Respiratory — USMLE Step 2 CK Notes

Acute Respiratory Failure: hypoxia (<60mmHg), hypercapnic (PaCO2 >50mmHg) or both

V/Q mismatch AND Diffusion impairment (eg COPD/ILD) —->> RESPOND to O2

Diffuse Shunting: Only one that does not respond to O2!

Pulmonary oedema/ARDs

Localised shunting does respond eg lobar pneu/Atelecstasis

Massive PE or R->L Cardiac shunt also dont respond to O2

Hypercapnia d/t Increased CO2 production: Sepsis, DKA, Hyperthermia Or alveolar hypoventilation

Decreased minute ventilation/increased physiological dead space

Low V/Q —> High CO2

Aa gradient normal if hypoventilation or low inspired PO2 the mechanism

Ventilation is monitored by PaCO2: RR or Tidal Volume

Oxygenation monitored by O2 SATS and PaO2 -> FiO2 or PEEP

Ventilation and oxygenation are unrelated

To improve oxygenation:

Decubitus, upright or prone positioning bronchodilation

Decrease O2 requirement

Remove pulmonary vasodilator eg nitroprusside

NPPV

Pt must be neurologically intact, awake and cooperative and able to protect airway

If no improvement: intubate and mechanical ventilation!

ARDS

Diffuse inflamm process involving both lungs ——> Pulmonary oedema

Neutrophil activation in the systemic or pulm circulation is primary mechanism

Bilateral chest infiltrates

PCWP <18mmHg

Massive intrapulmonary shunting of blood

Severe hypoxaemia w/o improvement with 100% O2

Needs high PEEP to prop open airways!

Shunting d/t widespread atelectasis, collapse of alveoli and surfactant dysfunction

Causes stiff lungs, increase Aa gradient and ineffective gas exchange

Decreased pulm compliance: increased work of breathing; high PEEP needed

Increased dead space secondary to obstruction and destruction of pulm capillary bed

No fever

Causes: SEPSIS most common (LPS driven)

Aspiration; trauma, multiple/massive transfusions, near drowning

Initially resp alkalosis which gives way to resp acidosis as work of breathing increases

Metabolic acidosis if pt SEPTIC

Tx: Oxygenation sats >90%

Mechanical ventilation: high PEEP with low tidal volumes

Complications: Perm lung injury: scarring or honeycomb lung

Barotrauma; Critical illness myopathy

Mechanical ventilation:

Impaired consciousness with inability to protect airway

Significant hypoxaemia (70), hypercapnia (50) or resp acidosis (pH<7.2)

Goal is to reduce likelihood of barotrauma (overinflation) and atelectasis (underinflation)

Theoretically FiO2 <60% safe

PEEP is P maintained at end of passive exhalation (keeps alveoli open)

5cmH2O appropriate initial setting

High levels decrease cardiac output —>> decreased venous return

Increased plateau pressure (pulmonary compliance)

Complications:

Tracheomalacia (softening of tracheal cartilage) d/t prolonged presence of endotrach tube ## (>2wks):

——-> SOB, non productive cough and expiratory stridor

GI effects: increased risk of stress ulcers and cholestasis (pts should be on PPI/H2 blocker)

Low tidal Volume: decreases likelihood of overdistending alveoli

——> improves mortality in ARDS

Pulmonary HTN (Dx of exclusion)

Mean pulm arterial P>25mmHg

Causes:

Passive d/t resistance in pulm venous system (HF, atrial myxoma)

Hyperkinetic: Shunts such as ASD or PDA

Obstruction: PE or pulm artery stenosis

Pulm vascular obliteration (collagen vascular diseases)

Pulm vasoconstriction (chronic hypoxaemia)

Limited cutaneous systemic sclerosis

Loud pulmonic component of P2 and subtle lift of sternum/RV heave

Dx: ECG: RV Hypertrophy (Right axis deviation)

CXR: Enlarged pulm arteries

Echo: estimates pulm artery systolic P

Right heart catheterisation reveals increased pulm artery P and confirms dx

Tx: Continuous O2 therapy

Inhaled phosphodiesterase I (Sildenafil), oral CCBs, prostacyclins (eg epoprostenol)

Endothelin R antag (bosentan)

Cor Pulmonale

RV hypertrophy with eventual RV Failure d/t pulm HTN secondary to pulm disease

Excludes pulm HTN d/t left sided heart disease

Causes: COPD most common

ILD, asthma, CF, sleep apnea and pneumoconioses, PE

Dx: Echo (R heart cath gold standard)

Tx: Use diuretics cautiously as pts may be preload dependent; CPAP if hypoxic

Pulmonary Embolism

Risk factors: Nephrotic syndrome, >60yrs

Sources of emboli: Femoral Vein MCC

Often clinically silent. Recurrences common causing chronic pulm HTN and cor pulmonale

Pleuritic chest pain (d/t pulm infarction), nonproductive Cough, Hemoptysis, Syncope

Tachypnea, Rales

S4, increased JVP, Increased P2

Can cause prepulmonary obstructive shock (PCWP low/norm) with rapid circulatory collapse

Low grade fever, decreased breath sounds, dullness on percussion

R heart strain on ECG, decreased vascular markings on CXR, wedge infarct

Small pleural effusions common d/t hemorrhage/inflamm

Troponin increase d/t myocardial demand ischaemia

Dx: CT angiography (CTA) (/spiral CT) initial study of choice (shows filling defect)

PaO2 and PaCO2 are low and pH high

Aa gradient elevated

CXR normal: Atelectasis or pleural effusion may be present

V/Q scan if CTA CI: renal insufficiency —> CTA have lower accuracy in pregnant women so V/Q scan preferred

Chest CT shows WEDGE infarct (follows vascular distribution (cf pneumonia -> bronchial)

If high suspicion negative D Dimer does not exclude PE (false negative rate high)

D Dimer elevated in MI, CHF, pneumonia and postoperative state

If clinical suspicion of PE high and all tests negative PE still possible!

Tx: DVT/PE

O2, intubation etc

Acute anticoagulation with IV heparin

—> Start immediately on basis of clinical decision, do not await tests!

—> DOAC; Warfarin; thrombolytic/embolectomy (unstable pt)

CI to heparin: active bleeding, uncontrolled HTN, recent stroke, HIT

LMWH better bioavailability and less complications (but renally cleared)

THEN DOACs with warfarin for LT tx -> Continue for 3-6 months/ lifelong

Thrombolytic therapy: streptokinase, tPa -> No evidence this improves mortality

IVC interruption (IVC filter): CI to anticoagulation or complication/failure of current anticoagulation

Acute massive PE: underlying malignancy RV Dysfunction: Decreased ability to pump blood ==> hemodynamic collapse

Bowing of septum d/t RV P exceeding LVDP and RV free wall hypokinesis

Pulmonary Aspiration

Lower segments of Right upper lobe and upper segments of Right lower lobe

Extubation (impaired pharyngeal/laryngeal Function) and esophageal disorders predispose

Aspiration pneumonia occurs 2-4 days after aspiration

Aspiration pneumonitis:

Infiltrates acutely on CXR whereas pneumonia takes a few days to develop

->>>> Pneumonia may follow pneumonitis anyway

If obstruction early bronchoscopy indicated

Poor dental hygiene pre-disposes -> foul smelling sputum indicates anaerobes

Dyspnea

Chest wall abnormalities (kyphoscoliosis), rib fracture, ankylosis spondylitis

Neuromuscular Disease that weak resp muscles: MG, MD

COPD: PND: excessive secretions in day accumulate at night

—->. PND: Paroxysmal nocturnal dyspnea not specific for heart disease

Hemoptysis

Bronchitis (50% of cases)

Pneumonia; PE + Pulm infarction

Mitral stenosis (elevated pulm venous P) -> pulm oedema

Dx: CXR

Fiberoptic bronchoscopy (identify bleeding source and small tumours not obvious on CXR)

—> can be therapeutic

CT of chest (supplements bronchoscopy if CI)

PULMONARY contusion

SOB, hemoptysis, tachypnea, rhonchi, wheezes, hypoxemia, and hypercarbia

Alveolar hemorrhage and oedema —->> impaired oxygen diffusion

May not exhibit these symptoms for hours to days following trauma:

Nonlobar lung groundglass opacification/ irregular (nonlobular) patchy infiltrates

—->> initial X-RAY may be normal —-> infiltrates not diffuse/restricted by borders (nonlobar)

Tx supportive: Pain, Incentive Spirometry and supplemental O2

Fat embolism Syndrome

Triad: Resp distress, neuro dysfunction and petechial rash —-> rash only present in 50%

Similar to ARDS but has petechiae D/t fracture of BM contains bone (femur); Ortho surgery or pancreatitis

Systemic inflammatory micro vascular response to fat emboli

Respiratory alkalosis cf metabolic acidosis in ARDS

Prevention: Early immobilisation of fracture

Pulmonary oedema -> Cough + pink frothy sputum (Hemoptysis), wheeze

Negative P Pulm edema

When pt has upper airway obstruction (eg laryngospasm during extubation)

Large negative intrathoracic P d/t inspiration against obstruction

Non cardiogenic oedema

More common in young M or after head/neck surgery

Pulm auscultation findings:

Breath Sounds. Tactile Fremitus. Percussion. Mediastinal ## Shift

Normal: Bronchovesicular (hilar). N. Resonance. None

Vesicular (periph)

Consolidation: Increased. Increased. Dullness. None

Pleural Effusion: Decreased/absent. Decreased. Dullness. Away

Pneumothorax: Decreased/absent. Decreased. Hyperresonance. Away

Atelecstasis: Decreased/absent. Decreased Dullness. Toward

Normal: Quiet inspiration w almost inaudible expiratory phase

Consolidation: sound conducts more rapidly through consolidated lung (solid) cf effusion ## (fluid)

Atelecstasis: D/t shallow breathing —-> increased work of breathing/tachypnea ensue

Amiodarone induced interstitial pneumonitis: restrictive. -> Decreased DLCO Progressive dyspnea, nonproductive cough, bilateral Inspiratory wheezes, pulmonary infiltrates

New reticular/ground glass opacities on chest x ray —> can be migratory

Within months of treatment

COPD

2 Types: Chronic bronchitis or Emphysema

Chronic bronchitis: BLUE BLOATER

Excess mucus production narrows airways

Productive cough for min 3 months a year for min 2 consecutive years

Enlargement of mucous glands and SM hyperplasia lead to obstruction

Emphysema: PINK PUFFER

Relative excess protease (elastase) activity or relative deficiency of antiprotease (alpha1 antityrpsin)

PULMONARY CACHEXIA w disease progression —> sys inflamm + increased work of breathing

Elastase released from PMNs and macrophages, digests human lung

Tobacco smoke increases number of activated PMNs and macrophages, inhibits alpha1 antitypsin and increases oxidative stress on lung by free radical production

Centrilobular is most common type: SMOKERS

Destruction limited to resp bronchioles (proximal acini); upper lung zones

Panlobular: Alpha1 antitypsin deficiency

Destruction of both proximal and distal acini; lung bases

Smokers present in their 30s; non smokers 40s

Paraseptal —> most commonly involves young, otherwise healthy males

—-> associated with bullae —> increased risk for spontaneous pneumothorax

DX: GOLD staging (mild, moderated, severe, v severe) based on FEV1 -> Best Px indicator

CXR: Decreased vascular markings Tx: Smoking cessation has greatest impact on mortality Improves resp sx plus slows disease progression (decrease mortality)

Inhaled anticholinergics > Inhaled beta 2 agonists > Inhaled corticosteroids: anti inflammatory

Oxygen therapy: LT O2 -> prolongs survival

Theophylline: refractory COPD

Pulmonary Rehabilitation: Improves QOL

Vaccination: Influenza, S Pneu every 5-6 years (booster)

Surgery: Lung resection/transplantation

Acute Exacerbation: Antibiotics + Oxygen (target SpO2 of 88-92%)

Antibiotic: dependent on pseudomonas risk

Ipratropium + Albuterol

Systemic corticosteroids (not inhaled): promote shorter hospital stay and improve lung function O2: > 93% pt at risk of CO2 retention -> loss of hypoxaemic drive and the Haldane effect

Magnesium relaxes SM

Physical therapy not indicated in acute exacerbations

Oseltamivir if evidence of Influenza; NPPV

Risk of symptomatic hypercapnia (BIPAP/CPAP discontinued too early)

——-> shallow breathing means CO2 retention despite tachypnea =====> sx are neurological

HA; somnolence; delirium; lethargy; coma; seizure (d/t vasodilation)

Complications of COPD: Secondary Polycythemia: Pulm HTN and cor pulmonale

DLCO reduced d/t alveolar destruction

Preope PT reduces risk of postop pneumonia and shortens hospital stay

Preop Abs have no effect unless active infection

Asthma

Triad: Airway inflamm; Airway Hyperresponsiveness; Reversible airflow obstruction

Extrinsic asthma: Atopic, produce IgE to environmental Ags; Presents at young age

Intrinsic asthma: Not related to Atopy

Triggers: beta blockers

Sx typically worse at night

Wheezing during insp and exp is most common finding

Attack: Paradoxical movement of abdomen and diaphragm on inspiration -> impending resp failure

Dx: PFTs: Increase in FEV1 >12% with albuterol

Decreases in FEV1 >20% with methacholine or histamine

Decreased FEV1/FVC

Chest X-RAY usually normal, hyperinflation in severe asthma

Tx: SABA

LABA (Salmeterol) are esp good for nighttime asthma and exercise induced asthma

Inhaled corticosteroids-> sore throat and hoarseness d/t oropharyngeal deposition

Montelukast useful prophylaxis for exercise induced asthma (if exercise daily)

Can allow for reductions in dose of steroids (steroid alternative)

Cromolyn sodium/nedocromil sodium -> Only for prophylaxis (eg exercise); Rarely used in

adults

Exercise Induced Asthma

Tx: SABA (Albuterol) 10-20 min prior to exercise if required only a few times per wk

If exercising daily: Inhaled corticosteroids or antileukotriene agents (eg montelukast)

Acute exacerbation: SABA, IV Corticosteroids, ipratropium bromide

Third line: IV Magnesium, helps with bronchospasm if not responded to others

Supplemental oxygen (>90%); Intubation

Antibiotics if severe or infection suspected

Increased A-a gradient

Complications: Status astmaticus (does not respond to standard meds)

Acute resp failure d/t resp muscle fatigue

Pneumothorax, atelecstasis, pneumomediastinum

Aspirin sensitive asthma: asthma+nasal polyps -> Avoid aspirin and NSAIDs

Intermittent: Sxs twice a wk, night cough <2 x wk and norm PFTs: Albuterol

Mild Persistent: Sxs >2 x wk, night cough 3-4 month and norm PFTs: Albuterol + inhaled steroid

Moderate: Sxs daily, night cough >1 per week and reduced FEV1 (60-80%):

Albuterol + inhaled Steroid + LABA

Severe: Sxs daily, night cough >4 x wk and FEV1 <60%:

Albuterol, inhaled steroid, LABA, Montelukast and Oral Steroid

Aspirin exacerbated respiratory disease (AERD): Not d/t IgE

Pseudo allergic reaction to NSAIDs

Asthma chronic rhinosinusitis with nasal polyposis or Chronic urticaria D/t increased production of leukotrienes (inflamm) and decreased PGs (anti inflamm)

——> NSAIDs block COX and thus PG production (arachidonic acid diverted to leukotriene path)

Presents with asthmatic sx, nasal and ocular sx and facial flushing post NSAID

Tx: Avoidance of NSAIDs/desensitisation if NSAID use needed

Leukotriene R Blockers (Montelukast) and leukotriene I (zileuton)

Bronchiecstasis:

Permanent, abnormal dilation and destruction of bronchial walls with chronic inflammation

Airway collapse and ciliary loss/dysfunction leading to impaired clearance of secretions

A variety of recurrent infections can cause this eg chronic bronchitis

Cystic Fibrosis most common cause

Primary ciliary dyskinesia (Kartageners), alpha 1 antitrypsin def

Idiopathic; airway obstruction (eg cancer); autoimmune

Sx: Chronic cough with large amounts of mucopurulent, foul smelling sputum, SOB

Hemoptysis d/t rupture of fragile bronchial bvs nr bronchial wall surfaces

Dx: High resolution CT: bronchial wall thickening and bronchial dilation

CXR: Multiple cysts and bronchial crowding, linear atelecstasis, dilated/thickened airways

Tx: Antibiotics for acute exacerbations

Bronchial hygiene: Hydration

Chest physio (postural drainage, chest percussion) to remove mucus

Inhaled bronchodilators

Cystic Fibrosis

AR, predominantly Caucasians

Defect in chloride channel protein impairs chloride and water transport

Excessively thick secretions in resp tract, exocrine pancreas, sweat glands, GIT and Genitourinary tract

Obstructive pattern with chronic lung infections (Pseudomonas), Hemoptysis

Pancreatic insufficiency and other GI complications; Polyps poss; Vas deferens agenesis d/t clogging

MCC pneumonia is kids is Staph Aureus (Pseudomonas in adults)

Dx: elevated sweat Cl on 2 occasions (>60)

Lung Cancer

SCLC (25%), not surgery! Radon (basements) and COPD are RFs

SCLC staged differently to NSCLC (TNM)

Limited: confined to chest + supraclavicular nodes, but not cervical or axillary

Extensive: outside of chest and supraclavicular node

SCLC: Central (hilar/perihilar) mass; Mediastinal LAD

Adenocarcinoma can occur in scars of previous pneumonia; nodule

Characteristic exudative pleural effusion with high hyaluronidase

Large Cell: Peripheral Cavitation with metastases

Squamous cell: Large cavitary lesion (periph/apical or central)

Local manifestations (squamous cell most commonly associated extrinsic compression of bronchi)

Recurrent pneumonia (postobstructive pneumonia); hemoptysis

SVC Syndrome: Mediastinal tumour obstructs SVC

Most commonly seen with SCLC

Facial fullness, facial and arm edema, dilated veins over ant chest, arms n face, JVD

Phrenic nerve palsy : Destruction of phrenic nerve by tumour -> Hemidiaphragmatic paralysis

Recurrent laryngeal nerve palsy —hoarseness

Horner Syn d/t invasion of sym chain by apical tumour

Pancoast tumour: Superior sulcus tumour: Apical. Tumour involving C8 and T1-2 nerve roots

Shoulder pain radiating down arm -> Pain, arm weakness d/t brachial plexus invasion

Usually squamous cell (can be small cell)

Associated with Horner Syn in 60%

Malignant pleural effusion: poor px (equiv to distant metatastases)

Metastasis: Brain, bone, adrenals, liver

Screening: Low dose Chest CT annually for those who have smoked 30 or more pack years

AND Ages 55-80 AND Pt still smokes or quite within last 15 years

Paraneoplastic syndromes:

SIADH (SCLC): euvolemic hyponatremia

Ectopic ACTH (SCLC)

PTH like hormone (squamous)

Hypertrophic pulm osteoathropathy: adenocarcinoma and squamous

Eaton Lambert (SCLC): Decreased DTRs

Digital clubbing d/t thickened subungual tissue

Dermatomyositis NSCLC

DIC, thrombophlebitis Adenocarcinoma

Dx: CXR: Stability of abnormality over a 2 year period likely benign (INITIAL TEST OF CHOICE)

CT with IV contrast (staging), shows lymphadenopathy in mediastinum

Fibre optic bronchoscopy: useful in central tumours

Transthoracic needle biopsy -> peripheral

Always perform biopsy for intrathoracic LAD

Squamous can show cavitation on CXR

Carcinoid and SCLC both test + chromogramin A

Tx: Chemo fo SCLC

Radiation good adjunct, prophylaxis in SCLC decreases brain metastasis

NSCLC can have surgery unless metastatic disease is outside chest -> radiation, chemo

FEV1 and DLCO best px indicators of postop outcomes following lung resection

Solitary Nodule: GRANULOMA, HAMARTOMA, CANCER, CARCINOID OR PNEUMONIA Features of round opacity up to 3cm

No associated mediastinal or hilar LN involvement

Hamartomas most common benign: Popcorn Calcification

GRANULOMA: Concentric calcification (poss old TB infection)

GET PREVIOUS X-RAY!

Change in size: If not changed in 2 years follow yearly (malignancy ruled out)

If changed but CT (thin sections) suggests benign then follow every 3 months

Malignant lesions tend to grow rapidly however growth over days usually infect/inflamm

If no previous X-RAY then Chest CT to characterise lesion:

Benign Features: <0.8 cm; diffuse, central, popcorn, concentric

Malignant features: irregular borders; eccentric calcification, speculated, ground glass

Age: Older pt (>50) more likely malignant; Smoking

Low probability nodule eg <0.8 cm: serial CT

Int risk nodule 1cm or more: PET, if Positive then biopsy/surgical excision

High risk of malignancy: Excision

Mediastinal Masses:

Metastatic cancer esp lung cancer

Anterior mediastinum 4 T’S: Thyroid, teratogenic, thymoma, terrible lymphoma

Middle mediastinum: Lung cancer, aneurysm, cong diaphragmatic hernia

Posterior mediastinum: Neurogenic tumour

Sx d/t compression or invasion of adj structures (see lung cancers)

Dx: CT

LARYNGEAL Cancer

Squamous cell

Alcohol and tobacco use

Hoarseness that worsens over time (several wks), dysphagia, ear pain, hemoptysis

Tx laryngectomy, radiation,+/- chemo

Interstitial Lung Diseases:

Rales at bases, digital clubbing Reticular -> Fibrotic -> aFibrosis tends to encroach from periph Dx: High resolution CT

CXR shows honey comb lung

Idiopathic Pulmonary Fibrosis

Inflamm causes fibrosis, unknown cause

Pts >50 years (more common in M and smokers)

Abnormal S2 d/t pulm HTN

TX: Oxygen, Corticosteroids + azathioprine/ cyclophosphamide, lung transplant

Pneumoconioses

Digital clubbing; Cor pulmonale and pulm HTN

Acute or chronic

CXR shows multinodular opacities; CT shows fibrosis

Tx: Prevention/remove trigger

Caplans Syn: Coal workers/asbestos pneumoconiosis + rheumatoid nodules in lung

Silicosis: Nodules in UPPER Lobes with Eggshell calcification of hilar LNs

Increased risk of TB and lung cancer: get annual test!

Tx: remove exposure

Coal worker disease: UPPER nodular opacities

No increased risk of cancer

Centrilobular emphysema

Berylliosis: Noncaseating granulomas, diffuse infiltrates, hilar adenopathy

Increased risk of lung cancer

Chronic similar to sarcoidosis: skin lesions, hypercalcaemia, granulomas

Tx: Glucocorticoids

Dx: beryllium lymphocyte proliferation blood test

Asbestosis: DEVELOPS >15-20YRS POST EXPOSURE

CXR shows hazy infiltrates with bilateral linear opacities

Reticulonodular process

Pleural plaques esp in lower lung regions

Fibrosis cause sx not plaques

ILD associated with granulomas: ## Sarcoidosis

Noncaseating granulomas

Cough, arthritis, erythema nodosum, Vision blurred/loss, Uveitis, CN7 Palsies, arrthymias + heart block

Increased ACE, Alkaline phos, ESR and calcium, hypercalcaemia (macrophages produce Vit D)

Bilateral hilar LAD with ground glass appearance (pulm infiltrates) on CT

Upper lobes

Dx: Biopsy

TX: Self resolves, systemic corticosteroids, cytotoxic drugs (methotrexate) if no response,

Patients frequently show ANERGY (not reaction) to a skin or PPD test

Histiocytosis X: Chronic interstitial pneumonia

D/t abnorm proliferation of histiocytes (related to Langerhans cells of skin)

Most are cigarette smokers

Variants: eosinophilia granuloma (localised to bone/lung)

2 systemic forms: Letterer-Siwe disease and Hand-Schuller-Christian syndrome

SOB and cough

Spontaneous pneumothorax, lytic bone lesions, diabetes insipidus

CXR has honeycomb appearance, CT shows cystic lesions

Tx: Corticosteroids, lung transplant

Wegener’s (Granulomatosis with polyangiitis)

Necrotising Granulomatous inflamm and necrosis of lung and other organ systems

Noncaseating granulomas (Biopsy); Multiple lung nodules with cavitation

Ulcerations of nasopharynx and auditory canal

CNS (hearing loss, sensory neuropathy, corneal ulceration, diplopia)

Livedo Reticularis

Arrhythmia, myalgia, SOB, hemoptysis, chronic sinusitis

Systemic Sx

Positive cANCA

Dx: Renal biopsy shows vasculitic process

Tx: cytotoxic, corticosteroids

Rapidly fatal if untreated

Chugg-Strauss

Granulomatous vasculitis in pts with asthma

Pulmonary infiltrates, rash and eosinophilia

Systemic vasculitis: skin, muscle and nerve lesions

P-ANCA

Tx: systemic glucocorticoids

ILD associated with hypersensitivity (significant overlaps with ILD associated with granuloma)

Hypersensitivity pneumonitis (extrinsic allergic alveolitis)

Inhalation of antigenic agent to alveolar level induces immune-mediated pneumonitis

Chronic exposure may cause restrictive lung disease -> Fibrosis

Often mistaken for recurrent pneumonia

Can be caused by HOT TUBS!!!!

Transient attacks w Ag exposure: Fine Crackles

Abrupt onset fever, chills, cough, SOB, fatigue and leukocytosis

CXR: Scattered micronodular interstial opacities

Presence of serum IgG and IgA to inhaled Ag is hallmark finding, eosinophilia and leukocytosis

Dx: PFT; BAL; Biopsy (granulomas; lymphocytic infiltrate)

Tx: remove offending agent, glucocorticoids

Association: spores of Thermopylae actinomycetes

Nitrofurantoin-induced pulm injury: erythematous rash and effusion also

Acute form has flu like features (CXR shows pulm infiltrates); Chronic form harder to dx

Statin can also cause iatrogenic pulmonary fibrosis

Eosinophilic pneumonia

Fever and peripheral eosinophilia

CXR shows periph pulm infiltrates

Tx: Glucocorticoids effective but relapses may occur

Diseases of Pleura

Transudative: Low protein (peritoneal dialysis, cirrhosis) or high hydrostatic P

Exudative: Light’s Criteria: If any point violated then its positive!

Pleural protein/serum protein >0.5

Pleural LDH/serum LDH >0.6

LDH > 2/3 upper limit of normal serum LDH

PE can cause exudative or transudative effusion

Exudative d/t inflammation

Post CABG

Chylothorax (milky + TG)

RA Effusion has v low glucose (<50) and v high LDH (>700)

—-> usually resolve spontaneously/asymp

Elevated Pleural fluid amylase: Esophageal rupture, pancreatitis, malignancy

Bloody effusion: Malignancy

Exudative and primarily LYMPHOCYTIC: TB

Low Glucose d/t high WBC (use glucose) -> Glucose <60 consider RA

Dx: CXR (PA and lateral): opacity w Blunting of costophrenic angle

Lateral decubitus films more reliable than PA/Lateral CXRs for detecting small effusions

====> layering fluid on lateral decubitus

Tx: Thoracentesis if causing SOB

Transudative: Diuretics and sodium restriction

Exudative: Chest thoracostomy if empyema or complicated Parapneumonic

Parapneumonic effusions: Pleural effusion in presence of pneumonia

Uncomplicated (noninfected/no need for drainage): antibiotics:

-> pH >7.2 + WBC <50K; Glucose >60

Complicated (infected/needs draining): Chest tube

-> Gram stain positive; very acidic (pH<7.2), glucose <60

-> Empyema (type of complicated Parapneumonic effusion): PUS

Dx: CXR and CT

Tx: Aggressive drainage and antibiotics

Pneumothorax:

Spontaneous: Primary or secondary:

Primary (simple) pneumothorax: No underlying lung disease

Spontaneous rupture of subpleural bleb

Pts have sufficient pulm reserve so severe resp distress rarely occurs

Mediastinal/tracheal shift TOWARD side of pneumothorax

Secondary (complicated) pneumothorax: d/t underlying lung disease

COPD most common -> Lack of pulm reserve…..life threatening

Rupture of apical alveolar bleb

Tracheal shift RARE but if present: TOWARD side of pneumothorax

Dx: CXR

Tx: Primary can resolve spontaneously within 10 days

Secondary: Chest tube

<20% in size with no signs of resp/circ collapse will resolve spontaneously

-> 100% O2 will speed this up

Tension pneumothorax:

Tissues surrounding opening into pleural cavity act as valves only allowing air in

Mediastinum shifts AWAY from side of pneumothorax

Do not obtain CXR if suspected, immediate decompression via large bore needle/chest tube!!!

Subcutaneous crepitus/emphysema suggests tracheobronchial injury

==> large quantity of air escapes per breath ==> rapid reaccumulation

=====> persistent pneumothorax/pneumomediastinum

Dx: Bronchoscopy

Spontaneous pneumomediastinum RF: Asthma exacerbation; Respiratory infection; Tall thin adolescent boy

Acute Chest Pain; SOB; cough paroxysms (high intralveolar P)

Subcutaneous emphysema -> Hamman sign (crunching sound over heart)

Spontaneous pneumothorax can co-occur

Dx: Mediastinal gas on Chest X-RAY

Tx: Rest, analgesics, avoid Valsalva manoeuvres

Malignant mesothelioma

Bloody pleural fluid

SOB, weight loss and cough

NB Not all mesothelioma are malignant

Benign ones have excellent px and are unrelated to asbestos

Alveolar Filling Disease:

Good pastures Syndrome: (Type 2 hypersensitivity)

Progressive autoimmune disease of lungs and kidneys

D/t antiglomerular and antialveolar BM antibodies

Intraalveolar hemorrhage (haemorrhagic pneumonitis) and glomerulonephritis

Restrictive lung pattern with increased DLCO d/t presence of Hb in alveoli

Dx: Tissue biopsy and serology: AutoAbs

Tx: Plasmapheresis to remove autoantibodies, corticosticosteroids, cyclophosphamide

Pulmonary alveolar proteinosis

Accumulation of surfactant like protein and phospholipids in alveoli

D/t autoimmunity to GCSF mainly

Dry cough, SOB, hypoxia, rales

CXR has ground glass appearance with bilateral alveolar infiltrates that resemble a bat shape

Dx: lung biopsy

Tx: Lung lavage and G-CSF

Increased risk of infection so do not give steroids!

MISCELLANEOUS ILDs

Cryptogenioc organising pneumonitis

Inflamm lung disease with features similar to infectious pneumonia

Associated with multiple entities; Most idiopathic

Cough, SOB, Flu like sx, bilateral patchy infiltrates on CXR

Antibiotics ineffective

Spontaneous recovery may occur, corticosteroids more commonly used

Radiation Pneumonitis

Interstitial pulm infamm d/t thoracic irradiation

Acute form occurs 1-6 months post irradiation

Chronic form develops 1-2 years later: alveolar thickening and pulm fibrosis

CXR often norm

CT shows diffuse infiltrates (hallmark), pleural/pericardial effusions

Tx: corticosteroids

Aspiration Pneumonitis

Inflamm of lung parenchyma d/t gastric acid

Resolves w/o antibiotics

Atelecstasis: Tracheal deviation!

Lung looks white on X-RAY

Airway obstruction —> distal air trapping in alveoli -> diffuses into blood

—> alveoli collapse as devoid of matter

Mucous plug; tumour; foreign body —> surgery and smoking increase risk of mucus plug

Shallow breathing limits recruitment of alveoli at lung base

Weak cough predisposes to small airway mucus plugging

Chest physio used to prevent mucus plugging/ tx minor atelecstasis

Incentive spirometry decrease incidence postoperatively

Bronchoscopy needed to remove large mucus plugs

PFTs in chronic lung disease

Asthma. COPD. ILD. Pulm A HTN. Restrictive chest wall

TLC. N/H. H. L. N. L

FEV1/FVC. L. L. N. N. N

DLCO. N/H. N/L. L. L. N

Egophony: consolidated lung