Week 3: Respiratory medicine (4) (common conditions con) Flashcards
Pleural cavity
- Potential space between the visceral and parietal pleura- two lays which surround the lungs- tiny bit of fluid
outer pleura –> parietal (attached to chest wall)
inner pleura –> visceral (covers lungs)
pleural diseases
- Pneumothorax’s= air in pleural cavity
- Pleural effusion= fluid in pleural cavity
- Empyema= infected fluid in pleural cavity
- Pleural tumours= benign vs malignant
- Pleural plaques= discrete fibrous areas
- Pleural thickening= scarring/calcification caused by
pneumothoraxs can be split into
- Spontaneous
- Primary (no lung disease)
- Secondary (lung disease
- Traumatic
- TENSION: emergency (haemodynamic instability
- Iatrogenic (e.g. post central line or pacemaker insertion)
risk factors of pneumothorax
- Pre-existing lung disease
- Being tall and slim
- Smoking/cannabis
- Diving
- Trauma/chest procedure
- Other conditions e..g marfans
management of primary pneumo
- If symptomatic and rim of air >2cm on CXR give O2 and aspirate. If unsuccessful consider re-aspiration or intercostal drain. Remove drain after full re-expansion / cessation of air leak.
management of secondary pneumo
as above but lower threshold for ICD If persistent air leak >5 days (bronchopleural fistula) refer to thoracic surgeons
discharge advice after pneumothorax
no flying or diving until resolved
simple pneumothorax
- Tiny rim of air within pleural cavity that doesn’t impair haemodynamic stasis
tension pneumothorax
- Causes haemodynamic instability
- Hypotensive and tachycardic
- Caused by the one-way flow of air
- More and more air accumulating in pleural cavity
- Life threatening- quick intervention
- Causes e.g. trauma to the chest
primary vs secondary pneumo
Primary
- No underlying lung pathology
- Risk factors
- Male young
- Family history of pneumothorax
- Smoking (x9 risk)
Secondary
- Underlying lung pathology
- COPD
- Asthma
- Bronchiectasis – inc CF
- Lung cancer
- Infections: TB, pneumonia
- Marfans syndrome, Ehlers Danlos syndrome
- RA
Spontaneous vs iatrogenic vs traumatic pneumo
Spontaneous
- Disruption of the subpleural blebs/bulla (air filled sac)
Iatrogenic
- Insertion of central/pacing wires
- Esp internal jugular vein
Trauma
- Severe chest wall injury- stab wound or gunshot wound allows air to enter the pleural space
- Rib fractures puncture the visceral pleura
- May not be easily visible
presentation of tension pneumothorax
Symptoms
- Chest pain
- Pleuritic in nature
- Sudden onset
- Sharp pain
- +/- SOB
- History of trauma/liung disease
- Respiratory distress
- Cyanosis
- Tachycardia
- Marked hypoxemia
Signs
- Low BP
- Tachycardic
- Cyanotic
- Coma
- Trachea deviation
- Away from the affected side
- Chest movement
- Reduced on affected side
- Auscultation
- Reduced/ absent breath signs
- Will not have time to do percussion
(which would be hyper resonant on affected side)
or vocal/tactile resonance (which would be reduced
on affected side)
treatment if you suspect tension
if you suspect tension- do not wait to x-ray
Emergency needle decompression
- First site
- 2nd intercostal space, mid-clavicular line
- Just lateral to the nipple
- If first site doesn’t work
- 5th ICS
- Anterior axillary line, lateral to the nipple
- Remember to go over the rib to avoid the nerve, artery and vein bundle
symptoms of simple pneumothorax
-
Symptoms
- Chest pain
- Pleuritic in nature- sharp stabbing
- Sudden onset
- Sharp pain
- +/- SOB
- History of trauma/lung disease
- Chest pain
-
Signs
- Trachea deviation – usually normal, can push the trachea to the other side
- Chest movement reduced on affected side- collapsed lung
- Percussion
- Hyper resonant or resonant on affected side
- Auscultation
- Reduced or absent breath signs on affected side
- Vocal/tactile resonance
- Reduced on affected side
radiological finding of simple pneumo
- Left lung
- Absent lung markings
- Collapsed lung borders seen
management of simple pneumo
-
Conservative treatment
- Small pneumothorax
- Pt goes home
- Comes back to see if resolved
-
Pleural aspiration
- Needle in pleural cavity to drain air out
- 2.5l maximum
- Chest drain insertion
Chest drain insertion
- Under ultrasound guidance
- Safe triangle
- Superior: base of the axilla
- Inferior: 6th rib/5th intercostal space
- Anterior: lateral edge of pectoralis major muscle
- Posterior: lateral edge of latissimus dorsi muscle
pathophysiology of pleural effusion
In normal pleural cavity there is tightly controlled production and absorption of pleural fluid.
-
Excess fluid in the pleural cavity
- Imbalance between rate of production and absorption
simple effusion
when there is fluid in the pleural fluid- can be transudate or exudate
haemothorax
when the fluid is blood e.g. trauma
chylothorax
when the fluid is lymph e.g. leak from lymphatic duct
empyema
when the fluid is pus
examination for pleural effusion
- CXR
- ECG
- Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting
- ECHO (if suspect heart failure)
- Staging CT(with contrast) if suspect exudative cause
presenting symptoms and signs of pleural effusion
- SOB (gradual onset)
- Pleuritic chest pain – irritation of pleural lining to the fluid e.g. blood or lymph
- Features of clinical disease
- Congestive cardiac failure – pulmonary oedema
- Lung malignancy
signs of pleural effusion
- Tracheal deviation
- Away from the affected side
- Chest movement
- Reduced on affected side
- Percussion notes
- Stony dull on affected side
- Breath sounds
- (Vesicular) reduced/ absent on affected side
- Vocal resonance
- Reduced on affected side
radiological findings of pleural effusion
Criteria for PE
- Meniscus showing fluid in the pleural cavity (right base)
- Beneath the yellow line= fluid
- Loss of costophrenic angle
- Loss of left heart border
PE and tracheal deviation
If no tracheal deviation then pathology may be a mixture of atelectasis and effusion (pull + push = no deviation)
- Will need to do a bedside US to determine if fluid or collapse
Pleural effusion diagnosis
Ultrasound guided pleural aspiration
- Biochemistry (protein, pH, LDH)
- Cytology
- Microbiology (including AAFB)
N.B. Never insert a chest drain unless the diagnosis is well established (e.g. known metastatic lung cancer) otherwise draining all fluid off may hinder the opportunity to obtain pleural biopsies. Only indication for urgent chest drain insertion for a new effusion would be an underlying empyema (pH of pleural fluid <7.2 or visible pus on aspirate).
Consider Thoracoscopy or CT Pleural Biopsy
Causes of Transudate effusions (pleural protein <30 g/L)
Common:
- Heart failure
- Cirrhosis
- Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)
Less common:
- Hypothyroidism, mitral stenosis, pulmonary embolism
Rare:
- Constrictive pericarditis, superior vena cava obstruction, Meig’s syndrome
Causes of Exudate effusions (pleural protein >30 g/L)
Common:
- Malignancy
- Infections – parapneumonic, TB, HIV (kaposi’s)
Less common:
- Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease
Rare:
- Yellow nail syndrome, fungal infections, drugs
Interstitial library disease (ILD)
Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner including:
- Usual Interstitial Pneumonia (UIP)
- Non-specific Interstitial Pneumonia (NSIP)
- Extrinsic Allergic Alveolitis
- Sarcoidosis
- Several other conditions
- Important to take a comprehensive occupational / environmental history – inhalation can lead to conditions such as silicosis (dust), asbestosis (asbestos) or pneumoconioisis (coal workers)
diagnosis of ILD
- Typically restrictive lung diseases on PFT’s (above 70%)
- Harder to breath in than out
- Reduced DLCO due to thickening of the lung parenchhyme due to fibrosis
pathophysiology of ILD
- Lung compliance reduced
- Lungs are stiff and hard to expand
- Elastic recoil of lungs is increase, the resting lung volume is smaller than normal, but rate of airflow not impaired
- Restrictive type of ventilatory defect on spirometry
clinical symptoms of ILD
- Dry cough
- Dyspnoea (short of breath) on exertion progressing to at rest
- Fatigue
- Typically gradual, insidious progression Sx
clinical signs of ILD
- Decreased lung excursion on palpation
- Bi-basal end inspiratory lung crackles
- Finger clubbing small pleural effusions
Usual interstitial pneumonia (UIP)
Commonest type of pulmonary fibrosis usually idiopathic
Signs and symptoms
- SoB on activity
- Dry cough
- Reduced appetite
- Clubbing
- Reduced chest expectation
Examination
- Auscultation
- Fine inspiratory creptiations (VELCRO)- usually best heard in basal/ axillary areas
- Cardiovascular- features of pulmonary hypertension
Extrinsic Allergic Alveolitis
Also known as Hypersensitivity Pneumonitis
Background
Inhalation of organic antigen to which the individual has been sensitised
Clinical presentation
- ACUTE – short period from exposure, 4-8 hrs. Usually reversible: spontaneously settle 1-3 days. Can recur.
- CHRONIC – chronic exposure (months – years). Less reversible.
Common Drug causes:
- Amiodarone
- Bleomycin
- Methotrexate
- Nitrofurantoin
- Penicillamine
ILD Treatment Principles
Earlier treatment is started the better the outcomes
- Depends on underlying pathology
- Occupational exposure – remove
- Environmental exposure – remove (e.g. pet birds)
- Drug associated – avoid
- Stop smoking
- MDT approach – maybe suitable for specialist medications such as Pirfenidone to slow progression
- Treatment of infective exacerbations
- Oxygen if respiratory failure
- Palliative care
- Transplantation
sarcoidosis
- Multisystem inflammatory condition of unknown cause
- Non-caseating granulomas (Histology important)
- Immunological response
- Commonly involves Resp system BUT can affect nearly all organs
- 50% get spontaneous remission, others get progressive disease
investigations for sarcoidosis
- PFTs: (obstructive until) fibrosis
- CXR: 4 stages
- Bloods: renal function, ACE, Calcium
- Urinary Calcium
- Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI
- CT/MRI head: headaches – Neuro sarcoid
Lung cancer
- Lung Cancer is the biggest cause of cancer related death worldwide and in the UK
- 48,000 new cases / year in the UK
- 35,000 deaths / year in the UK
- Number of cases in women continue to rise
- 5 year survival approximately 16%
- 72% of LC in the UK caused by smoking
Lung Cancer Clinical Features / Presentations
Usually present late- higher risk of metastasis- poor outocmes
- general: weight loss, chronic cough, SoB
- Asymptomatic, incidental finding
- Any respiratory symptom/systemic deterioration
- Superior Vena Cava Obstruction
- Horner’s syndrome
- Metastatic disease – liver, adrenals (Addison’s), bone, pleural, CNS
- Paraneoplastic – clubbing, hypercalcaemia, anaemia, SIADH, Cushing’s syndrome, Lambert-Eaton myasthenic syndrome
- Increased risk of thrombo-embolic disease
signs of lung cancer
- Clubbing
- Enlarged lymph nodes
- Dysponea
- cachexia
RF for lung cancer
- Large number of smoking pack years
- Airflow obstruction
- Increasing age
- Family history of lung cancer
- Exposure to other carcinogens, e.g. asbestos
Investigations for lung cancer
MDT approach vital (Physicians, Oncologists, Surgeons, Radiologists, Pathologists, Palliative Care Team, Specialist Nurses, Primary Care)
- Bloods – FBC, U&E, Calcium, LFT’s, INR
- CXR
- Staging CT – Spiral CT Thorax and Upper Abdo – helps to stratify TNM stage
Histology options for lung cancer
*
- US guided neck node FNA for cytology if lymphadenopathy
- Bronchoscopy – endobronchial, transbronchial, endobronchial ultrasound (if mediastinal lymphadenopathy)
- CT Biopsy
- Thoracoscopy if pleural effusion present
PET Scan - lung cancer
- MDT Decision if patient is a surgical candidate and initial CT suggestive of low stage
- Helps to detect small metastases not seen on staging CT
TNM staging
Histological Classification
Classified primarily into two groups which account for about 95% of cases
- Small cell (oat cell) lung cancer (SCLC)
- Non-small cell lung cancer (NSCLC)
Includes squamous cell, adenocarcinoma- NON SMOKERS, and large cell carcinoma, bronchoalveolar cancer
Others -, bronchial gland ca, carcinoid tumour
Small Cell LC Treatment & Prognosis
- Rapid growth rate and almost always too extensive for surgery at time of diagnosis
- Mainstay of treatment is chemotherapy
- Also palliative radiotherapy
- Untreated – median survival is 8-16 weeks
- Combination chemotherapy – median survival 7- 15 months
Lung Cancer Treatment Summary
- Curative surgery for stages I & II – assuming fit for surgery
- Surgery & adjuvant chemotherapy clinical trial for stage IIIa – assuming fit for surgery & chemo
- Chemotherapy – consider in patients with stage III/IV disease and PS 0-2
- Radiotherapy – curative (CHART = continuous hyperfractionated accelerated radiotherapy) for people not fit for surgery OR palliative
- Palliative Care
- Do nothing / watch & wait
LC Metastasis commonly to:
- Liver
- Bone
- Brain
- Adrenal gland
- Pleura
Paraneoplastic syndromes associated with lung cancer
Small cell lung cancer
- Ectopic ACTH
- SIADH
- hyponatraemia
Squamous cell carcinoma
- Hypercalcaemia (PTH secreting hormones)
- Stones moans and groans)
Obstructive sleep apnoea
- Upper airway obstruction during sleep
- Clinical definition = upper airway narrowing, provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness
RF of OSA
- Male
- High BMI
- Undersized or set back mandible
Pathophysiology of OSA
- Upper airway patency depends on dilator muscle activity. All muscles relax during sleep (including pharyngeal dilators).
- Some narrowing of the upper airway is normal
- Excessive narrowing can be due to either an already small pharyngeal size during awake state which undergoes a normal degree of muscle relaxation during sleep causing critical narrowing OR excessive narrowing occurring with relaxation during sleep
Causes of small pharyngeal size
- Fatty infiltration of pharyngeal tissues and external pressure from increased neck fat and/or muscle bulk
- Large tonsils
- Craniofacial abnormalities
- Extra submucosal tissue, e.g. myxoedema
Causes of excessive narrowing of the airway during sleep
- Obesity may enhance residual muscle dilator action
- Neuromuscular disease with pharyngeal involvement may lead to greater loss of dilator muscle tone, e.g. stroke, MND, myotonic dystrophy
- Muscle relaxants – sedatives, alcohol
- Increasing age
Clinical Effects of sleep apnoea
- Severe OSA leads to repetitive upper airway collapse, with arousal required to re-activate the pharyngeal dilators. i.e. you have to wake uo
- There may be associated hypoxia and hypercapnia which are corrected during the inter-apnoeic hyperventilatory period.
- Chronic hypoxia can cause pulmonary hypertension e.g. cor pulmonale
- Recurrent arousals lead to highly fragmented and unrefreshing sleep – snoring and apnoea attacks often witnessed by partner
- Excessive daytime sleepiness results (Epworth Sleepiness Scale score >9)
- With every arousal there is a rise in BP, often over 50 mmHg. It is not clear if this damages the CVS. There is also a rise in daytime BP.
- Nocturia
- Less common - Nocturnal sweating, reduced libido, oesophageal reflux
Epworth Sleepiness Scale
used in sleep apnea diagnosis
Points for following:0=would never doze, 1=slight chance, 2=moderate chance, 3=high chance
- Sitting & reading
- Watching TV
- Sitting in a public place, e.g. theatre
- Passenger in a car for an hour
- Lying down to rest in the afternoon Sitting & talking
- Sitting quietly after lunch without alcohol In a car, while stopped in traffic
Diagnosis – Sleep Study – Types
- Overnight oximetry alone
- Limited sleep study – oximetry, snoring, body
movement, heart rate, oronasal flow, chest/abdominal movements, leg movements – usual study of choice
- Full polysomnography – limited study plus EEG, EMG
sleep apnoea management
Treatment is given based on symptoms/quality of life – NOT on severity seen on sleep study - Also consider livelihood, e.g. driving as occupation
SIMPLE APPROACHES:
Weight loss, sleep decubitus rather than supine, avoid/reduce evening alcohol intake
FOR SNORERS & MILD OSA:
- Mandibular advancement devices, consider pharyngeal surgery as last resort
FOR SIGNIFICANT OSA:
- Nasal CPAP, consider gastroplasty/bypass, and rarely tracheostomy
FOR SEVERE OSA & CO2 RETENTION:
- May require a period of NIV (non invasive ventilation) prior to CPAP if acidotic, but compensated CO2 may reverse with CPAP alone
Sleep apnoea and driving
- Do not drive while sleepy- stop and have a nap
- Should notify DVLA on diagnosis
- Doctors can advise to stop driving altogther
CPAP
- Usually given via nasal mask, but can use mouth/nose masks
- Upper airways splinted open with approximately 10cm H2O pressure – this prevents airways collapse, sleep fragmentation, and ultimately daytime somnelence
- Also opens collapsed alveoli and improves V/Q matching
