraces
- cardiac and pulmonary exam — **asymmetric decreased breath sounds
- hyperresonance to percussion of the ipsilateral side**
- etiology to consider — idiopathic
- airway disease (COPD, asthma, cystic fibrosis)
- infections (necrotizing bacterial pneumonia, TB, fungal pneumonia, Pneumocystis carinii)
- neoplasm
- interstitial lung disease (sarcoidosis, idiopathic pulmonary fibrosis, lymphangiomyomatosis, tuberous sclerosis)
- pneumoconioses
- connective tissue diseases
- pulmonary infarction
- endometriosis
- blunt chest trauma
- penetrating trauma to the neck or trunk
- iatrogenic (central line placement, other vascular access procedures)
⭐ severity of symptoms is generally proportional to the size of the pneumothorax; chest pain on the ipsilateral side — sharp, pleuritic, sudden onset (dull ache in delayed presentations); shortness of breath; rarely cough, asymptomatic, or generalized malaise; tachypnea; ⭐ heart rate <120 bpm is generally seen in simple spontaneous pneumothoraces; cardiac and pulmonary exam — asymmetric decreased breath sounds; hyperresonance to percussion of the ipsilateral side; etiology to consider — idiopathic; airway disease (COPD, asthma, cystic fibrosis); infections (necrotizing bacterial pneumonia, TB, fungal pneumonia, Pneumocystis carinii); neoplasm; interstitial lung disease (sarcoidosis, idiopathic pulmonary fibrosis, lymphangiomyomatosis, tuberous sclerosis); pneumoconioses; connective tissue diseases; pulmonary infarction; endometriosis; blunt chest trauma; penetrating trauma to the neck or trunk; iatrogenic (central line placement, other vascular access procedures) | - ⭐ imaging is the mainstay of the workup
- ⭐ DO NOT delay chest decompression if the patient is hemodynamically unstable and there is sufficient clinical evidence of pneumothorax
- arterial blood gas offers little over oxygen saturation
- upright chest radiograph (patients unable to tolerate an upright film can be taken in the decubitus position with the suspected side up) — ⭐ **absence of lung markings distal or peripheral to the visceral pleural white line
- displacement of the mediastinum or anterior junction line
- deep sulcus sign** (a larger lateral costodiaphragmatic recess than on the opposite side on frontal view, and the diaphragm may be inverted on the side with the deep sulcus)
- ⭐ a rough estimate of pneumothorax size is sufficient to make clinical decisions
- expiratory film may demonstrate a small pneumothorax but has not been shown to increase the yield of detection
- chest CT is very sensitive for small pneumothorax but has little practical advantage over chest radiograph
- **US — rapid at bedside
- lack of lung sliding and comet-tail artifact signifies pneumothorax
- M-mode confirms pneumothorax with smooth lines above and below the pleural line
- with experience, sensitivity surpasses chest radiograph**
- ECG is often necessary to rule out cardiac etiologies of chest pain — nonspecific changes include T-wave inversion, left axis deviation, and decreased R-wave amplitude
⭐ imaging is the mainstay of the workup; ⭐ DO NOT delay chest decompression if the patient is hemodynamically unstable and there is sufficient clinical evidence of pneumothorax; arterial blood gas offers little over oxygen saturation; upright chest radiograph (patients unable to tolerate an upright film can be taken in the decubitus position with the suspected side up) — ⭐ absence of lung markings distal or peripheral to the visceral pleural white line; displacement of the mediastinum or anterior junction line; deep sulcus sign (a larger lateral costodiaphragmatic recess than on the opposite side on frontal view, and the diaphragm may be inverted on the side with the deep sulcus); ⭐ a rough estimate of pneumothorax size is sufficient to make clinical decisions; expiratory film may demonstrate a small pneumothorax but has not been shown to increase the yield of detection; chest CT is very sensitive for small pneumothorax but has little practical advantage over chest radiograph; US — rapid at bedside; lack of lung sliding and comet-tail artifact signifies pneumothorax; M-mode confirms pneumothorax with smooth lines above and below the pleural line; with experience, sensitivity surpasses chest radiograph; ECG is often necessary to rule out cardiac etiologies of chest pain — nonspecific changes include T-wave inversion, left axis deviation, and decreased R-wave amplitude | - Initial stabilization — cardiac monitor, pulse oximetry, oxygen 100% via nonrebreather face mask, IV access
- suspected tension pneumothorax requires either immediate needle thoracostomy or tube thoracostomy
- see the tension, treatment-pathway, and disposition rows
Initial stabilization — cardiac monitor, pulse oximetry, oxygen 100% via nonrebreather face mask, IV access; suspected tension pneumothorax requires either immediate needle thoracostomy or tube thoracostomy; see the tension, treatment-pathway, and disposition rows | - DO NOT delay chest decompression if the patient is hemodynamically unstable and there is sufficient clinical evidence of pneumothorax
- small pneumothoraces, particularly in mechanically ventilated patients, must not be missed — recognizing them is crucial to preventing tension pneumothorax
- arterial blood gas offers little over oxygen saturation
- expiratory film — has not been shown to increase the yield of detection
- chest CT — very sensitive for small pneumothorax but has little practical advantage over chest radiograph
- ultrasound — user experience required
DO NOT delay chest decompression if the patient is hemodynamically unstable and there is sufficient clinical evidence of pneumothorax; small pneumothoraces, particularly in mechanically ventilated patients, must not be missed — recognizing them is crucial to preventing tension pneumothorax; arterial blood gas offers little over oxygen saturation; expiratory film — has not been shown to increase the yield of detection; chest CT — very sensitive for small pneumothorax but has little practical advantage over chest radiograph; ultrasound — user experience required |
| Pneumothorax — aspiration, Heimlich valve & suction | - Nontraumatic pneumothorax — apply the pathway by collapse size and stability
- simple aspiration is an option for a simple pneumothorax with only 15–30% collapse, or for increase in size of a small pneumothorax during observation
Nontraumatic pneumothorax — apply the pathway by collapse size and stability; simple aspiration is an option for a simple pneumothorax with only 15–30% collapse, or for increase in size of a small pneumothorax during observation | - Repeat chest radiograph to confirm resolution at each step — after aspiration and after catheter removal
- **if the pneumothorax is no longer visible on 2 subsequent chest radiographs at 4 hr intervals, remove the catheter
- if a final chest radiograph is normal 2 hr after the catheter is removed, the patient may be discharged**
Repeat chest radiograph to confirm resolution at each step — after aspiration and after catheter removal; if the pneumothorax is no longer visible on 2 subsequent chest radiographs at 4 hr intervals, remove the catheter; if a final chest radiograph is normal 2 hr after the catheter is removed, the patient may be discharged | - ⭐ nontraumatic pneumothorax estimated at <15% collapse and no cardiovascular or respiratory compromise — observe with 100% oxygen support for 4–6 hr, repeat chest radiograph, and discharge if unchanged
- ⭐ **simple aspiration — place an aspiration catheter (typically 8F) with a 3-way stopcock and aspirate air until resistance or 3 L of air aspirated
- a 2nd aspiration may be attempted if the pneumothorax does not resolve**
- ⭐ **Heimlich valve — indicated when <30% collapse after failure of aspiration
- attach the Heimlich valve to the aspiration catheter or chest tube**
- ⭐ **suction — indicated when the Heimlich valve fails
- attach the aspiration catheter to suction at 20 cm H₂O and observe for 1 hr**
⭐ nontraumatic pneumothorax estimated at <15% collapse and no cardiovascular or respiratory compromise — observe with 100% oxygen support for 4–6 hr, repeat chest radiograph, and discharge if unchanged; ⭐ simple aspiration — place an aspiration catheter (typically 8F) with a 3-way stopcock and aspirate air until resistance or 3 L of air aspirated; a 2nd aspiration may be attempted if the pneumothorax does not resolve; ⭐ Heimlich valve — indicated when <30% collapse after failure of aspiration; attach the Heimlich valve to the aspiration catheter or chest tube; ⭐ suction — indicated when the Heimlich valve fails; attach the aspiration catheter to suction at 20 cm H₂O and observe for 1 hr | — |
| Pneumothorax — disposition, follow-up & procedural pitfalls | - **Admission criteria — tension pneumothorax
- chest tube required**
Admission criteria — tension pneumothorax; chest tube required | - Follow-up chest radiograph to assure re-expansion
- ⭐ **at the 48 hr follow-up — clamp the catheter, observe for 2 hr, and repeat chest radiograph
- remove the thoracic vent or catheter if there is no re-expansion
- observe for 2 hr and repeat the radiograph
- if there is no re-expansion, discharge with 24 hr and 1 wk follow-up**
- ⭐ patients without re-expansion at 1 wk require a cardiothoracic surgery consult
Follow-up chest radiograph to assure re-expansion; ⭐ at the 48 hr follow-up — clamp the catheter, observe for 2 hr, and repeat chest radiograph; remove the thoracic vent or catheter if there is no re-expansion; observe for 2 hr and repeat the radiograph; if there is no re-expansion, discharge with 24 hr and 1 wk follow-up; ⭐ patients without re-expansion at 1 wk require a cardiothoracic surgery consult | - ⭐ discharge criteria — <15% collapse with no expansion while in the ED, or successful aspiration with the catheter removed: discharge with follow-up in 24 hr and 1 wk for chest radiograph to assure re-expansion
- reliable patients with a thoracic vent and successful aspiration, or a secured catheter and Heimlich valve: discharge with 24 and 48 hr follow-up
- **discharge instructions should include prompt return for new onset chest pain or dyspnea
- follow up with pulmonary medicine and/or chest surgery**
- ⭐ **pearls and pitfalls — delay in chest decompression in the unstable patient leads to rapid hemodynamic compromise
- avoid poor tube placement involving kinks or improper depth, which may necessitate repeating the procedure
- avoid placement of the catheter or tube too low on the lateral chest wall, which may lead to iatrogenic abdominal injuries
- failure to detect associated mediastinal or lower neck injuries — if pneumomediastinum is detected, evaluate for esophageal pathology**
⭐ discharge criteria — <15% collapse with no expansion while in the ED, or successful aspiration with the catheter removed: discharge with follow-up in 24 hr and 1 wk for chest radiograph to assure re-expansion; reliable patients with a thoracic vent and successful aspiration, or a secured catheter and Heimlich valve: discharge with 24 and 48 hr follow-up; discharge instructions should include prompt return for new onset chest pain or dyspnea; follow up with pulmonary medicine and/or chest surgery; ⭐ pearls and pitfalls — delay in chest decompression in the unstable patient leads to rapid hemodynamic compromise; avoid poor tube placement involving kinks or improper depth, which may necessitate repeating the procedure; avoid placement of the catheter or tube too low on the lateral chest wall, which may lead to iatrogenic abdominal injuries; failure to detect associated mediastinal or lower neck injuries — if pneumomediastinum is detected, evaluate for esophageal pathology | - Avoid poor tube placement involving kinks or improper depth, which may necessitate repeating the procedure
- avoid placement of the catheter or tube too low on the lateral chest wall — it may lead to iatrogenic abdominal injuries
- do not delay chest decompression in the unstable patient — it leads to rapid hemodynamic compromise
- if pneumomediastinum is detected, evaluate for esophageal pathology
- do not miss associated mediastinal or lower neck injuries
- patients without re-expansion at 1 week require a cardiothoracic surgery consult
Avoid poor tube placement involving kinks or improper depth, which may necessitate repeating the procedure; avoid placement of the catheter or tube too low on the lateral chest wall — it may lead to iatrogenic abdominal injuries; do not delay chest decompression in the unstable patient — it leads to rapid hemodynamic compromise; if pneumomediastinum is detected, evaluate for esophageal pathology; do not miss associated mediastinal or lower neck injuries; patients without re-expansion at 1 week require a cardiothoracic surgery consult |
| Pleural effusion — normal pleural space & classification | - Normally the pleural space contains 0.1–0.2 mL/kg (30 mL in an adult) of clear, low-protein fluid that facilitates movement of the pulmonary parenchyma within the thoracic space
- **fluid formation and reabsorption are governed by hydrostatic and oncotic forces — the sum of these forces moves fluid into the pleural space from the parietal surface and reabsorbs it at the visceral surface, and lymphatics help remove any excess
- alteration of any of these factors results in abnormal fluid accumulation**
Normally the pleural space contains 0.1–0.2 mL/kg (30 mL in an adult) of clear, low-protein fluid that facilitates movement of the pulmonary parenchyma within the thoracic space; fluid formation and reabsorption are governed by hydrostatic and oncotic forces — the sum of these forces moves fluid into the pleural space from the parietal surface and reabsorbs it at the visceral surface, and lymphatics help remove any excess; alteration of any of these factors results in abnormal fluid accumulation | - Small effusions are often asymptomatic
- **dyspnea, pleuritic chest pain, and/or cough
- tachypnea, hypoxia, decreased breath sounds, and/or dullness to percussion**
- **history — the underlying primary pathologic process (CHF, pneumonia, pulmonary embolus, pancreatitis) is often the source of complaints
- dyspnea on exertion or at rest
- cough with a large effusion
- pleuritic chest pain with inflammation of the pleura
- empyema causes fever, fatigue, weight loss**
- **exam — decreased breath sounds, decreased tactile fremitus, increased egophony for large effusions, dullness to chest percussion, and pleural friction rub
- examine for the primary cause of the pleural effusion**
Small effusions are often asymptomatic; dyspnea, pleuritic chest pain, and/or cough; tachypnea, hypoxia, decreased breath sounds, and/or dullness to percussion; history — the underlying primary pathologic process (CHF, pneumonia, pulmonary embolus, pancreatitis) is often the source of complaints; dyspnea on exertion or at rest; cough with a large effusion; pleuritic chest pain with inflammation of the pleura; empyema causes fever, fatigue, weight loss; exam — decreased breath sounds, decreased tactile fremitus, increased egophony for large effusions, dullness to chest percussion, and pleural friction rub; examine for the primary cause of the pleural effusion | - ⭐ **classification — transudative: an ultrafiltrate of serum containing low protein and cells, resulting from an increase in hydrostatic pressure and/or a decrease in oncotic pressure
- the pleural surface is not involved in the primary pathologic process**
- ⭐ exudative: contains high protein and cells, resulting from pathologic disease of the pleural surface leading to membrane permeability and/or disruption of lymphatic reabsorption
- ⭐ identify and treat the underlying cause of the pleural effusion (see the treatment-by-cause and management-ladder rows)
⭐ classification — transudative: an ultrafiltrate of serum containing low protein and cells, resulting from an increase in hydrostatic pressure and/or a decrease in oncotic pressure; the pleural surface is not involved in the primary pathologic process; ⭐ exudative: contains high protein and cells, resulting from pathologic disease of the pleural surface leading to membrane permeability and/or disruption of lymphatic reabsorption; ⭐ identify and treat the underlying cause of the pleural effusion (see the treatment-by-cause and management-ladder rows) | — |
| Pleural effusion — transudative | - ⭐ a pressure problem — due to increased hydrostatic or decreased oncotic pressure
- causes: congestive heart failure, cirrhosis with ascites, peritoneal dialysis, pulmonary embolism, acute atelectasis, nephrotic syndrome, myxedema, hypoproteinemia, superior vena cava syndrome, Meigs syndrome (triad of ascites, benign ovarian tumor, and pleural effusion), and hypoalbuminemia
⭐ a pressure problem — due to increased hydrostatic or decreased oncotic pressure; causes: congestive heart failure, cirrhosis with ascites, peritoneal dialysis, pulmonary embolism, acute atelectasis, nephrotic syndrome, myxedema, hypoproteinemia, superior vena cava syndrome, Meigs syndrome (triad of ascites, benign ovarian tumor, and pleural effusion), and hypoalbuminemia | - ⭐ a transudate typically has a serum glucose equal to pleural fluid glucose and a pH between 7.40 and 7.55
- meets none of Light's criteria (see Light's criteria row)
- CXR shows blunting of the costophrenic angles
⭐ a transudate typically has a serum glucose equal to pleural fluid glucose and a pH between 7.40 and 7.55; meets none of Light's criteria (see Light's criteria row); CXR shows blunting of the costophrenic angles | - ⭐ if the risk of infection is small and the effusion is likely due to CHF — initiate diuresis and follow with serial chest X-rays to assess resolution
- observation if asymptomatic, with serial chest X-rays
⭐ if the risk of infection is small and the effusion is likely due to CHF — initiate diuresis and follow with serial chest X-rays to assess resolution; observation if asymptomatic, with serial chest X-rays | — |
| Pleural effusion — exudative | - ⭐ a permeability problem — due to increased production of fluid from abnormal capillary permeability, or decreased lymphatic clearance from the pleural space
- causes: malignancy, rheumatoid arthritis, vasculitis, lupus
- ⭐ lecture etiology — pulmonary or pleural infection (bacterial, viral, fungal, tuberculosis, parasitic), primary lung cancer, mesothelioma, metastasis (often from breast cancer, ovarian cancer, or lymphoma), pericarditis, pulmonary embolism, intra-abdominal disorders (pancreatitis, hepatitis, cholecystitis, subdiaphragmatic abscess, esophageal rupture, peritonitis), Meigs syndrome, rheumatologic disease (systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis), trauma (hemothorax, chylothorax), and drugs (drug-induced lupus, nitrofurantoin, methysergide, dantrolene, amiodarone, bromocriptine, crack cocaine)
⭐ a permeability problem — due to increased production of fluid from abnormal capillary permeability, or decreased lymphatic clearance from the pleural space; causes: malignancy, rheumatoid arthritis, vasculitis, lupus; ⭐ lecture etiology — pulmonary or pleural infection (bacterial, viral, fungal, tuberculosis, parasitic), primary lung cancer, mesothelioma, metastasis (often from breast cancer, ovarian cancer, or lymphoma), pericarditis, pulmonary embolism, intra-abdominal disorders (pancreatitis, hepatitis, cholecystitis, subdiaphragmatic abscess, esophageal rupture, peritonitis), Meigs syndrome, rheumatologic disease (systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis), trauma (hemothorax, chylothorax), and drugs (drug-induced lupus, nitrofurantoin, methysergide, dantrolene, amiodarone, bromocriptine, crack cocaine) | - ⭐ meets one or more of Light's criteria
- fluid pH tends to be low in empyema due to tuberculosis or anaerobic pathogens, and in rheumatoid involvement of the pleura
- cytology to assess for metastatic cancer to the pleura
⭐ meets one or more of Light's criteria; fluid pH tends to be low in empyema due to tuberculosis or anaerobic pathogens, and in rheumatoid involvement of the pleura; cytology to assess for metastatic cancer to the pleura | - Thoracentesis to identify the cause — infectious, malignancy, chylothorax — or to relieve dyspnea
- ⭐ repeated thoracentesis is acceptable for malignant effusions that reaccumulate, especially when needed infrequently
- ⭐ **pleurodesis — malignant effusions drained by chest tube may be sclerosed to prevent recurrence
- the sclerosing agent is introduced through the chest tube (slurry) or by thoracoscopic surgical procedure (talc poudrage) after drainage is complete**
Thoracentesis to identify the cause — infectious, malignancy, chylothorax — or to relieve dyspnea; ⭐ repeated thoracentesis is acceptable for malignant effusions that reaccumulate, especially when needed infrequently; ⭐ pleurodesis — malignant effusions drained by chest tube may be sclerosed to prevent recurrence; the sclerosing agent is introduced through the chest tube (slurry) or by thoracoscopic surgical procedure (talc poudrage) after drainage is complete | - Pleurodesis — the sclerosing agent is introduced only after drainage is complete (slurry through the chest tube or talc poudrage)
Pleurodesis — the sclerosing agent is introduced only after drainage is complete (slurry through the chest tube or talc poudrage) |
| Parapneumonic effusion | - ⭐ pleural effusions that form in the pleural space adjacent to a pneumonia
- fever, especially if the fluid is infected
- dullness on percussion with diminished or absent breath sounds over the affected area
- pleural friction rub
⭐ pleural effusions that form in the pleural space adjacent to a pneumonia; fever, especially if the fluid is infected; dullness on percussion with diminished or absent breath sounds over the affected area; pleural friction rub | - Thoracentesis with laboratory evaluation — cell count and differential including WBC
- chemistries (serum and pleural fluid total protein, glucose, LDH, amylase, triglycerides)
- Gram stain and cultures (aerobic and anaerobic bacteria, acid-fast bacilli, fungi)
- fluid pH
- cytology
Thoracentesis with laboratory evaluation — cell count and differential including WBC; chemistries (serum and pleural fluid total protein, glucose, LDH, amylase, triglycerides); Gram stain and cultures (aerobic and anaerobic bacteria, acid-fast bacilli, fungi); fluid pH; cytology | - Thoracentesis as indicated
- treat the underlying pneumonia (see CAP and HAP/VAP rows)
- ⭐ empyema requires chest tube insertion and probable surgical intervention — antimicrobials alone are not curative when empyema is present
Thoracentesis as indicated; treat the underlying pneumonia (see CAP and HAP/VAP rows); ⭐ empyema requires chest tube insertion and probable surgical intervention — antimicrobials alone are not curative when empyema is present | - Empyema — antimicrobials alone are not curative
- it requires chest tube insertion and probable surgical intervention
Empyema — antimicrobials alone are not curative; it requires chest tube insertion and probable surgical intervention |
| Empyema | - ⭐ infection and pus in the pleural space
- fever, especially if the fluid is infected
- dullness on percussion with diminished or absent breath sounds over the affected area
- pleural friction rub
⭐ infection and pus in the pleural space; fever, especially if the fluid is infected; dullness on percussion with diminished or absent breath sounds over the affected area; pleural friction rub | - Thoracentesis — ⭐ fluid pH tends to be low in empyema due to tuberculosis or anaerobic pathogens
- Gram stain and cultures — bacteria (aerobic and anaerobic), acid-fast bacilli, fungi
- ⭐ select all antimicrobials on pleural fluid culture results, including sensitivity data
Thoracentesis — ⭐ fluid pH tends to be low in empyema due to tuberculosis or anaerobic pathogens; Gram stain and cultures — bacteria (aerobic and anaerobic), acid-fast bacilli, fungi; ⭐ select all antimicrobials on pleural fluid culture results, including sensitivity data | - ⭐ requires chest tube insertion and probable surgical intervention
- ⭐ antimicrobials alone are not curative when empyema is present
- select all antimicrobials on pleural fluid culture results, including sensitivity data
⭐ requires chest tube insertion and probable surgical intervention; ⭐ antimicrobials alone are not curative when empyema is present; select all antimicrobials on pleural fluid culture results, including sensitivity data | - Antimicrobials alone are not curative when empyema is present — chest tube insertion and probable surgical intervention are required
- select all antimicrobials on pleural fluid culture results, including sensitivity data
Antimicrobials alone are not curative when empyema is present — chest tube insertion and probable surgical intervention are required; select all antimicrobials on pleural fluid culture results, including sensitivity data |
| Hemothorax | - ⭐ accumulation of blood in the intrapleural space after blunt/penetrating chest trauma or other nontraumatic etiology
- results in decreased vital capacity, hypoxia, and respiratory compromise
- loss of large intravascular volume causes hemodynamic instability and hemorrhagic shock
- massive hemothorax can increase intrathoracic pressure, resulting in compromised venous return and decreased cardiac output
- ⭐ **small amount (<400 mL) — little or no change in the patient's appearance, vital signs, or physical findings
- large amount (>1,000 mL) — restlessness, anxiety, pallor, pleuritic chest pain, hemoptysis, dyspnea, or air hunger
- signs of shock with loss of blood volume ≥30% (1,500–2,000 mL) — tachycardia, tachypnea, hypotension**
- with insidious onset (e.g., malignancy) dyspnea is the most common presenting sign, since blood loss is usually not acute enough to produce a visible hemodynamic response
- exam — **asymmetric chest expansion, gross deformity, paradoxical wall movement, abrasion, hematoma, contusion
- tenderness or crepitus over ribs, clavicles, scapulae, or the sternum
- SC emphysema
- dullness to percussion
- decreased or absent breath sounds over the ipsilateral side (best appreciated in the upright patient)
- JVD if increased intrathoracic pressure
- tracheal deviation**
⭐ accumulation of blood in the intrapleural space after blunt/penetrating chest trauma or other nontraumatic etiology; results in decreased vital capacity, hypoxia, and respiratory compromise; loss of large intravascular volume causes hemodynamic instability and hemorrhagic shock; massive hemothorax can increase intrathoracic pressure, resulting in compromised venous return and decreased cardiac output; ⭐ small amount (<400 mL) — little or no change in the patient's appearance, vital signs, or physical findings; large amount (>1,000 mL) — restlessness, anxiety, pallor, pleuritic chest pain, hemoptysis, dyspnea, or air hunger; signs of shock with loss of blood volume ≥30% (1,500–2,000 mL) — tachycardia, tachypnea, hypotension; with insidious onset (e.g., malignancy) dyspnea is the most common presenting sign, since blood loss is usually not acute enough to produce a visible hemodynamic response; exam — asymmetric chest expansion, gross deformity, paradoxical wall movement, abrasion, hematoma, contusion; tenderness or crepitus over ribs, clavicles, scapulae, or the sternum; SC emphysema; dullness to percussion; decreased or absent breath sounds over the ipsilateral side (best appreciated in the upright patient); JVD if increased intrathoracic pressure; tracheal deviation | - ⭐ **CXR is the ideal diagnostic tool — in the hemodynamically stable patient an upright posteroanterior (PA) projection at full inspiration is optimal
- fluid collections >200–300 mL can usually be seen on upright or decubitus CXR, shown as a meniscus/fluid level blunting the costophrenic angle**
- ⭐ in the supine anteroposterior (portable) radiograph up to 1,000 mL of blood may not be readily apparent — only a slight hazy infiltrate over the involved hemothorax may be seen
- look for associated injuries (pneumothorax, rib fractures, pulmonary contusion, widened mediastinum)
- ⭐ the pleural fluid removed should reveal a hematocrit >50% of the blood hematocrit
- **hematocrit may be helpful if it shows a drop or changes on serial evaluations
- type and cross-match
- pulse oximetry, ABG**
- **US — an extended FAST scan can diagnose hemothorax with a higher sensitivity than a portable CXR in trained hands
- CT is useful in detecting small amounts of intrapleural fluid not visible on the chest radiograph**
- ⭐ **delayed hemothorax can occur hours to days later without initial evidence of intrathoracic pathology on CXR
- it may be related to rupture of a chest wall hematoma or disruption of intercostal vessels by rib fracture edges during movement**
- **history — acute blunt or penetrating trauma to the chest
- recent rib fracture or flail chest
- malignancy or metastatic disease
- recent surgical procedure (thoracentesis, thoracostomy)**
⭐ CXR is the ideal diagnostic tool — in the hemodynamically stable patient an upright posteroanterior (PA) projection at full inspiration is optimal; fluid collections >200–300 mL can usually be seen on upright or decubitus CXR, shown as a meniscus/fluid level blunting the costophrenic angle; ⭐ in the supine anteroposterior (portable) radiograph up to 1,000 mL of blood may not be readily apparent — only a slight hazy infiltrate over the involved hemothorax may be seen; look for associated injuries (pneumothorax, rib fractures, pulmonary contusion, widened mediastinum); ⭐ the pleural fluid removed should reveal a hematocrit >50% of the blood hematocrit; hematocrit may be helpful if it shows a drop or changes on serial evaluations; type and cross-match; pulse oximetry, ABG; US — an extended FAST scan can diagnose hemothorax with a higher sensitivity than a portable CXR in trained hands; CT is useful in detecting small amounts of intrapleural fluid not visible on the chest radiograph; ⭐ delayed hemothorax can occur hours to days later without initial evidence of intrathoracic pathology on CXR; it may be related to rupture of a chest wall hematoma or disruption of intercostal vessels by rib fracture edges during movement; history — acute blunt or penetrating trauma to the chest; recent rib fracture or flail chest; malignancy or metastatic disease; recent surgical procedure (thoracentesis, thoracostomy) | - ⭐ if the fluid is bloody, insertion of a chest tube is often required
- thoracentesis is both diagnostic and therapeutic (relieves dyspnea)
- ⭐ **cautions — it is difficult to differentiate hemothoraces from pneumothoraces clinically, since all may present with dyspnea, pleuritic chest pain, decreased breath sounds, and hemodynamic instability
- clues are SC emphysema for pneumothorax and dullness to percussion for hemothorax**
- see the hemothorax management row for tube size, thoracotomy indications, and sedation doses
⭐ if the fluid is bloody, insertion of a chest tube is often required; thoracentesis is both diagnostic and therapeutic (relieves dyspnea); ⭐ cautions — it is difficult to differentiate hemothoraces from pneumothoraces clinically, since all may present with dyspnea, pleuritic chest pain, decreased breath sounds, and hemodynamic instability; clues are SC emphysema for pneumothorax and dullness to percussion for hemothorax; see the hemothorax management row for tube size, thoracotomy indications, and sedation doses | - It is difficult to differentiate hemothoraces from pneumothoraces clinically — all may present with dyspnea, pleuritic chest pain, decreased breath sounds and hemodynamic instability
- clues — subcutaneous emphysema for pneumothorax, dullness to percussion for hemothorax
- a bloody effusion often requires chest tube insertion
It is difficult to differentiate hemothoraces from pneumothoraces clinically — all may present with dyspnea, pleuritic chest pain, decreased breath sounds and hemodynamic instability; clues — subcutaneous emphysema for pneumothorax, dullness to percussion for hemothorax; a bloody effusion often requires chest tube insertion |
| Hemothorax — etiology & complications | - ⭐ bleeding is usually the result of disruption of the tissues/vessels of the chest wall, pleura, or intrathoracic structures
- traumatic injuries (including iatrogenic) to major blood vessels — intercostal artery, internal mammary artery, pulmonary artery, pulmonary vein, aorta, vena cava, and heart
- traumatic lung parenchymal injuries often stop spontaneously as a result of low pulmonary pressures and high concentrations of thromboplastin in the lung, and are often associated with pneumothorax
- ⭐ nontraumatic or spontaneous hemothoraces are very rare — consider coagulation disorder, malignancy, primary vascular event (such as aortic dissection, ruptured aneurysm), PE with infarction, infection (TB), bullous emphysema, pulmonary AV malformation, or lobar sequestration
- torn pleural adhesions as a complication of spontaneous pneumothorax or tube thoracostomy
⭐ bleeding is usually the result of disruption of the tissues/vessels of the chest wall, pleura, or intrathoracic structures; traumatic injuries (including iatrogenic) to major blood vessels — intercostal artery, internal mammary artery, pulmonary artery, pulmonary vein, aorta, vena cava, and heart; traumatic lung parenchymal injuries often stop spontaneously as a result of low pulmonary pressures and high concentrations of thromboplastin in the lung, and are often associated with pneumothorax; ⭐ nontraumatic or spontaneous hemothoraces are very rare — consider coagulation disorder, malignancy, primary vascular event (such as aortic dissection, ruptured aneurysm), PE with infarction, infection (TB), bullous emphysema, pulmonary AV malformation, or lobar sequestration; torn pleural adhesions as a complication of spontaneous pneumothorax or tube thoracostomy | - ⭐ rarely a solitary finding in blunt trauma — commonly associated with pneumothorax (25% of cases), extrathoracic injuries (73% of cases), and pulmonary contusion
- large hemothoraces cause the release of substances that can act as anticoagulants and contribute to continued intrathoracic bleeding
⭐ rarely a solitary finding in blunt trauma — commonly associated with pneumothorax (25% of cases), extrathoracic injuries (73% of cases), and pulmonary contusion; large hemothoraces cause the release of substances that can act as anticoagulants and contribute to continued intrathoracic bleeding | - ⭐ if left untreated, hemothorax can lead to empyema and fibrothorax (lung trapping due to adhesions)
- provide definitive treatment promptly — see the hemothorax management row
⭐ if left untreated, hemothorax can lead to empyema and fibrothorax (lung trapping due to adhesions); provide definitive treatment promptly — see the hemothorax management row | - If left untreated, hemothorax can lead to empyema and fibrothorax (lung trapping due to adhesions)
- delayed hemothorax can occur hours to days later without initial evidence of intrathoracic pathology on CXR
- without a clear history of trauma, the CXR may be incorrectly read as pneumonia
- if there is a concurrent diaphragmatic injury, a hemothorax may have an intra-abdominal origin
If left untreated, hemothorax can lead to empyema and fibrothorax (lung trapping due to adhesions); delayed hemothorax can occur hours to days later without initial evidence of intrathoracic pathology on CXR; without a clear history of trauma, the CXR may be incorrectly read as pneumonia; if there is a concurrent diaphragmatic injury, a hemothorax may have an intra-abdominal origin |
| Hemothorax — management, thoracotomy indications & pearls | - ⭐ the pleural cavity of an average 70 kg man can hold over 4 L of blood, so an exsanguinating hemorrhage can occur without any evidence of external blood loss
- auscultation and percussion of a supine trauma patient with substantial hemothorax may produce equivocal findings due to distribution of blood along the entire posterior aspect of the pleural space
- without a clear history of trauma, the chest radiograph may be incorrectly read as pneumonia
⭐ the pleural cavity of an average 70 kg man can hold over 4 L of blood, so an exsanguinating hemorrhage can occur without any evidence of external blood loss; auscultation and percussion of a supine trauma patient with substantial hemothorax may produce equivocal findings due to distribution of blood along the entire posterior aspect of the pleural space; without a clear history of trauma, the chest radiograph may be incorrectly read as pneumonia | - Obtain an upright chest radiograph as quickly as possible, but if the patient is unstable do not wait to administer definitive therapy
- correct placement and adequate drainage is confirmed via chest radiograph
- type and cross-match and serial hematocrit
Obtain an upright chest radiograph as quickly as possible, but if the patient is unstable do not wait to administer definitive therapy; correct placement and adequate drainage is confirmed via chest radiograph; type and cross-match and serial hematocrit | - **Manage airway, breathing, circulation — control the airway as needed with endotracheal intubation for impending respiratory failure
- supplemental oxygen
- 2 large-bore IV access sites and a fluid bolus to restore circulating blood volume**
- **needle thoracostomy should be performed in patients with hemodynamic instability unless a chest tube kit is immediately available
- position the patient sitting upright unless contraindicated**
- ⭐ hemothorax is treated by evacuating the accumulated blood — tube thoracostomy evacuates blood, allows re-expansion of the lung, and provides constant monitoring of blood loss: use a large-bore chest tube (36–40Fr), insert in the 4th–5th intercostal space at the mid-axillary line aiming posteriorly and superiorly, then connect to underwater-seal drainage and suction (20–30 mL H₂O)
- autotransfusion should be used if available to replace blood loss — prepare for it early, as most blood loss occurs on initial chest tube insertion
- ⭐ **indications for OR thoracotomy — initial tube drainage >20 mL/kg of blood (or 1,000 mL of blood for adults from the pleural cavity)
- persistent bleeding at a rate >7 mL/kg/hr (or 200 mL/hr for 4 hr)
- increasing hemothorax seen on chest radiography
- patient remains hypotensive despite adequate blood replacement and other sites of blood loss have been ruled out
- patient decompensates after initial response to resuscitation**
- ⭐ **indications for ED thoracotomy — penetrating trauma: traumatic arrest in the ED or within 10 min of ED arrival, or severe shock with clinical signs of cardiac tamponade
- blunt trauma: traumatic arrest in the ED at a trauma center or with a surgeon available within 10 min**
- **medication — local anesthetics for cutaneous anesthesia prior to tube thoracostomy in awake, conscious patients
- procedural sedation and analgesia for stable, awake patients: fentanyl 2–5 μg/kg per dose and midazolam 0.02–0.04 mg/kg per dose**
- ⭐ **be sure all chest tube fenestrations are within the thoracic cavity
- prophylactic antibiotics administered with chest tube insertion do not decrease the risk of pneumonia or empyema
- in the supine trauma patient a common error is chest tube placement too anterior and superior, making complete drainage difficult
- if there is a concurrent diaphragmatic injury, a hemothorax may have an intra-abdominal origin**
Manage airway, breathing, circulation — control the airway as needed with endotracheal intubation for impending respiratory failure; supplemental oxygen; 2 large-bore IV access sites and a fluid bolus to restore circulating blood volume; needle thoracostomy should be performed in patients with hemodynamic instability unless a chest tube kit is immediately available; position the patient sitting upright unless contraindicated; ⭐ hemothorax is treated by evacuating the accumulated blood — tube thoracostomy evacuates blood, allows re-expansion of the lung, and provides constant monitoring of blood loss: use a large-bore chest tube (36–40Fr), insert in the 4th–5th intercostal space at the mid-axillary line aiming posteriorly and superiorly, then connect to underwater-seal drainage and suction (20–30 mL H₂O); autotransfusion should be used if available to replace blood loss — prepare for it early, as most blood loss occurs on initial chest tube insertion; ⭐ indications for OR thoracotomy — initial tube drainage >20 mL/kg of blood (or 1,000 mL of blood for adults from the pleural cavity); persistent bleeding at a rate >7 mL/kg/hr (or 200 mL/hr for 4 hr); increasing hemothorax seen on chest radiography; patient remains hypotensive despite adequate blood replacement and other sites of blood loss have been ruled out; patient decompensates after initial response to resuscitation; ⭐ indications for ED thoracotomy — penetrating trauma: traumatic arrest in the ED or within 10 min of ED arrival, or severe shock with clinical signs of cardiac tamponade; blunt trauma: traumatic arrest in the ED at a trauma center or with a surgeon available within 10 min; medication — local anesthetics for cutaneous anesthesia prior to tube thoracostomy in awake, conscious patients; procedural sedation and analgesia for stable, awake patients: fentanyl 2–5 μg/kg per dose and midazolam 0.02–0.04 mg/kg per dose; ⭐ be sure all chest tube fenestrations are within the thoracic cavity; prophylactic antibiotics administered with chest tube insertion do not decrease the risk of pneumonia or empyema; in the supine trauma patient a common error is chest tube placement too anterior and superior, making complete drainage difficult; if there is a concurrent diaphragmatic injury, a hemothorax may have an intra-abdominal origin | - Position the patient sitting upright unless contraindicated
- if the patient is unstable, do not wait for an upright CXR to administer definitive therapy
- prophylactic antibiotics administered with chest tube insertion do not decrease the risk of pneumonia or empyema
- a common error in the supine trauma patient is chest tube placement too anterior and superior, making complete drainage difficult
- be sure all chest tube fenestrations are within the thoracic cavity
- auscultation and percussion of a supine trauma patient with substantial hemothorax may produce equivocal findings
- an exsanguinating hemorrhage can occur without any evidence of external blood loss — the pleural cavity of an average 70 kg man can hold over 4 L
Position the patient sitting upright unless contraindicated; if the patient is unstable, do not wait for an upright CXR to administer definitive therapy; prophylactic antibiotics administered with chest tube insertion do not decrease the risk of pneumonia or empyema; a common error in the supine trauma patient is chest tube placement too anterior and superior, making complete drainage difficult; be sure all chest tube fenestrations are within the thoracic cavity; auscultation and percussion of a supine trauma patient with substantial hemothorax may produce equivocal findings; an exsanguinating hemorrhage can occur without any evidence of external blood loss — the pleural cavity of an average 70 kg man can hold over 4 L |
| Chylothorax | - ⭐ thoracic duct injury — injury of the thoracic ducts with accumulation of chyle in the pleural space
- dyspnea, pleuritic chest pain, tachypnea
- dullness on percussion with diminished or absent breath sounds over the affected area
⭐ thoracic duct injury — injury of the thoracic ducts with accumulation of chyle in the pleural space; dyspnea, pleuritic chest pain, tachypnea; dullness on percussion with diminished or absent breath sounds over the affected area | - ⭐ thoracentesis is indicated when you need to identify the cause — infectious, malignancy, chylothorax
- laboratory evaluation of pleural fluid includes triglycerides (serum and pleural fluid chemistries — total protein, glucose, LDH, amylase, triglycerides)
⭐ thoracentesis is indicated when you need to identify the cause — infectious, malignancy, chylothorax; laboratory evaluation of pleural fluid includes triglycerides (serum and pleural fluid chemistries — total protein, glucose, LDH, amylase, triglycerides) | - Thoracentesis to identify the cause and to relieve dyspnea (the source states no other chylothorax-specific therapy)
Thoracentesis to identify the cause and to relieve dyspnea (the source states no other chylothorax-specific therapy) | — |
| Pleural effusion — CXR detection volumes by view | - CXR: ⭐ blunting of the costophrenic angles — a linear shadow ascending vertically and clinging to the ribs in a meniscus pattern
- fluid may layer out on decubitus films, or loculate along the lateral chest wall (confirmed by ultrasound or CT)
- also dyspnea, pleuritic chest pain, tachypnea, dullness on percussion with diminished or absent breath sounds over the affected area, pleural friction rub, fever especially if the fluid is infected
CXR: ⭐ blunting of the costophrenic angles — a linear shadow ascending vertically and clinging to the ribs in a meniscus pattern; fluid may layer out on decubitus films, or loculate along the lateral chest wall (confirmed by ultrasound or CT); also dyspnea, pleuritic chest pain, tachypnea, dullness on percussion with diminished or absent breath sounds over the affected area, pleural friction rub, fever especially if the fluid is infected | - ⭐ lateral decubitus view — as little as 5 mL may blunt the costophrenic angle (most sensitive view)
- ⭐ lateral chest X-ray — at least 75 mL of pleural fluid needed (intermediate)
- ⭐ posteroanterior chest X-ray — at least 200 mL of pleural fluid needed (least sensitive)
- ⭐ lecture — the upright chest film requires at least 200–250 mL of fluid to blunt the costophrenic angle, and the lateral decubitus film can identify as little as 5–10 mL
- **subpulmonic effusions may be indicated by loss of supradiaphragmatic vascular markings or an increased space between the gastric bubble and the pulmonary parenchyma
- suspect a loculated effusion or alternative diagnosis if the effusion fails to layer**
- **US — has similar sensitivity to the lateral decubitus film and can detect as little as 5–10 mL
- can differentiate simple effusions from loculated fluid collections
- improves patient safety and decreases the risk of pneumothorax for thoracentesis**
- ⭐ CT chest with IV contrast is the most sensitive study for detecting pleural fluid collections and identifying loculated effusions, and is useful for determining an underlying lung process such as masses and pleural thickening
- ⭐ **ALERT — consider pulmonary embolism as a cause of unexplained pleural effusion
- obtain lateral decubitus films or bedside US prior to performing thoracentesis to avoid misdiagnosis and procedural complications**
⭐ lateral decubitus view — as little as 5 mL may blunt the costophrenic angle (most sensitive view); ⭐ lateral chest X-ray — at least 75 mL of pleural fluid needed (intermediate); ⭐ posteroanterior chest X-ray — at least 200 mL of pleural fluid needed (least sensitive); ⭐ lecture — the upright chest film requires at least 200–250 mL of fluid to blunt the costophrenic angle, and the lateral decubitus film can identify as little as 5–10 mL; subpulmonic effusions may be indicated by loss of supradiaphragmatic vascular markings or an increased space between the gastric bubble and the pulmonary parenchyma; suspect a loculated effusion or alternative diagnosis if the effusion fails to layer; US — has similar sensitivity to the lateral decubitus film and can detect as little as 5–10 mL; can differentiate simple effusions from loculated fluid collections; improves patient safety and decreases the risk of pneumothorax for thoracentesis; ⭐ CT chest with IV contrast is the most sensitive study for detecting pleural fluid collections and identifying loculated effusions, and is useful for determining an underlying lung process such as masses and pleural thickening; ⭐ ALERT — consider pulmonary embolism as a cause of unexplained pleural effusion; obtain lateral decubitus films or bedside US prior to performing thoracentesis to avoid misdiagnosis and procedural complications | - Choose the lateral decubitus view when a small effusion is suspected
- confirm loculation with ultrasound or CT
- proceed to thoracentesis for diagnosis or symptom relief
Choose the lateral decubitus view when a small effusion is suspected; confirm loculation with ultrasound or CT; proceed to thoracentesis for diagnosis or symptom relief | - Obtain lateral decubitus films, or bedside ultrasound, before performing thoracentesis to avoid misdiagnosis and procedural complications
- suspect a loculated effusion or an alternative diagnosis if the effusion fails to layer
- consider pulmonary embolism as a cause of unexplained pleural effusion
Obtain lateral decubitus films, or bedside ultrasound, before performing thoracentesis to avoid misdiagnosis and procedural complications; suspect a loculated effusion or an alternative diagnosis if the effusion fails to layer; consider pulmonary embolism as a cause of unexplained pleural effusion |
| Light's criteria | - ⭐ exudate if one or more of the three criteria is present — the classification drives the entire workup
⭐ exudate if one or more of the three criteria is present — the classification drives the entire workup | - ⭐ pleural fluid protein : serum protein > 0.5
- ⭐ pleural fluid LDH : serum LDH > 0.6
- ⭐ pleural fluid LDH more than two-thirds the upper limit of normal serum LDH
- ⭐ a transudate typically has a serum glucose equal to pleural fluid glucose and a pH between 7.40 and 7.55
⭐ pleural fluid protein : serum protein > 0.5; ⭐ pleural fluid LDH : serum LDH > 0.6; ⭐ pleural fluid LDH more than two-thirds the upper limit of normal serum LDH; ⭐ a transudate typically has a serum glucose equal to pleural fluid glucose and a pH between 7.40 and 7.55 | - Use the result to direct therapy: transudate likely due to CHF → initiate diuresis and follow with serial chest X-rays
- exudate → identify the cause (infectious, malignancy, chylothorax) with thoracentesis and fluid analysis
Use the result to direct therapy: transudate likely due to CHF → initiate diuresis and follow with serial chest X-rays; exudate → identify the cause (infectious, malignancy, chylothorax) with thoracentesis and fluid analysis | — |
| Thoracentesis — indications & fluid analysis | - Indicated when you need to identify the cause — infectious, malignancy, chylothorax — and when the patient is dyspneic (therapeutic, and can be diagnostic when fluid is sent for laboratory evaluation)
Indicated when you need to identify the cause — infectious, malignancy, chylothorax — and when the patient is dyspneic (therapeutic, and can be diagnostic when fluid is sent for laboratory evaluation) | - ⭐ cell count and differential including WBC
- chemistries — serum and pleural fluid levels of total protein, glucose, LDH, amylase, triglycerides
- Gram stain and cultures — bacteria (aerobic and anaerobic), acid-fast bacilli, fungi
- ⭐ fluid pH tends to be low in empyema due to tuberculosis or anaerobic pathogens, and in rheumatoid involvement of the pleura
- cytology to assess for metastatic cancer to the pleura
⭐ cell count and differential including WBC; chemistries — serum and pleural fluid levels of total protein, glucose, LDH, amylase, triglycerides; Gram stain and cultures — bacteria (aerobic and anaerobic), acid-fast bacilli, fungi; ⭐ fluid pH tends to be low in empyema due to tuberculosis or anaerobic pathogens, and in rheumatoid involvement of the pleura; cytology to assess for metastatic cancer to the pleura | - ⭐ **management ladder: 1) observation if asymptomatic, with serial chest X-rays
- 2) if the risk of infection is small and the effusion is likely due to CHF, initiate diuresis and follow with serial chest X-rays
- 3) thoracentesis
- 4) if bloody → chest tube
- 5) empyema → chest tube and probable surgery**
- repeated thoracentesis is acceptable for malignant effusions that reaccumulate, especially when needed infrequently
- pleurodesis for malignant effusions drained by chest tube
⭐ management ladder: 1) observation if asymptomatic, with serial chest X-rays; 2) if the risk of infection is small and the effusion is likely due to CHF, initiate diuresis and follow with serial chest X-rays; 3) thoracentesis; 4) if bloody → chest tube; 5) empyema → chest tube and probable surgery; repeated thoracentesis is acceptable for malignant effusions that reaccumulate, especially when needed infrequently; pleurodesis for malignant effusions drained by chest tube | — |
| Thoracentesis — technique, contraindications & complications | - No absolute contraindications
- ⭐ **relative contraindications — platelets <50,000/mm³
- prothrombin and partial thromboplastin time >2 × normal level
- serum creatinine >6
- correct coagulopathy if present**
- **indications — diagnose a new effusion in a toxic patient
- relieve symptomatic dyspnea caused by large effusions
- diagnostic thoracentesis in a stable patient can be deferred until after the patient has been admitted**
No absolute contraindications; ⭐ relative contraindications — platelets <50,000/mm³; prothrombin and partial thromboplastin time >2 × normal level; serum creatinine >6; correct coagulopathy if present; indications — diagnose a new effusion in a toxic patient; relieve symptomatic dyspnea caused by large effusions; diagnostic thoracentesis in a stable patient can be deferred until after the patient has been admitted | - **Position the patient upright with arms crossed in front to elevate the scapula
- identify the superior border of the effusion with US, percussion, or egophony, then mark the area 1 interspace below this in the posterior axillary line or the midscapular line
- prepare the area with Betadine, dry, and drape for a sterile field
- anesthetize with 2% lidocaine
- attach a 3-way stopcock between needle and syringe
- enter the superior border of the rib with the needle bevel down, aspirating while advancing**
- ⭐ **use a 20G needle for diagnostic aspiration and a 16G–18G needle/catheter (commercial kit) for therapeutic aspiration
- advance the catheter once the pleural space is entered**
- ⭐ **a minimum of 100 cc is required for basic studies (protein, LDH, cell count, Gram stain and culture) — more for cytology/additional studies
- avoid withdrawing >1,500 cc to prevent re-expansion pulmonary edema**
Position the patient upright with arms crossed in front to elevate the scapula; identify the superior border of the effusion with US, percussion, or egophony, then mark the area 1 interspace below this in the posterior axillary line or the midscapular line; prepare the area with Betadine, dry, and drape for a sterile field; anesthetize with 2% lidocaine; attach a 3-way stopcock between needle and syringe; enter the superior border of the rib with the needle bevel down, aspirating while advancing; ⭐ use a 20G needle for diagnostic aspiration and a 16G–18G needle/catheter (commercial kit) for therapeutic aspiration; advance the catheter once the pleural space is entered; ⭐ a minimum of 100 cc is required for basic studies (protein, LDH, cell count, Gram stain and culture) — more for cytology/additional studies; avoid withdrawing >1,500 cc to prevent re-expansion pulmonary edema | - ⭐ intraprocedural chest pain may indicate trapped lung or pneumothorax — stop the procedure and obtain a chest radiograph
- after obtaining fluid, withdraw the needle, apply pressure, dress, and obtain a post-procedural chest radiograph for pneumothorax
- bedside US improves patient safety and decreases the risk of pneumothorax
⭐ intraprocedural chest pain may indicate trapped lung or pneumothorax — stop the procedure and obtain a chest radiograph; after obtaining fluid, withdraw the needle, apply pressure, dress, and obtain a post-procedural chest radiograph for pneumothorax; bedside US improves patient safety and decreases the risk of pneumothorax | - No absolute contraindications
- relative contraindications — platelets < 50,000/mm³, prothrombin and partial thromboplastin time > 2 × normal, serum creatinine > 6 — correct coagulopathy if present
- avoid withdrawing more than 1,500 cc to prevent re-expansion pulmonary edema
- intraprocedural chest pain may indicate trapped lung or pneumothorax — stop the procedure and obtain a chest radiograph
- bedside ultrasound improves patient safety and decreases the risk of pneumothorax
No absolute contraindications; relative contraindications — platelets < 50,000/mm³, prothrombin and partial thromboplastin time > 2 × normal, serum creatinine > 6 — correct coagulopathy if present; avoid withdrawing more than 1,500 cc to prevent re-expansion pulmonary edema; intraprocedural chest pain may indicate trapped lung or pneumothorax — stop the procedure and obtain a chest radiograph; bedside ultrasound improves patient safety and decreases the risk of pneumothorax |
| Pleural effusion — treatment by underlying cause | - ⭐ emergency — ABCs, high-flow oxygen for shortness of breath, and emergent thoracentesis for significant respiratory compromise
- bloody effusion is not a contraindication to anticoagulation
⭐ emergency — ABCs, high-flow oxygen for shortness of breath, and emergent thoracentesis for significant respiratory compromise; bloody effusion is not a contraindication to anticoagulation | - **Differential diagnosis to consider — intraparenchymal densities (lobar collapse, mass/tumor/infiltrative disease, pneumonia)
- pleural densities (pleural scarring, mesothelioma, metastatic disease)
- other (herniated abdominal contents, paralyzed diaphragm)**
- ⭐ **consider pulmonary embolism as a cause of unexplained pleural effusion
- obtain lateral decubitus films or bedside US prior to performing thoracentesis to avoid misdiagnosis and procedural complications**
Differential diagnosis to consider — intraparenchymal densities (lobar collapse, mass/tumor/infiltrative disease, pneumonia); pleural densities (pleural scarring, mesothelioma, metastatic disease); other (herniated abdominal contents, paralyzed diaphragm); ⭐ consider pulmonary embolism as a cause of unexplained pleural effusion; obtain lateral decubitus films or bedside US prior to performing thoracentesis to avoid misdiagnosis and procedural complications | - Identify and treat the underlying pathologic process
- ⭐ **CHF — diuresis
- parapneumonic effusion — antibiotics
- pulmonary embolism — anticoagulation
- rheumatologic disease — NSAIDs and steroids
- loculated effusion — injection of streptokinase or urokinase into the pleural space by a thoracic surgeon or pulmonologist**
- **surgical consult for tube thoracostomy if empyema is found
- consult interventional radiology or pulmonology for loculated effusions**
- ⭐ **indications for tube thoracostomy — loculated effusion
- aspiration of pus
- complicated parapneumonic effusion with pH <7, or pleural glucose <60 mg/dL, or positive pleural Gram stain or culture
- hemothorax**
Identify and treat the underlying pathologic process; ⭐ CHF — diuresis; parapneumonic effusion — antibiotics; pulmonary embolism — anticoagulation; rheumatologic disease — NSAIDs and steroids; loculated effusion — injection of streptokinase or urokinase into the pleural space by a thoracic surgeon or pulmonologist; surgical consult for tube thoracostomy if empyema is found; consult interventional radiology or pulmonology for loculated effusions; ⭐ indications for tube thoracostomy — loculated effusion; aspiration of pus; complicated parapneumonic effusion with pH <7, or pleural glucose <60 mg/dL, or positive pleural Gram stain or culture; hemothorax | - A bloody effusion is not a contraindication to anticoagulation in pulmonary embolism
A bloody effusion is not a contraindication to anticoagulation in pulmonary embolism |
| Pleural effusion — disposition & admission criteria | - ⭐ **admission criteria — respiratory compromise
- unknown cause of the effusion
- primary process requires hospitalization
- presence or suspected parapneumonic effusion or empyema
- ICU admission for severe hemodynamic and respiratory compromise**
⭐ admission criteria — respiratory compromise; unknown cause of the effusion; primary process requires hospitalization; presence or suspected parapneumonic effusion or empyema; ICU admission for severe hemodynamic and respiratory compromise | - Observation for 6 hr or admission for potential complications of thoracentesis — pneumothorax, re-expansion pulmonary edema
Observation for 6 hr or admission for potential complications of thoracentesis — pneumothorax, re-expansion pulmonary edema | - ⭐ **discharge criteria — the source of the pleural effusion is known
- no evidence of respiratory compromise exists
- the majority of effusions will resolve if the primary process is treated appropriately
- the patient must be reliable and have access to a telephone, a supportive social environment, and adequate follow-up**
- **arrange appropriate follow-up with an oncologist or pulmonologist prior to discharge
- instruct patients to return to the ED for worsening dyspnea, fever/chills, or other symptoms of respiratory distress**
- ⭐ **pearls — the most common causes of pleural effusion are CHF, pneumonia, and malignancy
- failure to identify fatal causes such as pulmonary embolism, esophageal rupture, or hemothorax, and failure to drain large effusions causing respiratory or circulatory compromise**
⭐ discharge criteria — the source of the pleural effusion is known; no evidence of respiratory compromise exists; the majority of effusions will resolve if the primary process is treated appropriately; the patient must be reliable and have access to a telephone, a supportive social environment, and adequate follow-up; arrange appropriate follow-up with an oncologist or pulmonologist prior to discharge; instruct patients to return to the ED for worsening dyspnea, fever/chills, or other symptoms of respiratory distress; ⭐ pearls — the most common causes of pleural effusion are CHF, pneumonia, and malignancy; failure to identify fatal causes such as pulmonary embolism, esophageal rupture, or hemothorax, and failure to drain large effusions causing respiratory or circulatory compromise | - Observation for 6 hr or admission for the potential complications of thoracentesis — pneumothorax and re-expansion pulmonary edema
- ICU admission for severe hemodynamic and respiratory compromise
- do not fail to identify fatal causes of pleural effusion — pulmonary embolism, esophageal rupture, or hemothorax
- do not fail to drain large effusions that are causing respiratory or circulatory compromise
- a patient must be reliable and have telephone access, a supportive social environment and adequate follow-up to be discharged
Observation for 6 hr or admission for the potential complications of thoracentesis — pneumothorax and re-expansion pulmonary edema; ICU admission for severe hemodynamic and respiratory compromise; do not fail to identify fatal causes of pleural effusion — pulmonary embolism, esophageal rupture, or hemothorax; do not fail to drain large effusions that are causing respiratory or circulatory compromise; a patient must be reliable and have telephone access, a supportive social environment and adequate follow-up to be discharged |
| Pleuritis (pleurisy) | - ⭐ **inflammation of the lung pleura causing pain
- the pain is typically localized, sharp, and fleeting, and made worse by coughing, sneezing, and deep breathing**
- pleural friction rub
⭐ inflammation of the lung pleura causing pain; the pain is typically localized, sharp, and fleeting, and made worse by coughing, sneezing, and deep breathing; pleural friction rub | - Pleural friction rub on exam
- etiologies to consider — autoimmune disease, viral infections, pneumonia, lung cancer, and certain medications
Pleural friction rub on exam; etiologies to consider — autoimmune disease, viral infections, pneumonia, lung cancer, and certain medications | - ⭐ treatment depends on the cause
⭐ treatment depends on the cause | — |
| Chest wall — scoliosis, kyphosis, ankylosing spondylitis | - ⭐ **congenital scoliosis — S-shaped curvature
- may induce a restrictive ventilatory defect
- risk of respiratory failure rises if the curvature is severe or superimposed chest disease makes breathing difficult**
- ⭐ **kyphosis — accentuated dorsal curve
- may coexist with scoliosis
- acquired kyphosis results from osteoporosis and vertebral collapse with pain — and treating that pain may introduce the additional risk of ventilatory compromise**
- ⭐ **ankylosing spondylitis — chronic inflammatory disease of the axial skeleton joints
- pain and progressive stiffening, with chest expansion becoming limited as it progresses**
⭐ congenital scoliosis — S-shaped curvature; may induce a restrictive ventilatory defect; risk of respiratory failure rises if the curvature is severe or superimposed chest disease makes breathing difficult; ⭐ kyphosis — accentuated dorsal curve; may coexist with scoliosis; acquired kyphosis results from osteoporosis and vertebral collapse with pain — and treating that pain may introduce the additional risk of ventilatory compromise; ⭐ ankylosing spondylitis — chronic inflammatory disease of the axial skeleton joints; pain and progressive stiffening, with chest expansion becoming limited as it progresses | - Restrictive ventilatory defect on pulmonary function testing (scoliosis)
- chest expansion becomes limited as ankylosing spondylitis progresses
- assess for superimposed chest disease that raises respiratory failure risk
Restrictive ventilatory defect on pulmonary function testing (scoliosis); chest expansion becomes limited as ankylosing spondylitis progresses; assess for superimposed chest disease that raises respiratory failure risk | - The source gives no spine-specific therapy
- ⭐ the key caution is that treating kyphotic pain may introduce the additional risk of ventilatory compromise
The source gives no spine-specific therapy; ⭐ the key caution is that treating kyphotic pain may introduce the additional risk of ventilatory compromise | - Treating kyphotic pain may introduce the additional risk of ventilatory compromise
- the risk of respiratory failure rises if the curvature is severe or superimposed chest disease makes breathing difficult
Treating kyphotic pain may introduce the additional risk of ventilatory compromise; the risk of respiratory failure rises if the curvature is severe or superimposed chest disease makes breathing difficult |
| Chest wall — rib & sternal fractures | - ⭐ rib or sternal fracture can occur spontaneously or from trauma or surgery
- ⭐ chest wall instability with flailing outward during inspiration limits movement, especially with multiple fractures — causing hypoventilation and poor secretion clearance
- sternal dehiscence after open heart surgery or mediastinal procedures can similarly compromise respiration
⭐ rib or sternal fracture can occur spontaneously or from trauma or surgery; ⭐ chest wall instability with flailing outward during inspiration limits movement, especially with multiple fractures — causing hypoventilation and poor secretion clearance; sternal dehiscence after open heart surgery or mediastinal procedures can similarly compromise respiration | - Clinical: flail segment with outward movement during inspiration, hypoventilation, poor secretion clearance
- assess oxygenation/ventilation for evolving ventilatory failure
Clinical: flail segment with outward movement during inspiration, hypoventilation, poor secretion clearance; assess oxygenation/ventilation for evolving ventilatory failure | - ⭐ pain medication may facilitate breathing, but excessive analgesia may lead to hypoventilation and ventilatory failure
- ⭐ milder injuries may be stabilized with chest wall binders
- ⭐ significant impairment may require positive pressure ventilation to stabilize the wall
⭐ pain medication may facilitate breathing, but excessive analgesia may lead to hypoventilation and ventilatory failure; ⭐ milder injuries may be stabilized with chest wall binders; ⭐ significant impairment may require positive pressure ventilation to stabilize the wall | - Excessive analgesia may lead to hypoventilation and ventilatory failure — pain medication may facilitate breathing, but over-sedation is a risk
- chest wall instability with flailing outward during inspiration limits movement, causing hypoventilation and poor secretion clearance
- sternal dehiscence after open heart surgery or mediastinal procedures can similarly compromise respiration
Excessive analgesia may lead to hypoventilation and ventilatory failure — pain medication may facilitate breathing, but over-sedation is a risk; chest wall instability with flailing outward during inspiration limits movement, causing hypoventilation and poor secretion clearance; sternal dehiscence after open heart surgery or mediastinal procedures can similarly compromise respiration |
| Costochondritis | - ⭐ **may be confused with serious chest conditions
- more common in young women
- tenderness over the area**
- costosternal junction inflammation can also come from autoimmune arthritis (rheumatoid disease, SLE) or Tietze syndrome
⭐ may be confused with serious chest conditions; more common in young women; tenderness over the area; costosternal junction inflammation can also come from autoimmune arthritis (rheumatoid disease, SLE) or Tietze syndrome | - Tenderness over the area on palpation
- consider autoimmune arthritis (rheumatoid disease, SLE) and Tietze syndrome in the differential
Tenderness over the area on palpation; consider autoimmune arthritis (rheumatoid disease, SLE) and Tietze syndrome in the differential | ⭐ NSAIDs and heat help | - Costochondritis may be confused with serious chest conditions — keep the serious causes on the differential
Costochondritis may be confused with serious chest conditions — keep the serious causes on the differential |
| Duration-of-therapy rules & the CAP stopping rule | - ⭐ CAP treatment minimum 5–7 days
- ⭐ HAP & VAP duration 7 days
- the infiltrate may lag symptoms by 48 h, justifying a repeat chest X-ray 24–48 hours after presentation
- blood cultures for endocarditis — 3 sites
⭐ CAP treatment minimum 5–7 days; ⭐ HAP & VAP duration 7 days; the infiltrate may lag symptoms by 48 h, justifying a repeat chest X-ray 24–48 hours after presentation; blood cultures for endocarditis — 3 sites | - ⭐ **before stopping CAP therapy the patient must be: afebrile for 48–72 hours
- hemodynamically normal (HR < 100, systolic BP > 90, RR < 24, SpO₂ > 90% on room air)
- tolerating an oral diet
- with preserved mentation**
⭐ before stopping CAP therapy the patient must be: afebrile for 48–72 hours; hemodynamically normal (HR < 100, systolic BP > 90, RR < 24, SpO₂ > 90% on room air); tolerating an oral diet; with preserved mentation | - ⭐ extend HAP/VAP therapy beyond 7 days only if the clinical condition fails to improve or another uncovered organism is identified
- sequence: culture first, then empiric therapy, then narrow — revise as culture data returns and use the narrowest spectrum that covers the known organism
- CAP treatment minimum 5–7 days
⭐ extend HAP/VAP therapy beyond 7 days only if the clinical condition fails to improve or another uncovered organism is identified; sequence: culture first, then empiric therapy, then narrow — revise as culture data returns and use the narrowest spectrum that covers the known organism; CAP treatment minimum 5–7 days | - Do not stop CAP therapy before the patient is afebrile 48–72 hours, hemodynamically normal (HR < 100, systolic BP > 90, RR < 24, SpO₂ > 90% on room air), tolerating an oral diet, and with preserved mentation
- CAP treatment minimum 5–7 days
- HAP/VAP — do not extend beyond 7 days unless the clinical condition fails to improve or another uncovered organism is identified
- do not use procalcitonin or CRP to initiate therapy — clinical criteria guide that decision
- culture first, then empiric therapy, then narrow
Do not stop CAP therapy before the patient is afebrile 48–72 hours, hemodynamically normal (HR < 100, systolic BP > 90, RR < 24, SpO₂ > 90% on room air), tolerating an oral diet, and with preserved mentation; CAP treatment minimum 5–7 days; HAP/VAP — do not extend beyond 7 days unless the clinical condition fails to improve or another uncovered organism is identified; do not use procalcitonin or CRP to initiate therapy — clinical criteria guide that decision; culture first, then empiric therapy, then narrow |