Management



AsthmaAsthma is suggestive if Peripheral blood eosinophiliaChest tightness whilst exercising History of eczemaDiagnosisThere is particular emphasis on the use of?fractional exhaled nitric oxide (FeNO). Nitric oxide is produced by 3 types of nitric oxide synthases (NOS). One of the types is inducible (iNOS) (↑↑inflammatory cells, particularly eosinophils. Levels of NO correlate with levels of inflammation.Spirometry and peak flow variability are still important.All patients >= 5 years should have objective tests to confirm the diagnosis.Diagnostic testingPatients >= 17 years?Better symptoms on days away from work/during holidays referred to a specialist as possible occupational asthma (Serial peak flow measurements at work and at home all patients should have spirometry with a bronchodilator reversibility (BDR) testall patients should have a FeNO tesPatients 5-16 yearsall patients should have spirometry with a bronchodilator reversibility (BDR) testFeNO test if there is Normal spirometry or obstructive spirometry with a Negative bronchodilator reversibility (BDR) test.Patients < 5 yearsclinical judgementSpecific points about the testsFeNOAdults level of >= 40 parts per billion (ppb) is positiveChildren level of >= 35 parts per billion (ppb) positiveSpirometryFEV1/FVC ratio < 70% (or below the lower limit of normal if this value is available) obstructiveReversibility testingin adults positive test is indicated by an?improvement in FEV1 ≥ 12% and increase in volume of 200 ml or morein children a positive test is indicated by an?improvement in FEV1 ≥ 12% Asthma: occupationalChemicals at work are worsening their asthma or you may notice in the history that symptoms seem better at weekends / when away from work.Exposure to the following chemicals is associated with occupational asthma:Isocyanates the most common cause. ( spray painting and foam moulding using adhesive)Platinum saltsSoldering flux resinGlutaraldehydeFlourEpoxy resinsProteolytic enzymesSerial measurements of peak expiratory flow are recommended at work and away from work.Referral should be made to a respiratory specialist for patients with suspected occupational asthma.Management in adultsStepNotes1 Newly-diagnosed asthmaShort-acting beta agonist (SABA)2Not controlled on previous step ORNewly-diagnosed asthma (symptoms ≥ 3 /W or night-time wakingSABA + low-dose inhaled corticosteroid (ICS)3SABA + low-dose ICS + leukotriene receptor antagonist (LTRA) "Montlucast" 4SABA + low-dose ICS + long-acting beta agonist (LABA)Continue LTRA depending on patient's response to LTRA5SABA +/- LTRASwitch ICS/LABA for a maintenance and reliever therapy (MART)(low-dose ICS) 6SABA +/- LTRA ICS MART (medium-dose) OR Consider changing back to a fixed-dose of a moderate-dose ICS and separate LABA7SABA +/- LTRA + one of the following options:High-dose ICS (only as part of a fixed-dose regime, not as a MART)Additional drug (long-acting muscarinic receptor antagonist or theophylline)seeking advice from a healthcare professional with expertise in asthmaMaintenance and reliever therapy (MART)Combined ICS +LABA single inhaler, containing both ICS and a fast-acting LABA, (Daily maintenance therapy and relief of symptoms as requiredMART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (Ex: formoterol)Adult inhaled corticosteroid dosesLow Dose ≤ 400 ?g budesonide or equivalent Moderate Dose 400 - 800 ?g budesonide or equivalent High Dose > 800 ?g budesonide or equivalentThe BNF advises that 'inhaled drugs, theophylline and prednisolone can be taken as normal during pregnancy and breast-feeding'.Leukotriene receptor antagonistse.g. Montelukast, zafirlukasthave both anti-inflammatory and bronchodilatory propertiesshould be used when patients are poorly controlled on high-dose inhaled corticosteroids and a long-acting b2-agonistparticularly useful in aspirin-induced asthmaassociated with the development of Churg-Strauss syndromeEosinophilia and a Mononeuritis multiplex,(Foot drop, Wrist drop) .montelukast can unmask underlying Churg-Strauss syndrome, of which prior to treatment the only symptom is asthma.Acute asthma:ModerateSevereLife-threateningPEFR 50-75% best or predictedSpeech normalRR < 25 / minPulse < 110 bpmPEFR 33 - 50% best or predictedCan't complete sentencesRR > 25/minPulse > 110 bpmPEFR < 33% best or predictedOxygen sats < 92%'Normal' pC02?(4.6-6.0 kPa)?less severe asthma lower than normal pCO2Silent chest, cyanosis or feeble respiratory effortBradycardia, dysrhythmia or hypotensionExhaustion,?confusion?or Coma4th category ('Near-fatal asthma)' ↑↑pC02 > 6 / PH< 7.35 and/or requiring MV with↑↑ inflation pressures.Further assessmentABG for patients with oxygen Sats < 92%Chest x-ray is not routinely recommended, unless:life-threatening asthmasuspected Pneumothoraxfailure to respond to treatmentManagementAdmissionall patients with life-threatening should be admitted in hospitalpatients with features of Severe acute asthma if they fail to respond to initial treatment.Previous near-fatal asthma attack,?pregnancy, an attack occurring despite already using oral corticosteroid and presentation at nightOxygenif patients are hypoxaemic. Acutely unwell started on 15L via a non-rebreathe mask then be titrated down to to maintain SpO? 94-98%.Bronchodilation with short-acting beta?-agonists (SABA)high-dose inhaled SABA (salbutamol, terbutaline)NO life-threatening or near-fatal asthma, given by a standard pressurised metered-dose inhaler (pMDI) or by an oxygen-driven nebulizerLife-threatening exacerbation of asthma ?nebulised SABA?is recommendedCorticosteroidall patients 40-50mg of prednisolone orally (PO) daily (continued for at least 5 days OR until the patient recovers from the attack)During this time, patients should continue their normal medication (inhaled corticosteroids)Ipratropium bromideSevere or life-threatening asthmapatients who have not responded to beta?-agonist and corticosteroid treatment or nebulised ipratropium bromide, a short-acting muscarinic antagonistIV magnesium sulphateSevere/life-threatening asthma.IV Aminophylline may be considered following consultation with senior medical staffPatients who fail to respond ?senior critical care support?and should be treated in an appropriate ITU/HDU setting. Treatment options include:intubation and ventilationextracorporeal membrane oxygenation (ECMO)Criteria for dischargebeen?stable on their discharge medication (No nebulisers or oxygen) for 12–24 hoursinhaler technique checked and recordedPEF >75% of best or predictedCOPDDestruction of alveolar walls 2ry to proteinases such as elastase irreversible damage to the supporting CT of the alveolar septa.Smoking accelerates this process CausesSmokingAlpha-1 antitrypsin deficiencyOther causesCadmium (used in smelting)CoalCottonCementGrain?Investigation and diagnosisPatients > 35 years + Smokers or Ex-smokers + Symptoms (Exertional breathlessness/ Chronic cough/ Regular sputum production).Post-bronchodilator spirometry to demonstrate airflow obstruction FEV1/FVC < 70%Chest x-ray hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancerCBC exclude 2ry polycythaemia(BMI) calculationThe severity of COPD is categorised using the FEV1Post-bronchodilator FEV1/FVCFEV1 (of predicted)Severity< 0.7> 80%Stage 1 – Mild + (symptoms "must")< 0.750-79%Stage 2 - Moderate< 0.730-49%Stage 3 - Severe< 0.7< 30%Stage 4 - Very severePeak expiratory flow limited value in COPD, as it may underestimate the degree of airflow obstruction.Most useful for monitoring the progression FEV1Stable managementGeneral managementSmoking cessation?the single most important intervention in patients with COPDincluding offering nicotine replacement therapy, varenicline or bupropionAnnual influenza vaccinationone-off pneumococcal vaccinationpulmonary rehabilitation?to all people functionally disabled by COPD (usually Medical Research Council [MRC] grade 3 and above)Bronchodilator therapyShort-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatmentNext step is determined by whether the patient has?'asthmatic features/features suggesting steroid responsiveness' ↓↓ Exacerbationsany previous, secure diagnosis of asthma or of atopy↑↑Blood eosinophil count.Variation in FEV1 over time (at least 400 ml)Diurnal variation in peak expiratory flow (at least 20%)Routine spirometric reversibility testing is not necessary as part of the diagnostic process or to plan initial therapyLABA + inhaled corticosteroid (ICS)if patients remain breathless or exacerbations 3 therapy (LAMA + LABA + ICS)if already taking a SAMA discontinue and switch to a SABAUse of combined inhalers where possible No asthmatic features/features suggesting steroid responsivenessAdd a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)if already taking a SAMA discontinue and switch to a SABAOral TheophyllinesOnly after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy↓↓ Dose if Macrolide or fluoroquinolone antibiotics are co-prescribedOral prophylactic antibiotic therapyAzithromycin prophylaxis is recommended in select patientsFor patients? not smoke, have optimised standard treatments continue to have exacerbationsPrerequisites include CT thorax (to exclude bronchiectasis) and sputum culture (Exclude atypical infections and T.B)LFTs +?ECG exclude QT prolongation should also be done as azithromycin can prolong the QT intervalMucolyticsW chronic productive cough and continued if symptoms improveCor pulmonaleperipheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2loop diuretic for oedema, consider long-term oxygen therapyACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICEFactors which may improve survival in patients with stable COPDsmoking cessation - the single most important intervention in patients who are still smokinglong term oxygen therapy in patients who fit criterialung volume reduction surgery in selected patientsLong-term oxygen therapyincrease survival in hypoxic patients Patients receive LTOT breathe supplementary oxygen for at least 15 hours/dDay. Oxygen concentrators are used to provide a fixed supply for LTOT.Assess patients if any of the following:↑↑↑↑ Airflow obstruction (FEV1 < 30% predicted). 'considered' for patients with (FEV1 30-49% predicted)CyanosisPolycythaemiaPeripheral oedema↑↑ JVPO2 saturations ≤ 92% on room airAssessment measuring ABGs on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.Offer LTOT to patients with a PO2 of < 7.3 kPa OR PO2 of 7.3 - 8 kPa + 1 of the following:2ry polycythaemiaPeripheral oedemaPulmonary HTNIn terms of smokingDo not offer LTOT to people who continue to smoke despite offered smoking cessation advice and treatment, and referral to specialist stop smoking services.Risk assessment before LTOT:The risks of falls from tripping over the equipmentThe risks of burns and fires, and ↑↑ risk of these for people who live in homes where someone smokes (including ecigarettes)Acute exacerbation of COPDFeatures↑↑dyspnoea, cough, wheezesputum suggestive of an infective causeHypoxic and in some cases have acute confusionThe most common bacterial organisms that cause infective exacerbations of COPD are:Haemophilus influenzae?(most common cause) show no consolidation patchStreptococcus pneumoniae X-Ray will show consolidation patch Moraxella catarrhalisRespiratory viruses ( 30% of exacerbations) (human rhinovirus being the most important pathogen).Management↑↑ frequency of bronchodilator use and consider giving via a nebuliserPrednisolone 30 mg/ day/ 7-14 daysAntibiotics. NICE do not support this approach giving oral antibiotics?'if sputum is purulent or there are clinical signs of pneumonia'First-line:?amoxicillin or clarithromycin or doxycycline.H. Influnza Amoxicillin or Tetracycline together with prednisolone.indication for non-invasive ventilation.Acidosis (pH <7.35),rising pCO2 respiratory rate >30 breaths per minute despite best medical management (steroids, nebulised bronchodilators and standard oxygen Intubation and ventilation pH is below 7.26 pCO2 is rising on non-invasive ventilation (NIV).Smoking cessationpatients should be offered nicotine replacement therapy (NRT), varenicline or bupropion ( Not to favour one medication over another)NRT, varenicline or bupropion should normally be prescribed as part of a commitment to stop smoking on or before a particular date (target stop date)Prescription sufficient to last only until 2 weeks after the target stop dateafter 2 weeks of NRT therapyAfter 3-4 weeks for varenicline and bupropion, to allow for the different methods of administration and mode of action. Further prescriptions should be given only to people who have demonstrated that their quit attempt is continuing.if unsuccessful (using NRT, varenicline or bupropion) do not offer a repeat prescription within 6 months unless special circumstances have intervenedDo not offer NRT, varenicline or bupropion in any combinationNicotine replacement therapyS/E nausea & vomiting, headaches and flu-like symptomsOffering a combination of nicotine patches + another form of NRT (gum, inhalator, lozenge or nasal spray) For ↑↑↑ dependence on nicotine ORwho have found single forms of NRT inadequate in the pastVareniclinea nicotinic receptor partial agonistStarted 1 week before the patients target date to stopCourse of treatment 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)More effective than bupropionNausea is the most common adverse effect. Other common problems include headache, insomnia, abnormal dreamsUsed with caution patients with a history of depression or self-harm.CI pregnancy and breast feeding\Cautionsrisk of relapse, irritability, depression, and insomnia on discontinuation (consider dose tapering on completion of 12-week course); history of psychiatric illness (may exacerbate underlying illness including depression);predisposition to seizures, including conditions that may lower seizure threshold; history of cardiovascular diseaseBupropionNorepinephrine and dopamine reuptake inhibitor, and nicotinic antagonistshould be started 1 to 2 weeks before the patients target date to stopSmall risk of seizures (1 in 1,000)CI? epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindicationPregnant womenall pregnant women tested for smoking using?carbon monoxide detectors ('some women find it difficult to say that they smoke the pressure not to smoke during pregnancy is so intense.'.Offering NHS Stop Smoking Services.All women who smokeStopped smoking within the last 2 weeks CO reading of ≥ 7 ppm Interventions1st-line cognitive behaviour therapy, motivational interviewing or structured self-help and support from NHS Stop Smoking Servicesthe evidence for the use of NRT in pregnancy is mixed but it is often used if the above measures failure. There is no evidence that it affects the child's birthweight. Pregnant women should remove the patches before going to bedas mentioned above, varenicline and bupropion are contraindicatedAllergic bronchopulmonary aspergillosisAn allergy to?Aspergillus spores. In the exam often give a history of bronchiectasis and eosinophilia.FeaturesMajor criteria for the diagnosis are:Clinical features of asthmaProximal bronchiectasisBlood EosinophiliaImmediate skin reactivity to Aspergillus antigen + Ve Radioallergosorbent (RAST) test to Aspergillus↑↑ serum IgE (>1000 IU/ml)Minor criteria:Fungal elements in sputumBrown flecks in sputumDelayed skin reactivity to fungal antigensBronchoconstriction wheeze, cough, dyspnoea.?Patients may have a previous label of asthmabronchiectasis (proximal)Investigationsflitting CXR changes+ Ve IgG precipitins (not as positive as in aspergilloma)ManagementSteroids such as prednisolone, which is slowly tapered over the course of 3 to 12 months depending on regimen.Oral antifungals (often as an adjunct)May help ↓↓ long-term glucocorticoid use. Both Itraconazole and Voriconazole may be hepatotoxic and patients should be monitored for evidence of hepatotoxicity.Extrinsic allergic alveolitisalso known "Hypersensitivity Pneumonitis" caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles. Largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.ExamplesBird fanciers' lung Avian Proteinsfarmers lung spores of?Saccharopolyspora Rectivirgula?(formerly?Micropolyspora faeni) "Hay is the commonest source"Malt workers' lung ?Aspergillus ClavatusMushroom workers' lung Thermophilic Actinomycetes*PresentationAcute: occur 4-8 hrs after exposure, SOB, Dry Cough, FeverChronicInvestigationChest x-ray upper/mid-zone fibrosisBronchoalveolar lavage lymphocytosisBlood NO eosinophilia*here the terminology is slightly confusing as thermophilic actinomycetes is an umbrella term covering strains such as?Micropolyspora faeniPulmonary eosinophilia↑↑↑ Eosinophils in the lung airways and parenchyma. This is generally associated with a blood eosinophilia. Causes Churg-Strauss syndromeallergic bronchopulmonary aspergillosis (ABPA)Loffler's syndromeEosinophilic pneumoniaHypereosinophilic syndromeTropical pulmonary eosinophiliaDrugs ?Nitrofurantoin, Sulphonamidesless common: Wegener's granulomatosisLoffler's syndrometransient CXR shadowing and blood eosinophiliathought to be due to parasites such as?Ascaris lumbricoides?causing an alveolar reactionFever, cough and night sweats which often last < 2 weeks.generally a self-limiting diseaseAcute eosinophilic pneumonia↑↑ responsive to steroidsTropical pulmonary eosinophilia associated with?Wuchereria bancrofti?infectionCryptogenic organizing pneumoniaA diffuse interstitial lung disease distal bronchioles, respiratory bronchioles, alveolar ducts and alveolar walls. Incidence 2 for 100,000. Male = Female. 5th or 6th decadeEtiology is unknown is not associated with smoking.Features cough, shortness of breath, fever and malaise (Weeks or Months). Haemoptysis is rareClinical examination is often normal but inspiratory crackles can be heard. Wheeze and clubbing are rare.History of non-response to antibiotics.Investigations CBC ↑↑ (WBCs, ESR and CRP).X-Ray Bilateral patchy OR Diffuse consolidative OR ground glass opacities. Lung function most commonly restrictive but can be obstructive or normal. The transfer factor is reducedTreatment is watch and wait if mild or high dose oral steroids if severe.Churg Strauss SyndromeEosinophilic granulomatosis W polyangiitis (Churg-Strauss syndrome) Chestgranulomatosis with polyangiitis (Wegner granulomatosis)Initial Phase Allergy W history of asthma or allergic rhinitis inflammation of the nasal passages lead to nasal polyps.2nd phase Eosinophilia?> 10%3rd stageVasculitis small and medium-sized vessels kidney failureLung, Petechial rash, GIT, Heart Association PANCA(60%)Leukotriene receptor antagonists?may precipitate the disease.Vacuities, Sinusitis DyspneaEpistaxis, Hemoptsis cANCA Granulomatosis with polyangiitis "Wegener's granulomatosis" Autoimmune condition W necrotizing granulomatous vasculitis, Affect both the upper and lower respiratory tract as well as the kidneys.Featuresupper respiratory tract Epistaxis,?Sinusitis, Nasal crustinglower respiratory tract Dyspnoea,?HaemoptysisKidney rapidly progressive glomerulonephritis?('pauci-immune', 80% of patients)saddle-shape nose deformityVasculitic rash, Eye involvement (proptosis), cranial nerve lesionsInvestigationscANCA positive in > 90%, pANCA positive in 25%chest x-ray wide variety of presentations, including cavitating lesions (Nodules W central Cavities)Renal biopsy ?epithelial crescents in Bowman's capsuleManagementSteroidsCyclophosphamide (90% response)plasma exchangemedian survival = 8-9 yearsLofgren's syndromeAcute form sarcoidosis young females and carries an excellent prognosis.characterised bybilateral hilar lymphadenopathy (BHL) Bulky MediastinumErythema nodosum Painful shin lesionsFever and Polyarthralgia.?N.B Loffler's syndrome is a cause of pulmonary eosinophilia caused by parasites such as Ascaris lumbricoidesIdiopathic pulmonary fibrosisPreviously termed "Cryptogenic Fibrosing Alveolitis" a chronic lung progressive fibrosis of the interstitium of the lungs. Many causes of lung fibrosis (medications, connective tissue disease, asbestos) the term IPF is reserved when no underlying cause exists.Aged 50-70 years and is twice common in men.Featuresprogressive exertional dyspnoeabi-Bibasal fine end-inspiratory crepitations on auscultationDry coughClubbingDiagnosisSpirometry: classically a?restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)↓↓ gas exchange ↓↓ transfer factor (TLCO)ImagingX-Ray Bilateral interstitial shadowing (1st changes small, irregular, peripheral opacities - 'Ground-glass' later progressing to 'Honeycombing') High-Resolution CT investigation of choice?required for diagnosis of IPF Reticular changes ↑↑ at bases. Honeycombing traction bronchiectasis, and architectural distortionGround-glass opacities are less?ANA positive in 30%Rheumatoid Factor (10%) but this does not necessarily mean that the fibrosis is secondary to a CT disease. Titres are usually lowManagementPulmonary RehabilitationFew medications give any benefit in IPF?Pirfenidone (an antifibrotic agent) may be useful in selected patients.many patients will require supplementary oxygen and eventually a lung transplantPrognosispoor, average life expectancy is around 3-4 yearsAcute respiratory distress syndromeCaused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli non-cardiogenic pulmonary oedema. It mortality 40% and is associated with significant morbidity in those who survive.Causesinfection sepsis, pneumoniamassive blood transfusiontraumasmoke inhalationacute pancreatitiscardio-pulmonary bypassClinical features are typically of an acute onset and severe:dyspnoeaelevated RRbilateral lung crackles↓↓ O2 saturationsA chest x-ray and arterial blood gases are the key investigations.Criteria (American-European Consensus Conference)Acute onset (within 1 week of a known risk factor)Pulmonary oedema: bilateral infiltrates on chest x-ray ('not fully explained by effusions, lobar/lung collapse or nodules)Non-cardiogenic (pulmonary artery wedge pressure needed if doubt)PO2/FiO2 < 40kPa (200 mmHg) hypoxia despite oxygen therapyManagementgenerally managed in ITUoxygenation/ventilation to treat the hypoxaemiageneral organ support e.g. vasopressors as neededtreatment of the underlying cause e.g. antibiotics for sepsiscertain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDSAlpha-1 antitrypsin deficiencyA common inherited condition lack of a protease inhibitor (Pi) normally produced by the liver.The role of A1AT is to protect cells from enzymes such as?neutrophil elastase. It classically causes emphysema (chronic obstructive pulmonary disease) in patients who are?young?and?non-smokers.Geneticslocated on chromosome 14inherited in an?AR / co-dominant fashion*alleles classified by their electrophoretic mobility M for normal, S for slow, and Z for very slownormal = PiMMhomozygous PiSS (50% normal A1AT levels) ( SS and SZ) more risk of developing symptoms over MZ have a more marked deficiency.Heterogenou PIMZ ?35% of normal Asymptomatichomozygous PiZZ (10% normal A1AT levels)Featurespatients who manifest usually have PiZZ genotypelungs panacinar emphysema, most marked in?lower lobesliverAdults cirrhosis and?HCC?Children cholestasis in InvestigationsA1AT concentrationsspirometry:?obstructive pictureManagementno smokingsupportive bronchodilators, physiotherapyIV alpha1-antitrypsin protein concentratesSurgery ?lung volume reduction surgery,( removes the worst affected part of the lungs in order to improve airflow and alveolar gas exchange in the remaining portion of the lung. lung transplantationKartagener's syndrome"primary ciliary dyskinesia" its association with dextrocardia ('quiet heart sounds', 'small volume complexes in lateral leads') Pathogenesis Dynein arm defect results in immotile cilia Features\Recurrent chest infections + subfertility - think primary ciliary dyskinesia syndrome (Kartagener's syndrome)Dextrocardia or complete situs inversusBronchiectasis generalized Crepitation and wheezy chest Recurrent SinusitisSubfertility (↓↓sperm motility and defective ciliary action in the fallopian tubes)-Ve sweat test ruled out Cystic fiberosis Altitude related disorders3 main types of altitude related disorders due to the chronic hypobaric hypoxia which develops at high altitudesAcute mountain sickness (AMSSelf-limiting conditionFeatures start > 2,500 - 3,000m gradually over 6-12 hours and potentially last a number of days:Headache, nausea, fatiguePrevention and treatment of AMSRisk may be correlated to physical fitnessgain altitude at no > 500 m per dayAcetazolamide (a carbonic anhydrase inhibitor) used to prevent AMS .Treatment descentA minority of people above 4,000m pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE),high altitude pulmonary edema (HAPE) DescentNifedipine/ dexamethasone/ acetazolamide phosphodiesterase type V inhibitors* ↓↓systolic pulmonary artery pressureOxygen if availablehigh altitude cerebral edema (HACE).headache, ataxia, papilloedemaManagement descent + dexamethasoneAsbestos and the lungvariety of lung disease from benign pleural plaques to mesothelioma.Pleural plaquesThe most common form of asbestos related lung disease latent period of 20-40 years. Benign and do not undergo malignant changePleural thickeningThe underlying pathophysiology is not fully understood.similar pattern to that seen empyema or haemothorax. AsbestosisThe severity of asbestosis is related to the length of exposure. latent period is typically 15-30 yearsAsbestosis typically lower lobe fibrosis. The most common symptoms are shortness-of-breath and reduced exercise tolerance.MesotheliomaMesothelioma is a malignant disease of the pleura Not related to severity of exposure Crocidolite (blue) asbestos is the most dangerous form.?Possible featuresprogressive shortness-of-breathchest painpleural effusionpalliative chemotherapy and there is also a limited role for surgery and radiotherapy. Prognosis is very poor, with a median survival from diagnosis of 8-14 months.Lung cancerAsbestos exposure is a risk factor for lung cancer and also has a synergistic effect with cigarette smoke.AtelectasisCommon postoperative complication basal alveolar collapse Respiratory difficulty. (Airways become obstructed by bronchial secretions).Features it should be suspected in the presentation of?dyspnoea and hypoxaemia around 72 hours postoperativelyManagementpositioning the patient uprightchest physiotherapy: breathing exercisesSevere cases bronchoscopy.Bilateral Hilar LymphadenopathyThe most common causes ?Sarcoidosis?and?Tuberculosis.Other causes include:lymphoma/other malignancyPneumoconiosis (berylliosis) Inflammation due to inhalation ofdust.fungi Histoplasmosis, CoccidioidomycosisChest x-ray: cavitating lung lesionAbscess Staph aureusKlebsiella Middle-aged alcoholic men, Abscess (middle/upper lobes and empyema). The mortality 30-50%?PseudomonasSQ. cell lung cancerT.BWegener's granulomatosisPERAAspergillosis, Histoplasmosis, CoccidioidomycosisChest x-ray: lung metastasesBreast cancerProstate cancerColorectal cancerRenal cell cancerBladder cancerMultiple, round well-defined lung secondaries 'cannonball metastases'. Most commonly ?renal cell cancer?but may also occur secondary to choriocarcinoma and prostate cancer.Calcification in lung metastases is uncommon?except Characteristic for Chondrosarcoma OR Osteosarcoma.Consolidation like pneumonia Adenocarcinoma (spread along the walls of alveoli, instead of destroying the lung parenchyma)Cavitation "commonest" SQ. cell carcinoma.Haemorrhagic metastases Choriocarcinoma and Angiosarcoma.Miliary pattern Renal cell carcinoma and Malignant Melanoma.Lung fibrosisMore common causes (idiopathic pulmonary fibrosis, drugs) tend to affect the lower zonesFibrosis predominately affecting the upper zones (CHRTS)Hypersensitivity pneumonitis?(also known as extrinsic allergic alveolitis)Coal worker's pneumoconiosis/progressive massive fibrosisSilicosisSarcoidosisAnkylosing spondylitis?(rare)HistiocytosisTuberculosisFibrosis predominately affecting the lower zonesidiopathic pulmonary fibrosisMost connective tissue disorders (except ankylosing spondylitis) e.g.?SLEAsbestosisDrug-Induced]Amiodarone,?Typically with doses > 400mg daily after ≥ 2months of therapy. 1 to 5% in the patients who are on long term amiodarone. The mechanism is not entirely understood (direct toxic injury to the lung or an indirect immunological reaction).Bleomycin?immunosuppressant inhibiting calcineurin. gum hypertrophy, nephrotoxicity and hepatotoxicity.Methotrexate, Cyclophosphamide, Nitrofurantoin, and penicillamine Bronchiectasis: causespermanent dilatation of the airways secondary to chronic infection or inflammation. Associated W HLA-DR1 post-infective: tuberculosis, measles, pertussis, pneumoniacystic fibrosisBronchial obstruction e.g. lung cancer/foreign bodyimmune deficiency selective IgA, hypogammaglobulinaemiaAllergic bronchopulmonary aspergillosis (ABPA)Ciliary dyskinetic syndromes: Kartagener's syndrome, Young's syndromeyellow nail syndrome?Most common organisms isolated from patients with bronchiectasis:Haemophilus influenzae?(most common)Pseudomonas?aeruginosaKlebsiella spp.Streptococcus?pneumoniaeAfter assessing for treatable causes (e.g. immune deficiency) management is as follows:Physical training (inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasispostural drainageantibiotics for exacerbations + long-term rotating antibiotics in severe casesbronchodilators in selected casesimmunisationsSurgery in selected cases (Localised disease)HLA-DR2: systemic lupus erythematous (SLE)HLA-DR3: autoimmune hepatitis, primary Sjogren syndrome, type 1 diabetes Mellitus, SLEHLA-DR4: rheumatoid arthritis, type 1 diabetes MellitusHLA-B27: ankylosing spondylitis, postgonococcal arthritis, acute anterior uveitisChest drainA tube inserted into the pleural cavity which creates a one-way valve, allowing movement of air or liquid out of the cavity.?IndicationPleural effusionPneumothorax not suitable for conservative management or aspirationEmpyemaHaemothoraxHaemopneumothoraxChylothoraxIn some cases of penetrating chest wall injury in ventilated patientsRelatively contraindication:INR > 1.3Platelet count < 75Pulmonary bullaePleural adhesionsTechnique?Triangle of safety: SUP Base of the axilla, ANT Lateral edge pectoralis major, INF5th intercostal space and Post anterior border of latissimus dorsiOnce patient consent has been obtained and patient imaging assessed positioned in a supine position or at a 45? angle. The patient's forearm may be positioned behind the patient's head easy access to the axilla. Identify the?5th intercostal space in the midaxillary line OR ultrasound guidance local anaesthetic injection (lidocaine, up to 3mg/kg). The drainage tube should then be inserted using a Seldinger technique. Positioning confirmed by aspiration of fluid from the drainage tubing, by 'swinging' of the fluid when the patient inspires and on chest x-ray.?Complications Failure of insertionthe drain may be abutting the apical pleura pulled backMay be subcutaneous or in rare cases could enter the abdominal cavity removed and re-sited.Bleeding - around the site of the drain or into the pleural spaceInfectionPenetration of the lungRe-expansion pulmonary oedemaPreceded by the onset of a cough and/or shortness of breath.Chest drain should be clamped and an urgent chest x-ray should be obtained.Prevention drain tube clamped regularly if rapid fluid output (not exceed 1L/ short period of time (less than 6 hours).?Removal of the chest drain is dependent upon the indication for insertion:?Drainage from the pleural cavity removed when no output for > 24 hours and imaging shows resolution of the fluid collection.Pneumothorax No longer bubbling spontaneously or when the patient coughs and imaging shows resolution of the pneumothorax.Penetrating chest injury should be reviewed by the specialist to confirm an appropriate time for removal.Pneumonia: assessment and managementPrimary care setting CRB65 criteria:CriterionMarkerCConfusion (abbreviated mental test score <= 8/10)RRespiration rate >= 30/minBBlood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg65Aged >= 65 yearsPatients are stratified for risk of death as follows:0 low risk ( < 1% mortality risk) home-based care1 or 2 intermediate risk (1-10% mortality risk) hospital assessment3 or 4 high risk ( > 10% mortality risk) hospital assessmentUse of antibiotic therapy:CRP < 20 mg/L NO routine antibiotic therapyCRP 20 - 100 mg/L consider a delayed antibiotic prescriptionCRP > 100 mg/L offer antibiotic therapySecondary care setting in hospital CURB65 extra criterion of urea > 7 mmol/L:CriterionMarkerCConfusion (abbreviated mental test score <= 8/10)Uurea > 7 mmol/LRRespiration rate >= 30/minBBlood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg65Aged >= 65 yearsNICE recommend, in conjunction with clinical judgement:CURB65 score of 0 or 1 low risk ( < 3% mortality risk) Home CURB65 score of ≥ 2 intermediate risk (3-15% mortality risk) HospitalCURB65 score of ≥ 3 high risk (> 15% mortality risk) ICUInvestigationschest x-rayin intermediate or high-risk patients blood and sputum cultures, pneumococcal and legionella urinary antigen testsCRP monitoring response to treatmentManagement of community acquired pneumonialow-severity Moderate and High-severity Amoxicillin is first-lineif penicillin allergic macrolide or tetracycline5 day course of antibiotics Dual antibiotic (amoxicillin and macrolide)7-10 day course is recommendedHigh-Severity Pneumonia (CURB > 3) Beta-lactamase stable penicillin IVCo-amoxiclav, Ceftriaxone or Piperacillin W Tazobactam + Macrolide Discharge criteria and advice post-dischargePatients are not routinely discharged if in the past 24 hours ≥ 2 or more of the following findings:Abnormal mental statustemperature > 37.5°Crespiratory rate 24 breaths per minute or moreheart rate > 100 beats per minutesystolic blood pressure ≤ 90 mmHg or lessO2 Sat. < 90% on room airinability to eat without assistance.how quickly their symptoms should symptoms should resolve:TimeProgress1 weekFever should have resolved1 month↓↓↓ Chest pain and sputum production 6 weeks↓↓↓ Cough and breathlessness 3 monthsMost symptoms but fatigue may be present6 monthsMost people will feel back to normal.Klebsiella Pneumonia Gram -Ve rod "normal gut flora" Pneumonia (typically following aspiration) and UTI.Features More common in?alcoholic and diabetics (Debilitating condition of respiratory defenses)may occur following aspiration'red-currant jelly' sputum A human neutrophil interacting with?Klebsiella pneumoniae(pink)often affects upper lobesPrognosiscommonly causes Lung abscess formation and?Empyemamortality is 30-50%Haemophilus influenzae?is common in older patients with chronic obstructive pulmonary disease (COPD) and can present as a hospital-acquired pneumonia. It does not cause 'red-currant jelly' sputum.Mycoplasma?is an atypical pneumonia which classically presents with a gradual onset dry cough and occasionally other features, such as autoimmune haemolytic anaemia and erythema multiforme.Staphylococcus aureus?pneumonia commonly occurs after influenza and can also be a complication of measles infection. On chest x-ray, multi-lobar consolidation, cavitation or a pneumothorax might be seen.Streptococcus pneumoniae?is the most common cause of pneumonia and characteristically presents with a high fever and pleuritic chest painPsittacosisInfection caused by?Chlamydia psittaci. The most common presentation is as a cause of atypical pneumonia. (Combination of typical fever +?history of bird contact (84%)?OR Pneumonia + Severe headache/ Organomegaly + failure to respond to penicillin- antibiotics.?EpidemiologyPsittacosis is present throughout the world, including the United Kingdom↑↑young adultsPathologyObligate intracellular bacterium Transmission (birds "pet birds and wild birds" Bird secretions) including urine and faeces after cleaning bird cagesTransmission from other animals or humans is possible but very rare and no strong female or male predisposition has been notedIt is rare; in the US there are roughly 10 cases reported annuallyPresentation with a subacute onset of:Flu-like symptoms (90%) fever, headache and myalgiaRespiratory symptoms (82%): dyspnoea, dry cough and chest painAcute or chronic conjunctivitisSignsChest unilateral crepitations and vesicular breathing (common), evidence of pleural effusion (uncommon)Abdomen Hepatomegaly and splenomegaly (rare)Investigations:↑↑ inflammatory markersChest X-ray: consolidation (90%)Confirmation with serology (usually as part of atypical pneumonia screening)Treatment:1st-line: tetracyclines e.g. doxycycline2nd-line: macrolides e.g. erythromycinMiddle East respiratory syndromeCaused by the betacoronavirus MERS-CoV. limited to the Arabian Peninsula and its surrounding countries, Incubation period of 2-14 days travellers returning from this region may present with MERS in other parts of the world.?Contact with?camels?(including camel products such as milk) is a significant risk factor for MERS-CoV.The clinical syndrome of MERS is varied (only mild symptoms through to life-threatening multi-organ failure.TuberculosisInfection caused by?Mycobacterium tuberculosis?that most commonly affects the lungs. Primary tuberculosisNon-immune exposed to M. tuberculosis A small lung lesion known as a Ghon focus (composed of tubercle-laden macrophages. The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex calcific peri-hilar nodularity,Immunocompotent intially lesion usually heals by fibrosis. Immunocompromised disseminated disease (miliary tuberculosis).Secondary (post-primary) tuberculosisHost becomes immunocompromised the initial infection may become reactivated. Reactivation generally occurs in the apex of the lungs spread locally or to more distant sites. Possible causes of immunocomprise include:immunosuppressive drugs including?steroidsHIVmalnutritionThe lungs remain the most common site for secondary tuberculosis. Extra-pulmonary infection may occur in the following areas:CNS (tuberculous meningitis - the most serious complication)vertebral bodies (Pott's disease) most common in the lower thoracic and upper lumbar vertebraecervical lymph nodes (Scrofuloderma)renalgastrointestinal tractiliopsoas abscess history of likely TB and back pain. more likely display inguinal tenderness and pain on hip flexion/extension, due to irritation of the muscle during contraction/relaxation respectivelyLung cancer: investigationChest x-raythis is often the first investigation done in patients with suspected lung cancerin?around 10% of patients subsequently diagnosed with lung cancer the chest x-ray was reported as normalCT?is the investigation of choice to investigate suspected lung cancerBronchoscopythis allows a biopsy to be taken to obtain a histological diagnosis sometimes aided by endobronchial ultrasoundPET scanningis typically done in non-small cell lung cancer to establish eligibility for curative treatmentuses 18-fluorodeoxygenase which is preferentially taken up by neoplastic tissuehas been shown to improve diagnostic sensitivity of both local and distant metastasis spread in non-small cell lung cancerBloodsraised platelets may be seenLung cancer: referralUrgent referral (for an appointment within 2 weeks) for lung cancer if they:Chest x-ray findings that suggest lung cancer≥ 40 W unexplained haemoptysisUrgent chest x-ray (within 2 weeks) for lung cancer ≥ 40if ≥ 2 of unexplained symptoms OR have ever smoked + have ≥ 1 of the following unexplained symptoms:coughfatigueshortness of breathChest painWeight lossAppetite lossUrgent chest x-ray (2 weeks) for lung cancer in people ≥ 40 with any of the following:Persistent or recurrent chest infectionFinger clubbingSupraclavicular lymphadenopathy OR persistent cervical lymphadenopathyChest signs consistent with lung cancerThrombocytosisLung cancer: risk factorsSmoking↑↑ risk of lung ca by *10 15% of lung cancers W passive smokingOther factorsAsbestos increases risk of lung ca by a factor of 5 (Smoking and asbestos are synergistic 10 * 5 = 50 times)ArsenicRadonNickelChromateAromatic HydrocarbonCryptogenic Fibrosing AlveolitisFactors that are NOT relatedCoal dustLung cancer: carcinoidThe majority of bronchial adenomas are carcinoid tumours, arising from amine precursor uptake and decarboxylation (APUD) system, Ex: small cell tumours.Lung carcinoid accounts 1% of lung tumours and for 10% of carcinoid tumours. The term bronchial adenoma is being phased out.typical age = 40-50 yearssmoking not risk factorSlow growing: . long history of cough, recurrent haemoptysisoften centrally located and not seen on CXR'cherry red ball' often seen on bronchoscopycarcinoid syndrome itself is rare (associated with liver metastases)Managementsurgical resectionif no metastases then 90% survival at 5 yearsLung cancer: small cellFeaturesusually centralOrigin APUD cells (Amine- high amine content) (Precursor Uptake- high uptake of amine precursors) (Decarboxylase- ↑content of the enzyme decarboxylaseassociated with ectopic ADH, ACTH secretionADH → hyponatraemiaACTH → Cushing's syndromecan cause bilateral adrenal hyperplasia, ↑↑cortisol can lead to hypokalaemic alkalosisLambert-Eaton syndrome antibodies to voltage gated calcium channels causing myasthenic like syndromeManagementusually metastatic by time of diagnosisvery early stage disease (T1-2a, N0, M0) are now considered for surgery. Most patients with limited disease receive a combination of chemotherapy and radiotherapypatients with more extensive disease are offered palliative chemotherapyLung cancer: Non-small cell managementManagementonly 20% suitable for surgeryMediastinoscopy d prior to surgery as CT does not always show mediastinal lymph node involvementCurative or palliative radiotherapypoor response to chemotherapySurgery contraindicationsassess general healthstage IIIb or IV (metastases present)FEV1 < 1.5 litres is considered a general cut-off point*malignant pleural effusiontumour near hilumvocal cord paralysisimplies extracapsular spread to mediastinal nodes?SVC obstruction* However if FEV1 < 1.5 for lobectomy or < 2.0 for pneumonectomy further lung function tests as operations may still go ahead based on the resultsAdenocarcinomaNot necessarily associated with smoking can present as primary lung cancers or as secondaries from adenocarcinomas elsewhere in the body.Squamous cell lung cancersStrongly associated with smoking They can cavitate and sometimes appear as cavitating lesions on chest x-ray. Associated with hypercalcemia.Alveolar cell carcinomasRare and present W productive cough with copious sputum and fluffy infiltrates on chest x-ray.Small cell carcinomas20% of lung cancers. They are the most aggressive type usually metastasized by the time of diagnosis. Because of this surgery is very rarely an option but they can be very chemosensitive. Also associated with hyponatraemia.Mesothelioma Associated with exposure to asbestos.Lung cancer: paraneoplastic featuresSmall cellSquamous cellAdenocarcinomaADHACTH?- not typicalHypertension, Hyperglycaemia, ↓↓ K+, alkalosis and muscle weakness are more common than buffalo hump Lambert-Eaton syndrome.hyperthyroidism due to ectopic TSHParathyroid hormone-related protein (PTH-rp)?secretion ↑↑ Ca++ClubbingHypertrophic Pulmonary Osteoarthropathy (HPOA)GynaecomastiaHypertrophic pulmonary Osteoarthropathy (HPOA) "Most common"Pulmonary Function TestsObstructive lung diseaseRestrictive lung diseaseFEV1 - significantly ↓↓FVC - reduced or normal?FEV1% (FEV1/FVC) - ↓↓FEV1 ↓↓FVC - significantly ↓↓↓↓FEV1% (FEV1/FVC) - normal or ↑↑AsthmaCOPDBronchiectasisBronchiolitis obliteransPulmonary fibrosisAsbestosisSarcoidosisAcute respiratory distress syndromeInfant respiratory distress syndromeKyphoscoliosis ?ankylosing spondylitisNeuromuscular disordersSevere obesityFlow volume loops most suitable way of assessing compression of the upper airway.A normal flow volume loop is often described as a 'triangle on top of a semi circle'Respiratory physiology: lung volumesTidal volume (TV)volume inspired or expired with each breath at rest500ml in males, 350ml in femalesVital capacity (VC) = 5Lmaximum volume of air that can be expired after a maximal inspiration4,500ml in males, 3,500 mls in femalesdecreases with ageVC = inspiratory capacity + ERVResidual volume (RV) = 1.2Lvolume of air remaining after maximal expirationincreases with ageRV = FRC - ERVInspiratory reserve volume (IRV) = 2-3 Lmaximum volume of air that can be inspired at the end of a normal tidal inspirationinspiratory capacity = TV + IRVFunctional residual capacity (FRC)the volume in the lungs at the end-expiratory positionFRC = ERV + RVExpiratory reserve volume (ERV) = 750mlmaximum volume of air that can be expired at the end of a normal tidal expirationTotal lung capacity (TLC) is the sum of the vital capacity + residual volumePhysiological dead space (VD)VD?= tidal volume * (PaCO2?- PeCO2) / PaCO2where PeCO2?= expired air CO2Respiratory acidosisCausesCOPDDecompensation in other respiratory conditions e.g.?life-threatening asthma?/ pulmonary oedemaNeuromuscular diseaseObesity hypoventilation syndromeSedative drugs Benzodiazepines,?Opiate overdoseRespiratory alkalosisCausesAnxiety leading to hyperventilation (NO hypoxia)Pulmonary embolism (↓↓ PO2)Salicylate poisoningMixed respiratory alkalosis and metabolic acidosisEarly stimulation of the respiratory centre respiratory alkalosis?Later direct acid effects of salicylates (combined with acute renal failure) may lead to acidosisCNS disorders: stroke, subarachnoid haemorrhage, encephalitisaltitudepregnancyNon-invasive ventilationNon-invasive ventilation - key indicationsCOPD with respiratory acidosis pH 7.25-7.35NIV W BiPAPcan be used in more acidotic (pH < 7.25) but a greater degree of monitoring (HDU) and a lower threshold for intubation and ventilation Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoeaCardiogenic pulmonary oedema unresponsive to CPAPWeaning from tracheal intubationN.B trial of NIV may be undertaken in bronchiectasis it should not be used routinely as its effectiveness is likely to be limited by excessive secretionsInitial settings for bi-level pressure support in COPDExpiratory Positive Airway Pressure (EPAP) 4-5 cm H2OInspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2OBack up rate: 15 breaths/minBack up inspiration:expiration ratio: 1:3Oxygen dissociation curveThe oxygen dissociation curve (Relationship between % of saturated Hb and partial pressure of oxygen in the blood. It is not affected by haemoglobin concentrationshifts to left = for given oxygen tension ↑↑saturation of Hb with oxygen i.e. ↓↓ oxygen delivery to tissuesshifts to right = for given oxygen tension ↓↓saturation of Hb with oxygen i.e. ↑↑ oxygen delivery to tissuesShifts to?L?→?Lower oxygen delivery, caused by Low [H+] (alkali) Low pCO2/ Low 2,3-DPG/ Low temperatureShifts to Left = Lower O2 deliveryShifts to Right = Raised O2 deliveryHbF,?methaemoglobin,?carboxyhaemoglobin↓↓ [H+] (alkali)↓↓ pCO2↓↓ 2,3-DPG↓↓ TemperatureRaised [H+] (acidic)Raised pCO2Raised 2,3-DPG*Raised temperature↑↑ Altitude 2,3-diphosphoglycerate (DPG) A glycolytic intermediate, (↑↑)in acidosis. It selectively binds to deoxyhaemoglobin and shifts the O2dissociation curve to the right.Myo-inositol trispyrophosphate (ITPP) is a performance-enhancing substance which shifts O2 dissociation curve to the right.Transfer factorThe transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion. Results given as Total gas transfer (TLCO) OR Corrected for lung volume (transfer coefficient, KCO)Causes of a raised TLCOasthmapulmonary haemorrhage (Wegener's, Goodpasture's) due to ↑↑uptake of CO by intra-alveolar Hbleft-to-right cardiac shunts (↓↓ O2delivar)Polycythaemiahyperkinetic statesmale gender, exerciseCauses of a lower TLCO (Tissue damage)pulmonary fibrosispneumoniapulmonary embolipulmonary oedemaemphysemaanaemialow cardiac outputKCO measure of the efficiency of gas exchange into the blood stream. TLCO = KCO x Alveolar volume (VA)↓↓↓ if the lungs are damaged ↓↓ lung volume (VA), but the fibrosis of alveoli also ↓↓ gas exchange in the alveoli (KCO) ↓↓↓ TLCO .↑↑↑ if there is additional blood in the lungs to remove carbon monoxide. ↑↑ with age Some conditions may cause an ↑↑ KCO with a normal or ↓↓ TLCO alveolar volume (↓↓) (↓↓) TLCO, but gas exchange is unaffected KCO will be normal or possibly high (as capillary blood flow is shunted to the areas of lung that are adequately perfusedPneumonectomy/lobectomyScoliosis/kyphosisNeuromuscular weakness Ankylosis of costovertebral joints ankylosing spondylitisOxygen therapyIn patients who are critically ill (anaphylaxis, shock etc) oxygen should initially be given via a reservoir mask at 15 l/min. Hypoxia kills.? The BTS guidelines specifically exclude certain conditions where the patient is acutely unwell (myocardial infarction) but stable.Oxygen saturation targetsAcutely ill patients: 94-98%patients at risk of hypercapnia (COPD patients): 88-92% (see below)oxygen should be reduced in stable patients with satisfactory oxygen saturationManagement of COPD patientsPrior to availability of blood gases use a 28% Venturi mask at 4 l/min and aim for an O2 Sat. 88-92% (if risk factors for hypercapnia) but no prior history of respiratory acidosisAfter ABG results target range to 94-98% if the pCO2 is normalSituations where oxygen therapy should not be used routinely if there is no evidence of hypoxia:myocardial infarction and acute coronary syndromesstrokeobstetric emergenciesAnxiety-related hyperventilationObstructive sleep apnoea/hypopnoea syndromePredisposing FactorsObesityMacroglossia Acromegaly,?Hypothyroidism, Amyloidosislarge tonsilsMarfan's syndromeFeatures excessive snoring and may report periods of apnoea.Consequencedaytime somnolencecompensated respiratory acidosis (Co2 retension)HypertensionAssessment of sleepinessEpworth Sleepiness Scale? questionnaire completed by patient +/- partnerMultiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria)Diagnostic testsSleep studies (Polysomnography)?- ranging from monitoring of pulse oximetry at night to full polysomnography where a wide variety of physiological factors (EEG/ respiratory airflow/ Thoraco-abdominal movement/ Snoring/ Pulse oximetry)Other tests ?Cinematic MRI and sleep endoscopy are useful in investigating the anatomical basis of disease. These tests aid in the diagnosis and are important for potential candidates for surgery. Managementweight loss, stopping smoking and avoiding alcohol.Continuous positive airway pressure (CPAP)?is first line for moderate or severe OSAHSIntra-oral devices (mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS ( no daytime sleepiness)DVLA should be informed?if OSAHS is causing excessive daytime sleepinesslimited evidence to support use of pharmacological agentsPleural effusion: causesdyspnoea, non-productive cough or chest pain are possible presenting symptomsclassic examination findings include dullness to percussion, reduced breath sounds and reduced chest expansion.Transudate (< 30g/L protein)Exudate?(> 30g/L protein)Heart Failure (most common transudate cause)Hypoalbuminaemia (liver disease/ nephrotic syndrome/ Malabsorption)HypothyroidismMeigs' syndromeInfectionPneumonia (most common exudate cause)TB, subphrenic abscessConnective tissue disease: RA, SLENeoplasia: lung cancer, mesothelioma, metastasesPancreatitispulmonary embolismDressler's syndromeyellow nail syndrome.Investigation Imagingposterioranterior (PA) chest x-rays should be performed in all patientsU/S ↑↑ likelihood of successful pleural aspiration and is sensitive for detecting pleural fluid septationsContrast CT is now increasingly performed to investigate the underlying cause, particularly for exudative effusionsPleural aspirationU/S recommended to reduce the complication rate21G needle + 50ml syringe should be usedPH, protein, lactate dehydrogenase (LDH), cytology and microbiologyLight's criteria?(DD. between a transudate and an exudate. criteria for borderline cases: Protein ( 25-35 g/L)An exudate is likely if ≥ 1 :Pleural protein/ serum protein > 0.5pleural LDH / serum LDH > 0.6Pleural LDH > 2/3 upper limits of normal serum LDHOther characteristic pleural fluid findings:↓↓ glucose rheumatoid arthritis, tuberculosis↑↑ amylase pancreatitis,?oesophageal perforationHeavy blood staining Mesothelioma, PE, TBPleural infectionAll patients with a pleural effusion + sepsis or a pneumonic illness require diagnostic pleural fluid samplingPurulent or turbid/cloudy chest tube should be placed to allow drainageNon-purulent pleural fluidClear but the?pH < 7.2 in patients with suspected pleural infection a chest tube should be placedOrganisms identified by Gram stain and/or culture (pleural infection is established) prompt chest tube drainage.Management of recurrent pleural effusionOptions for managing patients with recurrent pleural effusions include:Recurrent aspirationPleurodesisIndwelling pleural catheterDrug management to alleviate symptoms e.g. opioids to relieve dyspnoeaPneumothorax: featuresRisk factorspre-existing lung disease COPD (Commonest cause 2ry Pneumothorax)/ Asthma/ ?Cystic fibrosis/?Lung cancer, Pneumocystis pneumoniaconnective tissue disease Marfan's syndrome, Rheumatoid ArthritisVentilation, including?non-invasive ventilationCatamenial pneumothorax?3-6% of spontaneous pneumothoracesoccurring in menstruating women 32-35 years caused by endometriosis within the thoraxSymptoms tend to come on suddenly. Features include:dyspnoeachest pain: often pleuriticsweatingtachypnoeatachycardiaManagementPrimary Pneumothorax if the rim of air is < 2cm and the patient is not short of breath discharge and outpatient X-Ray (otherwise aspiration should be attempted)if this fails (defined as > 2 cm or still short of breath) chest drain should be insertedAvoid smoking↓↓ risk of further episodes the lifetime risk of developing a pneumothorax in healthy smoking men (10%) compared with around 0.1% in non-smoking menSecondary pneumothorax:< 1cm giving oxygen and admitting for 24 hoursAir (1-2cm) aspirationIf aspiration fails (pneumothorax > 1cm) chest drain should be inserted. All patients should be admitted for at least 24 hours> 50 years old + air > 2cm and/or Short of breath ?chest drain?should be inserted.Scuba Diving Avoided for life unless patient undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively.'Air travel acceptable once the pneumothorax has fully resolved2 weeks after successful drainage if there is no residual air.1 week post check x-rayIatrogenic pneumothoraxless likelihood of recurrence than spontaneous pneumothoraxmajority will resolve with observation, if treatment is required Aspiration should be usedventilated patients need chest drains, as may some patients with COPDRe-expansion Pulmonary EodemaDue to over-rapid re-expansion of the lung after large volume thoracocentesis for pneumothorax or effusion.?Uncommon within 1-2 hours of thoracocentesis but up to 24 hours after. RPE may progress over 1-2 days and usually resolves several days later.?Risk factors Longer duration of lung collapseLarger volume of lung collapseRapid drainage of pleural fluid/airApplication of negative pleural pressure (suction)Younger age of patientPulmonary hypertensionSustained elevation in mean pulmonary arterial pressure of >?25 mmHg?at rest OR 30 after Exercise. Group 1Group 2 (Heart)Group 3 (lung hypoxia)Group 4 Group 5: MiscellaneousIdiopathic*FamilialAssociated conditionsCollagen vascular diseaseCongenital heart disease W systemic to pulmonary shuntsHIVDrugs and toxinsSickle cell diseasePersistent pul. HTN of newbornleft-sided atrial, ventricular or valvular disease LV systolic and diastolic dysfunction mitral stenosis mitral regurgitationCOPDInterstitial Lung Disease Sleep Apnoea High AltitudeThromboembolicEvents Lymphangiomatosis 2ry Carcinomatosis SarcoidosisRheumatoid arthritis: respiratory manifestationsPulmonary fibrosisCaplan's syndrome - massive fibrotic nodules with occupational coal dust exposureComplications of drug therapy methotrexate Pneumonitis (1-5% of patients?)Pulmonary nodulesBronchiolitis obliterans Obstructive pattern Pleural effusionPleurisyInfection (possibly atypical) secondary to immunosuppressionSarcoidosisMultisystem disorder of unknown aetiology W non-caseating granulomas. ↑↑ young adults/ African descentFeaturesacute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgiainsidious: dyspnoea (History of Asthma) , non-productive cough, malaise, weight lossskin: lupus pernio↑↑Ca++ macrophages inside the granulomas ↑↑conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)Syndromes associated with sarcoidosisLofgren's syndrome?acute form of the disease bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgiaIt usually carries an excellent prognosis?Mikulicz syndromeEnlargement of the parotid and lacrimal glands sarcoidosis, tuberculosis or lymphomaHeerfordt's syndrome?(uveoparotid fever) there is parotid enlargement +fever + uveitis (painful eye) 2ry to sarcoidosisInvestigationThere is no one diagnostic test clinical. ACE levels have a sensitivity of 60% and specificity of 70% not reliable in the diagnosis of sarcoidosis (monitoring disease activity).Routine bloods ↑↑ (Ca++ (10%) and ESR)A chest x-ray may show the following changes:stage 0 = normalstage 1 = bilateral hilar lymphadenopathy (BHL)stage 2 = BHL + interstitial infiltratesstage 3 = diffuse interstitial infiltrates onlystage 4 = diffuse fibrosisOther investigationsSpirometry: may show a restrictive defecttissue biopsy: non-caseating granulomasgallium-67 scan - not used routinelyManagementIndications for steroidsChest x-ray stage 2 or 3 + Symptoms. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatmentHypercalcaemiaEye, Heart or Neuro involvementPrognosis Sarcoidosis remits without treatment in 2/3 of peopleFactors associated with Poor PrognosisAge>40Black peopleInsidious "Gradual" onset symptoms > 6 monthsAbsence of erythema nodosumHypercalcaemiaExtrapulmonary manifestations lupus pernio, splenomegalyCXR stage III-IV featuresHLA B13 subtypeGood Prognosis (Spontanous improvement)HLA B8Lofgren's syndrome (bilateral hilar lymphadenopathy, erythema nodosum, polyarthritis and fever)SilicosisA fibrosing lung disease inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing TB (Toxic to macrophages).As the disease progresses the hilar retracts upwards and cavitation can occur leading to the potential for a secondary tuberculosis infectionOccupations at risk of silicosisminingslate worksfoundriespotteriesFeaturesfibrosing lung diseaseX-Ray FindingThe typical chest findings in chronic silicosis Calcified multiple and small well-rounded nodules, particularly in the upper zone.Hilar lymph nodes 'Egg-Shell' calcification DD. Berylliosis Occuoitional Exposure AeronauticalMetal Electronics industry. Berylliosis and sarcoidosis have similar clinical features such as bilateral hilar lymphadenopathy, shortness of breath, and dry cough. ................
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