A 22-year-old with asthma

• ACUTE ( lasting 3 weeks or less)
• Acute viral upper respiratory tract infection (common cold): cough, sore throat, runny nose, headache, low-grade fever, sneezing, malaise and myalgia.
• Acute bronchitis: persistent productive cough, low grade fever, malaise, difficulty in breathing and wheezing.
• Acute rhinosinusitis: cough due to post-nasal drip, purulent nasal discharge, nasal obstruction, facial pain (pressure), ear fullness, dental pain, hyposmia (anosmia in some cases) and fatigue.
• Pertussis: paroxysmal intense coughing followed by forceful inspiration (whoop) and post tussive emesis, syncope or apnea. Fever, fatigue, runny nose and conjunctival injection.
• Acute exacerbation of COPD: productive cough(more sputum than normal), worsening dyspnea, fatigue. A history of cigarette smoking with more than 20 pack years should increase your suspicion.
• Allergic rhinitis: cough secondary to post-nasal drip, nasal congestion, sneezing, clear rhinorrhea, watery eyes and a history of exposure to allergic triggers.
• Asthma: dry cough (though production of small amounts of thick non-purulent sputum is common), breathlessness, wheezing and chest tightness. Symptoms worsen at night and when exposed to triggers.
• Congestive heart failure: cough (due to orthopnea), shortness of breath (exertional and positional – orthopnea), chest pain, exertional fatigue, paroxysmal nocturnal dyspnea, anorexia, lower limb swelling.
• Pneumonia: cough (dry or productive with purulent sputum), fever, chills, myalgia, malaise, dyspnea, dull note on percussion, crackles on auscultation, increased tactile fremitus.
• Aspiration: presence of risk factors such as neurological impairment, impaired swallowing, mechanical ventilation, patients with a nasogastric tube and tracheostomy, frequent high volume vomiting. Acute dyspnea, tachypnea, cough, low oxygen saturation, rhonchi and rales on auscultation or absent breath sounds if obstruction is complete.
• Pulmonary embolism: cough, hemoptysis, pleuritic chest pain, dyspnea as well as risk factors for venous thromboembolism such as surgery, trauma, long distance travel, pregnancy, oral contraceptives, malignancy, thrombophilia as well as a prior history of DVT.
• Inhaled foreign body: sudden onset of cough, dyspnea, choking, generalized wheezing, unilateral hyperinflation, common in young children.
• Tracheitis: insidious development of raw, retrosternal pain with cough in the setting of prodromal symptoms suggesting a upper viral respiratory tract infection.
• Laryngitis: dry cough, voice changes (raspy or hoarse), early vocal fatigue, throat pain. History of a previous upper respiratory illness.
• Tonsillitis: sore throat, fever, malaise, tender anterior cervical lymphadenopathy, odynophagia and dysphagia
• Pulmonary migraine – spastic narrowing of the lumen of the lobar bronchus leading to cough with a thick sputum, lower back pain radiating to the shoulder, chest pain, atelectasis, migraine headache, nausea and vomiting.
• NSAID hypersensitivity – history of taking aspirin and other NSAIDS. Acute exacerbation of bronchoconstriction in individuals with a history of asthma, nasal congestion.
• SUBACUTE (lasting 3 to 8 weeks)
• Post-infectious following a viral upper respiratory tract infection: presents similarly to upper viral respiratory tract infection.
• CHRONIC (lasting more than 8 weeks)
• Gastro-esophageal reflux disease: asthma and GERD often occur together. Cough**,** heart burn, acid regurgitation, chest pain. Symptoms commonly occur after meals and are triggered by exercise or lying in a recumbent position.
• Upper airway cough syndrome: longstanding post-nasal drip seen in allergic and non-allergic rhinitis, post-infectious rhinosinusitis causes chronic cough. Presents as above.
• Chronic bronchitis: productive cough of more than 3 months occurring within a span of 2 years, malaise, chest and abdominal pain from chronic coughing. History of exposure to inhaled irritants such as smoke
• Post-infectious cough: history of previous pulmonary infection
• Angiotensin-converting enzyme inhibitor intolerance
• Malignancy: Chronic cough, hemoptysis, unintentional weight loss, night sweats. Imaging will reveal a mass.
• Interstitial lung diseases: long term exposure to hazardous materials such as asbestos, silicone and coal dust. Gradual onset of dyspnea and cough as well as hemoptysis. Bibasilar crackles heard on auscultation.
• Obstructive sleep apnea: Loud snoring, cessation of breathing, gasping or choking and coughing while asleep and witnessed by a bed partner. Excessive daytime somnolence is a common complaint.
• Chronic sinusitis: Purulent nasal discharge, nasal obstruction, facial and dental pain/ fullness, hyposmia present for more than 12 weeks.
• Bronchiectasis: longstanding cough with excessive amounts of sputum produced as well as progressive dyspnea, intermittent wheezing, hemoptysis, pleuritic chest pain, and associated fatigue and weight loss. A history of repetitive pulmonary infections in the past.

• Details about duration
• Diurnal variation
• Relieving factors
• Aggravating factors
• Productive with sputum or nonproductive, if productive, what is the color of phlegm
• Cigarette smoking
• Use of angiotensin-converting enzyme inhibitors
• Weight loss
• Occupation
• Associated hemoptysis
• Associated fever
• Associated shortness of breath
• Presence of an upper respiratory tract infection at the onset of a cough

Respiratory causes

• Asthma
• COPD
• Pneumonia
• Pulmonary embolism
• Lung malignancy
• Pneumothorax: sudden onset of dyspnea, sharp pleuritic chest pain that radiates to ipsilateral shoulder. On examination: asymmetrical lung expansion, increased respiratory rate, decreased tactile fremitus, hyperresonant percussion note, decreased breath sounds. Mediastinal shift can be seen in tension pneumothorax.
• Aspiration
• Foreign body aspiration

Secondary spontaneous pneumothorax is associated with asthma.

Cardiovascular causes

• Congestive heart failure
• Pulmonary edema: progressively worsening dyspnea, tachypnea, crackles on auscultation, hypoxia
• Acute coronary syndrome: ischemic cardiac chest pain (central, radiating to jaw and arm, tight and choking in character, triggered by exertion and emotion, relieved by rest and nitrates), breathlessness.
• Pericardial tamponade: chest pain, palpitations, shortness of breath, or in more severe cases, dizziness, syncope, and altered mental status. On examination: Beck’s triad – hypotension, jugular venous distention and muffled heart sounds.
• Valvular heart defect: Angina type of chest pain, dyspnea, dizziness, fatigue, palpitations, lower limb edema and murmurs on heart auscultation.
• Pulmonary hypertension: worsening dyspnea on exertion, hemoptysis, fatigue, palpitations, dizziness, syncope. In severe cases, signs of right sided heart failure such as ascites, lower limb swelling, hepatomegaly, pallor, peripheral cyanosis are present. On examination: right sided S3 and S4 sounds.
• Cardiac arrhythmia: chest pain, dyspnea, palpitations, fatigue, syncope as well as concomitant findings on ECG.
• Superior vena cava obstruction: face/neck swelling, distended neck veins, cough, dyspnea, orthopnea, upper extremity swelling, distended chest vein collaterals, and conjunctival suffusion

Neuromuscular causes

• Chest trauma with fracture or flail chest: History of trauma, acute onset of dyspnea and chest pain. On examination: Asymmetrical chest expansion, tender chest.
• Massive obesity
• Kyphoscoliosis: uneven shoulders or hips, prominence of part of the spine or the scapula, uneven waist, change in gait, back pain and progressively worsening dyspnea.
• Central nervous system (CNS) or spinal cord dysfunction
• Phrenic nerve paralysis: shortness of breath, recurrent pneumonia, anxiety, insomnia, morning headache, excessive daytime somnolence, orthopnea, fatigue, and difficulty weaning from mechanical ventilation. On examination: decreased breath sounds on the affected side, dullness to percussion of the affected side of the chest and inward movement of the epigastrium during inspiration.
• Myopathy: motor impairment without involvement of sensation. Complaints of muscle weakness which interferes with daily activities such as walking, climbing stairs, rising from a chair.
• Peripheral neuropathy: numbness and paresthesias; pain, weakness, and loss of deep tendon reflexes.

Psychogenic causes

• Hyperventilation syndrome: Sudden onset of dyspnea, chest pain, dizziness, agitation, anxiety, bloating, carpopedal spasm, positive Chvostek and Trousseau signs (hypocapnia induces hypocalcemia)
• Vocal cord dysfunction: breathing difficulties (stridor), voice changes (hoarseness, vocal fatigue), intermittent wheezing (inspiratory monophonic wheeze), chronic cough, chest and throat tightness.

Other systemic causes

Epiglottitis: Sudden onset of dyspnea, muffled voice, drooling, dysphagia, distress. History of preceding URTI. In severe cases signs of respiratory distress such as intercostal or suprasternal retractions, tachypnea, and cyanosis may be seen.

Anemia: Fatigue, weakness, palpitations, breathlessness, chest pain, pica. On examination: pallor of the mucous membranes.

Metabolic acidosis: dyspnea, nausea, vomiting, chest pains, palpitations and general weakness. Specific symptoms pointing to certain etiologies: history of diarrhoea(loss of bicarbonate), alcohol intake, polyuria, polydipsia, epigastric pain (DKA) etc.

Thyrotoxicosis: weight loss, palpitations, heat intolerance, tremors, anxiety, dyspnea, sweating. Women present with oligomenorrhea or amenorrhea, men may present with gynecomastia.

Liver cirrhosis: dyspnea, ascites, jaundice, fatigue, weakness, gastrointestinal bleeding, nausea, vomiting, unintentional weight loss.

Anaphylaxis: difficulty breathing, hoarseness, wheezing, and stridor, cutaneous flushing and urticaria

Is it related to exertion? If yes, then to what extent?

Variability – are there good days and days where they are particularly affected. Does it worsen at any time of day?

Respiratory infections

Asthma

Chronic obstructive pulmonary disease (COPD)

Anaphylaxis

Congestive heart failure

Vocal cord dysfunction

Postnasal drip

Airway compression: Intrinsic or extrinsic (squamous cell carcinomas, goiter)

Tracheobronchomalacia

Foreign body inhalation

Does the patient notice any sounds coming from the chest?

Variability

• Asthma is a chronic inflammatory disorder of the airways that is defined by recurrent episodes of dyspnoea, cough, and wheezing together with reversible airflow obstruction
• Reversible, recurrent small airway inflammation
• Can occur with triggers or spontaneously
• In Kenya, it is estimated that 7.5% (about 4 million) of the population suffer from asthma with the majority either being improperly and inadequately managed or not treated at all.

• Bronchial muscle contraction
• Mucosal swelling/inflammation
• Increased mucus production
• Bronchial muscle contraction is triggered by a variety of stimuli. Loss of epithelial lining due to eosinophil and neutrophil action can cause activation of the autonomic nerves and reflex smooth muscle constriction to minimise mucosal compromise
• There is also a thickening of the smooth muscle layer in asthmatics
• Mast cell and basophil degranulation release inflammatory mediators that cause mucosal swelling and inflammation
• Angiogenesis and vasodilatation are increased in patients with asthma which drives the increase in mucous secretion
• Eosinophils may be responsible for the increased concentration in NO seen in expired air of asthmatics (and possible the vasodilatation)

• Increased airway smooth muscle
• Fibrosis
• Angiogenesis
• Mucus production

• Gender
• Atopy
• Airway hyperresponsiveness
• It has been found that in early years, asthma is more common in boys (particularly first born boys) while in adulthood it is more common in women
• Individuals with a positive skin prick test to common allergies are at increased risk of developing asthma
• Individuals who react to a small dose of bronchoconstrictors with a reduction in the FEV in one second by 20% are at an increased risk of developing asthma
• Both atopy and airway hyperresponsiveness may be genetically determined (heritable predisposition)

Asthma is a type 1 hypersensitivity reaction characterised by:

• Airway inflammation
• Episodic airway obstruction
• Bronchial hyper responsiveness – the hallmark of asthma

Airway inflammation takes the following path:

• Sensitization to the allergen with antigen presenting cells presenting the allergen to CD4 + T cells which differentiate to T helper 2 cells. Th2 cells release IL-4, IL-5, IL-13 leading to the production of IgE antibodies which bind to specific receptors on mast cells, activation of eosinophils and mucus hypersecretion respectively.
• Re-exposure to the allergen leads to the release of mast cell mediators
• Immediate response is due to the release of histamine, leukotrienes and prostaglandins which leads to smooth muscle contraction, increased mucus production, vascular permeability and dilation
• Late phase response is characterised by inflammatory cells such as eosinophils, neutrophils and Th2 cells furthering inflammation by releasing cytokines and intracellular components that sustain the inflammation even in the absence of the allergen.

The above process leads to narrowing of the airways.

Neutrophils are seen in severe asthma that is not responding to common anti-inflammatory medications.

Pathological changes in the airways seen in asthma

• Epithelial denudation and shedding
• Basement membrane thickening
• Airway smooth muscle hyperplasia and hypertrophy
• Increase in goblet cells and submucosal glands leading to mucus hypersecretion
• Vascular proliferation
• Submucosal edema
• Cellular infiltration

With increasing severity and prolonged inflammation, airway remodelling will lead to fibrosis of the bronchial wall and fixed narrowing. There will be reduced response of bronchodilators.

• Associated symptoms: intermittent dyspnoea, wheezing, cough (often nocturnal), sputum
• Precipitants e.g. cold air, exercise, emotions, allergens, infection, smoking, and passive smoking, pollution, NSAIDs, Beta-blockers
• Diurnal variation of symptoms
• Exercise and quantification of exercise tolerance
• Disturbed sleep (classified as nights per week)
• Acid reflux
• Other atopic diseases e.g. eczema, hay fever, allergy, family history
• Environment at home
• Occupation
• Days per week spent off work or school
• Asthma symptoms may vary over the day. A marked morning drop in peak flow is common and can precipitate a serious attack despite having normal peak flow at other times
• Disturbed sleep is a sign of severe asthma
• 40-60% of patients with asthma have reflux. Treating reflux improves spirometry but may not improve symptoms
• For the home environment ask about pets, carpets and how regularly they are cleaned, feather pillows or duvets, floor cushions, and other “soft” furnishings

• This is the progressive worsening of symptoms and reduction in lung function in an individual previously diagnosed with asthma
• Disease control is lost
• Asthma exacerbations are common, despite adherence to treatment guidelines

• Viral respiratory infections
• Exposure to allergens such as house dust, mites, pollen etc.
• Cold, dry air
• Exercise/sports
• Extremes in weather
• Heightened emotions
• Exposure to cigarette smoke
• Exposure to diesel exhaust fumes
• Air pollution
• NSAIDS
• Beta blockers
• Incorrect use of inhalers
• Non-compliance to treatment
• Sinusitis
• Poorly controlled underlying illnesses such as diabetes
• Pregnancy
• Hormonal factors – symptoms may worsen during perimenopause. Thought to be due to estrogen fluctuation
• NSAIDS inhibits COX-1, activating the lipoxygenase pathway leading to increased production of cysteinyl leukotrienes which cause bronchospasm.
• Beta blockers inhibit the beta 2 receptors in the airway leading to bronchoconstriction

• The most common trigger is a viral upper respiratory infection. Common viruses include: Rhinovirus, adenovirus, enterovirus and respiratory syncytial virus.
• It has been shown that allergic individuals express reduced IFN-α (The most important anti-viral response) hence are unable to mount a sufficient immune response. This causes prolonged inflammation leading to exacerbation of asthma symptoms.
• Viral infections weaken the body’s immune response to bacterial infections hence when infected, chronic inflammation ensues leading to an exacerbation
• Exposure to environmental triggers and air pollutants increase the risk of suffering an exacerbation

• Intrinsic asthma
• More likely to have concomitant nasal polyps and be aspirin-sensitive
• May also develop asthma later in life

• Exercise-induced asthma
• Typically begins after exercise has ended and resolves within 30 minutes
• Worse in cold and dry climate

• Bronchodilators cause relaxation of the lower esophageal sphincter

• Neutrophilic and eosinophilic
• Eosinophilic is more treatable, and most research has focused on nullifying the eosinophilic response
• Neutrophilic type is more difficult to treat, is more debilitating, and has a higher fatality since not many treatment options are aimed at it

• Th 2
• IL-4, -5, and -13
• TNF-a and IL-1b amplify the inflammatory response in severe disease
• IL-10 and -12 are anti-inflammatory and are deficient in asthmatics

• Not always. In asthmatic individuals, eosinophils accumulate in sputum causing a purulent appearance with no infection present.
• Sputum smear microscopy and culture can confirm infection

• No. Her asthma is NOT adequately managed
• Use the rules of twos to remember how to know if asthma is being adequately treated. Ask the patient whether:
• They have asthma symptoms or use their quick-relief inhaler more than TWO times a week.
• They awaken at night with asthma symptoms more than TWO times a month.
• They refill their quick-relief inhalers more than TWICE a year.
• There is any limitation in physical activity.

Mild persistent

Supportive evidence: Symptoms occur 3 to 4 times a week as evidenced by her inhaler use. She awoke 3 times in the past night. She uses her inhaler 4 times a week but not more than once a day. There is minor limitation of her normal activity since she is still able to perform her duties as a teacher and chores at home.

• Also known as an orthopneic position.
• One sits or stands leaning forward and supports the upper body with hands on the knees or on another surface.
• Adopted by individuals experiencing respiratory distress
• Our patient has adopted this position as seen above hence is in respiratory distress

• Her airway is narrowed meaning she needs extra assistance to draw in air against this obstruction. At this stage of examination we can only see her sternocleidomastoid muscles being used.

• Sternocleidomastoid muscles which lift the sternum
• Trapezius and scalene muscles which lift the shoulder girdle
• Pectoralis major and minor which pull the ribs outwards
• External intercostal muscles which pull the ribs outwards
• Latissimus dorsi, serratus anterior and posterior muscles also play a role

• Abdominal muscles
• Internal intercostal muscles

• A change in voice quality to hoarse would alert you to vocal cord dysfunction while a muffled voice would point you towards epiglottitis.
• As such we have tentatively ruled out vocal cord dysfunction and epiglottitis as causes of her dyspnea and wheeze

A change in gait would alert you to the possibility of chest wall deformities such as kyphoscoliosis.

A decrease in chest wall compliance as seen in kyphoscoliosis restricts the chest wall leading to hypoventilation.

Further examination of her chest would be required to rule it out completely.

Massive obesity is a cause for dyspnea hence we have now ruled it out.

Under-weight: <18.5 kg/m2

Healthy weight range: 18.5 – 24.9 kg/m2

Overweight range: 25.0 – 29.9 kg/m2

Obese range: > 30.0 kg/m2

• Ask the patient to appose their fingers such that each fingernail lies against the other.
• Obliteration of Schamroth’s window identifies clubbing.
• Flattening of the Lovibond angle is diagnostic of clubbing.
• Schamroth’s window is a diamond shaped opening found at base of the nail beds when the dorsum of 2 fingers from the opposite hands are opposed.
• Lovibond angle is the angle made by the proximal nail fold and nail plate. It is typically less than or equal to 160 degrees. An angle between 160-180° may indicate early stages of clubbing. Anything more than 180 degrees indicates definitive clubbing.

Grade 1: Fluctuation and softening of the nail bed

Grade 2: Obliteration of the lovibond angle

Grade 3: Accentuated convexity of the nail

Grade 4: Fingertips develop a clubbed appearence. Drumstick appearance

Grade 5: Nail and surrounding skin develops a glossy change with longitudinal striations of the nail.

Carcinoma of the bronchus

Pulmonary fibrosis

Bronchiectasis

Lung abscess

Pleural empyema

Direct effect of prolonged use of high dose beta-agonists (in this case her rescue inhalers) on the skeletal muscle.

Also known as flapping tremor, it indicates an inability to maintain a sustained posture of muscle contraction causing short lapses during a sustained posture.

It commonly presents bilaterally and in the upper limbs however it is possible to have it occur unilaterally and in the lower limbs, trunk, face and tongue.

Upper limb

• Ask the patient to extend their arms and dorsiflex their wrists while extending their fingers all the while with their eyes closed.
• A brief flap (flexion of the wrist) indicates presence of asterixis.

To increase sensitivity of the test; gently push back the patient’s fingers (enhanced dorsiflexion)

Lower limb

• Ask them to dorsiflex their ankle; a flap at the ankle joint or a quick lowering of the leg indicates a positive asterixis.

• Ask the patient to lie down and lift their leg by flexing at the hip joint and extending the knee.

Metabolic encephalopathy

• Hepatic encephalopathy (decompensated liver disease)
• Uremic encephalopathy (renal failure)
• Carbon dioxide retention in lung disease

Electrolyte abnormalities

• Hypokalemia
• Hypomagnesemia

Medication side effects

• Antiepileptics – valproate, carbamazepine, phenytoin, gabapentin
• Antipsychotics – clozapine
• Antibiotics – cefepime

Brain lesions

• Stroke
• Tumors
• Encephalitis

The most common lesion site is the thalamus

Cardiac arrythmia

Congestive heart failure

Valvular heart defects

Pulmonary hypertension

Pericardial tamponade

In individuals using the sternocleidomastoid as an accessory muscle of respiration it may be difficult to see the internal jugular vein as it lies underneath the active muscle

Position the patient in a semi-recumbent position. Ensure they are comfortable and that the room is well lit.

Ask the patient to turn to the left so you have a clear view of the right side of the neck

Look for the internal jugular vein from the medial end of the clavicle up to the right ear lobe. Make sure you can see a pulsation.

Look for the highest point of pulsation

Extend a card or ruler horizontally from highest pulsation point, cross with ruler placed on the sternal angle (Angle of Louis)

Add 5 cm to the measurement and then report the JVP as centimetres of water

Normal JVP ranges from 6-8 cm H2O

We add 5cm to the value we get because the sternal angle of Louis lies 5cm above the right atrium. Measurement of the JVP ,at the end of day, is an attempt to estimate the central venous pressures and by extension the right atrial pressure.

Venous pulses have a double waveform pulsation (2 pulses) while arteries have a single waveform pulsation.

Venous pulses sink in when the patient inspires (changes associated with respiration)

The internal jugular venous pulse is not easily palpated unlike the carotid artery

Positive hepatojugular reflex

Right-sided heart failure caused by pulmonary hypertension

Tension pneumothorax

Large pulmonary embolism

Constrictive pericarditis – JVP increases with inspiration (Kussmaul’s sign)

Cardiac tamponade

Fluid overload – renal disease

Superior vena cava obstruction

Tumors found at the apex of the lung compress the cervical sympathetic chain leading to unilateral ptosis, pupillary constriction and anhydrosis on the affected side (Horner’s syndrome)

It is a sign of prolonged steroid inhaler use

Superior venous obstruction

She is tachypneic

Poor oxygen saturation

Elevated pulse

Normal respiratory rate for an adult ranges from 12 to 18 breaths per minute

Normal pulse rate ranges from 60-100

Normal oxygen saturation ranges from 95% to 100%

This is a drop in the systolic pressures exceeding 10 mm Hg during inspiration.

A drop in systolic pressure during inspiration is normal due to reduced preload in the left ventricle.

Conditions that increase intrathoracic and pericardial pressures (thus reducing left ventricular preload) such as cardiac tamponade, constrictive pericarditis, COPD, asthma and tension pneumothorax lead to an exaggerated drop in systolic BP during inspiration.

Moderately severe episode.

Supportive evidence: Breathless while talking, adopts a sitting position, respiratory rate is increased, accessory muscles are activated, heart rate is 100-120bpm pulsus paradoxus is present, oxygen saturation is between is below 95% but above 91%.

Central

• Thoracotomy – indicates removal of a piece (lobectomy) or the whole lung (pneumonectomy)
• Sternotomy
• Tracheostomy

Clavicular

• Pacemaker placement

Mid-axillary or posteriorly

• Intercostal drain insertion
• Biopsy or video assisted thoracoscopic surgery

Lateral chest wall (ask patient to raise arm)

• Lateral thoracotomy

Kyphosis

Scoliosis

Pectus Excavatum

Pectus Carinatum

Sternal clefts

Ectopia cordis

If movement is symmetrically reduced then it must be due to a condition that restricts lung elasticity

If movement seems to be diminished on one side; that is where the pathology is present.

Severe upper airway obstruction

• Cervical lymph nodes
• Examine with the patient sitting; from behind gently feel for the submental, submandibular, pre-auricular, tonsillar supraclavicular and deep cervical lymoh nodes (anterior triangle of the neck)
• From the front of the patient; gently palpate for the posterior auricular and occipital lymph nodes.
• Axillary lymph nodes
• Lift the patient’s arm with yours as you palpate the apex, medial, anterior and posterior walls of the axilla
• Note for size, site, tenderness, consistency, attachment to surrounding structures.
• Other sites to check include; inguinal and popliteal region.

Acute infection

Tuberculosis

HIV

Lymphoma

Metastatic cancer

Systemic inflammatory disorders

Place your second and fourth fingers onto the patient’s sternal notches and use your third finger to feel for the trachea’s position (should be central)

Dip your finger into the spaces beside the trachea. They should be equal in size.

Contralateral deviation

• Pleural effusion
• Pneumothorax

Ipsilateral deviation

• Lung fibrosis
• Lung collapse

Solid masses such as lung cancer can cause deviation

If the cardiac impulse is the only one deviated consider diseases of the vertebral column such as scoliosis and left or right ventricular enlargement.

Facing the patient; place your each hand on either side of the upper anterior chest wall with your thumbs meeting in the midline.

Ask the patient to take a deep breath in; each thumb should move an equal distance from the midline.

Repeat in the lower chest wall anteriorly

Symmetrically reduced

• Pulmonary fibrosis

Asymmetrically reduced

Pleural effusion

Place your palm over different area of the chest wall while asking the patient to repeat a phrase such as ninety nine.

Place the middle finger of your non-dominant hand flatly and firmly over the patient’s chest in an intercostal space, parallel with the ribs.

Strike the distal interphalangeal joint of your middle finger with the tip of your opposite right finger.

Compare each percussion note, as you work your way down the chest wall, with either side.

Pneumothorax

Emphysema

Acute asthma exacerbation

COPD

Lung consolidation

Lung collapse

Pleural effusion (stony dullness)

Use of the stethoscope

• Ensure the ear pieces are aligned with your auditory canals.
• Use the diaphragm of the stethoscope as its larger surface area is better equipped at picking up the quiet breath sounds.

When auscultating a hairy chest, use the bell of the stethoscope as movement of hair against the diaphragm can be easily mistaken for crackles.

Instructions to the patient

• Ask the patient to relax and take repeated, slow, deep breaths through an open mouth

Examination sequence

Auscultate the anterior chest wall; top to bottom making sure to compare the right side from the left.

Wheeze

Normal vesicular breath sounds

Normal bronchial breath sound

Stridor

Friction rub

Airway narrowing

Extensive loss of lung tissue such as in emphysema

Intervening pleural medium (such as pleural membrane thickening or fluid in the pleural space)

Consolidation

Breath sounds are transmitted better in airless medium (sound travels more efficiently through solids)

Localised narrowing of an airway by a foreign body or tumor

Widespread, polyphonic wheezes are heard in diffuse airway obstruction (COPD and asthma)

Stridor – seen in localised narrowing of the large airways

Crackles – associated with pulmonary edema, pulmonary fibrosis, cardiac failure

Pleural rub – seen in pleural inflammation

Stridor is higher pitched than wheezes

Wheezes are more musical sounding

Consolidation

Pleural effusion

Obesity

Pneumothorax

Hemothorax

Emphysema

Asking the patient to whisper words (such as one, two, three) then listening with a stethoscope

Consolidation causes the words to be heard very clearly (louder than normal)

Tachycardia

Tachypnoea

Nasal flaring

Purse lip breathing

Tracheal tug

Accessory muscle use

Intercostal retractions

Paradoxical breathing

Subcostal muscle use

Hyperinflation and hyper resonance

Severe dyspnoea (use of accessory muscles)

No lung sounds

Hyperresonance

This is a medical emergency

Mild episodes

• Breathless after walking a short distance
• Respiratory rate is increased however accessory muscles of respiration are not in use
• Heart rate is below 100 bpm
• Pulsus paradoxus is not present
• Oxygen saturation is greater than 95%
• Auscultation of the chest will show wheezing

Moderately severe episode

• Breathless while talking
• Adopts a sitting position
• Respiratory rate is increased, accessory muscles are activated
• Heart rate is 100-120bpm
• Pulsus paradoxus may be present (10-29mmHg)
• Oxygen saturation is between 91-95%
• Auscultation will reveal loud wheezing, end expiratory.

Severe episodes

• Breathless even while at rest
• Agitated and sit upright (take the tripod stand)
• Respiratory rate greater than 30 breaths per minute, accessory muscles are used (suprasternal retraction is seen)
• Heart rate is greater than 120bpm
• Pulsus paradoxus is present (20-40mmHg)
• Oxygen saturation is less than 91%
• Auscultation reveals loud inspiratory and expiratory wheezes

Imminent respiratory arrest

• Absent wheezing and almost no breath sounds on auscultation

• Patient struggles for air (I can’t breathe)

• Somnolence and patient lies down

• Reduced respiratory rate – shallow and slow breaths

• Bradycardia – sign of severe hypoxemia

• Pulsus paradoxus absent

• Diaphoresis

• Falling oxygen saturation

Acute infective exacerbation of bronchial asthma complicated with type 1 respiratory failure.

According to severity; Moderately persistent.

Pulmonary function tests

Spirometry before and after an inhaled bronchodilator

Reversal of airway obstruction suggests asthma

Partial or non-reversal suggests COPD

Asthma is also inducible with methacholine (methacholine challenge) which drops the FEV1/FVC

Marked decrease in flow and volume

Increases to 2.5 times that of normal

Due to airway narrowing (bronchoconstriction)

It increases

There is air-trapping

Carbon monoidoide diffusing capacity (DLCO) measures the lung’s ability to transfer gas in the blood.

Low DLCO is seen in alveolar damage (emphysema), pulmonary fibrosis, pulmonary congestion (CCF), reduced flow (pulmonary embolism), reduced carrying capacity (anaemia), obesity, myasthenia gravis

High DLOC is seen in hyperventilation (asthma), pulmonary hemorrhage (a lot of gas in the hemorrhaged blood) and polycythemia (increased carrying capacity)

This is a syndrome in which the respiratory system is unable to maintain normal arterial oxygen and carbon dioxide levels due to a failure of pulmonary gaseous exchange.

May be classified into hypoxemic (type 1) or hypercapnic (type 2), acute or chronic

Hypoxemic respiratory failure

Characterised by low PaO2 (<60 mmHg) and normal/low PaCO2

Seen in conditions where there is local impairment of ventilation e.g. pulmonary oedema, pneumonia, lobar collapse, pneumothorax, ARDS, COPD, pulmonary fibrosis, right-to-left shung, kyphoscoliosis, obesity

Poor ventilation to a region of the lung result in hypoxia and hypercapnia at first.

The lungs compensate by increasing ventilation to healthy regions, which increasing carbon dioxide excretion but hypoxia persists as the hemoglobin flowing through these healthy regions are fully saturated with oxygen. This results in hypoxia with normocapnia.

Treated with a high concentration of oxygen (40-60%) by mask to reduce hypoxia.

Hypercapnic respiratory failure

Characterised by PaCO2 of >50mmHg (> 6.0 kPa) and hypoxia (PaO2 < 8kPa)

Seen in conditions where there is reduced total ventilation of the lungs e.g. acute asthma exacerbation, emphysema, upper airway obstruction, flail chest, kyphoscoliosis, muscular dystrophy, tension pneumothorax, narcotic overdose, polyneuropathy, myasthenia gravis

This is an emergency that requires high oxygen concentration (60%) as the underlying cause is investigated

Increased work performed by respiratory muscles

Hypoxemia

Repeated treatment with beta-2 agonists (Salbutamol-induced lactic acidosis)

In this patient, note the increase in lactate levels when salbutamol therapy was started and how it reduced when it was stopped. This leads us to believe that salbutamol played a role in the development of lactic acidosis – Salbutamol induced lactic acidosis

This is an extreme form of an asthma exacerbation that is characterized by hypoxemia, hypercapnia, and respiratory failure

It responds poorly to therapy

Patients are usually tachycardic, tachypnoeic, and conversationally dyspnoeic

In severe cases, auscultation may not reveal a wheeze due to serious airflow impairment

Pulsus paradoxus on inspiration is present

History of past near-fatal asthma exacerbation with endotracheal intubation being required

Recurrent hospitalisations due to asthma exacerbations

Altered mental state and sleep deprivation

History of coronary artery disease

Non adherence to controller medication

Forced Expiratory Volumes (FEV) using spirometry

Peak Expiratory Airflow (PEF) using a Peak Expiratory Flow Meter

Low

Due to hyperventilation in response to mild hypoxia

Impending respiratory failure is predicted when PaCO2 is normal

> 12% increase or > 200mL increase

Poor adherence to medication

Poor inhaler use

Poor environmental control

4 puffs of reliever

Wait 4 minutes

4 puffs again

If still not breathing normally, call an ambulance and give 4 puffs every 4 minutes until ambulance arrives

4 puffs of reliver, if usng a spacer, 4 breaths from the spacer

Controller medication

Inhaled corticosteroids such as budesonide, beclomethasone

Long acting beta 2 agonists such as salmeterol

Reliever medication – short acting beta 2 agonists such as salbutamol and short acting muscarinic antagonists such as ipratropium bromide

Add-on medications

Long acting muscarinic antagonists

Leukotriene receptor antagonists

Oral steroids

Biological therapies

Rapid alleviation of hypoxia

Relieve airway obstruction

Prevent worsening

Prevent relapse

Restore lung function to normal or previous best

STEP ONE – infrequent symptoms(less than twice a month)

• Controller: Non-pharmacological e.g trigger avoidance
• Reliever: As needed ICS -Formoterol OR low dose SABA – ICS as needed

STEP 2 – Twice a month or more but not on most days

• Controller: Non-pharmacological e.g trigger avoidance OR add regular low dose ICS.
• Reliever: Low dose ICS-Formoterol (if not on regular ICS) OR SABA-ICS if on daily ICS as needed

STEP 3 – Most days or waking with asthma once a week or more

• Controller: Regular low dose ICS + Formoterol OR regular low dose ICS + LABA
• Reliever: As needed low dose ICS-Formoterol(If on regular ICS-Formoterol) OR as needed inhaled SABA-ICS(if on daily ICS +LABA)
• Refer to specialist

STEP 4 – Most days or waking with asthma once a week or more and low lung function. Acute asthma at diagnosis

• Controller: Regular medium dose ICS + Formoterol OR Regular medium dose or high dose ICS + LABA. May require short courses of oral corticosteroids
• Reliever: As needed low dose ICS – Formoterol (If on regular ICS+Formoterol) OR As needed inhaled SABA-ICS if on daily ICS+LABA

STEP 5 – Most days or waking with asthma once a week or more and low lung function. Acute asthma at diagnosis.

• Long acting muscarinic antagonist should be added onto Step 4 therapy.
• Substitution of the maintenance therapy from medium dose ICS to a high dose ICS
• Referral to a pulmonologist

STEP UP OR DOWN BASED ON ASSESSMENT

Age older than 40 years

Cigarette smoking with more than 20 pack years

FEV1 of 40-69%

What was the usual level of control?

Was the patient on appropriate therapy?

Was the patient adherent to therapy?

Was the inhaler technique correct?

Are there trigger factors that the patient may be going back to?

Was the patient being monitored adequately?

Hypoxia

Oxygen administration should commence to keep oxygen saturation close to 95%:

• Mild to moderate – oxygen via nasal cannula or a mask
• Severe – mechanical ventilation

Airway obstruction

Rapid dilation of the airways by giving bronchodilators should follow:

• Beta adrenoceptor agonists
• Anti-cholinergics
• Theophyllines
• Magnesium sulphate

A step-wise approach according to severity is advised.

In mild to moderate cases – inhaled SABA through the pMDI and spacer (Severe cases require nebulization)

Assess response to treatment after 15-30 minutes according to severity and repeat drug administration every 15-30 minutes till a response is obtained

Add a short acting muscarinic antagonist such as Ipratroprium if inhaled SABA is insufficient

If the patient does not respond to the inhaled SABA and anticholinergics then commence intravenous aminophylline

Adrenaline is reserved for patients who do not respond to the inhaled bronchodilators and intravenous aminophylline

Intravenous magnesium sulphate is adjuvant therapy for for unusual cases not responding to treatment

Oral steroids as at a dose of 0.5 – 1.0mg/kg for all patients suffering an asthma exacerbation for about 5 days or at least 2 days after the attack has resolved

Theophylline, cromolyn sodium, LTRAs, omalizumab and salmeterol are not effective in the management of acute asthma exacerbation

Cromolyn sodium and nedocromil are best used for extrinsic allergies

Oxygen

Albuterol/ipatropium nebulizer

Don’t waste time getting PFTs

PFTs can be ordered once the patient is stable or as outpatient

Endotracheal intubation

Decreased breath sounds, absent wheezing, declining mental status, hypoxia

Poor response to albuterol/ipatropium nebulizer, IV steroids, and Magnesium

Normal or elevated PaCO2 suggests impending Type 2 respiratory failure (inability to meet increased respiratory demands due to muscle fatigue → cannot blow out CO2)

Glucocorticoid-induced psychosis

Inflammation

Bronchoconstriction

All patients

LTRA (Montelukast)

Zileuton

Theophylline

LTRAs have fewer side effect

Any time

Cromolyn sodium

Nedocromil too

Thus prevents the release of histamine

Inhaled Corticosteroid

LABA without ICS increases mortality

Never use a LABA first or without ICS

SABA PRN

SABA PRN + low-dose ICS

SABA + low-dose ICS + LABA

SABA + medium- or high-dose ICS + LABA

If the patient has persistent symptoms despite adherence

If the patient uses SABA > 2 days per week for symptom relef

If there are any other comorbidities

If symptoms are controlled for ≥ 3 months

Whenever possible…

If the patient has symptoms (uses SABA) more than twice a week

Dysphonia

Oral candidiasis

Churg-Strauss Syndrome

Osteoporosis

Cataracts

Adrenal suppression

Fat redistribustion

Hyperlipidemia

Hyperglycemia

Acne

Hirsutism

Thinning of the skin/easy bruising

Striae

Mood swings

Influenza

Pneumococcal

Oxygen until SpO2 > 90%

Salbutamol/Ipatropium nebulizer q 20 x 3

IV or PO Corticosteroids

Continue the patient’s scheduled home medication (do not stop chronic asthma management during status asthmaticus)

Observe for 3 hours before deciding on the next step

If oxygen, duoneb and corticosteroids fail, give racemic, nebulised adrenaline or SQ adrenaline

Adrenaline is not any more effective than Salbutamol and has more systemic side effects

Magnesium helps to relieve bronchospasm and is only used in acute severe asthma exacerbation that does not respond to several rounds of albuterol while waiting for steroids to take effect

Peak expiratory flow rate (PEFR) and Physical exam

PEFR is based on height and age (not weight) and is an acute approximation of FVC

If PEFR > 70% of the patient’s max PEFR and there are no signs and symptoms the patient can be discharged home

If PEFR 50-70% of the patient’s max PEFR and there are mild/moderate signs and symptoms the patient is admitted

If PEFR < 50% of the patient’s max PEFR and there are severe signs and symptoms the patient is intubated and admitted to the ICU

The patient is also admitted to the ICU if PaCO2 > 42 mmHg (Type 2 respiratory failure)

Intubation

Continues nebuliser treatment

IV high-dose steroids

ECMO if indicated