Respiratory Flashcards
Specific Ix finding results of Asthma that are diagnostic:
-FeNO: An exhaled FeNO of 40 parts per billion or greater (indirect marker of eosinophil inflammation)
( children 35 parts per billion o greater)
- BDR: A post-bronchodilator improvement in lung volume of 200 ml or FEV1 of 12% or more (reversibility essentially)
- Spirometry: An FEV1/FVC ratio <70% (it is an obstructive lung disease)
- PEFR: A peak expiratory flow rate variability of 20% or more (normal between attack then reduced during symptoms).
- Challenge test using Histamine or methacholine: provokes symptoms of Asthma
- Skin-prick & serum IgE: to investigate Atopy. Normal = less likely Asthma
Asthma- definition, epidemiology & 3 screening Qs?
Definition: Airway hypersensitivity
o Chronic inflammation
o Bronchospasm
o Reversibility with bronchodilators
Epidemiology:
o Young/early onset
o Affects 5% of population
o Risk – Hx or FHx atopy
3 screening questions for asthma (by Royal College of Physicians): 1pt=med risk, 2-3pt=high risk
o In last month/week, have you had difficulty sleeping due to your asthma/cough?
o Have you had asthma symptoms (cough, wheeze, chest tightness) during the day?
o Have your asthma/symptoms interfered with your day-today activities (e.g. school, work)?
Symptoms of acute asthma exacerbation?
-Features of severe & life threatening:
Features of exacerbation: Wheeze, Cough, Chest tightness, SOB, ↑RR (Not responsive to salbutamol PRN)
Severe: • Inability to complete sentences • HR >110 • RR >25 • PEFR 33-50%
Life threatening – any one sign!: 33 92 CHEST Indication for intubation- REFER TO ITU!
<33% PEFR
<92% Sats
- Cyanosis
- Hypotension (& bradycardia)
- Exhaustion with poor effort (↓pH, Normal PaCO2, lowering or normalising of RR)
- Silent chest (no wheeze, chest can be hyper-resonant on percussion due to trapping of air unable to be breathed out I.e. obstructed disease from narrow airways)
- Thirty-three percent PEFR (or less)
*Near-Fatal: high PaCO2
Note: So basically don’t ever be fooled into false-reassurance if the patients wheeze starts to improve & their RR goes to normal alone with normalisation mug of PaCO2= they are worsening! Be guided by hypoxia levels (Sats & PaO2). L
Ix of acute asthma:
Ix patient age 5-16 & >17:
o *Best: PFTs/spirometry (with bronchodilator reversibility test (BDR)
o Normal PFTs, patient likely has asthma though: Salbutamol trial
o Consider: Serial peak flows (take home peak flow + record in diary x2wk)
-Fractional Exhaled Nitric oxide (FeNO) test
Note: patients >17yrs must rule out occupational asthma
Mx of acute asthma:
Management of acute exacerbation: (OShit, I Hate My Asthma)
o Oxygen – high flow 15L via non rebreathe mask
o Nebulised salbutamol 5mg + ipratropium (oxygen driven)
o IV Hydrocortisone /Oral prednisolone 40mg
o IV Mg sulphate
o IV Aminophylline 500mg/ IV salbutamol
o If all fails: ICU + mechanical ventilation
*if patient had previous ICU admission then they are likely to be high risk
Note: salbutamol shifts K into cells so on ABG might appear low & it’s something to think about replacing after patient is stable.
Chronic Rx of Asthma:
Chronic Rx for ADULTS: ALWAYS stop smoking, avoid allergens, wt loss, vaccines, ensure compliance w/ meds
o Step 1: SABA (e.g. salbutamol 100 mcg 2 puffs PRN)
o Step 2: ADD Inhaled corticosteroid low -dose (<400mcg) e.g 200mcg BD (Breathe=Beclomethasone dipropionate or budesonide)
o Step 3: Add LTRA (e.g. monteleukast)
o Step 4: Add LABA (e.g. Salmeterol 50mcg BD)
(NB: If no response to LTRA – stop. If response – continue)
o Step 5a: Keep SABA +/- LTRA if its working but switch LABA + low dose ICS for MART (maintenance and reliever therapy) (basically SMART ;) )
Step 5b: Increase ICS in MART to medium dose (400-800mcg/day)
Step 5c: Increase ICS to high dose (800- 2000 mcg) but not as type of MART anymore. Can add theophylline (LAMA)
o Step 6: Oral steroids + referral to respiratory physician
*pregnant + breastfeeding women must continue their inhaled meds, theophylline & prednisone
COPD: classification
Causes in old & young adults:
Classification
o Emphysema (histological) Permanent dilation and destruction of terminal bronchiole + alveoli
o Chronic Bronchitis (clinical) Permanent obstruction of airway
Cough+sputum on most days for 3months of two successive 2yrs
Cause o Of COPD: Old • Smoking o 50% of heavy smokers, but 10-15% of all smokers o Passive smoking also • Cooking with open fire indoors (e.g. India, Africa; 3 billion people cook like this + accounts for 1 million deaths worldwide) • Indoor and outdoor pollution
Young Alpha-1 Anti-trypsin deficiency (+ hepatitis)
Causes of acute exacerbation of COPD:
o Of acute exacerbations:
Bacterial: H influenza, S pneumo
Viral: Rhinovirus, influenza, parainfluenza, adenovirus, RSV
Other: Non-infective (e.g. allergic, continued smoking)
Presentation of COPD: Hx & of acute excacerbation
Presentation: o History: SOBOE + reduced exercise tolerance Wheeze Productive cough for few months (usually winter) in consecutive years Smoker
o Acute Exacerbation: ↑ SOB, ↑wheeze, ↑cough, ↓exercise capacity
Ix of COPD (acute & chronic)
Investigations:
o Acute: PFTs not useful in acute exacerbation
Blood
Blood cultures
ABG: ↓O2, ↑CO2 (Type 2 RF), if high Bicarb = chronic retention of CO2
CXR:
Fever + infective respiratory symptoms (i.e. productive cough/ purulent sputum/ SOB) = Infective exacerbation of COPD or LRTI
Fever + infective respiratory symptoms + X-ray consolidation = pneumonia
Sputum culture
Chronic
o PFTs: Obstructive pattern
For diagnosis:
Spirometry post-bronchodilator = FEV1/FVC <70% (obstructive)
CXR: • Hyperinflated • Flattened diaphragms • Bullous disease • Narrow cardiac silhouette (Also exclude lung Ca)
Blood: FBC to exclude secondary polycythaemia
Calculate BMI
For ongoing assessment of progression:
• FEV1 (best predictor of survival) – GOLD Classification
o Mild = >80%; Mod = 50-80%; Sev = 30-50%; Very Sev = <30%
Mx of acute exacerbation COPD
Treat: OSHIT
o Controlled O2 (keep between 88-92% sats) – nasal prongs or 24-28% venture
o Ipratropium + Salbutamol Nebs
o Oral Prednisolone 30 for 5 days
o If refractory: Aminophylline
o If still refractory (↓pH, ↑PaCO₂, ↓PaO₂ ): Ventilation (NIV Invasive)
NIV BiPAP
Invasive Intubation
o If infection suspected: Antibiotics (purulent sputum, fever, raised inflame markers)
First line: amoxicillin, second line clarithromycin or doxycycline
Chronic Mx of COPD (outline)
Chronic management
o Conservative:
Vaccines influenza (yearly), Pneumococ (one-off or 5 yearly if hypo/asplenism or CKD), H influ (once in life)
Stop Smoking – most important measure to reduce mortality (NRT, bupropion, varenicline)
-Chest physiotherapy
o Medical:
Inhalers
Mucolytics
Long Term Oxygen Therapy/LTOT IMPROVES OUTCOMES
-Surgery: bullectomy or lung transplant (final step)
Bronchiectasis: definition, causes & pathogens
• Definition: Permanent dilation of the airways which may be LOCAL (part of lung) or DIFFUSE (all of lung)
• Cause:
o Repeated infections (TB, Measles, pertussis, pneumonia), or
o Underlying disorders
CF, IBD, RA
Ciliary dyskinetic syndromes Kartagener’s, young syndrome
-ABPA: allergic bronchopulmonary aspergillosis (in asthmatics)
- Immune deficiency: selective IgA, hypogammaglobulinaemia
• Pathogens:
o H influ (35%)
o Pseudomonas aeruginosa (30%)
o Staph aureus
Features of bronchiectasis
• Features:
o Chronic cough with high volume sputum (can be intermittent, but more persistent than COPD)
o SOB, wheeze, hemoptysis (worse when infection present)
o Recurrent lung infection
-Signs: Coarse inspiratory crepitations + finger clubbing
Ix of bronchiectasis
• Investigate: o Bloods: Serum immunoglobulins, Aspergillus antigen test. o CXR: tram-tracks o PFTs/Spirometry -Sputum culture & microscopy -Genetic tests: CF, Young's, Kartagener
o Best: HRCT (high-resolution CT scan)= signet ring & tree bud appearance
Mx of bronchiectasis
o Acute:
Chest physio: airway clearance
Antibiotics in exacerbations
o Chronic
1-Conservative: Physio for both airway clearance & pulmonary rehabilitation to help with ADL, vaccines, stop smoking
• Chest physio MOST IMPORTANT Mx
2-Medical:
• All patients: Bronchodilators (sometimes no improvement though)= B2 agonists & anti-cholinergic bronchodilators.
• 3+ episodes/yr OR severe: Continuous Abx
* ICS not used
Surgery: If localised bronchiectasis – remove lobe!
Chronic COPD inhaler steps:
Step 1: SABA or SAMA (ipatropium) (PRN)
Step 2: Are they steroid responsive? OR have asthmatic features?
- previous diagnosis of asthma or atopy
- a higher blood eosinophil count
- substantial variation in FEV1 over time (at least 400 ml)
- substantial diurnal variation in peak expiratory flow (at least 20%)
Yes= Add ICS (beclomethasone )+ LABA (glycopyrronium)
Step 2b: Triple therapy: Add LAMA (formoterol or tiotropium) & discontinue SAMA (switch to SABA)
No= Add LABA + LAMA (stop SAMA & switch to SABA)
Step 3: Oral Theophylline (or if inhaled meds aren’t tolerated).
Chronic COPD: which antibiotic is used for prophylaxis, when can it prescribed?
What important Ix are needed before prescribing it?
How to monitor?
Azithromycin prophylaxis is recommended in select patients:
1-Dont smoke 2-Have optimized treatment 3-Still cont. to have infective exacerbations
Dose: 250mg daily or 500mg three times per week
Ix:
CT Thorax + Sputum culture = exclude bronchiectasis, atypical organisms & TB
LFT’s & ECG to exclude a QT prolongation as Azithromycin can prolong QT.
Note: - Abx and Pred for the patient to keep (rescue medication) , and then take when they have plurulent sputum and increased breathlessness.
- Abx prophylaxis (Azith 3 times a week) if they keep getting exacerbations despite optimal therapy.
Indication for LTOT in COPD?
1-If PaO2 <7.3 when stable or <7.3-8 WITH polycythemia, nocturnal hypoxaemia, pulmonary hypertension.
Hemoglobin >16.5 g/dL in men and >16 g/dL in women
*improves outcomes/mortality: must be used at least 15hrs/day - 20hrs.
Interstitial lung disease: definition, epidemiology & features?
Interstitial Lung Disease AKA Pulmonary Fibrosis
- Definition: A group of lung diseases damaging tissue of the lung between the bronchial tree + alveoli resulting in loss of lung elasticity
- Epidemiology: Relative rare, seen in age 50-70
• Features of ALL: Chronic inflammation => Fibrosis of interstitium => Poor gas exchange (↓O2)
o SOBOE with dry cough
o Fine end-inspiratory crackles (bibasal)
Finger clubbing
o NO FEVER OR SPUTUM (COPD); NO orthopnoea (CCF)
Ix of ALL interstitial lung diseases?
• Investigations of ALL:
o First:
- Blood (non-specific)
- X-ray: Reticular/mesh-like/ground-glass pattern (earlier) honeycombing (later)
- PFTs: Restrictive pattern (low FEV1, Low FVC, Low TLCO)
o Second – often BEST: HRCT (honeycombing)
o Third: Biopsy
-RARELY needed
General Mx for all Interstitial fibrosis:
Prognosis?
• General Treatment Measures:
o Conservative: Stop smoking, avoid exposures
o Medical:
- Immunosuppression (steroids)
- Oxygen
- pirfenidone (an antifibrotic agent)
o Surgical:
-Lung transplantation (the only treatment for patients with steroid-resistant disease :( )
• Prognosis: Life expectancy 3-4yr on average :(
Causes of Interstitial Fibrosis?
- Causes: Over 100!
- Idiopathic pulmonary fibrosis (previously: cryptogenic fibrosing alveolitis)
- Pneumoconioses/Occupational lung diseases: Asbestosis + Silicosis
- Extrinsic allergic alveolitis: Farmer’s, Bird fancier, mushroom/cheese worker lungs
Idiopathic Pulmonary fibrosis: Definition, Epidemiology, IX & Mx?
o Definition: Diagnosis of exclusion for fibrotic lung disease (i.e. NO risk factors for other ILDs)
o Epidemiology: Most common cause of fibrotic lung disease
o Ix: As above
o Treat: As above…
Pirfenidone (growth factor inhib)
(Steroids)
Pneumoconiosis/occupational lung disease:
Asbestosis: Features, Mx, Complications of Asbestos exposure?
o Asbestosis: Shipyard, insulation work
Features: symptoms of fibrosis.
Rx: Avoid further exposure + stop smoking
• NO medication available to slow or stop progression
• Will slowly progress
Complications (Asbestos exposure presents with a spectrum of complications):
1-Pleural plaques – benign!
2-Pleural thickening
3-Asbestosis (the pulmonary fibrosis-lower lobe fibrosis)
4-Mesothelioma (even from small asbestos exposure) = progressive shortness-of-breath,chest pain, pleural effusion.
5-Normal lung cancers
Silicosis: Features?
o Silicosis
Features:
• Sand blasting, glass/pottery work
o Silica dust = macrophage active = inflam = fibrosis
Extrinsic allergic alveolitis: Causes? Mx?
o Cause: Most often dust particles (often fungus spores)
Farmer’s lung Saccharopolyspora rectivirgula
Bird fancier’s lung Avian proteins
Malt worker’s lung Aspergillus clavatus
Mushroom worker’s lung Thermophilic actinomycetes/Micropolyspora faeni
o Rx:
Remove exposure
• Change location/job (rarely realistic), or
• Change duties at job, or
• Wear industrial respirator (filters 99% of environmental dust)
Steroids (usually for 1-2 months)
Sacroidosis: Definition, Epidemiology, Ix
o Definition: Multisystem chronic inflammatory disease characterised by NON-caseating granulomas
o Epidemiology:
3x higher in black population
o Ix:
Initial:
• PFT Restrictive lung defect
• Blood – high calcium
• CXR
o Bilateral hilar lymphadenopathy (BHL)
• HRCT
Best Ix – Biopsy of lymph nodes: Non-caseating (i.e. non-necrotic) granulomas
Mx of Sarcoidosis? (Indication)?
o Treat: Prednisolone
Indications are PUNCH
- Parenchymal Lung Disease (patients with chest x-ray stage 2 or 3 disease who are symptomatic. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment)
- Uveitis
- Neurological involvement or
- Cardiac involvement
- HyperCa
PE: Cause & risk factors?
• Cause: DVT
• Risk: PRINTS o Pregnancy/Pill o Renal failure o Immobility (e.g. flights) o Neoplasia/cancer o Thrombophilia o Surgery recently (esp orthopaedic)
PE Symptoms:
Most common PE signs?
SUDDEN ONSET SOB, pleuritic chest pain, cough (?hemoptysis), DVT symptoms
o Always take this history in conjunction with whether they have any risk factors or not
Tachypnea (RR>20/min), Tachycardia (HR>100bpm), crackles, Fever (>37.8C)
Less common: triad of pleuritic chest pain, dyspnoea, haemoptysis.
PE Ix (general):
• Investigate:
o ECG
Most common finding: Sinus tachycardia
Most specific finding: S1 Q3 T3
• Dominant S in lead I
• Q-wave and inverted T-wave in lead III
o Bloods – D-dimer?
o X-Ray Normal usually (R/O other lung pathology)
o Best test: Focused lung imaging
CTPA
VQ Scan (for young, renal failure, or pregnant)
PE, Mx (general)
• Acute Management:
o Not hypotensive:
Oxygen
DOAC(3mo if risk factor removed, 6mo if risk ongoing or unprovoked)
o Hypotensive:
ThrombolysisWell
Wells Score for DVT?
Wells Score for DVT (-2 to 9 Low: -2 to 0... Mod: 1,2... High 3+) • Cancer • Calf swelling • Swollen superficial veins • Unilateral pitting edema • Swelling of entire leg • Tenderness over deep venous system • Weakness of leg • Immobilisation >3d • Previous DVT • Alternative diagnosis at least as likely (-2)
Wells score for PE?
Wells Score for PE (0-12.5 0-4 = PE unlikely [consider D-Dimer]… 5-12.5 = PE likely [consider diagnostic imaging])
- Suspected DVT (3)
- Alternative diagnoses are LESS likely (3)
- Tachycardia (1.5)
- Immobilisation >3d (1.5)
- Prior DVT/PE (1.5)
- Hemoptysis (1)
- Malignancy (1)
Specific drug choices for PE:
1-PE in haemodynamically stable patient?
2-PE in patient with active cancer?
3-PE in severe renal impairment:
4-PE in Patient with anti-phospholipid syndrome (triple positive?)
5-PE in haemodynamically unstable patient (hypotensive)?
6-Repeat PE despite adequate anti-coagulation?
1-First-line: DOAC (Apixaban or Rivaroxaban) once Dx is suspected then continue if Dx is confirmed.
2-DOAC unless CI
3-LMWH, UH or LMWH followed by vitamin K antagonist (VKA)-warfarin.
4- LMWH, UH or LMWH followed by vitamin K antagonist (VKA).
5-This is considered massive PE
Thrombolysis is first line.
6-IVC filter= stops clots formed in the deep veins of the legs from moving to the pulmonary arteries.
Lung cancer: types & causes?
• Small (15%)
o ONLY associated with smokers
o Widespread, rapid growth
When caught EARLY, 2yr survival = 25% (poor prognosis)
o Paraneoplastic (ACTH Cushings; ADH SIADH)
• Squamous cell (35%) o Paraneoplastic (PTH hyperparathyroidism; TSH hyperthyroidism)
• Adenocarcinoma (30%)
o Associated mostly with smokers but by far the most common in non-smokers
• Large cell (10%)
Lung Ca risk factor?
o Smoking (10x risk of bronchial cancer over non-smokers) This includes passive smoking
Lung Ca features?
Cough (80%), haemoptysis (70%), SOB (60%), weight loss
o SVCO - Facial swelling, engorges vessels of the chest wall
o Brachial plexus compression - pain and numbness of arm
o Horner syndrome - Miosis (constricted pupil), Ptosis (lid droop), Anhidrosis (lack of sweating on that side)
Occurs with Pancoast tumour (affecting apex of lung)
o Recurrent laryngeal – hoarseness of voice
o Paraneoplastic
o Bony mets (high calcium, bone pain)
Lung Ca Ix?
o First:
CXR
CXR can be normal in some cases – if clinical suspicion, refer
o Second: CT chest
o Best: Bronchoscopy and biopsy
Lung Ca Mx?
o CURATIVE RESECTION
o RADIOTHERAPY
o CHEMOTHERAPY
CAP: Organisms, symptoms &signs?
Community Acquired Pneumonia (CAP)
S pneumo (most common), H influenza (2nd most com)
- Symptoms: Cough + Sputum, SOB, Pleuritic Pain, Fever/rigors, Confusion (may be only sign in elderly)
- Signs: Tachycardia, high RR, low sats, crackles on chest (unilateral)
CAP: Calculate severity?
o CURB65
0-1 = home treatment 2 = admit for 1d IV Abx ≥3 = severe pneumonia – 3d IV ± ITU
Confusion (AMTS ≤8, new onset) Urea >7 RR >30 BP <90 syst OR <60 diast 65 or older
CAP Ix?
• Diagnose:
o Initial:
Bloods
CXR – The patient MUST have radiological (CXR of CT chest) evidence of consolidation
o Secondary: Microscopy, culture, sensitivity (MC+S) Sputum
CAP Mx?
• Manage: Fluids + Oxygen + Antibiotics + Manage pain (FOAM)
Tb: Definition, organism & risk factors?
- Definition: Chronic granulomatous disease caused by Mycobacterium tuberculosis which is spread by droplet infection
- Pathogens: Mycobacterium tuberculosis
- Risk: Old, homeless, alcoholic, drug abuser, HIV, close contact with TB
TB: Features?
Ix?
• Features:
o Constitutional Fever, night sweats, weight loss
o Lung Chronic productive cough with purulent/blood-stained sputum
• Diagnose:
o Initial: CXR - Apical infiltrative cavitation
o Best: Sputum Acid-Fast Bacillus Stain + Culture
TB Mx?
• Treat:
o First two months: Rifamp, Isoniazid, Pyrizinamide, Ethambutol (RIPE)
o Next four months: Rifampin, Isoniazid + Prednisolone
Pneumothorax definition + classification? Features of pneumothorax?
Ix?
• Definition: Collection of air in pleural space resulting in lung collapse on affected side
• Classification + Causes/Risk Factors:
o Primary Tiny blebs of weakness in lung parenchyma
Risk Young, Tall, Marfan’s
o Secondary COPD, asthma, ILD
pneumothorax features?
• Features: Sudden onset chest pain + SOB (depends on size of lesion)
o Hyper-resonant chest to percussion
o Reduced or absent breath sounds
• Ix:
o CXR Clearly defined visceral pleura line with no lung markings peripheral to this
pneumothorax Mx?
• Rx: primary:
o <2cm, stable obs: Discharge + follow up in 2wk w/ repeat CXR
o >2cm OR needs O2 to maintain sats:
First: Aspirate
If aspiration fails: Chest drain
Secondary Pneumothorax:
*> 50 years old + rim of air is > 2cm and/or the patient is short of breath = a chest drain
- aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
- less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
Tension Pneumothorax: Mechanism, features, Ix & Mx?
o Mechanism: One-way valve created at rupture in lung tissue
o
o Features: ↓Sats, ↑HR, ↓BP, ↑JVP, trachea deviated away from side of lesion/midline shift
Much worse obs than normal pneumothorax
o Ix: Nil, DO NOT wait for CXR should be treating before they have an X-ray!
o Rx: Large bohr cannula into 2nd/3rd ICS in mid-clavicular line – gush of air confirms diagnosis
Causes of upper lobe fibrosis?
The causes of upper lobe fibrosis can be remembered with the mnemonic ‘CHARTS’
Coal workers’ pneumoconiosis
Histiocytosis
Ankylosing spondylitis/Allergic bronchopulmonary aspergillosis
Radiation
Tuberculosis
Silicosis (progressive massive fibrosis), sarcoidosis
Drugs that cause lung fibrosis:
Chronic illness that cause fibrosis:
Drug-induced: amiodarone, bleomycin, methotrexate, nitrofurantoin
ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)
Connective tissue diseases, SLE, RA, TB, sarcoidosis, ankylosing spondylitis
Bacteria causing Aspiration Pneumonia?
The bacteria often implicated in aspiration pneumonia are aerobic, and often include: Streptococcus pneumoniae Staphylococcus aureus Haemophilus influenzae Pseudomonas aeruginosa
Other aerobic, and anaerobic, organisms can also result in aspiration pneumonia, but are less common.
Aspiration Pneumonia: Definition, Risk factors, signs
Definition: Aspiration pneumonia is a pneumonia that develops as a result of foreign materials gaining entry to the bronchial tree, usually oral or gastric contents such as food and saliva. Depending on the acidity of the aspirate a chemical pneumonitis can develop, as well as bacterial pathogens adding to the inflammation.
Causes:
1-Incompetent swallowing mechanisms: stroke, multiple sclerosis and intoxication.
2-Iatrogenic causes: intubation
3-Other: Poor dental hygiene,
Prolonged hospitalization or surgical procedures
Impaired consciousness
Impaired mucociliary clearance
Sign: Right middle or lower lobe consolidation.
OSA: Predisposing factors, consequences, assessment of sleepiness, diagnostic tests, Mx?
Predisposing factors: obesity macroglossia: acromegaly, hypothyroidism, amyloidosis large tonsils Marfan's syndrome
The partner often complains of excessive snoring and may report periods of apnoea.
Consequence:
daytime somnolence
compensated respiratory acidosis
hypertension
Assessment of sleepiness:
- Epworth Sleepiness Scale - questionnaire completed by patient +/- partner
- Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria)
Diagnostic tests
-sleep studies (polysomnography)
Management:
- weight loss
- continuous positive airway pressure (CPAP) is first line for moderate or severe OSAHS
- intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated/daytime sleepiness isn’t an issue
- if daytime sleepiness= DVLA
Centor Criteria for patients with acute sore throat/acute pharyngitis/acute tonsillitis?
*if 3 or more of the criteria are present there is a 40-60% chance the sore throat is caused by Group A beta-haemolytic Streptococcus
The Centor criteria* are as follows: presence of tonsillar exudate tender anterior cervical lymphadenopathy or lymphadenitis history of fever absence of cough
Smoking cessation: Bupropion & Varenicline
Bupropion: norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist
CI=epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative CI
Varenicline: nicotinic receptor partial agonist
CI= pregnancy, breastfeeding, depression
Ix of pleural effusion?
Imaging:
posterioranterior (PA) chest x-rays should be performed in all patients
ultrasound is recommended: it increases the likelihood of successful pleural aspiration and is sensitive for detecting pleural fluid septations
contrast CT is now increasingly performed to investigate the underlying cause, particularly for exudative effusions
Pleural aspiration:
as above, ultrasound is recommended to reduce the complication rate
a 21G needle and 50ml syringe should be used
fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
Lights criteria components to distinguish b/w exudate vs transudate causes of pleural effusion?
exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L
If: the protein level is between 25-35 g/L, Light’s criteria should be applied. An exudate is likely if at least one of the following criteria are met:
pleural fluid protein divided by serum protein >0.5
pleural fluid LDH divided by serum LDH >0.6
pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
How would you manage a patient with pleural effusion associated with sepsis or pneumonia?
How you manage recurrent pleural effusions?
Must take pleural aspirate & check the color:
Purulent/turbid/cloudy = chest drain for drainage
Clear BUT pH is <7.2 = chest drain
Recurrent pleural effusions Mx: Recurrent pleural aspiration Insertion of indwelling pleural catheter Pleurodesis Drugs to manage dyspnoea e.g. opioids
How would you manage a patient with pleural effusion associated with sepsis or pneumonia?
How you manage recurrent pleural effusions?
Must take pleural aspirate & check the color:
Purulent/turbid/cloudy = chest drain for drainage
Clear BUT pH is <7.2 = chest drain
Recurrent pleural effusions Mx: Recurrent pleural aspiration Insertion of indwelling pleural catheter Pleurodesis Drugs to manage dyspnoea e.g. opioids