Respiratory pt 2 Flashcards
(25 cards)
Croup (all info)
- viral inflammation of the upper and lower respiratory tract causing respiratory distress
- Etiology: PAIR :: Parainfluenza virus type I (60% of cases), also types II-IV; Adenovirus; Influenza; RSV
- Age: typically occurs in children aged 6 mos to 3 yrs
- Sex: M:F ratio 2:1.
- Sx: prodrome–few days of mild URI with coryza, nasal congestion, sore throat, cough, low-grade fever
then developing: hoarse voice and harsh, brassy, seal bark-like cough
Respiratory stridor (often at night) - PE: distress: from minimal to severe respiratory failure due to airway obstruction
Mild cases: examination at rest usually is normal; may be mild expiratory wheezing
More severe cases: inspiratory stridor at rest with nasal flaring, suprasternal and
intercostals retractions. Lethargy or agitation from hypoxemia .Tachypnea, tachycardia out of proportion to fever, lethargy, pallor - Course: usually peaks over 3-5d, resolves in 4-7d.
- Laboratory: leukocytosis with left shift
- Diagnosis: A-P X-ray of the C-spine, “steeple sign”
- Prognosis: self-limited disease, but can very rarely result in death from complete airway obs
- DDx: other causes of SOB and stridor:
-epiglottitis- hot potato voice, high fever, drool (emergency, don’t try to visualize!)
-foreign body–no hx URI, no fever
-retropharyngeal abscess–swelling at back of throat, seen on lateral xray
-diphtheria- grayish membrane over pharynx/larynx
ACUTE BRONCHITIS
- Self-limited inflammation the bronchus—usually from viral infection
Influenza A and B, parainfluenza, coronaviris (types 1-3), rhinovires, RSV
Rare pathogens: H flu, Mycoplasma pneumoniae, Chlamydophila pneumoniae, Pertussis
- SX: Cough > 5 days with sputum production (often starting with URI sx)
Sputum may be purulent from sloughing tracheobronchial and inflammatory cells
- PE:
- Generally afebrile or low grade fever
- Wheezing suggests bronchospasm
- Rhonchi indicates mucus in upper airways, clear with cough
- Normal percussion, no changes in transmitted voice tests
- Lab: CBC usually not warranted. No to mild leukocytosis
- Imaging: CXR usually not warranted. Only if developing signs of pneumonia, >75 yo, abnormal vitals, presence of crackles
- DDX: chronic bronchitis (persists), pneumonia, post-nasal drip, GERD, asthma
PNEUMONIA SPUTUM TO CAUSE
- Bloody/rust colored
- Green
- Foul-smelling
- Currant jelly
- Bloody/rust colored: pneumococcus
- Green: Pseudomonas, Haemophilus, and pneumococcal spp
- Foul-smelling: anaerobic
- Currant jelly: Klebsiella
PNEUMONIA CLASSIFICATIONS
a. Community-acquired pneumonia:
- 5-6 cases/1000 persons per year, worse in winter months
- Higher rates in males and in African Americans; in US, 8th most common cz of death
- Pre-disposing host conditions: level of consciousness, smoking, alcohol consumption,underlying lung disease, malnutrition, advancing age, peds, immunocompromised
- Most common organisms:
PAIR :: parainfluenza virus, adenovirus, influenza viruses A or B, RSV
Bacterial: S pneumoniae, H flu, S aureus, Group A strep, M catarrhalis, Klebsiella pneumoniae (rare), Legionella spp., M pneumoniae, Chlamydophila pneumoniae, P. aeruginosa
b. i Hospital-acquired (nosocomial) pneumonia
Pneumonia onset in >48hrs of hospital admission
ii Ventilator-associated pneumonia
Pneumonia onset 48-72 hrs after endotrachial intubation
iii Healthcare-associated pneumonia
Pneumonia occurs after extensive healthcare contact (IV therapy, chemotherapy, dialysis, nursing home residence)
Common organisms for above: E coli, Klebsiella, enterobacter spp, P aeruginosa, MRSA, H flu
General sxs of pneumonia
bacterial
viral
mycobacterium
bacterial: cough with thick greenish or rust-colored mucus; SOB; rapid breathing; sharp pleuritic pain–worse with deep breaths (S pneumoniae esp); abdominal pain, and severe fatigue. May be profuse sweating and mental confusion.
viral: malaise/headache/myalgia (flu-ike presentation), chest pain, sore throat, cough with scant sputum, dyspnea
mycobacterium: often very benign, slow progression, looks like URI (sore throat, fever, headache, malaise) and resolves without any treatment. possible violent attacks of coughing with scant mucus, chills/fever; occ. N/ V…..dry cough can persist for as long as a month; some pts can have a protracted
illness/weakness lasting as long as 6 weeks.
PE of pneumonia
bacterial
viral
mycobacterium
bacterial: Patient looks sick (fever, pallor, tachycardia, bradycardia, altered mental state) and lung exams point to consolidation (bronchial breath sounds, positive egophony, dullness to percussion, increased tactile fremitis, wheezes/rhonchi/crackles)
viral: most just have mild fever; some may have respiratory/multi-organ failure (decreased breath sounds, pleurisy, wheezing/rhonchi/crackles, tachypnea, tachycardia, sternal or intercostal retractions)
mycobacterium: non-toxic looking, CTAB, possibly rash, mild cervical LA, erythematous TM, pharyngeal erythem w/no exudate
This fungus is a frequent cause of morbidity and mortality in persons who are immunocompromised, may be AIDS-defining diagnosis. Rare in general population
(also give sxs and complications)
Pneumocystis jirovecii pneumonia (formerly P carinii)
Sxs: usually insidious onset of malaise, weight loss, night sweats and low-grade fever associated with a dry cough (sputum is too viscous to expectorate)
may be more severe: dyspnea, cyanosis, respiratory distress, chest pain, productive cough
Complications: spontaneous pneumothorax and hypoxemia Can also affect the liver, spleen and kidney.
Coccidioidomycosis (San Joaquin Valley fever or desert rheumatism)
Etiology: Coccidioides immitis, a soil fungus particularly adapted to arid condition. Southwest US (Utah, Ariz.), Mexico, S. America ….. Spores become airborne with soil disruption: construction, farming, quakes
Sxs: self-limited respiratory tract infx, occurs 1-3 weeks after exposure. most cases subclinical, never reaching the attention of a physician
common complaints are nonspecific: fever, cough, chest pain, fatigue, dyspnea, headache, arthralgias, and/or myalgias
May disseminate to other body systems in those immunocompromised
PE: Pulmonary: findings are generally nonspecific: crackles, pleural rubs, wheezing, and decreased breath sounds from effusions
Disseminated disease:
· Dermatologic; erythema nodosum
· CNS: disseminated CI may lead to meningitis - fever, altered mental status.
· Cardiovascular: endocarditis (rare but serious if involved)
· Musculoskeletal: osteomyelitis, septic arthritis, and synovitis.
Work-up:
· CBC - leukocytosis with eosinophilia, lymphocytosis, or monocytosis.
· CXR: Infiltrates can range from segmental or lobar to diffuse reticulonodular
· Skin testing - delayed-type hypersensitivity reactions may become pos in 1-3 wks.
· Serology tube precipitin assays for IgM may detect acute infection.
· Sputum culture results are usually delayed (5- to 7-day incubation period)
Diagnosis: clinical suspicion and history of possible exposure or travel to an endemic area.
Prognosis: General good, but poor if the patient is immunocompromised
Allergic Bronchopulmonary Aspergillosis
Eosinophilic pneumonia: Type I and II allergic rx. to Aspergillosis nigra or fumigatus (Fungus found in soil, decaying vegetation, dust, water)
Typical patient already has asthma- then develops cough, wheezing, dyspnea worse than normal, low-grade fever
Sputum- extremely tenacious, forms plugs with brown flecks filled with aspergillosis (colonized in the mucus)
CBC- diff. 50+% eosinophils, increased IgE, pos RAST skin test to aspergillosis
CXR shows infiltrates (Alveoli packed with eosinophils)
Histoplasmosis “spelunker’s lung”
Etiology:Histoplasma capsulatum, a fungus found in soil enriched with bird or bat droppings (caves) In US: Ohio and Mississippi river valleys, and Southeast. Spores inhaled into alveolar spaces, budding yeast seen within cells. Infx varies in sxs and seriousness (short-term, treatable infection to a disseminated disease)
Sxs:
- Acute (short term, mild) - fatigue, fever, chills, chest pain, dry cough (~10 d post exp)
- Chronic (long term, serious) – persistent or relapsing
- Disseminated histoplasmosis leads to serious symptoms, multiple body organs
PE: related to the extent and duration of infection.
- Acute pulmonary histoplasmosis
- Lung auscultation: crackles or wheezes (rarely)
- Heart auscultation: may be pericardial friction rub (~5% of pts develop pericarditis)
- Skin: erythema multiforme or erythema nodosum(~5-6% of pts develop)
- Chronic pulmonary histoplasmosis:
- Lung auscultation: crackles, wheezes
- Chronic progressive disseminated histoplasmosis:
- Mouth: ulcers on the buccal mucosa, tongue, gingiva, and larynx.
- Eyes: May be vision loss
- Abdomen: hepatosplenomegaly is possible
Work-up: sputum culture for the organism; positive histoplasma skin test, useful only for outbreak investigations; PCR to identify DNA; CXR: calcified hilar lymph nodes, lung scarring seen in chronic forms
Prognosis: acute pulmonary histoplasmosis is associated with a good outcome; chronic progressive disseminated histoplasmosis has a protracted course, lasting up to years, with long asymptomatic periods. If untreated may result in death
Two forms of non-infectious pneumonia
Aspiration from: esophageal dz., seizures, chronic hiccups, while under general anesthesia, post-surgery, alcoholism, drug abuse, disturbances of consciousness, vomiting
-local structures having problems leading to liquid in the lungs; severe inflamx process ensues, potentially fatal
Lipoid aspiration (fat or oil)- e.g. mineral oil (elderly pt.), nasal ointments, nose drops, furniture polish into lungs
- Oil causes inflammation, secondary infection
SX: acute: fever, cough, oil droplets in sputum, chronic wt loss, night sweats
CXR reveals infiltrates throughout lung
LUNG ABSCESS
- Sequestration of anaerobic bacteria leading to necrosis of lung parynchema, typically as a complication of aspiration pneumonia, or severe bacterial pneumonia
- SX: history of unresolving pneumonia, fever, cough, sour-tasting sputum for > 2wks; night sweats, weight loss, hemoptysis, pleurisy
- Work-up: Seen as cavitation on CXR and CT
Considerations with unresolved bacterial pneumonia
- Comorbidities: alcoholism, COPD, CHF, CKD, Malignancy, DM, HIV
- Advancing age >65
- Aggressive organism: Klebsiella, Legionella, S Aureus
- Drug-resistant organism: eg S pneumoniae
- Non-bacterial agents: TB, fungi
- Underlying neoplastic dz
- Misdiagnosis of: connective tissue dz, sarcoidosis, pulmonary embolism, pulmonary edema, drug-induced lung dz
Complications include: lung abscess, pleural effusion, empyema
Important points about top five bacteria causing pneumonia
i) Streptococcus pneumoniae (Pneumococcus pneumonia) (60-80%)
- Prognosis: overall mortality 5%
- Complications: meningitis, endocarditis
- REFER if: BUN >70, WBC <5000, other underlying dz. (heart, COPD)
ii) Klebsiella pneumoniae
- gram negative bacilli causes aggressive necrotizing lobar pneumonia
- risk factors: alcoholism, malnutrition, DM, recent tx with antibiotic, COPD, >40yo, hospitalized individuals
- Prognosis: 40-60% if untreated
- Sx: Cough, fever, pleuritic chest pain, dyspnea; spreads quickly, “currant jelly” sputum, Relative bradycardia: pulse rate does not increase as much with fever (usually with every degree in temp rise is inc 10 in heart rate)
iii) Haemophilus influenzae
- most commonly arises in the winter and early spring
- risk factors: asthma, COPD, smoking, immunocompromised
iv) Staphylococcus aureus
* in IV drug abusers and other individuals with debilitations infx often spread hematogenously to the lungs from contaminated injection sites.
v) Legionella pneumophila (gram negative bacterium) “Legionnaire’s disease”
- outbreaks from aerosolized organisms from air conditioning system or contaminated shower heads, more often in hotels and hospitals
- associated GI symptoms >50% of the time: anorexia, nausea, vomiting, and diarrhea.
Groups with higher prevalence of TB:
Homeless or marginally housed persons
Foreign-born or freq travel to endemic areas
Persons in group living
Elderly
Health care workers serving high risk grps
Medically underserved, low income
Children exposed to adults at high risk
Groups with higher risk of progression to active TB:
Those infected within 2 previous years
Kids < 4 yrs
Persons with history of untreated/undertreated TB
Immunocompromised
Underlying medical conditions: silicosis, DM, CKD, gastrectomy, underweight
Primary vs Active TB Infection
i. Primary TB infection:
- Organism enters lungs, inflammatory reaction holds organisms in check
- Only 10% of people infected with TB will develop active disease. Remaining 90% will show no signs of infection, nor will they spread the disease to others (latent TB)
ii. Active TB (from either primary infection, or reactivation from latent)
Sxs:
- Chronic productive cough (>3 wks duration)
- yellow-green sputum – usu in AM (late in dz)
- hemoptysis (late in dz)
- malaise, fatigue
- anorexia, wt loss
- low grade fever coming on in late afternoon
- night sweats
- Note: classic symptoms are often absent, esp in patients who are elderly or immunocomp
PE:
- fever
- cachexia
- hypoxia
- tachycardia
- lymphadenopathy
- abnormal lung sound
Lab: PPD test, Quantiferon Gold
PLEURISY
Inflammation of the pleura, may lead to pleural effusion (fluid in pleural space)
Layers of pleura rub with inhalation, causing sharp pain ie “pleuritic chest pain”
Etiologies:
- infections: bacterial, TB, fungus, parasites, or viruses (most common)
- inhaled chemicals or toxic substances
- collagen vascular diseases: lupus SLE, rheumatoid arthritis RA
- cancers - spread of lung cancer or breast cancer to the pleura, mesothelioma
- congestion: heart failure (CHF)
- pulmonary embolism (PE)
- trauma - rib fractures or irritation from chest tubes
- abdominal conditions such as pancreatitis, cirrhosis of the liver
- lung infarction: lung tissue death due to lack of oxygen from poor blood supply
Sxs:
- usually sudden onset of pain (vague or sharp stabbing pain)
- pain worse coughing, deep breathing—leading to rapid, shallow breathing, holding breath, splinting of chest. May refer to shoulder or diaphragm
- SOB
- when an effusion develops, pain usu. subsides but dyspnea increases
PE:
- fever if infectious cause
- tachycardia
- limited chest motion on that side
- decreased breath sounds
- Pleural friction rub is characteristic, may not hear until 24-48 hrs after onset of pain (crackles, harsh grating, or leathery creaking on inspiration and expiration)
- Compared to Pericardial friction rub– pathognomonic for pericarditis (rub will be constant, have pt hold breath and the sound will persist)
- With pleural effusion, decreased or absent breath sounds, percussion dullness, decreased tactile fremitus, egophony at upper border of fluid
Laboratory: CBC, Arterial blood gases (ABGs)
Imaging studies
- CXR: may be normal, fluid blunting of costo-phrenic angle if effusion
- Ultrasound can detect the presence of pleural fluid
- CT scan can be very helpful in detecting trapped pockets of pleural fluid
Pleurisy DDx:
- acute abdomen- N/V, abd. pain
- intercostal neuritis- no friction rub
- costo-chondritis- hx of trauma?, localized pain, reproducible with palpation
- herpes- if no eruptions yet may be difficult to tell!
- MI- location of pain, concomitant sx, risk history, cardiac enzymes
- pneumothorax- tracheal deviation, R/O by x-ray,
pericarditis- rub with heart beat (constant) instead of breath, precordial pain radiating to neck, shoulders, also < resp, cough, heart sounds are lowered as fluid in sac muffles heart sounds
Pleural Effusion Classification
a. transudate - from increased microvascular pressure or decreased oncotic pressure (containing normal levels of these body chemicals, from a systemic problem).
b.exudate – local pleural inflammation with increased permeability of pleural space to protein (high in protein, low in sugar, high in LDH enzyme, and high WBCs; characteristic of a local inflammatory process)
Types of pleural fluid:
Lymph:
Pyogenic:
Blood:
Serous:
Types of pleural fluid:
Lymph: chylothorax
Pyogenic: empyema*
Blood: hemothorax
Serous: hydrothorax
PLEURAL EFFUSION
Normal pleural space contains approximately 1 ml of fluid
Sxs:
- Dyspnea (most common) related more to distortion of the diaphragm and chest wall during respiration than to hypoxemia.
- mild, nonproductive cough, chest pain
PE: (findings do not usually manifest until pleural effusions exceed 300 mL )
- decreased breath sounds
- dullness to percussion over effusion
- decreased tactile fremitus
- egophony (E-to-A change) (at top of fluid)
- pleural friction rub with breathing
- mediastinal shift away from the effusion (with effusions >1000 mL)
Laboratory/procedure: CMP (protein, albumin, LDH) and Removal of pleural fluid by thoracentesis is essential in diagnosing (referral to perform)
Analysis of fluid color, consistency, and clarity; presence of organisms and/or cancer cells
Pleural Effusion Causes
EXUDATE
Lung infections
Malignancy (carcinoma, lymphoma, mesothelioma)
Pulmonary embolism
Collagen vascular (RA, SLE)
TB
Asbestos
Chest trauma
Esophageal perforation
Radiation pleuritis
Sarcoidosis
TRANSUDATE
Congestive heart failure CHF
Cirrhosis (hepatic hydrothorax)
Atelectasis (malignancy, pulmonary embolism)
Hypoalbuminemia
Nephrotic syndrome
Peritoneal dialysis
Myxedema
Constrictive pericarditis
PLEURAL EMPYEMA
common organisms: Strep pneumoniae, Haemophilus influenzae, and S aureus.
Sxs: symptoms of pneumonia: fever, cough, fatigue, SOB, chest pain, bad breath
