Acute Bronchiolitis
-Inflammation of the bronchioles, usu. occurs in children <2yrs.
Etiology:
RSV = Most common cause
Infants 2 months - 2 yrs = MOST at risk.
Clinical manifestations:
Viral prodrome (URI) for 1-2days followed by resp. distress. (Wheezing, tachypnea, nasal flaring, cyanosis)
Signs of severity: Hypoxemia, apnea, resp. failure.
Dx: Clinical.
CXR nonspecific, Pulse oximetry = single best predictor.
Management:
Supportive measures = mainstay of treatment. (Humidified O2, IV fluids)
Mech. ventilation may be indicated
Corticosteroids NOT indicated unless hx of underlying reactive airway.
Prevention:
Palivizumab
Handwashing
Acute/Chronic Bronchitis
Acute: Cough >5 days; can last 1-3wks.
Sx: Fever is unusual. MC is viral
Bacterial → M. catarrhalis
Dx: CXR
Tx: symptomatic/supportive
Hydration, B2 agonist, expectorant
abx → elderly, underlying dz, cough >7-10 days
Chronic:
Results from enlargement of mucus glands and goblet cell hypertrophy in large airway (>3 months!)
Tx:
Acute exacerbation: O2, beta-agonist, steroids
Chronic: Smoking cessation = best
Asthma
-Chronic inflammatory disease of the airways characterized by persistent variable symptoms that include dyspnea, cough, and wheezing.
-Most common chronic lung disease in the US. (COPD most common in the world)
-More common in women and children and poor
-Environmental factors and genetic factors.
Pathophysiology:
Bronchospasm (Hyperreactivity)
Bronchial wall edema (bronchoconstriction)
Increased mucus secretion (inflammation)
-T2-High → allergic (Allergens)
-T2-Low → non-allergic (meds, stress, exercise, GERD)
Risk factors:
Atopy = Strongest risk factor
Samter’s triad: (Aspirin-exacerbated resp. disease)
Asthma + Chronic rhinosinusitis w/ nasal polyps + Sensitivity to Aspirin/NSAIDs
Atopic Triad: Asthma, Atopic disease, Allergies
Clinical Manifestations of Asthma
Symptoms:
Classic Triad (Esp. @ night)
Dyspnea, Cough, wheezing
-PE: Prolonged expiration w/ wheezing, hyperresonance to percussion.
Severe asthma & Status asthmatics: inability to speak in full sentences, “tripod” positioning. Silent chest.
Altered mental status = ominous.
Dx: Made in office
Pulmonary Function test → Methacholine challenge (>20% decrease in FEV1) followed by bronchodilator (increase of FEV1 by 12%)
Dx Criteria of Asthma severity
Components:
Daytime symptoms > 2x week
Nighttime awakenings due to asthma
Interference with normal activity
Reliever meds needed >2x per week
-Apparently mild Asthma (well controlled) → meets none of the above.
-Moderate Asthma (Partly-controlled) → 1-2 components within the last 4 weeks
-Severe Asthma (Not controlled) → 3-4 components within the last 4 weeks.
-Life-threatening →
Exhausted
Cyanotic
Pulse ox. < 90% (severe under 94%)
Absent breath sounds
Accessory muscle use/tripod position
General Line of Treatment for Asthma
1.) Long-term controller
Reduce airway inflammation, symptoms, and risk of exacerbation
Inhaled corticosteroids (foundation of treatment)
2.) Reliever
Used PRN to relieve breakthrough symptoms
SABAs (albuterol)
Low-dose ICS-formoterol (LABA)
3.) Add-on therapies
For severe asthma
Systemic corticosteroids
Anticholinergics
Max doses:
Budesonide-formoterol (Symbicort)→ 12 for adults, 8 for children.
Beclometasone-formoterol (Fostair)→ 8 for everyone.
Steps 1-2
-Symptoms less than 4-5 days a week
-Take 1 puff low dose ICS-formoterol PRN
+rescue inhaler
Step 3
-Symptoms most days, or waking with asthma once a week or more.
-Take 1 puff low dose maintenance ICS-formoterol 2x/day + 1 puff inhalation PRN
+rescue inhaler (low dose ICS-formoterol)
Step 4
-Daily symptoms, or waking with asthma once a week or more, AND low lung function.
-Take 2 puffs 2x daily + 1 puff PRN
+Rescue inhaler (low dose ICS-formoterol PRN)
Step 5
Step 4 +
Add-on LAMA
Refer for assessment of phenotype
Consider High dose maintenance ICS-formoterol + antibodies
Cystic Fibrosis
-Autosomal Recessive trait → abnormal mucus production → obstruction of glands and ducts
Patho:
CTFR gene mutation → abnormal chloride & water transport → thick, viscous secretions.
Clinical Manifestations
Infancy: Meconium ileus, failure to thrive, diarrhea from malabsorption.
Pulmonary: Most common cause of Bronchiectasis.
GI: Malabsorption → fatty stools, foul smelling.
Dx:
Elevated Tripsinogen in neonatal screening = Red flag.
Elevated Sweat chloride = Test of Choice (most accurate)
NaCL 60mmol/L or greater on 2 occasions after Pilocarpine administration.
Pulmonary function test → obstructive pattern. (irreversible)
Cystic Fibrosis Management
Management:
Abx are often needed: Macrolides, Cephalosporins….(all broad spectrum)
Airway clearance treatment
Supportive (Pancreatic enzymes, fat-soluble vits., vaccinations.)
General measures:
Mean survival is 47yrs
First few years of life → resp infx from staph and H. flu
P. aeruginosa = major cause of infection after first years of life.
Foreign Body Aspiration
-Peanuts are MC FB aspirated in children
MC age is 2yrs, MC cause of death is hypoxic brain injury.
-Most common on the right side (position may influence locations:
Supine → MC in sup. segment of right lower lobe
Sitting/standing: MC in posterobasal of RLL
Lying on right side → MC in right/middle lobe or Post. seg. of RUL.
Clinical Manifestations:
Sudden onset of choking, cough, and dyspnea.
Wheezing or asymmetric breath sounds.
Inspiratory stridor if FB is high in airway
Wheezing & decreased breath sounds if in low airway.
Dx: CXR or CT (air trapping MC finding)
Right bronchoscopy = definitive dx. (also therapeutic)
Management:
Rigid Bronchoscopy → removal of FB
Thoracotomy if refractory
Emergency → Heimlich maneuver
Tracheostomy if unsuccessful
Hyaline Membrane Disease
(Resp. distress syndrome)
-Atelectasis & pulm. perfusion w/o ventilation d/t insufficiency of surfactant production by an immature lung.
Patho:
Lack of surfactant production (if born before 35wks = very high risk)
Airways collapse => struggle to breath until MOD and death
MC single cause of death in 1st month of life.
Risk factors:
Caucasians, Males, Multiple births, maternal diabetes.
Clinical Manifestations: Present @ birth (tachypnea, chest wall retractions, expiratory grunting, nasal flaring, cyanosis.
Dx: CXR → bilateral reticular atelectassi (ground glass appearance) + air ronchograms
ABG → hypoxia
Management:
Exogenous surfactant via endotracheal tube + Mechanical Vent (CPAP)
This opens up the alveoli
Prevention:
Antanatal glucocorticoids given to mature lungs if premature birth suspected (24-36 wks.)
Croup (Laryngotracheitis)
Etiology: MCC = parainfluenza type 1, RSV, Adenovirus, and Rhinovirus
MC between 6months-6 years, esp in fall/winter
Clinical Manifestation:
Upper airway involvement: Harsh “seal-like barking cough” = Hallmark of disease
Inspiratory stridor, hoarseness in older children.
URI symptoms
Dx: Clinical diagnosis (once epiglottitis & FB aspiration are excluded)
Frontal cervical radiograph: Steeple sign (subglottic narrowing of the airway)
Management:
Mild (no stridor @ rest, no resp. distress)
Supportive care (cool humidified air), Dexamethasone/Prednisone
Moderate (Stridor @ rest, mild/mod retractions)
Dexamethasone or PRednisone
nebulized epi (racemic epi)
Severe (Stridor @ rest, marked retractions)
Dexamethasone + nebulized epi and Hospitalization
Hemoptysis
MC causes:
Bronchitis (50%)
Hemoptysis, dry cough, cough w/ phlegm
Tumor mass (20%)
Hemoptysis, chest pain, rib pain, smoking hx, wt. loss, clubbing
TB (8%)
Hemoptysis, chest pain, sweating
Other
Pulmonary Nodules
<3cm = Nodule, >3cm = Mass
-Typically incidental findings, if found get CT (best imaging)
Suspicious → biposy
Not suspicious → monitor @ 3mo, 6mo, then yearly.
smooth, calcifications, not in upper lobe
Carcinoid tumors:
Most pt. have a centrally located tumor that are symptomatic (wheezing, cough, hemoptysis…)
Carcinoid syndrome:
Diarrhea (Serotonin release), flushing, tachy, wheezing, hypotension.
DX: Chest CT and bronchoscopy (pink/purple well vasc. central tumor)
TX:
Surgicla = definitive
Octreotide = symptom management.
Pleural Effusion
Pathologic accumulation of fluid
Transudate effusions: (CHF (MC), nephrotic syndrome, Cirrhosis)
Increased hydrostatic pressure
Decreased oncotic pressure
Exudate effusions: (increased capillary perm.)
any condition assoc. w/ Infection or inflammation.
Clinical presentation:
Dullness to percussion, decreased fremitus, decreased breath sounds
Dx:
Xray → inital test of choice (lateral decubitus = best postion)
Blunting of costophrenic angles (Menisci sign)
Thoracentesis = dx standard
Light’s criteria: exudate present if any of three are present
Pleural fluid protein (>0.5)
Pleural fluid LDH (>0.6)
Pleural fluid LDH >2/3 normal limit.
CT scan or U/S = mrore accurate than lateral decubitus.
Tx:
Treat underlying disease = mainstay
Chest tube fluid drainage if empyema
Pneumothorax
-Accumulation of air in the pleural space, leading to lung collapse from the positive pressure.
Types:
Primary spontaneous → atraumatic and idiopathy
Secondary spont. → underlying disease (COPD/Asthma)
Tension → Any type in which positive air pressure pushes the trachea, great vessels, &/or heart to the contralateral side.
Sx: sudden onset dyspnea & chest pain (usu. pleuritic, ipsilateral, unilateral, non-exertional.
PE:
Air: Hyperresonant, decreased fremitus and breath sounds.
Tension: Increased JVP, systemic hypotension, pulsus paradoxus.
Dx: Chest XR → initial test of choice (expiratory upright)
Management:
Small PSP (<3cm from chest wall):
Small & first episode: Obsv. for 4-6hrs if pt. is reliable
Large PSP:
Needle aspiration (chest tube if fails)
Stable, Secondary PT:
Chest tube placement (tube thoracostomy) and hospitalization.
Tension PT:
Needle aspiration followed by chest tube thoracostomy
VATS if a persistent leak or no regression
Pt. Ed: Avoid pressure changes for a minimum of 2 weeks.
Pulmonary Embolism
-70% arise from DVT
-Virhcow’s triad
Clinical Manifestations:
Sudden onset dyspnea (MC) followed by pleuritic chest pain and cough (sometimes hemoptysis)
Dx:
CXR: Westermark sign (sharp cut-off of pulm. vessels, Hampton’s hump (wedge-shaped, pleural-based opacity at periphery of lung)
ECG: S1Q3T3 pattern not common but most specific for PE.
D-Dimer, ABG, Well’s criteria
Pulmonary angiography = Gold standard
Tx: (anticoag should continue for at least 3 months.)
Anticoagulation = mainstay of treatment.
IV heparin then switch to oral after 5 days.
Oral monotherapy (Rivaroxaban or Apixaban) (preferred to warfarin for prophylaxis)
IV heparin “bridged” to warfarin.
IVC filter
For those who fail anticoagulation or it is contraindicated in.
Unstable → Thrombolytic therapy or embolectomy
Pregnant/malignancy → LMWH
RSV
MCC of lower resp. tract infection in children. MCC of pneumonia and bronchiolitis.
Sx of viral infection
Dx: RSV test or CXR shows diffuse bilateral infiltrates.
Tx: Supportive (should resolve in 5-7 days)
Hospitalize → Tachypnea w/ feeding, Visible retractions, decreased O2
Vaccine for children w/ lung issues or premature/immunocom.
TB
Sx: Fever, night sweats, wt. loss
Dx:
>5mm: + for high risk pts.
CXR w/ evident findings, HIV, steroids daily, contact w/ infectious pt.
>10mm: Some risk factors
IVDU, recent immigrants, renal dz, prison/homeless, diabetes, head/neck cancer, GI bypass surgery.
>15mm: no risk factors
Tx:
PPD+ and CXR negative = latent → Isonazide x9mo
PPD+ and CXR+ = Active. → quad therapy
RIPE x8 wks, RI x 16wks
Rifampin: Orange body fluids, hepatitis
Isoniazid: Peripheral neuropathy (B6 to help)
Pyrazinamide: Gout (hyperuricemia)
Ethambutol: Optic neuritis, red-grn color blindness.