Flashcards in Pulmonary Emergencies Deck (119):
Air way obstruction is most common in _________.
Children, children 1-3 yo are most susceptible. They more frequently place things in their mouths and lack molars for properly grinding their food. They are often running or playing at the time of aspiration.
What is the most common food item aspirated?
After foreign body aspiration where can the foreign body settle? Which place is the most common
The FB can settle into 3 anatomical sites, the larynx, trachea or bronchus. 80-90% of aspirated FBs become lodged in the bronchi (the right one being most common).
Where are larger foreign bodies more likely to be lodged?
The trachea or larynx
How do patients with laryngeal foreign bodies present?
Present with airway obstruction and hoarsness or aphonia
How do patients with tracheal foreign bodies present?
Present with coughing and can also demonstrate wheezing similar to asthma
How do patients with bronchial foreign bodies present?
Present with cough, unilateral wheezing and decreased breath sounds. Only 65% of patients have all 3.
Foreign body evaluation:
Two view CXR, findings that may be suggestive would be: unilateral hyperexpansion and lobar atelectasis or pneumonia
Suspected FB aspiration requires ____________. (Treatment)
bronchoscopic evaluation (aka: broncoscopy)
Angioedema is aka a _____________
Hypersensitivity reaction/allergic reaction
What are possible drug mediated hypersensitivity reactions?
ACE inhibitors and ASA
How do we treat angioedema?
Treat with antihistamines, steroids +/- epinephrine
What are the various etiologies of airway obstruction?
FB aspiration, Angioedema, Burns/Trauma, Mass (cancer) or Infectious (Croup, Epiglottitis and Peritonsillar Abscesses)
What are the symptoms of Croup?
Barking cough, stridor, prodromal URI symptoms
How do we treat Croup?
Single dose dexamethasone (PO or IM). Epinephrine indicated in moderate to severe cases.
____________ is the pathogen most commonly identified with epiglottitis. It causes a _____________ presentation.
H. influenza b; more severe
Lesser pathogens associated with epiglottitis:
Staph and Strep
What is the gold standard for the diagnosis of epiglottitis?
Besides the gold standard for diagnosis for epiglottitis, what are other diagnostic criteria?
lateral soft tissue neck x-rays are up to 90% sensitive.
Think thumbprint sign!
What is the treatment for epiglotittis?
Children are more likely to require airway protection, awake fiberoptic intubation is ideal.
Begin 3rd gen. cephalosporin + vancomycin or clindamycin
Who is more likely to develop a Retropharyngeal abscess?
Increasingly more common in adults.
What are the most common organisms associated with Retropharyngeal abscess?
Typically polymicrobial: anaerobes, Staph are most common flora
How does a patient with a Retropharyngeal abscess present?
Classically presents with sore throat, neck pain/stiffness, dysphagia and “hot-potato” voice
How do we diagnose a Retropharyngeal abscess?
On normal lateral soft tissue neck X-ray, soft tissue anterior to C1-C4 should be < 40% of the diameter of the adjacent vertebral body. Widening of this space suggests infection.
What is the treatment for a Retropharyngeal abscess?
Treatment is IV antibiotics and operative I and D
What is Ludwig’s Angina?
A progressive infection of the connective tissues of the floor of the mouth and neck which begins in the submandibular space.
What is the pathophysiology of Ludwig’s Angina?
Most commonly caused by infection originating in the area of the 2nd or 3rd molars
What is the patient presentation of Ludwig’s Angina?
Exam reveals bilateral submandibular swelling, elevation of the tongue, dysphonia
What is the treatment for Ludwig’s Angina?
Airway should be secured, preferably via fiberoptic guidance. Antibiotic coverage for oral flora, e.g. ampicillin-sulbactam, clindamycin.
How is a Peritonsillar Abscess diagnosed?
Diagnosed on the basis of infero-medial displacement of the infected tonsil with resulting uvular deviation. Needle aspiration confirms the diagnosis and is therapeutic.
Peritonsillar Abscess Treatment:
Larger abscesses may require I and D by ENT. Typical antibiotic coverage is amoxicillin/clavulanate, clindamycin also commonly utilized.
What is Aspiration pneumonitis?
Aspiration pneumonitis represents an acute, chemical lung injury resulting from the inhalation of gastric contents.
What is the pathophysiology of Aspiration pneumonitis?
It occurs when a patient inhales material from the oropharynx that is colonized by upper airway flora.
Diagnosing Aspiration pneumonitis:
Consider this diagnosis in patients with even transient alterations in level of consciousness resulting from dementia, delirium, seizures, CVAs, drug intoxication or head trauma.
Includes impairment of gag reflex, coughing, ciliary movement, and immune mechanisms, all of which aid in removing infectious material from the lower airways.
Who is most likely to develop Aspiration pneumonitis?
Most commonly occurs in individuals with chronically impaired airway defense mechanisms.
Causative organism of Aspiration pneumonitis:
Once thought to be primarily caused by anaerobic organisms but newer data suggests typical URI flora are more common
• S. pneumoniae
• S. aureus
• H. influenzae
Hospital-acquired cases are more likely to involve Staph, Pseudomonas
How is aspiration pneumonitis treated?
Prophylactic antibiotics generally not recommended in case of aspiration pneumonitis. No role for corticosteroids.
Treat aspiration pneumonia as you would pneumonia based on the setting it was contracted in (community vs. healthcare-associated).
In addition, anaerobic coverage is typically used to complement traditional pneumonia treatment.
What is Hyperventilation?
Not limited to tachypnea-may also refer to abnormally deep respirations.
What causes hyperventilation?
While anxiety is a very common cause of this presentation, must consider organic etiologies:
• PE, along with other causes of hypoxemia
• Acidemia (i.e. DKA)
• Obstructive lung disease
• Interstitial lung disease
• Salicyclate overdose
How do we treat hyperventilation?
Treatment depends on underlying etiology. Consider administration of a benzodiazepine in the ED once organic illness excluded.
T/F: Pulmonary embolisms need to be diagnosed early. They are easy to diagnose but can be life threatening.
False, PE is traditionally difficult to diagnose. Missed diagnosis results in a large number of malpractice claims. Fear of missing the diagnosis results in frequent (negative) testing-with potential negative outcomes for patients.
Hypercoagulability, Stasis, Vessel injury
Risk Factors for a PE
Hypercoagulability, Venous Stasis, Venous Injury
What puts a person at risk for Hypercoagulability?
- Nonmalignant thrombophilia: Pregnancy, Postpartum status (<~4wk), Estrogen/ OCP’s, or Genetic mutations (Factor V Leiden, Protein C & S deficiency, Factor VIII, prothrombin mutations, AT-III deficiency).
What puts a person at risk for Venous Stasis?
Bedridden status, Recent cast or external fixator and Long-distance travel
What puts a person at risk for Venous Injury?
Recent surgery requiring general anesthesia or Recent trauma (especially the lower extremities and pelvis).
Pathophysiology of a Pulmonary Embolism:
Venous emboli (typically from the lower extremities) may become dislodged from their site of origin, embolizing to the pulmonary arterial circulation or, paradoxically to the arterial circulation through a patent foramen ovale.
Pulmonary vascular resistance abruptly increases, causing increased RV wall tension and RV dilation and dysfunction
Elevated troponin and BNP predict mortality. Progressive right heart failure is the usual immediate cause of death from PE.
What is the Clinical Presentation of a Pulmonary Embolism?
Most common symptoms present in patients with proven PE: Dyspnea (84%), Chest Pain, pleuritic (74%), Anxiety (59%), Cough (53%).
The Classic Triad: (Hemoptysis, Dyspnea, Pleuritic Pain). Not very common (Occurs in less than 20% of patients with documented PE).
How do we diagnose a PE?
Using vital signs, history and physical and chest X-ray, determine your pretest probability (PTP) of PE.
1. High PTP: Patients in whom PE can be reliably excluded only by imaging
2. Low-Moderate PTP: Patients safe for exclusion via negative D-dimer
3. Patients with such low pretest probability that no testing is indicated
EKG findings in a patient with a PE:
Moderate to severe PE results in increased PA and RV pressures, resulting in evidence of right heart strain on the EKG.
• Q wave in lead III
• Precordial T wave inversions
EKG in association with PEs
Limited sensitivity and specificity
• Primary utility lies in identification of alternative explanation for patient’s symptoms (i.e. pneumothorax)
• Westermark's sign
• A dilation of the pulmonary vessels proximal to the embolism along with collapse of distal vessels, sometimes with a sharp cutoff.
• Hampton’s Hump
• A triangular or rounded pleural-based infiltrate with the apex toward the hilum, usually located adjacent to the hilum.
• Neither are commonly observed
What are the Wells Criteria?
Clinical evidence of DVT
PE most likely diagnosis
Immobilization > 3d; surgery within 4 wk
Prior DVT or PE
Wells Score of 4 or greater suggest the patient should undergo imaging, score less than 4 implies D-dimer testing is appropriate first step in diagnosis
PE Rule-Out Criteria
Identifies a very low risk population for which the authors advocate no testing for PE
• Low clinical suspicion for PE in addition to:
• Age < 50 years
• Pulse < 100 bpm
• SaO2 > 94%
• No prior PE or DVT
• No unilateral lower extremity edema
• No hemoptysis
• No use of exogenous estrogen
• No trauma or surgery within 4 weeks
• If high pretest probability, proceed directly to CT scanning
• If low-moderate pretest probability, obtain D-dimer as first step in workup
• If D-dimer is below cutoff, PE is effectively excluded
• If D-dimer is elevated, proceed to CT scanning
• Fibrin split product
• Circulating half-life of 4-6 hours
• Quantitative test have 80-85% sensitivity, and 93-100% negative predictive value
• False Positives:
Pregnant Patients Post-partum < 4 weeks
Malignancy Surgery within 1 week
Advanced age > 80 years Sepsis
AMI Collagen Vascular Diseases
• Noninvasive and rapid
• May provide alternative diagnosis
• Risk of contrast nephropathy
• Risk of radiation
• If concerns regarding risks of CT preclude this modality, may consider:
• V/Q Scan (limited availability at some institutions)
• Lower extremity venous dopplers (if DVT identified, anticoagulation is indicated anyway)
• Empiric treatment if sufficiently high pretest probability
• Low molecular weight heparin (e.g. enoxaparin 1 mg/kg IV/SC bid)
• Unfractionated heparin (bolus with subsequent drip)
• Recent guidelines support preferential use of LMWH (no need for monitoring PTT)
• Works though activation of antithrombin III, resulting in inhibition of proteases necessary for coagulation cascade. Clot resolution will take days/weeks
• Consideration of thrombolysis/mechanical clot removal
• Definitely indicated in patients with hypotension
• Consider in patients with RV dysfunction on echo, elevated troponin/BNP
• IVC filter placement in patients with contraindication to anticoagulation or recurrent thrombus despite adequate anticoagulation
Traditional Stratification of PE Severity
• Massive PE
• Defined as PE resulting in systemic hypotension
• 5% of patients diagnosed with PE
• 30-60% mortality
• General consensus that lysis is indicated if no contraindications
• Submassive PE
• 95% of patients
• Mortality rate of <5%
• Most patients will go on to have an unremarkable course, require only anticoagulation if no contraindication
Means of Risk-Stratifying Patients with Submassive PE
• Markers of RV Dysfunction
• Echocardiography (best method, but limited availability)
• Biomarkers (Good sensitivity, limited specificity)
• Patients with abnormal RV function may benefit from more aggressive treatment (thrombolytics)
Acute Respiratory Distress Syndrome:
Accumulation of fluid in alveoli of lungs with resulting severe hypoxia, with non-cardiac etiology.
Complex pathophysiology involving endothelial damage, loss of surfactant, inflammation and accumulation of proteinaceous material in the lung parenchyma. May result from direct insult or systemic illness.
• Inhalational injury
• DIC, TTP
• Embolic phenomena:
• Amniotic fluid
• Transfusion reaction
• Drug reaction
• ASA, phenothiazines, TCAs, opioids, chemo drugs, amiodarone
• Radiation injury
• High altitude exposure
• Near drowning
• Bilateral pulmonary infiltrates
• PaO2/FiO2 ratio < 200
• Non-cardiogenic etiology
• Primarily supportive-address the underlying cause
• Mechanical ventilation-avoid barotrauma and oxygen toxicity
• Limit peak inspiratory pressure (ideally <30 mmHg)
• Low tidal volume (4-6ml/kg)
• Titrate FiO2 to keep SaO2 in the 85-90% range
• Leads to approximately 1.8 million ED visits/year
• Nearly 500,000 hospital admissions/year
• Approximately 40% of hospitalizations are in those under 18 years of age
• Shortness of breath
• Chest tightness
• Sputum production
• End-expiratory wheezing w/ a prolonged expiratory phase
• Decreased breath sounds
• Peak flow rate assists in triaging severity of exacerbation
• Chest X-ray
• Little utility in patients with established diagnosis, no history/physical findings consistent with pneumonia
• Should be obtained in patients with status asthmaticus or patients with no prior history of wheezing
• BMP - useful for those on continuous nebulizers to monitor K+
• CBC - little/no utility (WBC increase with left shift is expected within 2 hours of steroid administration)
• In general, patients presenting to the ED should receive corticosteroids
• PO formulation preferred if able to tolerate (60 mg prednisone, or 2 mg/kg in children)
• Simultaneously, inhaled bronchodilators should be administered
• Inhaled β-agonists
• Systemic β-agonists
• Patients with peak flow rate (PFR) <40% of predicted after ED therapy generally require admission
• Patients with a PFR of 70% or greater can generally be safely discharged
• Discharged patients should receive 5 days of Prednisone 2 mg/kg up to 60 mg PO daily
• Ensure adequate supply of albuterol and provide teaching on use if necessary
• Ensure close follow-up with PCP and discuss return precautions.
• 4th leading cause of death in the U.S., 6th in the world
• 3rd most common cause of hospitalization
• Rare in persons younger than 40, approx 10% prevalence in those 55-85 y/o
• Cigarette smoking accounts for approximately 90% of cases of COPD
• Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough being excluded).
• Emphysema, is defined physiologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, without obvious fibrosis.
• Productive cough
• Accessory muscle usage
• Pulse oximetry-change from baseline values more useful than absolute value
• ABG-not routinely performed unless severe exacerbation, altered mental status
• PFTs-of much lesser role in COPD compared with asthma (less airway obstruction reversibility)
• Sputum Gram’s stain-little/no utility
• BMP, CBC-limited utility
• BNP-may be of use if CHF is in the differential
• Routinely ordered in patients with COPD exacerbations
• Most commonly reveals chronic changes
• Decreased vascular markings
• Small cardiovascular silhouette
• May demonstrate an acute treatable cause of deterioration
COPD- ED Treatment
• Intubation/Non-invasive ventilatory support if needed
• Oxygen to maintain SaO2 ≥ 90%
• Short-acting inhaled β-agonists and anticholinergics are mainstays of ED therapy
• Commonly, albuterol and ipratropium are administered simultaneously, owing to synergistic effects.
• Typical dose of albuterol is 2.5-5 mg inhaled Q 20 minutes
• Ipratropium 0.5 mg inhaled q 30 minutes X up to 3 doses
• May consider Magnesium sulfate 2 g IV in severe exacerbations with minimal response to inhaled medications
• In contrast to acute bronchitis, antibiotics have been shown to benefit patients with moderate to severe acute COPD exacerbations
• Initial trials established efficacy using amoxicillin, tetracycline, trimethoprim-sulfamethoxazole, however, resistance patterns have since changed
• Target therapy to S. pneumoniae, H. influenzae, M. catarrhalis, based on local resistance patterns
• 3rd generation cephalosporins
• Levofloxacin, pipericillin/tazobactam, or cefepime may be considered in patients with high risk for Pseudomonas
• General Criteria for Admission
• Significant worsening of symptoms from baseline
• Inadequate response to ED treatment
• Significant comorbidities
• Worsened hypoxia or hypercarbia from baseline
• Difficult social situation, inability to ensure follow-up
• If discharged
• Corticosteroids (Prednisone 40-60 mg PO daily X5 days)
• Appropriate follow up with PCP
• 4 million cases, 1 million hospitalizations/year
• 6th leading cause of death in U.S.
• 90% of deaths in patients over 65 years old
• Cough, dyspnea, fever, rigors, malaise
• Hemoptysis, night sweats
• Chest pain, AMS, decline in function
• Duration of symptoms
• Comorbid conditions
• Immunosuppression, pulmonary disease, exposures
• Immunization (Pneumococcal, influenza)
• Smoking status
Pneumonia Physical Exam
• Vital signs including pulse oximetry
• Tachypnea, tachycardia, fever, hypotension with severe illness
• Evidence of alveolar fluid and/or consolidation
• Dullness to percussion
• Diminished breath sounds
• Bronchial congestion causes rhonchi, wheeze
Pneumonia Lab and Diagnostic Studies
• Chest radiograph
• Laboratory evaluation (BMP, CBC)
• Not necessary in all patients
• Blood cultures
• Of greatest use in the immunocompromised, those with severe sepsis or septic shock, or risk factors for endovascular infection
• Sputum cultures
• Minimal/no value in patients with obvious CAP
• Use should be limited to patients with suspected infection by unusual pathogens
Health Care-Associated Pneumonia
• Hospitalization for 2 or more days within the preceding 90 days
• Nursing home residents
• Hemodialysis patients
• Patients who have received IV antibiotics, chemotherapy, or wound care within 30 days of infection
Health Care-Associated Pneumonia
• P. aeruginosa
• K. pneumoniae (including ESBL producers)
Pneumonia- CAP Microbiology
• S. pneumoniae - overall most common
• H. influenzae - common in those with COPD, immune compromise
• M. pneumoniae - very common in previously healthy, young patients
• Klebsiella - alcoholics, diabetics
• S. aureus - Uncommon cause of CAP
• Legionella-commonly seen in clusters, GI symptoms are common
• Anaerobes-generally due to aspiration associated with poor dentition
• S. pneumoniae
• K. pneumoniae
• H. influenzae
• Occasionally can be caused by atypicals
• Atypical organisms
• M. pneumoniae
• C. pneumoniae
• S. aureus
• Gram negative rods
• Associated with CD4 count < 200
• Often presents with more indolent course than bacterial pneumonia
• Classic radiographic appearance is bilateral interstitial infiltrates
• Wide variation in appearance, may be lobar pattern or completely normal
• Serum LDH level of >220 U/L has high sensitivity
• Treatment with corticosteroids in addition to antibiotics recommended in those with HIV and hypoxemia
• At risk populations include the immunocompromised, incarcerated, homeless
• CXR may reveal hilar lymphadenopathy
• Upper lobe consolidation is also suggestive
• Initiate respiratory isolation early
• Several risk-stratification tools exist to guide the disposition decision
• PORT Score
• Hypoxemic patients are generally admitted
• Clinical judgment must always supersede
• 1-point each assigned for
• Urea (BUN > 20 mg/dl)
• Respiratory rate > 30/minute
• Blood Pressure <90 mmHg
• Age ≥ 65
Antibiotic Choice-CAP Outpatient
• No significant comorbidities or recent antibiotics
• Doxycycline (most suitable for atypicals, variable activity against S. pneumoniae)
• Comorbidities or antibiotics in last 3 months
• 3rd generation cephalosporin + azithromycin
• CAP, immunocompetent:
• Ceftriaxone + azithromycin; Levofloxacin
• CAP, severe (ICU admission):
• Levofloxacin + vancomycin + ceftriaxone
• HCAP or neutropenia (risk of Pseudomonas):
• Cefepime or antipseudomonal penicillin + quinolone or aminoglycoside + vancomycin
• Suspected Pneumocystis:
• Trimethoprim-sulfamethoxazole 240/1200 mg IV q6hr
CHF and Acute Pulmonary Edema
• Approximately 4.7 million people diagnosed
• 400,000 new cases each year
• Less than 1 percent of Americans younger than 50 years are affected, but prevalence doubles each decade until, by age 80 years, nearly 10 percent carry the diagnosis.
• Leading cause of hospitalization in those over 65 years of age
CHF and Acute Pulmonary Edema
• Congestive Heart Failure(CHF) is an imbalance in pump function in which the heart fails to adequately maintain normal cardiac output.
• The most severe presentation of CHF, pulmonary edema, develops when this imbalance causes an increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung.
CHF and Acute Pulmonary Edema History:
• Dyspnea at rest
• Dyspnea on Exertion
• Orthopnea and/or PND (although only 20-30% sensitive)
• Lower extremity edema
• Inquire about dietary indiscretion, medication compliance
• S3 gallop
• Basilar rales
• Diminished breath sounds at bases
• Lower extremity pitting edema (typically bilateral)
CHF and Acute Pulmonary Edema-Diagnostic Evaluation
• Cardiac Enzymes
CHF and Acute Pulmonary Edema Treatment:
• Typically double patient’s PO dose and give IV
• Nitrates (reduce myocardial oxygen demand by lowering preload and afterload)
• Sublingual, transcutaneous or IV nitroglycerin
• Analgesics (In addition to anxiolytic and analgesic effects, also results in venodilation, reducing preload)
• Positive pressure ventilation (CPAP/BiPAP or mechanical ventilation)
• Inotropic Agents (increase myocardial contractility)
• Dopamine or Dobutamine
Indications for Intubation
• Failure to protect airway
• Failure to oxygenate
• Failure to ventilate
• Anticipated clinical deterioration
Rapid Sequence Intubation
• Paralysis and induction
• Placement and proof
• Post intubation management
• Place oxygen on patient
• Assess for difficult airway
• Good suction
• Good IV access
• Monitors in place
• Respiratory therapist in room
• Gather necessary equipment (and assess functionality)
• Begin positioning patient
• Place high flow O2 on spontaneously breathing patient for at least 3 minutes
• Alternatively, can have an alert patient take 8 full vital capacity breaths with high flow O2
• Consider additional placement of nasal cannula with high flow oxygen
Paralysis and Induction: Induction agents:
• No cardiovascular depression
• Theoretical risk of adrenal suppression
• Mild cardiovascular depression
• Cardiovascular depression
• May increase intracranial pressure
• May be of benefit in reactive airway disease
• No cardiovascular depression
• Fast onset
• Short duration of action
• Malignant hyperthermia history
• Burn or crush injuries >3 days old
• Non-depolarizing agents (rocuronium, vecuronium)
• Slightly slower onset
• Longer duration of action, especially for vecuronium
Placement and Proof
• Direct visualization of tube passing through cords
• Fogging of tube
• Bilateral axillary and epigastric auscultation
• Secure tube
• CXR to evaluate placement
• Place NG/OG tube to decompress stomach
• Continue sedation