Basal Cell Carcinoma (BCC) is a slow-growing locally invasive malignant tumour (malignant skin ulcer) arising from basal epidermis and hair follicles – hence affecting the pilosebaceous skin!
90% of the lesions are found on the face above a line from the lobe of the ear to the corner of the mouth.
It rarely metastasize.
Micrograph of a BCC, showing the characteristic histomorphologic features
By Nephron – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=22082605
First of all, one should understand the difference between the fat embolism and fat embolism syndrome (FES).
Presence of fat globules in pulmonary and peripheral circulation usually following a long bone fracture or major trauma.
A serious consequence of fat embolism producing a distinct pattern of symptoms and signs.
Following trauma, fat cells in the bone marrow enter into damaged veins and venous sinusoids → reach femoral vein and IVC → reach the pulmonary circulation → obstruct pulmonary capillaries → interstitial haemorrhages and oedema → alveolar collapse → reactive hypoxaemic vasoconstriction → pulmonary symptoms.
Some fat cells reach the systemic circulation through the patent foramen ovale → neurological and dermatological manifestations.
Fat globules in the plasma are broken down to FFA by the trauma-related hormonal mechanism → FFA intermediaries form (chylomicrons, VLDL etc.) → CRP causes chylomicrons to coalesce → larger chylomicrons go and obstruct capillaries as above.
When they go and obstruct pulmonary capillaries, FFA induce capillary endothelial damage → ARDS.
The same may happen to cerebral circulation → encephalopathy and neurological deﬁcit.
Sometimes, the capillaries of skin is obstructed, conjunctiva and oral mucosa get obstructed → thin walled capillaries rupture → petechiae.
Fat globules are proinﬂammatory and prothrombotic → they cause the generation of thrombin and ﬁbrin, platelet aggregation, consumption of coagulative factors → thrombocytopaenia, anaemia and DIC.
Since it takes time for this pathological process to occur, symptoms and signs appear within 24-72 hours of the primary injury.
At least 1 major and 4 minor should be present to the diagnosis of fat embolim syndrome.
Urine, sputum, serum (specially pulmonary arterial wedge blood sample) – fat globules
Auscultation for heart sounds is mainly done in 4 areas, namely Mitral, Tricuspid, Aortic & Pulmonic. Remember these areas do not correspond to the location of heart valves, but the areas where the cardiac sounds are best heard. Some cardiac sounds can be heard with the unaided ear (e.g. Prosthetic valve clicks).
Use your stethoscope for cardiac auscultation. Apart from the 3rd and 4th heart sounds and the mid-diastolic murmur of Mitral Stenosis, all the other heart sounds are best heard with the diaphragm of your stethoscope. You should firmly press your “diaphragm” to chest wall whereas apply only light pressure when you are auscultating with the “bell” of your stethoscope.
There is no standard order for auscultation. But starting from Apex and proceeding with Tricuspid (LLSB), Aortic & Pulmonic areas is easy to practice.
You should first concentrate only on “heart sounds” (carefully assess their intensity & splitting). Then auscultate for “added sounds” (Murmurs, Clicks, Opening Snaps & Pericardial rubs). If you hear a murmur, completely assess it with regards to its timing, duration, location, intensity, pitch, character, radiation, change with position and respiration.
Murmurs are caused by the blood flow across the valve (either from increased blood flow or defective valve).
It refers to the timing of the murmur in relation to the cardiac cycle.
It refers to the length of the murmur in relation to the phase of the cardiac cycle.
It refers to the location of the precordium where the murmur is best heard.
It refers to the loudness of the murmur and graded according to the Levine scale 1-6.
The shape refers to the change of intensity of the murmur over time as seen in phonocardiograms.
It refers to where the sound of the murmur radiates from the main location of it. As a rule of thumb, the murmur radiates in the direction of the blood flow.
It can be low, medium or high pitches. Depending on the pitch you select the chestpeice of the stethoscope you place to hear the murmur best.
It refers to unusual characteristics of the murmur which makes it unique in quality.
Right-sided murmurs are louder in inspiration (due to increased venous return) and left side murmurs are louder in expiration.
Some murmurs are best heard using some maneuvers which should be performed when you auscultate.
Usually, the opening of cardiac valves does not make any sound. Opening snap occurs due to forceful “Opening” of a stenosed valve and it is described in Mitral stenosis (Refer MS). Hence it is always pathological. It is a high-pitched sound that occurs after S2.
The pericardial rub is a pathognomic physical sign of Pericarditis. It is characterized by a “scratchy or grating” sound best appreciated along the sternal border with respiration suspended and the patient leading forward.
Pleural Effusion is one of the commonest (if not the commonest), respiratory short cases you would get at the undergraduate level. The clinical findings are usually prominent and well defined in patients with Pleural effusions.
Reduced chest expansion, reduced vocal fremitus, stony dull to percussion, absent breath sounds and bronchial breathing above the effusion is very classical of a pleural effusion.
Always try to figure the out possible aetiology for the pleural effusion. Unilateral large effusions are usually caused by underlying malignancies (Lung CA, Breast CA, Lymphoma) or maybe even Dengue hemorrhagic fever.
Bilateral mild effusions are usually caused by organ failures (Cardiac failure, Liver failure, Renal failure) & hypoalbuminaemia. Rheumatological diseases can also cause pleural effusions.
Pleural effusion is a pretty straightforward diagnosis with the characteristic clinical findings you would get in your chest examination. But finding the aetiology for the effusion should be done in your General Examination.
So, after completing your chest examination, you may come back to your General Examination in order to make sure you did not miss anything which would be suggestive of the primary pathology causing the pleural effusion.
This average build middle-aged patient is breathless at rest. There is no finger clubbing or tar staining. There is cervical, axillary lymphadenopathy and the epitrochlear node is palpable indicative of generalized lymphadenopathy. There are no features suggestive of CLCD or Rheumatological disease and there is no ankle oedema.
There are no surgical scars, aspiration marks or radiotherapy marks. There is reduced chest expansion on the right side. The vocal fremitus and the vocal resonance on the right lower zone are reduced where the percussion note is stony dull up to the mid zone. Trachea is slightly deviated to the left side. Breath sounds are markedly diminished over the right lower zone and Bronchial breathing is heard in the right upper zone.
So, my clinical findings are compatible with a Right side moderate pleural effusion, possibly due to underlying malignancy. Lymphoma is more likely than a Lung malignancy and I would like to examine for hepatosplenomegaly.
1. Lung Collapse 2. Lung Consolidation (Pneumonia, Pulmonary Infarction) 3. Pleural Thickening 4. Lower Lobectomy 5. Raised Hemidiaphragm
Using Tidal Percussion.
1. Pleural Effusion – stony dull, absent breath sounds, trachea may be deviated to the opposite side (in large effusions). 2. Lung Collapse – dull, absent breath sounds, trachea deviated to the same side 3. Lung Consolidation – increased vocal resonance, trachea not deviated, bronchial breathing, crepitations 4. Pleural Thickening – breath sounds heard, trachea not deviated. 5. Lobectomy – surgical scar, absent breath sounds
1. Exudate Effusion. 2. Transudate Effusion.
Analyzing pleural fluid protein level. When proteins < 30 g/L – “Transudate”. When proteins > 30 g/L – “Exudate”.
1. Cardiac Failure 2. Liver Failure 3. Renal Failure 4. Hypothyroidism 5. Nephrotic Syndrome (Hypoalbuminemia)
1. Neoplasia – Bronchial CA, Mesothelioma, Lung Secondaries, Lymphoma 2. Connective tissue disorders – SLE, RA 3. Infections – Pneumonia, Tuberculosis 4. Drugs – Methotrexate, Bromocriptine 5. Other – Asbestosis, Oesophageal rupture, Chylothorax, Yellow nail syndrome
1. Chest X-ray / USS Chest 2. Pleural fluid analysis 3. Blood Investigations – FBC, ESR, CRP, LFT, U&E, LDH, TSH, Rheumatoid factor 4. ABG (Arterial Blood Gas)
1. Pleural Biopsy 2. CECT Chest 3. Bronchoscopy
1. Lateral decubitus X-ray 2. Ultrasound Chest
1. Detect smaller effusions 2. Detect loculated effusions 3. Guided aspiration of pleural fluid & pleural biopsy 4. Differentiate pleural thickening from effusions
• pH – 7.6 to 7.64 • Proteins < 1-2g/L • WBC < 1000/mm3 • LDH < 50% of Plasma • Glucose = Plasma Glucose level
1. Pleural fluid full report 2. Culture & ABST 3. Gram staining 4. Pleural fluid LDH 5. Pleural fluid cytology 6. Pleural fluid ADA (if TB is highly suspected) 7. Pleural fluid pH (if Empyema is suspected)
Post aspiration Chest X-ray.
2 out of 3 of the following, 1. Pleural fluid protein: Serum protein > 0.5 2. Pleural fluid LDH: Serum LDH > 0.6 3. Pleural fluid LDH > 2/3 of upper limit of normal serum LDH
Presence of inflammatory fluid or pus within the pleural space.
Urgent IC tube insertion.
Milky white pleural fluid, when fluid cholesterol >4 g/L. Occurs due to lymphatic obstruction and Nephrotic syndrome.
1. Malignancy 2. Tuberculosis 3. Trauma
1. Empyema 2. Malignant Effusions 3. Rheumatoid Effusions
1. Empyema 2. Malignant Effusions 3. Rheumatoid Effusions 4. Tuberculosis 5. SLE
Pleurodesis is a medical procedure in which the pleural space is artificially obliterated. It involves the adhesion of the two pleurae. It can be done chemically or surgically.
1. Recurrent malignant effusions 2. Recurrent pneumothorax
1. Talc 2. Doxycycline 3. Bleomycin
It is defined as the triad of benign ovarian tumor with ascites and pleural effusion (right side) that resolves after resection of the tumor.
Oculomotor nerve (CN III) palsy is a common short case at the neurology station and it is usually evident with a distant because of unilateral complete ptosis.
As the name implies, the oculomotor nerve supplies the majority of the extraocular muscles apart from Lateral Rectus (supplied by VI nerve) and Superior Oblique (supplied by IV nerve). In addition, it supplies Levator Palpebrae Superioris muscle of upper eyelid and Sphincter Pupillae muscles which is responsible for pupillary constriction. This innervation is vital for understanding the clinical signs in III CN palsy, namely ptosis (often complete), dilated pupil and ophthalmoplegia.
There are two clinical entities, “Medical” and “Surgical” third nerve palsies. In a case of Surgical third nerve palsy, you are expected to do an extended examination to clinically locate the site of nerve compression to obtain full allocated marks.
This is obvious! You have to manually and gently elevate the upper eyelid when you carry on your examination to look for ophthalmoplegia.
Due to Medial Rectus palsy and unopposed action of Lateral Rectus supplied by the VI nerve.
In fact, the eye will be “Down & Out” because the Superior Oblique (supplied by IV nerve) is unantagonized by the paralyzed Superior Rectus, Inferior Rectus and Inferior Oblique muscles.
Impaired adduction of eye due to paralysis of Medial Rectus.
Due to the involvement of the parasympathetic nerve supply from the Edinger-Westphal nucleus. These fibers are located superficially, thus in external compression, they are affected first, making the pupil dilated.
Due to the involvement of the Ciliary muscle.
This is especially important when the pupil is affected (Surgical Third Nerve palsy) which would indicate an external compression of the Oculomotor nerve somewhere along its cause. You should do a targeted neurological examination to find out the possible location of the nerve.
Due to the involvement of Corticospinal tracts usually due to a Brainstem infarction.
Sometimes associated with tremor and involuntary movements (Benedikt Syndrome) when the red nucleus of the midbrain is involved.
It is seen without the involvement of other adjacent nerves. Here, the nerve is in close relationship with the posterior communicating artery and can be compressed with aneurysms of the above-mentioned artery.
At the cavernous sinus the oculomotor nerve is closely related to Trochlear and Abducens nerves and ophthalmic and Maxillary branches of Trigeminal nerves. Those nerves are affected together in case of Cavernous sinus thrombosis.
At the orbit, the Maxillary branch of the Trigeminal nerve is not in close relationship with the Oculomotor nerve, hence unaffected. It can occur in intraorbital cellulitis.
This patient has right complete ptosis and a divergent strabismus at neutral position. The right eye movements are impaired especially the adduction and it is fixed in down & out position. The right pupil is fixed and dilated. The accommodation reflex of the right eye is lost.
On my extended limited neurological examination, there are no associated IV or VI nerve palsies on the right side. There is no sensory deficit over the areas supplied by the maxillary and ophthalmic divisions of the Trigeminal nerve. The patient is having left hemiplegia. There are no hand tremors or involuntary movements.
So, my diagnosis is right oculomotor nerve palsy secondary to brainstem (midbrain) stroke. So, this is a case of Weber Syndrome.
It arises from the anterior aspect of the midbrain and originates from two nuclei. • Oculomotor nucleus – Originates at the level of the superior colliculus. • Edinger-Westphal nucleus – supplies parasympathetic fibres via the ciliary ganglion.
It originates at the midbrain at the level of superior colliculus —> passes between superior cerebellar and posterior cerebral arteries —> pierces the dura matter anterior and lateral to the posterior clinoid process —> transverses the cavernous sinus —> divides into two branches (Superior and inferior) at the orbit.
◦ Superior branch supplies the superior rectus and levator palpebrae superioris. ◦ Inferior branch divides into three divisions and supplies to medial rectus, inferior rectus, inferior oblique and ciliary ganglion (Sphincter pupillae & Ciliary muscle)
1. Weber Syndrome – Third nerve palsy + Contralateral Hemiplegia 2. Benedikt Syndrome – Third nerve palsy + Contralateral Involuntary Movements
1. Brainstem Tumours 2. Brainstem Strokes (Ischemic/ Haemorrhagic) 3. Brainstem Demyelination 4. Cavernous Sinus Thrombosis 5. Tentorial Herniation 6. Posterior Communicating Artery Aneurysms 7. Superior Orbital Fissure Lesions 8. Subacute Meningitis 9. Mononeuritis Multiplex (in Diabetes)
Lung fibrosis (Interstitial Lung Disease) commonly appears at undergraduate examinations, as it is a relatively straightforward case. But just diagnosing it won’t help you to acquire full marks allocated for the case.
You have to diagnose it as Lung fibrosis, find the possible aetiology & complications and also try to find outside effects of the current treatment if you really want to impress your examiner. Quite often they will be the cases of Idiopathic Pulmonary Fibrosis (IPF) or Rheumatic Arthritis (RA) associated lung fibrosis.
Suspect lung fibrosis in any patient with finger clubbing. But remember, clubbing may be absent in some patients with lung fibrosis.
If your clinical findings are compatible with Lung Fibrosis, try to find the possible aetiology in your general examination.
If you found “bilateral basal fibrosis” with “no evidence of” Rheumatological disease (RA, SLE mainly) you can safely mention “Idiopathic Pulmonary Fibrosis (IPF)” as your first differential diagnosis at undergraduate level (although there are many other causes except in rheumatological origin – refer FAQs).
Out of above mentioned ones, 1-3 causes predominantly “Basal fibrosis” and 4-6 causes “Apical fibrosis”.Basal Fibrosis Vs Apical Fibrosis
The patient is not breathless at rest and no evidence of peripheral cyanosis. He has finger clubbing, Swan neck deformity & Rheumatic nodules. No lymphadenopathy. There are cushingoid features like moonlike face and steroid purpura.
Chest expansion is equal but symmetrically reduced bilaterally. Percussion note is dull and vocal fremitus and resonance are reduced. Breath sounds are of reduced intensity and there are Fine-end inspiratory basal crepitations in base of the both lung fields.
Pulmonary component of the second heart sound is loud in intensity and there is parasternal heave.
My, probable diagnosis is bilateral basal lung fibrosis secondary to Rheumatoid Arthritis complicated with pulmonary hypertension and right heart failure. The presence of cushingoid features are suggestive of patient is on a high dose of steroids. I would like to extend my examination to look for tender hepatomegaly and proximal myopathy.
The patient is not breathless at rest and no evidence of peripheral cyanosis. He has finger clubbing, No lymphadenopathy. There are no features suggestive of underlying rheumatological disease like rheumatoid arthritis, SLE.
Chest expansion is equal but symmetrically reduced bilaterally. Percussion note is dull and vocal fremitus and resonance are reduced. Breath sounds are of reduced intensity and there are Fine-end inspiratory basal crepitations in base of the both lung fields.
Pulmonary component of the second heart sound is of normal intensity and there is no parasternal heave.
My, probable diagnosis is bilateral basal lung fibrosis secondary probably due to Idiopathic Lung Fibrosis (IPF)
1. Idiopathic Pulmonary Fibrosis (IPF) 2. Rheumatological diseases (RA, SLE, AS) 3. Infections – TB, Aspergillosis 4. Inhaled Agents – Asbestosis, Silicosis 5. Drugs – Methotrexate, Amiodarone 6. Vasculitis – Chrug-Strauss, Goodpasture’s
It is the other name for Idiopathic Pulmonary Fibrosis (IPF), a chronic progressive lung disease of unknown aetiology which is characterized by inflammation and fibrosis of lung parenchyma. It is diagnosed only when the other causes of lung fibrosis are excluded.
1. Acute Interstitial Pneumonia (AIP) 2. Usual Interstitial Pneumonitis (UIP) 3. Non-Specific Interstitial Pneumonia (NSIP)
1. SLE 2. Rheumatoid Arthritis 3. Systemic Sclerosis 4. Ankylosing Spondylitis 5. Psoriasis
1. Polyarteritis Nodosa 2. Wegner’s Granulomatosis 3. Chrug-Strauss Syndrome 4. Goodpasture’s Syndrome
. Methotrexate (MTX) 2. Amiodarone 3. Gold 4. Nitrofurantoin
1. Tuberculosis 2. Allergic Bronchopulmonary Aspergillosis (ABPA) 3. Ankylosing Spondylitis 4. Psoriasis 5. Sarcoidosis 6. Radiation 7. Langerhans Cell Histiocytosis
1. Idiopathic Pulmonary Fibrosis (IPF) 2. Rheumatic Arthritis 3. Drugs 4. Asbestosis
1. Interstitial Lung Disease 2. Lung CA 3. Bronchiectasis 4. Mesothelioma 5. Lung Abscess 6. Cystic Fibrosis
• Bi-basal reticulonodular infiltrates • “Honeycomb” appearance in advanced cases
• FBC, CRP, ESR • Chest X-ray, HRCT, MRI • Arterial Blood Gas (ABG) • Rheumatoid Factor, ANA, ANCA • Immunoglobulin levels
1. Respiratory Failure 2. Recurrent Pneumonia 3. Pulmonary Hypertension 4. Cor pulmonale 5. Lung CA
Type 1 Respiratory Failure.
1. Identify the aetiology and treat/prevent 2. Aggressive treatment of chest infections 3. Immunosuppressive therapy 4. Antifibrotic therapy 5. Long term oxygen therapy (LTOT)
1. Prednisolone 2. Azathioprine 3. Methotrexate 4. Cyclophosphamide
1. Colchicine 2. D-Penicillamine
Hepatomegaly simply means enlargement of the liver. Mean Liver size is 10.5 cm for an adult male and 7 cm for an adult female. Liver size depends on sex, age, body size. Hepatomegaly is considered only when the liver is enlarged at least 3cm from its normal size.
Sometimes the liver is “pushed down” by the hyperexpanded lungs (Emphysema). This is where the “Liver span” (distance from the upper border of the liver to lower border of the liver at the right midclavicular line) is more important than the “liver extension” below the costal margin. So, always confirm whether the liver is actually enlarged or just pushed down before you come to a conclusion.
80% of the abdominal cases given at the exams have organomegaly. But Isolated Hepatomegaly is different from Hepatosplenomegaly. Latter is discussed as a separate case in the app. It has its own differential diagnosis. So, once you have detected hepatomegaly, always exclude a co-existing splenomegaly.
Sometimes hepatomegaly may be due to venous congestion secondary to right heart failure. Look for,
This cachectic patient is not pale, icteric and there are no peripheral stigmata of CLCD. There is finger clubbing. There is left supraclavicular lymphadenopathy which are hard, fixed and non-tender. There is a palpable umbilical nodule (Sister-Mary-Joseph). There are no surgical scars or distended superficial abdominal veins. Abdomen is non-tender to superficial palpation. There is a right hypochondrial mass which I cannot get above and moves with respiration. Its dull to percussion and its dullness continues with the Liver dullness. It is enlarged 5cm below the costal margin in the right midclavicular line. It is nontender, irregular and hard in consistency and has a nodular surface. The upper border of the liver is at 5th intercostal space in the midclavicular line. There is a hepatic bruit.
There is no splenomegaly or ballotable loin masses or shifting flank dullness. The JVP is not elevated, and there is no evidence of heart failure.
My diagnosis is Hepatomegaly probably due to secondary metastasis from underlying intra-abdominal malignancy. GI lymphoma is highly likely as evident by Sister-Mary-Joseph nodule and Finger clubbing.
This patient is not pale, not icteric and there are no peripheral stigmata of CLCD. There is finger clubbing. There is no ankle oedema or lymphadenopathy.
The abdomen is not distended. There are no surgical scars or distended superficial abdominal veins. Abdomen is non-tender to superficial palpation.
There is a right hypochondrial mass which I cannot get above and moves with respiration. Its dull to percussion and its dullness continues with the Liver dullness. It is enlarged 2cm below the costal margin in the right midclavicular line. It is tender, regular and firm in consistency and has a smooth surface. The upper border of the liver is at 5th intercostal space in the midclavicular line. There is no hepatic bruit.
There is no splenomegaly or ballotable loin masses or shifting flank dullness.
The JVP is elevated. There is loud second heart sound. There are coarse late-inspiratory crepitations in the lower zones of both lung fields.
My diagnosis is Tender Hepatomegaly probably secondary to hepatic congestion due to right heart failure. The cause for the right heart failure could well be due to pulmonary hypertension secondary to bronchiectasis.
Ideally, the patient should be examined in the sitting position. Position the patient before you begin your “Examination Proper”. Examination of respiratory system consists of all 4 conventional steps – namely inspection, palpation, percussion and auscultation preceded by relevant general examination.
But these 4 steps can (should) be done both anteriorly and posteriorly. Usually, the examiner will guide you at the exam from which side you may examine the patient due to time limitation. Most of the physical signs are easily detected when the examination is done from posterior aspect. Hence, unless the examiner specifically asked, always begin your examination from the posterior aspect and keep in mind to examine the patient anteriorly if the time permits.
Suspect an upper lobe pathology if an examiner commands you “You may examine anteriorly!”, he might be giving you a clue to the diagnosis.Upper lobe pathologies are easier to detect when the patient is examined anteriorly.
Carefully look for the shape of the chest and chest deformities. For this you have to inspect the patient from both anteriorly and posteriorly. Remember the normal chest is elliptical and bilaterally symmetrical in shape.
Look for surgical scars. Never miss it! If you detect the lobectomy or pneumonectomy scar, you have your case there.
Usual respiratory pattern in adults is thoracic. Abdominal type of breathing is seen in children. But when respiratory muscles are weak, adults may show predominant abdominal type of respiration.
Approximately try to count the respiratory rate. You will get it with experience. You are not going to count this for one minute, Not in your exam! The normal respiratory rate in an adult is 12-20 breaths per minute.
You can get an idea of chest wall movement (Chest expansion) in inspection. Look whether there is a reduction in chest movements in one side or both sides asking the patient to take a deep breath in and out. You can confirm your findings at the next step, “Palpation”.
Chest expansion should be assessed in all three zones (Apex, Upper, Lower) of thorax both posteriorly (and anteriorly Ideally).
Have the patient seated erect with arms by the side. Stand directly behind the patient. First, gently grab the lower hemithorax on either side of the chest (with an equal amount of pressure) and bring your thumbs close together until they approximate each other in the midline. Have the patient slowly take a deep breath and expire. Assess the “Degree” of chest expansion & “Symmetry” of movement of each hemithorax simultaneously. Then repeat the technique over the upper chest and the apex.
Then if the time permits, repeat the whole process anteriorly, at least the apex. Expansion of the apex of the chest best felt anteriorly!
Normal Chest Expansion is 2-5 inches and chest wall should move symmetrically. That is the distance between the two thumbs should be at least 5 cm and both thumbs should be equal distance apart from the midline.
Half the times, your examination may be normal up to this point of the examination. But If you find unilateral reduction in chest expansion, then you know the abnormal side and you can significantly narrow down your possible diagnosis ie. Pleural effusion, Lung collapse, Pneumothorax, Unilateral Lung Fibrosis!You can further narrow down the possibilities by next step of palpation (Tracheal deviation & Mediastinal Shift) which is explained below.
Have the patient seated and position yourself directly in front of the patient and look for any deviation of the trachea. Keep your index and ring fingers of the right hand on the sternal heads of each sternocleidomastoid and then gently palpate the trachea above downwards with your middle finger along tracheal rings feeling its direction.
Then compare the empty space on both sides of the trachea. If the empty space is more on one side, it means the trachea is deviated to the opposite side. Normally there is a slight deviation of the trachea to the right side.
Trail’s Sign – It is the prominence of clavicular head of sternocleidomastoid muscle of the side in which trachea is deviated.Try to identify tracheal deviation before you even touch it!
Look for deviation of the apex beat indicative of a “mediastinal shift” when there is a tracheal deviation.
It is the palpation of the vibrations transmitted on to the chest wall (from larynx through the lungs).
To look for vocal fremitus palpate each side of the chest wall using the ulnar border of your hand at least at three levels (Upper, Middle, Lower zones).
Ask the patient to say “ninety-nine” and feel the vibrations on the chest wall. Always compare both sides. Ideally, the sequence should be repeated anteriorly if the time permits.
You can confirm your findings of vocal fremitus at the auscultation when you do “Vocal Resonance”.Vocal Resonance is the Better of the Two
Have the patient seated and approach from behind. Keep your middle finger of the left hand firmly over the intercostal spaces parallel to the ribs, with other four fingers lifted above, not touching the thoracic wall.
Then percuss (strike) the centre of the middle phalanx of the middle finger perpendicularly. Striking movement should be at the wrist joint, not the elbow. Striking finger should be taken off immediately to prevent dampening of the percussion note. Clavicles are percussed directly on the bone.
Always percuss bilaterally, comparing one side with the other. Always percuss from resonant area to dull (above downwards). Remember to percuss all three zones of bilateral chest wall, and ideally the whole process should be repeated anteriorly if time permits.
“Striking a surface over an air-filled cavity will produce a resonant sound, whereas striking a surface over a fluid / tissue filled cavity will produce a dull sound” That’s it!The Physcis Behind the Percussion
This is done to “exclude elevated hemidiaphragm causing basal dullness” from other causes like Lung Fibrosis, Basal Pneumonia, Lung Collapse or even Pleural effusion.
Percuss along the midclavicular line from the 2nd intercostal space downwards. Normally upper level of the liver dullness is met at 5th intercostal space in right side. If you encounter basal dullness, ask the patient to take a deep breath in, and percuss again. If the percussion note becomes resonant (being dull previously), it is due to elevated hemidiaphragm.
Usually with the diaphragm of the stethoscope firmly placed over the chest wall. Examine all three zones, apices in both lung fields. Make sure the patient is breathing in and out (preferably through the mouth). Auscultate a bit laterally (avoid the medial 3cm from midline).
Carefully try to assess one by one, concentrate only on the specific component you are looking for.
Keep the diaphragm of your stethoscope on chest wall and ask the patient to say “ninety nine”. Repeat this process in all three lung zones bilaterally, both anteriorly and posteriorly. The findings and interpretations are similar to vocal fremitus, but this is more sensitive. (Hence some examiners might ask you to skip Vocal Fremitus in percussion).
Normal breath sounds are low pitch vesicular in nature. There should be no added sounds. P2 should be of normal intensity.
Whishpering Pectoriloquy – Useful techninque to confirm Lung Consolidation if you heard a patch of bronchial breathing.You can confirm or exclude the presence of consolidation on dull patches you found during the Percussion
If you are not sure, ask the patient to cough; crepitations & ronchi may disappear, but not the pleural rub!Confirming a Pleural Rub
Most of the time students do miss this! Always exclude pulmonary hypertension secondary to chronic lung disease. To do this you just need to put your stethoscope over the pulmonary area and listen whether the second heart sound is louder or not. Be smart! Show the examiner that you are looking for possible complications of lung pathology.
If the second heart sound is loud, you may further extend your examination to look for signs of right heart failure to impress the examiner. If so, look for parasternal heave and tender hepatomegaly if time permits.
This average build patient is not breathless at rest. He is not plethoric or cyanosed and he has no finger clubbing, tar stains or lymphadenopathy. There is no ankle oedema.
There are no chest deformities or surgical scars. Chest expansion is normal bilaterally in all three zones. Trachea is not deviated and percussion note is resonant throughout both lung fields. Vocal fremitus and vocal resonance are normal. The breath sounds were heard in normal intensity and there were no added sounds over both lung fields. The pulmonary component of the second heart is not loud.
So, examination of the respiratory system is unremarkable in this patient.