Respiratory MedicineThis guide is intended to be used as a resource alongside many other sources

Knowledge: Anatomy &Physiology Normal ranges Respiratory failure Pleural diseases Asthma COPD Bronchiectasis Cystic Fibrosis Pneumonia Tuberculosis Lung cancer Pulmonary Fibrosis Occupational Thromboembolism Sleep Medicine

1

Anatomy & PhysiologyThe lungs are lined by visceral pleura which is continuous with the parietal pleura and facilitates movement for breathing. Pleura lubricated by surfactactant produced by type II pneumocytes.23 generations form bronchus to alveolar sacs, cartilage ends at generation 12 (bronchioles)

Trachea divides at carina @ T4Right bronchus wider, shorter & more vertical

Left lung – 2 lobesseparated by oblique fissure upper (mainly anterior) – 4 bronchial subdivisions lower (mainly posterior)– 4 bronchial subdivisions

Surface contacts1. Aortic arch2. Common carotid3. Thoracic duct4. Vagus & phrenic nerves

Right Lung – 3 lobes. U & M separated by transverse fissure, L separated by oblique fissure upper (mainly anterior) - 4bronchial subdivisions middle (small and only anterior) - 2bronchial subdivisions lower (mainly posterior) - 5 bronchial subdivisions

Surface contacts1. Oesophagus2. IVC & SVC3. Brachiocephalic &azygos veins4. Vagus & phrenic nerves

Normal ABG Ranges

2

Respiratory FailureA ventilation/perfusion mismatch causes pulmonary gas exchange to fail to maintain normal oxygen and carbon dioxide levels.

Type 1 – Hypoxia (PaO2<8 kPa)Type 2 – Hypoxia & Hypercapnia (PaCO2>6.6 kPa)

Causes

Type 1 Type 2Acute Chronic Acute Chronic

H+ Normal/Raised Normal Raised Normal/RaisedHCl- Normal Normal Normal RaisedCauses Acute asthma Emphysema Severe asthma COPD

Pulm oedema Fibrosis COPD exacerbation Sleep ApnoeaPneumonia Lymphangitis Airway obstruction KyphoscoliosisPneumothorax Carconomatosa Acute paralysis MyopathiesPE Right-to-Left shunt Narcotics Ankylosing spondylitisARDS Brain-stem Lesion Prim alveolar hypovent

InvestigationsABGCXR

ManagementOxygen (maximum unless severe COPD (24-28% with venture mask))Treat underlying conditionIf worsening/no improvement in ABG patient needs mechanical ventilation.

Long Term Oxygen Therapy (LTOT)Indications (+smoking cessation)-PaO2<7.3kPa & FEV1<1.5L-7.3kPa < PaO2< 8kPa & Pulm Hypertension/Peripheral Oedema Aim for PaO2> 8kPa without unacceptable rise in PaCO2

Therapy >15 hours/day

3

Pleural DiseasesPneumothorax–air in pleural spacePrimary – occurs in absence of underlying lung disease (Male, 20s, tall, thin, smoker w/ apical blebs)Secondary – occurs in presence of underlying lung disease (COPD & TB... others also)Traumatic – caused by surgery, chest wall injury etc.

Clinical featuresSymptomsSudden, unilateral pleuritic chest painBreathlessnessCough

SignsDecreased/absent breath sounds & vocal resonanceHyper-resonant percussionReduced expansionTracheal deviation & mediastinal shift (Tension)

InvestigationsCXR – complete translucency. Small <2cm Large >2cm (>2cm = 49% hemi-thorax)

ManagementTension & secondary = Intercostal tube drainage (ICD)Primary &>50 years old =ICDPrimary &<50 years old = Percutaneous aspirationPrimary &<15 % hemithorax = Observation for 6 hours and follow up as outpatientVideo assisted thoracoscopic surgery (VATS) indicated when:

Failure for lung to re-expand (5 days)1st contralateral PTX2nd ipsilateral PTXSpontaneous bilateral/haemothoraxProfessions at risk

No flying for 6 weeksNo diving (unless pleurectomy performed)

Pleural effusion – fluid in pleural spaceFluid - effusionPus – empyemaBlood – haemothorax

Clinical featuresSOBUnderlying disease

SignsReduced expansion/breath sounds & vocal resonanceStony dull percussion

Investigation & ManagementCXR - >200ml required before evidentUSS – useful for aspirationCT – distinguishes between benign & pleural disease

AspirationMicrobiology - cultureBiochemistry – protein, glucose, LDH, pHPathology – cytology

Biopsy (Abram’s or VATS)HistologyTB culture

4

Common causesPneumonia ExTB ExPE Ex (occasionally Trans)Malignancy ExCardiac failure TransRenal problems Trans

Light’s CriteriaPleural Fluid Protein:Serum protein ratio >0.5Pleural Fluid LDH:Serum LDH ratio >0.6Pleural Fluid LDH > 2/3 of normal upper limit serum LDH

Any positive = Exudative (infection/malig/inflamm/PE)

AsthmaNo universal definition. Paroxysmal airway obstruction caused by inflammation triggered by a specific stimulus.Airway narrowing due to bronchoconstriction & mucus plugging. Hypersensitive & increased inflame cells. Chronic leads to permanent remodelling.

Extrinsic – Specific allergen identified. 80%. IgE production esp to dust mites, pollen and pet dander

Intrinsic – Occurs in adults and does not improve Drug induced – NSAIDS (esp aspirin) inhibit COX = Leukotriene…think anti-leukotriene therapy Exercise induced –Hyperventilation = water loss = mediator production = asthma symptoms

Epidemiology – 8 million diagnosed (5.1 M on treatment). Prevalence increasing (300 M worldwide) possibly due to central heating, pollution, processed foods & hygiene hypothesis. 1/6 occupational.

Onset – Any age, but commoner in early decades. (Worse prognosis in adult-onset)

Symptoms – Breathlessness, chest tightness, wheeze & cough Think of variability, time of onset, provoking factors etc.

DiagnosisCharacteristic history

Diurnal symptoms (worse in early morning & disturbing sleep) Cough lasting >10 days & difficult to clear Recurrent episodes of wheezing esp. when associated with a provoking factor

FEV1>15% following bronchodilator>20% diurnal variationFEV1>15% decrease following 6 mins of exercise

ManagementStep 1 Step 2 Step 3 Step 4 Step 5

Education and environmental controlΒ2 agonist (salbutamol)

Low dose ICS 200µg -800µg (prednisolone)

High dose ICS 2000µg Glucocorticosteroid Low dose

Long acting β-agonist (salmeterol)

Leukotriene antagonist/inhibitor

Anti-IgE treatment

TheophyllineConsider if >2 exacerbations on step 1

Step up to control symptoms. Bear in mind non-complianceif symptoms worsening.If symptoms stable, step down therapy.

Acute exacerbationsPreceded by viral infections, moulds, pollen & pollution

Mild/Moderate–Generally worsening symptoms of PEF <60% of bestDoubling of ICS dose

Severe –PEF<50%Heart rate >110

5

Resp rate >25Inability to complete sentences in 1 breath

Life threatening - PEF <33%SpO2 <92%Silent chestBradychardiaCyanosis, exhaustion, confusion & coma

Near Fatal - Raised PaCO2 and/or requiring mechanical ventilation

Immediate treatmentABGOxygen – High concentration as possible. If not above 92%, mechanically ventilateBronchodilators – High dose salbutamol. Ipratropium bromide in life threatening casesSystemic Corticosteroids – O Prednisolone or IV hydrocortisone. Reduce inflame & hasten resolutionTheophylline – monitor serum levels if giving regularlyIV fluids – No evidence to support, but usually necessary. Esp K, as serum K can be low

If PEF remains below 30%, IV magnesium, aminophyllines&leukotriene RAs.

PEF measured every 15-30 mins and then 4-6hrs.

Discharge 24hrs after PEF >75%

Indications for Mech ventilationComa, exhaustion, drowsinessResp arrestABG deterioration despite best therapy (PaO2<8kPa & falling or PaCO2>6kPa & rising)

Pregnancy1/3 get better, 1/3 remain the same, 1/3 get worse. 90% no symptoms during labourBiggest threat to foetus is exacerbation, most drugs fine.

OccupationalSymptoms improve at weekends/holidays. Diagnosed by recording 2-hourly peak flows

Causative agents Occupations most at riskIsocyanates Paint sprayersFlour & grain BakersAnimals NursesAldehydes Chemical workersColophony & fluxes Animal workersLatex WeldersWood dust Food processing workers

Timber workers

6

COPDAirflow limitation that is not fully reversible. Characterized by chronic bronchitis (cough & sputum for >3 consecutive months over 2 years) and/or emphysema (permanent enlargement of airspaces distal to terminal bronchioles w/ wall destruction) which can be panlobular (Lower lobe.α1 ATD) or centrilobular (Upper lobe. Smokers)

Preventable & treatable with significant extra-pulmonary effects (muscle weakness, per oedema, weight loss, osteoporosis). Progressive with abnormal inflam response to noxious particles/gasses.

EpidemiologyDirectly related to tobacco smoking (and use of biomass fuels in low/middle income countries). 30,000 deaths per year. 5% of all deaths1/8 of all hospital admissions. 220,000 per year80 M worldwide

Risk FactorsTobacco (95% of cases in UK) & cannabis smokeBiomass fuelsOccupation – Coal minersAir pollutionLow birth weight – Lower maximal lung volumeLung growth - Lower maximal lung volume (maternal smoking & childhood infection)Infections – Accelerate decline of lung function. HIV asx w/ emphysemaGenetic – α1-antiprotease deficiency. Other COPD genes likely to be identified in future.

Clinical Features

Chronic bronchitis and/or breathlessnessPulmonary oedemaRR >20Accessory muscle usePursed lip breathingChest wall abnormalities – Horizontal ribs, barrel shaped chest, protruding abdomen, Intercostal in-drawing, flattened hemi diaphragm, decreased cricosternal distance. (All hyperinflation)Central cyanosis, signs of CO2 retention. Peripheral oedema & weight/muscle loss

Investigations

X-ray – Eliminate other causes: heart failure, lung cancer & identify bullaeFBC – Eliminate anaemia & Document polycythaemia. Assay α1AT in young patients. Spirometry – FEV/FVC <70%. Non reversible. Transfer factor/diffusing capacity. Low gas exchangeExercise testingHRCT

Management

7

α1-antiprotease deficiency

1/5000 live birthsα1-AT aggregates in liver = liver damage in some individualsEmphysema <50 years oldSome individuals normalPanlobar basal emphysemaSmoking cofactor

No COPD cure, but therapy can slow disease progression, ease symptoms and reduce exacerbations. Smoking cessation critical & reduction in other possible RFs (e.g. pollution)Β-agonist (better in asthma) & anticholinergics (better in COPD) improve symptoms & Spirometry. Theophylline improves exercise testing& blood gases.

Pulmonary rehabilitation improves exercise tolerance and QoL. No impact on Lung functionLong term oxygen therapy decreases mortality (>15 hours/day). Criteria: COPD

PaO2<7.3kPa (when well)Smoking is contraindication

Surgery: Bullectomy Lung volume reduction surgery Lung Transplantation

ExacerbationsTwo of following three symptoms: Breathlessness

Lung volume Change of sputum colour

ManagementOptimise bronchodilators (β-agonist +/- Ach + Oral glucocorticoids)Antibiotics (Think small, Amoxicillin 250mg/Doxycycline 500mg or Clarithromycin if penn aller or Co-amox if β-lactam +ve)Oxygen (Check ABG within 60 mins of Oxygen administration or any change)Ventilation (Non-invasive better)

Factors asx w/ death in acute on chronic resp failureAgeAcidosis (H+>55nmol/lHypotensionUraemia

8

Breathelessness & exercise limitationSABA/SAAChExacerbation and/or persistant breathlessnessFEV>50% - LAAChFEV<50% - LABA + ICSPersistent exacerbationsFEV>50% - LABA + ICSFEV<50% - LABA + LAMA + ICS

BronchiectasisAbnormal dilation of the bronchi w/ progressive scarring & lung damage

Causes Congenital

Cystic Fibrosis Ciliary Dysfunction Syndromes (primary ciliary dyskinesia & Kartanger’s) Primary Hypogabbaglobinaemia

Acquired – Children Pneumonia (complicating whooping cough/measles) Primary TB Inhaled foreign body

Acquired – Adult Supprative pneumonia (pneumonia w/ pus & perm lung damage, asx w/ abscess) Allergic broncho-pulmonary aspergillosis (complicating asthma) Pulmonary TB Bronchial tumours

Clinical FeaturesCough – Chronic and productive of copious purulent sputum. Worse in mornings & on changing posture. Asx w/ halitosisHaemoptysis – Slight or massive. Usually asx w/ sputum & purulence. Can be only symptom (dry bronchiectasis)Pneumonia & pleurisy – Inflammation causes fever & malaise as well as a sharp pain upon breathing, Poor general health – weight loss, anorexia & failure to thrive.

SignsFinger clubbingCoarse inspiratory cracklesWheeze

InvestigationSputum culture (Routine, fungal & TB)Blood tests – FBC, U&Es, LFTs, Immunological X-Ray – Not apparent unless severeCT – May show Bronchial dilation & wall thickeningCiliary dysfunction – Saccharin test

Management Smoking cessationAntibiotics 1st line Amox 500mg TDS

2nd line Clarithromycin 500mg bdVaccination (annual flu & 5yr pneumococcal)Pulmonary rehabilitation (>2 times daily)Pharmacology – SA-βA to improve function, then LA-βA if minimal improvement

ICS to reduce number of infectionsLT-Abx if >3 exacerbations/year w/ Ps Aeruginosa

Surgery – Only consider in patients with no co-morbidities with localised, unresponsive & severe bronchiectasis. (Emphysema is a CI)

9

Mild – CXR normal Diagnosis by CT scan

Severe – CXR abnormal -Cystic changes-Tramlining-Collapse

Mucus plugging Diagnosis by CT

scan

Bacterial colonisation 2/3 chronically colonised byH. influenzae β-lactam +ve Co-amox 375mg TDS

β-lactam -ve Amoxicillin 500mg bdS. Pneumonia Amoxicillin 500mg bdM. catarrhalis Co-amox 375mg TDSS. Aureus Flucoxicillin 250mg QDSPs. Aeruginosa See below

SputumSerous – frothy/clear. Pulmonary oedema Rusty - pneumococcal (lobar) pneumonia.Mucoid - clear, white or grey. Asthma, chronic bronchitis and in acute viral respiratory infections Mucopurulent – yellow/green/brown. Pulmonary infection. Darker = serious

Ps. Aeruginosa eradicationStep 1 Ciprofloxacin 750mg BD 2 weeksStep 2 Anti-pseudomonal abx IV 2 weeksStep 3 repeat ciproflox 4 weeks + nebulised colomycin 2MU bd 3 monthsStep 4nebulised colomycin 2MU bd 3 months

Cystic FibrosisMutation in CFTR (most common ΔF508) gene (on chromosome 7) resulting in abnormal sodium/chloride movement and dehydration in airway epithelium increasing chances of chronic infection, ciliary dysfunction & bronchiectasis.

EpidemiologyMost common fatal genetic disorder in Caucasians. Autosomal recessive. 1/25 carrier rate with 1/2500 live birth rate.

Clinical featuresAt birth, the lungs are macroscopically normal and lung function normal.

Respiratory-Infective exacerbations of bronchiectasis-Spontaneous Pneumothorax-Haemoptysis-Nasal Polyps-Resp failure-Cor pulmoale-Lobar Collapse

GI-Meconium ileus (14%)-Malabsorption-Steatorrhea-Distal intestinal obstruction syndrome-Biliary cirrhosis & portal hypertension-Gallstones-Rectal prolapse

Other-Diabetes (25%)-Delayed puberty-Male infertility (failure of vas deferens to develop)-Stress incontinence (due to persistent forced cough)-Osteoporosis-Arthropathy

InvestigationsScreening (detects ~50% of affected children)Sweat test (increased sodium chloride in sweat)Low elastase in stools

ManagementSimilar to severe bronchiectasisPulmonary physiotherapyS. Aureus infections managed with oral abxPs. Aeruginosa therapy managed with IV abx (@home through S/C vascular port)Regular nebulised abx therapy (colomycin/tobramycin) between exacerbations to suppress chronic Ps A colonisation.Many resistant strains develop & treatment becomes tailored to each patientHome Oxygen & NIV treat resp failure in latter stages of disease. Lung transplantation would be ideal, but limited by donors.

Non resp managementMalabsorption treated by oral pancreatic enzyme supplements & vitamins. High calorie diet

Somatic gene therapy to replace faulty gene with a working one is under trial and is an exciting research field.

10

Pneumonia (Community Acquired)A lower respiratory tract infection w/ new X-ray shadowing with no other cause.

Epidemiology5-11/1000Mortality <1% in community

6-12% in hospitalised patient>35% in ITU

Clinical FeaturesSymptomsCough (92%)Breathlessness (67%)Pleuritic pain (62%)New sputum production (54%)Haemoptysis (15%)

SignsFevers, rigors, tachypnoea, tachycardia, hypotension, rigors

Coarse crackles, reduced expansion, bronchial breathing, pleural rub

AetiologyCommunity Hospital

S. Pneumoniae 36% 39%H. Influenzae 10% 5%Legionella 0.4% 3.6%Atypicals 2.6% 27%Viruses 13% 13%No cause 45% 31%

CURB65–used to predict 30 day mortality (poor for very sick, very young & very old)

ConfusionUrea >7Resp Rate >30BP <90/60 (either one)>65 years old

1 point for each

0-1 Outpatient (mort <2%)2 In-patient; short stay (mort ~10%)>3 In-patient; consider ICU (mort 15-40%)

InvestigationsCXR – usually confirms diagnosis. Opacity occurs within 12-18 hours of onset in the affected lobe. (May take 6 weeks to clear)ABGFBC (WCC very high in severe but may be normal when caused by atypical organisms) U&Es & LFTsCRP usually elevatedMicrobiology:CURB 0-1– not necessary in mild pneumoniaCURB 2 – Blood & Sputum culture

Pneumococcal urine antigen test Pleural fluid (if present) aspirated for microscopy & culture

CURB >3 – As CURB 2DIF for atypical pathogen (eg M. pneumonia, adenovirus)

ManagementOxygen (>35% humidified)&IV fluids

11

Legionella suspected? Urine for legionella antigen Sputum sample for legionella culture

& Direct Immunofluorescence (DIF)

Abx 1st line therapyLow severity O amoxicillin 500mgMod severity (within 4 hours) O amoxicillin 500mg +

clarithromycin 500mgVery severe (asap) IV co-amoxiclav 1.2g + clarithromycin

500mgIf Legionella suspected, add in IV levofloxacin

PhysiotherapyPain control (beware opiates with poor resp funct)

TuberculosisInfection caused predominantly by Mycobacterium tuberculosis (Mtb)Epidemiology~10/100,000 in UK. Mortality 10%1/3 worldwide have latent Mtb infection with 2-3 million deaths /year

Risk FactorsTB contactVery young/elderlyEthnic minoritiesImmunosuppressed (HIV/chemotherapy)Health care workerSilicosis

Clinical FeaturesSeveral weeks/monthsWeight loss/anorexiaNight sweatsCough +/-sputum +/- haemoptysisGeneral Malaise

InvestigationsCXR – Upper lobes predominate (ΔΔ sarcoid, old infection & infection from other pathogen)

Consolidation, cavitation, military (<5mm nodules)Blood tests - ESR, Hb, Na, serum albumin & deranged LFTsTuberculin testEarly morning urineSputum samples

DiagnosisSputum x3 (including an early morning sample)& blood cultureBronchoscopy with washings (or BAL)Gastric washing (used for children)

ManagementRifampicinR 6 monthsIsoniazid H 6 monthsPyrazinamide Z 2 monthsEthambutamol E 2 monthsPyridoxine B6 6 months

Different regimes available based on patient resistance.Multi-Drug Resistant TB is resistant to Rifampicin & Isoniazid

Oral steroids to be used in extensive TB or with extensive extra-pulmonary features (2-3 months)

Control & preventionContact tracing to establish source

12

Tuberculin test 0-5mm –ve (or v severe)5-15mm immune>15mm active TB (or strong reaction to BCG)

Only useful to differentiate Sarcoid from TBResult read 48-72 hours after

Extra-pulmonary featuresLymphadenitisGI – esp lower tract & acute abdomenPericardial – effusion & constrictiveCNS – meningeal disease (high mort rates)Bone & joint – Lower spine, hip & kneeGU- renal symptoms for many years

Side effectsR H Z EP450 inducer P450 inhibitor Rash Retrobulbar neuritisBodily fluids orange Rash Hepatitis Dose halved in CRFRash Hepatitis ArthralgiaHepatitis GoutNausea & Vomiting

Lung cancerMalignant tumours more common than benign

Small cell lung cancer 20% (Many metastases)Non-small cell lung cancer

Squamous 30-40%Adenocarcinoma 20-30%Large cell 10%Undifferentiated 10%Mixed/other <5%

Clinical FeaturesAll 6Hoarseness, Horner’s (apical tumour), arm pain, SVCO

InvestigationCT scan better than CXR, used for stagingPET scan (must be done with CT)

StagingTNMPET scan more sensitive than CT

ManagementSCLC chemosensitive (80% responds)

Prolongs survival from 2 – 16 monthsNSCLC surgery (only stage T1 &T2)

Radiotherapy can be good, but can be bad

MesotheliomaPresents as pleural effusion w/ chest wall pain40 years between asbestos exposure and diagnosisCXR – Pleural thickeningThoracotomy to diagnoseChemotherapy may be usefulSurvival 9-12 months

13

CXR Nodule differentiation

Benign MalignantSmall LargeSmooth SpiculatedCalcified Non-calcifiedEqual distribution Upper lobes & Right side

more common

TNM StagingT1 Tumour <3cmT2 Tumour >3cm &<7cmT3 Tumour >7cm +/- invasion of diaphragm/chest wallT4 Invasion of heart/great vessels/mediastinum/trachea

N0 No nodal involvementN1 Ipsilateral but closeN2 Ipsilateral bit distantN3 Contralateral

M0 No distant metastasesM1 Distant metastases

Interstitial Lung Disease (ILD)(>200 types)

CXR shadowing Bi-basal -IPFILD asx w/ connective tissue disorder Asbestosis

Bilateral mid-zone – SarcoidosisBilateral upper – Sarcoidosis

SilicosisCoal workers pneumoconiosis Hypersensitivity pneumonitis

Peripheral bilateral – Eosinophilic pneumoniaFlitting shadows – Cryptogenic organising pneumonia (COP)

Idiopathic Pulmonary Fibrosis (IPF)Clinical FeaturesBreathlessnessCough (dry)

SignsClubbingFine bi-basal mid & late cracklesDull Percussion & Decreased vocal resonance

Epidemiology5-15/100,000. 4000-5000 new cases per year in UK (90 in Lothian)Median age presentation – 68M:F 2:1 Smokers:non-smokers

InvestigationsSpirometry – Restrictive. Lung volume & gas transferHRCT – bi-basal sub-pleural honeycomb cystsLung biopsy – if HRCT not conclusive, biopsy shows distorted lung architecture w/ honeycomb cysts

ManagementNo good therapy. Usually join an RCT & palliate with oxygen, opiates etc.Lung transplant if <65?Median survival 3-4 years after presentation

SarcoidosisSystemic disease characterised by non-caseating granulomas (small inflame nodules). Cause unknown

Clinical featuresSOBCough (dry)Fatigue& Skin lesionsHypercalcemia

InvestigationsSpirometry – Normal stage 1. Restrictive. Reduced TLC& KCOBlood tests generally normal. Serum ACE may monitor disease activity. Tuberculin skin test – ΔTBBiopsy – skin/lymph node/lung. Non caseating granuloma.

14

Staging1 – Bi-hilar lymphadenopathy (BHL). Asympt. 60-80% spontaneously remit with 1 year. Erythema Nodosum2 – BHL + infiltrates (=parenchymal disease) remits in 50-60%3 – Infiltrates. remits in 20-30%4 – Fibrosis. Occurs in 5-10%. Irreversible.

ManagementSarcoidosis is usually self-limiting. ICS possible & lung transplant is curative

Occupational lung disease

PneumoconiosisReaction of lung to inhaled dust

Coal Workers Pneumoconiosis (CWP) –small rounded opacities in upper & middle zonesProgressive Massive Fibrosis (PMF) – Irregular opacities

Risk of developing increases with increasing exposure to dusts

SilicosisA pneumoconiosis caused by inhalation of silica

Risk of developing increases with increasing exposure to silica

Progressive & irreversible

Can be complicated by pulm hypertension & cor-pulmonaleAppears 10 years after exposure

AsbestosisTiny blue fibresRequires much asbestos exposure

15-30 years after exposure before symptoms appear.

15

Venous Thromboembolism (VTE)PE & DVT – Most PEs arise from lower limb.

Annual risk 0.1-0.3%Mortality 1-2% (10% of hospital deaths)

Risk FactorsMajor Surgery –major surgery

Obstetrics –late pregnancy, C sectionLower limb problem -fracture. Varicose veinsMalignancyImmobilityPrevious VTE

Minor Cardio – Hypertension, CHFOestrogenLoads others

Thrombophilia (eg Factor V Leiden)Found in 25-50% of VTE <50 years old.

Clinical FeaturesSOBPainCoughHaemoptysis

SignsHS 4Loud P2Tachycardia

InvestigationsABG – Hypoxaemia&HypocapniaCXR – Normal/effusion/Westermarck’s/Hampton’s humpECG –S wave in lead I, Q wave and T wave inversion in lead III, and T wave inversion in leads V1 to V4. More commonly, the ECG demonstrates minor non-specific ST segment or T wave changesD-Dimer – Useful for exclusion (if –ve, PE unlikely)Well’s PE probability score >6 = high chanceVentilation/Perfusion scan CTPADoppler USSEcho – trans-oesophageal. Useful in massive PE

ManagementLMW HeparinWarfarin – 6 weeks to 6 monthsThrombolysis – tPA. Use if patient is shockedIVC filter –if anticoagulation is contraindicated.

16

Sleep Apnoea (Obstructive Sleep Apnoea/Hypo-apnoea Syndrome (OSAHS))Sleep disruption due to breathing pauses

Clinical featuresSleepinessSnoring/apnoeasUnrefreshing sleepAwake chokingPoor concentrationDepressionNocturia50% obese

EpidemiologyAffects 1-2% of western middle aged peopleOSAHS commonest resp patient referral90& cases undiagnosed

Obstruction arises from narrow pharynxwhich may be caused by: RetrognathiaObesityAlcohol

OSAHS is associated: Hypertension Increased chance of having an RTASudden nocturnal death (!)Cardiovascular eventsDiabetesLiver damageAcromegalyHypothyroidism

Investigations & DiagnosisEpworth Sleepiness score (>11 =referral)Overnight breathing study (>15 breathing pauses)

ManagementLifestyle –lose weightContinuous Positive Airway Pressure (CPAP) therapy - 1st line. Improves symptoms & blood pressureMandibular splints – 2nd line

17

Other causes of sleepinessInsufficient sleepShift workDrugsPsychiatric illnessNarcolepsy (autoimmune)