Pulmonary
Sara E. Erickson, M.D.
Stephen C. Lazarus, M.D.
Prediction rule for community-acquired pneumonia
Aspiration pneumonitis and pneumonia
Acute respiratory distress syndrome
1. Precipitants: irritants (pollen, dust, smoke, detergents), infection, gastroesophageal reflux disease, meds (b-blockers, aspirin).
2. Assessment: assess severity of attack (respiratory rate, peak flow (PF), absent breath sounds, accessory muscle use, initial response to bronchodilators). PF < 50% = severe (normal PF = 450-650 L/min man, 350-500 L/min woman)
· ABG: essential in severe attacks, elevated or normal pCO2 often indication for intubation.
3. Treatment:
· Nebs: albuterol (0.5cc/2.5cc NS) Q4h, Q2h, or continuous; add atrovent (0.5mg) if not responding to albuterol. Note that MDIs + spacer have been shown to be as effective as nebs. Use nebs in respiratory distress for ease of delivery. Start MDIs when patient has improved.
· Steroids: solumedrol 60-80 mg IV q6-8 hours (if not tolerating PO’s) or prednisone 60 mg PO QD until PF > 50%, then taper over next 8-10 days (IV not superior to PO). Start steroids early!
· Leukotriene receptor antagonists (LTRAs): beneficial in acute asthma as add-on therapy. Dose: Zafirlukast 160 mg PO in the emergency department reduced hospitalization by 34% in one trial.
· Heliox (mixture of O2+He): decreases turbulent flow through spastic airways; may reduce symptoms transiently, but no proven benefit in outcome.
· Magnesium: recent Cochrane systematic review did not support routine use. However, can consider in severe exacerbations since no significant adverse effects.
· Theophylline and aminophylline: don’t use them – no benefit in acute attacks and potential of harm from side effects.
· Frequent observation: order bedside peak flow meter to check q shift peak flows.
· Use hospitalization to educate patient on proper use of inhalers, preventive care, etc.
· Patients who frequently use their beta-agonists and don’t use steroid inhalers have a higher risk of hospitalization and ICU stay than those who use steroid inhalers. Make sure your patient is prescribed a steroid inhaler upon discharge and knows how to use it.
Gibbs MA, Camargo CA Jr, Rowe BH, Silverman RA. State of the art: therapeutic controversies in severe acute asthma. Acad Emerg Med. 2000 Jul;7(7):800-15.
Eisner MD, Lieu TA, Chi F, et al. Beta agonists, inhaled steroids, and the risk of intensive care unit admission for asthma. Eur Respir J 2001; 17:233-40.
1. Precipitants: commonly viral infection, bronchospasm, sedating medications.
2. Assessment: assess severity of attack (respiratory rate, accessory muscle use, inability to speak in full sentences), CXR, ABG to assess degree of acidemia and CO2 retention.
· O2: via NC or face mask – target oxygen saturation = 90-92% (prevents CO2 retention).
· Strongly consider positive pressure ventilation (i.e., BiPAP) in acute respiratory acidosis; contraindications are hemodynamic instability, respiratory arrest, patient unable to cooperate, patient unable to protect airway. See Critical Care: Noninvasive Positive Pressure Ventilation.
· Nebs: albuterol + atrovent (Q4-6h + PRN), change to MDIs as patient improves.
· Steroids: 80-125 mg IV Q6-8h x 3 days, then 60 PO QD. Tape over 8-14 days.
· Antibiotics: data supports use in patients hospitalized for COPD exacerbation: doxycycline 100 mg PO BID.
· Not useful: chest PT, mucolytics, methylxanthines (theophylline).
· Home O2 (patient qualifies by medicare criteria if O2 sat < 88% or PO2 < 55 on room air) and smoking cessation are the only interventions that reduce long-term mortality.
Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000 Jul 27;343(4):269-80.
McCrory DC, Brown C, Gelfand SE, Bach PB. Management of acute exacerbations of COPD: a summary and appraisal of published evidence. Chest 2001; 119:1190-209.
1. Diagnosis: Symptoms – fever, chills, cough, purulent sputum, SOB, pleuritic CP. Findings – infiltrate on CXR, WBC.
2. Microbiology:
|
Patient population |
Typical organisms |
|
Healthy young adult |
Pneumococcus, Mycoplasma, Chlamydia, viral |
|
HIV positive |
Pneumococcus, H. influenzae, PCP, TB, aerobic gram–negative rods (E. coli, Klebsiella), MAC, fungi (Cryptococcus, Histo, Aspergillus), CMV, Toxo |
|
Smoker (chronic bronchitis) |
Pneumococcus, H. flu, Moraxella catarrhalis |
|
Alcoholic or nursing home resident |
Pneumococcus, H. flu, Klebsiella, aspiration, S. aureus, tuberculosis |
|
Neutropenic |
Pneumococcus, gram–negatives (E. coli, K. pneumonia, Pseudomonas, H. flu, Enterobacter species), S. aureus, fungi (Candida, Aspergillus) |
3. Further evaluation:
· CBC with differential.
· Blood culture before antibiotic administration.
· ABG when patient is severely dyspnic or tachypneic.
· Consider testing for Legionella (culture and urinary assay), Mycoplasma (cold agglutinins), Chlamydia (acute and convalescent serology), or influenza if clinical course atypical or enigmatic.
· Sputum gram stain controversial, adequate sample has >25 PMNs and <10 epithelial cells.
· Consider HIV test in patients age 15-54.
· In HIV+ patients: induced sputum for PCP (1x), AFB (3x).
· Bronchoscopy with BAL if induced PCP or AFB sputum is negative.
4. Treatment: check your local antibiogram for susceptibility patterns at your hospital and in general, consult your hospital’s antibiotic guidelines.
· Floor patient – ceftriaxone 1g IV q24h; if unavailable can use cefuroxime 0.75-1.5g q8h, though not as effective. Add doxycycline 100 mg PO BID for atypical coverage.
· ICU patient: ceftriaxone + fluoroquinolone (levofloxacin 500 mg IV/PO QD).
· Underlying severe lung disease – anti-pseudomonal penicillin (Zosyn 3.375 g IV q6h or Timentin 3.1 g IV q4-6h).
· Aspiration: see Pulmonary: Aspiration Pneumonia/Pneumonitis.
Bartlett JG, Mundy LM. Community-acquired pneumonia. N Engl J Med 1995; 333:1618-24.
Niederman MS, Mandell LA, Anzueto A, et al. Guidelines for the management of adults with community-acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention. Am J Respir Crit Care Med 2001; 163:1730-54.
Risk factors for mortality:
|
Demographic factor |
Points |
|
Nursing home resident |
10 |
Coexisting illnesses |
|
|
· Neoplastic disease |
30 |
|
· Liver disease |
20 |
|
· Congestive heart failure |
10 |
|
· Cerebrovascular disease |
10 |
|
· Renal disease |
10 |
Physical exam findings |
|
|
· Altered mental status |
20 |
|
· Respiratory rate > 30/min |
20 |
|
· Systolic BP < 90 mm Hg |
20 |
|
· Temp < 35° or > 40° |
15 |
|
· Pulse > 125/min |
10 |
Laboratory and radiographic findings |
|
|
· Arterial pH < 7.35 |
30 |
|
· BUN > 30 mg/dL |
20 |
|
· Na < 130 mmol/L |
20 |
|
· Glucose > 250 mg/dL |
10 |
|
· Hematocrit < 30% |
10 |
|
· pO2 < 60 mm Hg |
10 |
|
· Pleural effusion |
10 |
Total score = age (or age – 10 for women) + points for above findings
· Score < 70 has low mortality (0 – 0.9%) and can consider outpatient therapy assuming patient can take oral antibiotics and can be compliant with regimen (homeless patients will often need to be admitted).
· Score 71–90 (2.8% mortality) consider brief hospitalization.
· Score 91-130 (8.2% mortality).
· Score >130 (29.2% mortality) will likely need ICU.
Note: many would add hypoxemia (O2 sat < 90%) and multilobar infiltrates as indications for admission.
Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med 1997; 336:243-50.
1. The evidence (forget what you’ve learned!):
· Aspiration pneumonitis can present with a fever, infiltrate, cough, elevated WBC. However, aspiration pneumonitis does not require treatment with antibiotics initially. Use the guidelines below to differentiate from aspiration pneumonia. Symptoms usually resolve within 24-48 hours.
· Aspiration pneumonia is not caused by anaerobes (for the most part). It’s mostly caused by gram negative rods, so make sure you cover with a broad spectrum antibiotic. Don’t use penicillin/clindamycin as this will not cover gram negatives!
· Percutaneous gastrostomy (PEG) tubes don’t prevent aspiration pneumonia and are not superior to nasogastric (NG) tubes.
2. Aspiration pneumonia:
· Patients at risk are those with dysphagia and gastric dysmotility.
· Usually affects elderly patients and usually is not witnessed.
· Results from aspiration of colonized oropharyngeal material and is therefore not sterile.
· Pathogens: mainly gram-negative rods and gram-positive cocci. Rarely due to anaerobic bacteria.
· Clinically presents as typical pneumonia with tachypnea, fever, cough.
3. Aspiration pneumonitis:
· Patients at risk are those with a depressed level of consciousness.
· Usually affects younger patients who are intoxicated, sedated, or have head injury/pathology and is usually witnessed.
· Results from aspiration of sterile gastric contents; acute lung injury results from acitidy and particulate material and not bacteria though superinfection later is always possible.
· Clnically can present with no symptoms, mild symptoms, or severe acute lung injury or ARDS with hypotension.
4. Management:
· Suction the upper airway after a witnessed aspiration event and if the patient can’t protect airway, intubate.
· Don’t blindly use prophylactic antibiotics for aspiration pneumonitis (this will simply select for more resistant bugs causing superinfection).
· Aspiration pneumonitis:
- If symptoms > 48 hours: treat with levofloxacin or ceftriaxone.
- If the patient is at risk for colonization of gastric contents (small bowel obstruction or on antacid therapy): use ceftriaxone, zosyn, or ceftazidime.
· Aspiration pneumonia:
- Community acquired: levofloxacin or ceftriaxone.
- Residence in long term care facility: zosyn or ceftazidime.
- Severe periodontal disease, putrid sputum, alcoholism, CXR with lung abscess: treat for anaerobes with zosyn, imipenem, or 2 drug therapy (levofloxacin or ceftriaxone plus clindamycin or metronidazole).
Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001; 344:665-71.
1. Definition:
· Acute onset of respiratory failure.
· Bilateral infiltrates on CXR. Note: some cases of ARDS do present unilaterally or with pleural effusion.
· PCWP < 18 mmHg or absence of any clinical evidence of left atrial hypertension. Exclude cardiogenic cause of pulmonary edema.
· If PaO2/FiO2 ratio < 300, patient has acute lung injury.
· If PaO2/FiO2 ratio < 200, patient has ARDS.
2. Causes:
· Direct lung injury: pneumonia and aspiration of gastric contents. Less common causes include pulmonary contusion, fat emboli, near-drowning, inhalational injury, reperfusion pulmonary edema after lung transplantation.
· Indirect lung injury: sepsis and severe trauma with shock/multiple transfusions. Less common causes include drug overdose, cardiopulmonary bypass, acute pancreatitis, transfusion of multiple blood products.
3. Treatment:
Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med 2000; 342:1334-49.
1. Thoracentesis is indicated for all new pleural effusions except those that are clearly a result of CHF (See Procedures: Thoracentesis). Suspected parapneumonic effusions should be tapped immediately.
2. Check bilateral decubitus films prior to thoracentesis. If effusion is small (layers less than 10 mm on decubitus film), ultrasound guidance may be necessary.
3. Note appearance of fluid when aspirated (straw colored, pus, etc.) Send fluid for total protein, LDH, cell count with differential, glucose, gram stain with culture (including AFB), cytology (if malignancy suspected), ± amylase, cholesterol, and triglycerides if indicated. Be sure to send serum for LDH and total protein (see below).
4. Light's criteria (exudates vs. transudate): to be an exudate, an effusion has to meet only one of the following criteria:
· Pleural fluid/serum LDH ratio > 0.6
· Pleural fluid/serum total protein ratio > 0.5
· Pleural fluid LDH > 2/3 the upper limit of normal
5. Transudative: CHF (90%), hepatohydrothorax, nephrotic syndrome, peritoneal dialysis, myxedema, acute atelectasis, constrictive pericarditis, SVC syndrome, PE, hypoalbuminemia.
6. Exudative: pneumonia (parapneumonic), cancer, PE, empyema, TB, connective tissue disease, chronic atelectasis, pancreatic disease, uremia, chylothorax, sarcoidosis, drug reaction, post MI, Meigs syndrome, viral/fungal/rickettsial/parasitic infection.
7. Differentiating causes of exudative effusions:
|
Parameter |
Associated effusion |
|
Glucose < 60 or ratio fluid/serum < 0.5 |
Complicated parapneumonic effusion vs empyema, tuberculous pleurisy, malignant effusion, lupus or rheumatoid pleuritis, esophageal rupture. Rheumatoid and empyema usually glucose <10. |
|
pH < 7.2 |
Empyema or complicated parapneumonic, rheumatoid, esophageal rupture (<6), TB, malignancy, hemothorax, systemic acidosis, parasitic |
|
High amylase |
Esophageal rupture, pancreatitis, malignancy |
|
Bloody (RBC > 100K) |
Trauma, malignancy, pulmonary embolism or infarction, TB |
|
Lymphocytes > 50% |
Lymphoma or other malignancy, TB or fungi, postpericardiotomy |
If TB suspected, consider pleural biopsy (approximately 75% sensitivity)
8. Parapneumonic effusions/empyema:
· Uncomplicated parapneumonic effusions have negative gram stain, no organisms on culture, no pus, glucose > 40-60, no loculations, and pH > 7.2.
· Complicated pleural effusions have LDH > 1000 U/L, glucose < 40 mg/dl, pH < 7.2, positive culture or gram stain.
· Empyema: pus in the pleural space.
9. Management of effusions:
· Transudative effusions don’t require therapeutic taps or chest tubes unless they are very large and are causing unmanageable dyspnea. Treating the underlying cause should result in resolution.
· Uncomplicated parapneumonic or tuberculous effusions usually resolve with antibiotics and do not require chest tubes.
· Complicated parapneumonic effusions and empyema require chest tube placement to prevent formation of pleural "peels" that may trap lung and cause loss of lung function. Loculated effusions may require multiple tubes, administration of t-PA or surgical decortication.
· Malignant effusions (which usually herald unresectable cancer) that recur after thoracentesis can be managed with serial therapeutic taps or talc pleurodesis (call pulmonary consult).
Light RW. Clinical practice. Pleural effusion. N Engl J Med 2002; 346:1971-7.
· Indications: pneumothorax, hemothorax, chylothorax, empyema, recurrent pleural effusion.
· Placement: typically pigtail (smaller caliber) chest tubes are placed by interventional radiology, larger chest tubes by thoracic surgery.
· Daily management: follow output (appearance and quantity) daily; positioning, dressing, etc. usually managed by physicians that placed the chest tube.
· Removal of chest tube: effusion draining < 50 cc/day (if empyema < 20cc/day). If chest tube placed for PTX and no further air leak ® place on water seal (4 hrs) ® CXR (if no residual PTX) ® clamp (4 hrs) ® CXR (if no recurrent PTX) ® pull tube.
Miller KS, Sahn SA. Chest tubes: Indications, technique, management, and complications. Chest 1987; 91:258.
1. Severe is defined as > 100-600 ml/day, massive > 600 ml/day.
2. Causes include BATTLE CAMP. Bronchitis, bronchietasis, Aspergilloma, Tumor, TB, trauma, LV failure, Embolism (PE), Connective tissue disease (Goodpasture’s, Wegener’s), Abscess AVM, Mitral stenosis, PNA.
3. Diagnostic tests: PT/PTT, CXR, CT, bronchoscopy, arteriography, ANCA, anti-GBM.
4. Management of severe hemoptysis:
· Call interventional radiology (IR) and pulmonary consult immediately. If IR not available, CT surgery can perform rigid bronchoscopy in the operating room.
Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med 2000; 28:1642-7.
1. Risk Factors: immobilization, recent surgery, CVA, prior DVT, malignancy, CHF, trauma, hormone replacement, oral contraceptives, obesity, smoking, HTN, hypercoagulability: (factor V Leiden, prothrombin 20210A, APC resistance, hyperhomocysteinemia, antiphospholipid antibody) .
2. Symptoms: dyspnea (73%), pleuritic pain (66%), cough (37%), leg pain or swelling (27%), hemoptysis (13%), lightheadedness, loss of consciousness.
3. Signs: tachypnea (~80%), tachycardia (~80%), rales (51%), S4, loud P2, elevated JVP, fever.
4. Work-up: Always think of PE in patients with new or unexplained dyspnea and/or hypoxemia. Studies should include:
· CXR: abnormal in 84% but non-specific: atelectasis, effusion, basilar opacity, elevated diaphragm, Westermark’s sign (focal decreased pulmonary vessel perfusion), Hampton’s hump (peripheral wedge shaped density).
· ECG: sinus tachycardia, S1Q3T3, right axis-deviation, RBBB, T wave inversions of V1-4, a-fib/flutter.
· ABG: mean PaO2 70mmHg, < 60 (25%), < 80 (74%). Normal ABG does not rule out PE if clinical suspicion high.
· D-Dimer: if ELISA test available, a low result has an extremely high negative predictive value.
· Spiral CT, V/Q Scan, LE doppler ultrasound. Echo can be useful in massive PE.
5. If V/Q scanning is available: In patients with a clear CXR and no focal extremity swelling, the current literature supports using V/Q scan for diagnosis: if normal ® stop, if high probability ® treat.
|
V/Q scan result |
High clinical suspicion |
Intermediate clinical suspicion |
Low clinical suspicion |
|
High |
96% |
88% |
56% |
|
Intermediate |
66% |
28% |
16% |
|
Low |
40% |
16% |
4% |
6. CT chest – PE protocol: If V/Q scanning is unavailable or presumed to be of limited use secondary to underlying lung pathology, a PE protocol chest CT can be obtained.
7. Treatment:
· Unfractionated heparin: see Sliding Scales: Heparin.
· Low molecular weight heparin (enoxaparin): preferred treatment for ease of use; dose at 1mg/kg q12h SQ. Continue for ~5 days, until INR is therapeutic (2.0-3.0) on warfarin. Relative contraindication if CrCl < 30 ml/min or weight > 120 kg. Can follow anti-factor Xa levels if available.
· Warfarin: start when patient is stable (which may be on admission).
· Thrombolytics: consider in massive PE with hemodynamic compromise (call pulmonary consult). Stop heparin and dose tPA at 100 mg IV over 2 hours. Can use up to 14 days after initial onset of PE. Obtain consent, review exclusion criteria, monitor frequently for neuro changes, and know full tPA protocol if you are going to proceed to thrombolysis.
· IVC filter: in patients who develop PE while anticoagulated, or in patients in whom anticoagulation is contraindicated (recent surgery, CVA). Not effective as long-term treatment.
· Start hypercoagulability workup when appropriate (i.e., when common risk factors are absent).
8. See also Hematology/Oncology: Deep vein thrombosis.
Goldhaber SZ. Pulmonary embolism. N Engl J Med 1998; 339:93-104.
Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753-9.
Rathbun SW, Raskob GE, Whitsett TL. Sensitivity and specificity of helical computed tomography in the diagnosis of pulmonary embolism: a systematic review. Ann Intern Med 2000; 132:227-32.
Goodman LR, Lipchik RJ, Kuzo RS, Liu Y, McAuliffe TL, O'Brien DJ. Subsequent pulmonary embolism: risk after a negative helical CT pulmonary angiogram--prospective comparison with scintigraphy. Radiology. 2000 May;215(2):535-42.
Perrier A, Howarth N, Didier D, et al. Performance of helical computed tomography in unselected outpatients with suspected pulmonary embolism. Ann Intern Med 2001; 135:88-97
Arcasoy SM, Kreit JW. Thrombolytic therapy of pulmonary embolism: a comprehensive review of current evidence. Chest 1999; 115:1695-707.
Decousus H, Leizorovicz A, Parent F, et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. N Engl J Med 1998; 338:409-15.
Modes of O2 delivery (room air FiO2=21%):
· Nasal cannula: 1-6 liters, with each liter increasing FiO2 by 3%. Actual FiO2 depends on minute ventilation (i.e.effective FiO2 drops as respiratory rate increases).
· Simple mask: 6-15 liters, maximum FiO2 is approximately 50%. Again, actual FiO2 depends on minute ventilation.
· Venturi mask: 1-4 liters, FiO2 preset at 24, 28, 31, 35, 40, and 50%.
· Non-rebreather (NRB): >15L, max FiO2 up to 90%.
· High humidity: >15 liters, max FiO2 ~100%.
· Face tent: FiO2 variable up to 50%; more comfortable than face mask.
1. Common measurements:
· FVC: Forced vital capacity. Reduced in restrictive disease or obstructive disease.
· FEV1: Forced expiratory volume in once second. Reduced in obstructive disease.
· FEV1/FVC: Reduced in obstructive disease, unchanged or increased in restrictive disease.
· TLC: Total lung capacity. Reduced in restrictive disease. Increased in emphysema.
· VC: Vital capacity. Reduced in restrictive disease.
· DLCO: Diffusing capacity for carbon monoxide. Reduced in PCP, interstitial lung disease, emphysema, or any other process with decreased capillary volume.
· MIF: Maximum inspiratory force. Decreased in progressive neuromuscular dysfunction (e.g. spinal cord injury) and can help predict which patients need mechanical ventilation.
2. Diagnostic approach:
· First make sure that the spirometry reading is of high quality (i.e. patient fully cooperated with exam).
· If FEV1/FVC is low, there is an obstructive defect. If there is improvement with FEV1 with bronchodilator challenge ® asthma. If there is no improvement in FEV1, consider COPD and check DLCO, lung volume measurements. If DLCO is low ® emphysema. If DLCO is normal ® chronic bronchitis. If DLCO is high ® asthma or possibly other lung pathology.
· If FEV1/FVC is normal and the patient has dyspnea, challenge with methacholine. If FEV1 decreases ® asthma.
· If vital capacity (or FVC) is low, there is a restrictive defect. Check the DLCO. If DLCO is low ® interstitial process. If the DLCO is normal, consider a chest wall process such as anatomic defect, pleural pathology, or diaphragmatic weakness.
Crapo RO. Pulmonary-function testing. N Engl J Med 1994; 331:25-30.