What is Fat Embolism?


What is Fat Embolism?

First of all, one should understand the difference between the fat embolism and fat embolism syndrome (FES).


Fat Embolism

Presence of fat globules in pulmonary and peripheral circulation usually following a long bone fracture or major trauma.

Fat Embolism Syndrome (FES)

A serious consequence of fat embolism producing a distinct pattern of symptoms and signs.


  • Trauma-related – 95%
    • Fractures and orthopaedic related
      • Long bone fractures – tibia and femur
      • Pelvic fractures
      • Vertebral fractures‣ IM nailing and arthroplasty
    • Non-orthopaedic related
      • Soft tissue trauma
      • Liposuction
      • BM harvesting and transplant
  • Non-trauma related – 5%


  • Young age
  • Multiple fractures
  • Conservative management of long bone fractures
  • Overzealous nailing◦ Reaming the medullary cavity
  • Increased gap between nail and cortical bone


Mechanical theory

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.

Biochemical theory

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.

Respiratory Symptoms (First to Appear)

  • Dyspnoea
  • Tachypnoea
  • Hypoxaemia – Occur in 75%
  • ARDS develops – Occur in about 10%

Neurological Symptoms (After Respiratory Symptoms)

  • Drowsiness
  • Confusion
  • Focal neurological signs (hemiplegia, aphasia etc.)

Dermatological Signs

  • Petechiae of skin of axilla and upper neck and chest
  • Petechiae of Conjunctivae and oral mucosa (emboli shooting from the ‣ aortic arch to non-dependent areas)

Other Signs

  • Fever
  • Tachycardia
  • Retinal changes – Purtscher’s retinopathy, fat globules seen on retina on fundoscopy
  • CVS – myocardial depression
  • Coagulopathy – mimicking DIC
  • Renal – oliguria, lipiduria, haematuria


At least 1 major and 4 minor should be present to the diagnosis of fat embolim syndrome.

Major Criteria

  • Axillary skin and subconjunctival petechiae
  • Hypoxaemia – PaO2 <60
  • CNS depression disproportionate to hypoxemia
  • Pulmonary oedema

Minor Criteria

  • Tachycardia
  • Fever
  • Fat globules in retina on fundoscopy
  • Fat globules in urine
  • Fat globules in sputum
  • FBC – thrombocytopenia, anaemia/drop of haematocrit
  • High ESR


Blood Tests

  • FBC – anaemia, thrombocytopenia, low haematocrit
  • ESR – high
  • Serum Lipase – elevated
  • Coagulopathy screening – DIC like picture
  • Serum Calcium – hypocalcaemia due to calcium binding to FF

Congo red/oil red O test

Urine, sputum, serum (specially pulmonary arterial wedge blood sample) – fat globules

Pulmonary Tests

  • CXR – snowstorm appearance in ARDS
  • CT chest – ground glass appearance
  • Pulmonary artery wedge pressure – increased → this is an early way to diagnose this condition.

Other Tests

  • MRI Brain – at the boundaries of major arterial territories there will be hyperintense punctate diffuse lesions “star ◦ field appearance” – petechiae in the white matter!
  • ECG
  • Transoesophageal Echocardiogram



  • Early immobilisation of the fractures
  • Early operative fixation of fractures
  • When reaming the BM for IM nailing, make sure not to increase the intraosseous pressure

Supportive therapy

  • Respiratory support – oxygenation, ventilation
  • Neurological support – the aim is to prevent secondary brain damage by maintaining cerebral perfusion and, oxygenation and minimise cerebral oedema
  • Renal support – proper fluid management with IP/OP monitoring and renal function assessment
  • CVS support – maintain stable haemodynamics, inotropes if necessary

General Measures

  • Physiotherapy
  • DVT prophylaxis
  • Skincare
  • Stress ulcer prophylaxis
  • Nutrition

Unproven Medication

  • Heparin – increases lipase activity and clears the lipaemic serum
  • Corticosteroids – limit FFA generation
  • Aspirin – prevents gas exchange abnormalities



Basal Cell Carcinoma

Basal Cell Carcinoma (BCC) is a slow-growing locally invasive malignant tumour (malignant [more]


Heart Sounds & Murmurs

Auscultation for heart sounds is mainly done in 4 areas, namely Mitral, Tricuspid, Aortic & [more]


Respiratory Examination (OSCE Guide)

Ideally, the patient should be examined in the sitting position. Position the [more]

Heart Sounds & Murmurs


Heart Sounds & Murmurs

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.



  • Produced by the closing of AV valves (Mitral & Tricuspid). Best heard in Mitral & Tricuspid areas on precordium. M1 is preceded T1 only slightly.
  • It marks the beginning of systole (or ventricular contraction).
  • High pitched – Hence auscultated using the Diaphragm of Stethoscope.


  1. Loud S1 – Mitral Stenosis
  2. Soft S1 – Mitral Regurgitation
  3. Widened-Split S1 – Right Bundle Branch Block (Delayed T1)


  • Produced by the closing of Semilunar valves (Aortic &Pulmonary).
  • Best heard in Aortic & Pulmonary areas on precordium.
  • A2 is preceded P2 only slightly. It marks the end of systole (& beginning of diastole).
  • High pitched – Hence auscultated using the Diaphragm of Stethoscope.


  1. Loud S2 – Pulmonary Hypertension
  2. Soft S2 – Pulmonary Stenosis
  3. Physiological Splitting of S2 – Normal in Inspiration (Young Patients)
  4. Fixed Splitting of S2 – Atrial Septal Defect (ASD)

THIRD HEART SOUND (S3 – Ventricular Gallop)

  • Produced by rapid filling (& expansion) of ventricles. It occurs just after S2 in diastole when the AV valves open.
  • It may be a normal finding in young patients & pregnancy, but almost always pathological after 40 years.
  • The most common cause of pathological S3 is a congestive cardiac failure.

FOURTH HEART SOUND (S4 – Atrial Gallop)

  • Produced by forceful atrial contractions forcing blood into stiff ventricles. It occurs immediately before S1 in late diastole.
  • Unlike S3, S4 is always pathological.
  • Low pitched – Hence auscultated using the Bell of Stethoscope.
  • It usually indicates atrial hypertrophy (seen in AS) or stiff ventricles (seen in myocardial infarction causing fibrous tissue formation)


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.

  • Systolic Murmurs – Heard between S1 & S2
  • Diastolic Murmurs – Heard between S2 & S1


It refers to the length of the murmur in relation to the phase of the cardiac cycle.

  • Early Systolic Murmurs – Heard in the early phase of systole
  • Pan Systolic – Heard throughout the systole
  • Mid diastolic – Heard in the middle part of diastole


It refers to the location of the precordium where the murmur is best heard.

  • Aortic – 2nd Right ICS
  • Pulmonic – 2nd Left ICS
  • Mitral – 5th Left ICS, midclavicular line (Apex)
  • Tricuspid – 4th left ICS


It refers to the loudness of the murmur and graded according to the Levine scale 1-6.

  • Grade 1 – Only audible when listening carefully
  • Grade 2 – Faint murmur, but immediately audible
  • Grade 3 – Loud murmur readily audible
  • Grade 4 – Loud murmur with a thrill
  • Grade 5 – Murmur loud enough to be heard with stethoscope just touching the chest
  • Grade 6 – Murmur loud enough to be heard even with stethoscope just lifted off the chest


The shape refers to the change of intensity of the murmur over time as seen in phonocardiograms.

  • Crescendo – Progressively increasing in intensity
  • Decrescendo – Progressively decreasing in intensity
  • Crescendo-Decrescendo – Progressively increasing in intensity followed by progressively decreasing in intensity (Diamond shaped)


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.

  • Axillary Radiation – Seen in Mitral Regurgitation
  • Carotid Radiation – Seen in Aortic Stenosis


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.

  • Low pitched Murmurs (eg: MS) – Auscultated using the Bell
  • High Pitched Murmurs (eg: MR) – Auscultated using the Diaphragm


It refers to unusual characteristics of the murmur which makes it unique in quality.

  • Rumbling Murmur – Seen in Mitral Stenosis
  • Blowing Murmurs – Seen in Mitral Regurgitation


Right-sided murmurs are louder in inspiration (due to increased venous return) and left side murmurs are louder in expiration.

  • Aortic Regurgitation – louder in expiration
  • Pulmonary Regurgitation – louder in inspiration


Some murmurs are best heard using some maneuvers which should be performed when you auscultate.

  • Lateral Decubitus Position – In Mitral Stenosis
  • Sitting & Leaning Forward – In Aortic Regurgitation


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.



Respiratory Examination (OSCE Guide)


Respiratory Examination (OSCE Guide)

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.

  • Barrel Chest – Seen in COPD
  • Harrison’s Sulcus – seen in Chronic Asthma
  • Pectus Carinatum
  • Pectus Excavatum
  • Scoliosis/ Kyphosis/ Kyphoscoliosis

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!

What is the Normal Chest Expansion?

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.

What are Abnormal Findings?
  • Reduced Chest Expansion (if the distance between the two thumbs less than 5 cm)
  • Asymmetrical Chest Expansion (if one thumb remains close to 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.

What are Abnormal Findings?
  • Trachea is shifted towards the side of pathology in Lung collapse, Lung Fibrosis.
  • Trachea is shifted away from the side of the pathology in Pleural effusion, Pneumothorax.
  • Trachea is not deviated in Lung consolidation.

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.

What are Abnormal Findings?
  • Vocal Fremitus is increased in Lung consolidation (Pneumonia, Pulmonary infarct) and Lung Fibrosis.
  • Vocal Fremitus is decreased in Pleural effusion, COPD, Chronic Asthma, Pneumothorax and thick pleura.

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

  • Hyper-resonant – Pneumothorax
  • Resonant – Normal Lung
  • Dull – Consolidation, Lung Fibrosis
  • Stony Dull – Pleural Effusion

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.

  1. Vocal Resonance
  2. Breath sounds
    • Character
    • Intensity
  3. Added Sounds
    • Crepitations – Fine or Coarse, Phase of respiration (Biphasic, Early- Inspiratory, End Inspiratory etc)
    • Ronchi
    • Pleural rub
    • Stridor (rare in the exam!)
  4. Pulmonary component of second heart sound (P2)

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).

What is Normal?

Normal breath sounds are low pitch vesicular in nature. There should be no added sounds. P2 should be of normal intensity.

What is Abnormal?
1. Breath Sounds – Abnormal Character
  • Bronchial Breathing – High pitched sound and inspiration & expiration duration are almost of the same duration. Three types of bronchial breathing are,
    • Tubular Bronchial Breathing – (Pneumonic Consolidation)
    • Cavernous Bronchial Breathing – (Lung Cavity)
    • Amphoric Bronchial Breathing – (Bronchopulmonary Fistula)

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
2. Breath Sounds – Abnormal Intensity
  • Absent Breath sounds – Pleural Effusion, Pneumothorax, Lung Collapse
  • Reduced Intensity – COPD, Asthma, Pleural Thickening
3. Crepitations (Crackles) – Added Sounds
  • Non-musical explosive interrupted sounds. Results from the collapse of peripheral airways on expiration.
  • Seen in Pulmonary Oedema, Bronchiectasis, Interstitial Lung Disease. It can be Fine or Corse in nature.
  • It can be Inspiratory (Early inspiratory, Mid inspiratory, End inspiratory), Expiratory or Biphasic in timing.
4. Ronchi – Added Sounds
  • Continous low picthed musical sounds. Occurs due to small airway obstruction.
  • Seen in Asthma, COPD, Bronchiectasis, Pneumonia.
  • It can be further subdivided to Monophonic & Polyphonic ronchi.
5. Pleural Rub – Added Sounds
  • Creaking or grating sounds. Occurs due to frictional resistance between two layers of inflamed pleura

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.



Mitral Stenosis (OSCE Guide)


Mitral Stenosis (OSCE Guide)

Mitral stenosis (MS) is a notoriously tricky case at the exam where most of the candidates failing to diagnose it because of the hardly audible low-pitched murmur needing the patient to be auscultated in the left lateral position. So, try to diagnose it even before you auscultate the patient!

Always suspect MS if the patient has irregularly irregular pulse indicative of atrial fibrillation (AF). Although MS patients are usually in AF, every AF is not having MS, and every MS patient is not in AF.

Mitral Valvotomy was carried out via a left lateral thoracotomy incision in the past. Although it is history now, there may be a handful of (elderly) patients who had undergone mitral valvotomy and having mitral restenosis with time. Suspect Before Auscultation!

  • Malar Flush
  • Irregularly Irregular Pulse

The most important finding would be the lateral thoracotomy scar if your clinical diagnosis is MS. If the scar is present you have to present the case as “Mitral Restenosis” instead of “Mitral Stenosis”.



  • Malar Flush – Indicate low cardiac output (Complication)
  • Running Fever – Suspect Infective Endocarditis (Complication)
  • Stigmata of IE – Clubbing, Splinter Hemorrhages, Osler’s Nodes, Janeway Lesions (Complication)
  • Joint Swelling – Rheumatic Fever (Aetiology)
  • Erythema Marginatum – Rheumatic Fever (Aetiology)
  • Bilateral Pitting Ankle Oedema – RHF (Complication)
  • Evidence of Hemiparesis – Thromboembolism (Complication)
  • Irregularly Irregular – Underlying Atrial Fibrillation (Complication)
  • Volume – Low volume in severe MS (Severity Marker)
  • Rate – may vary (Slow or Fast AF)
  • Narrow Pulse Pressure (PP) in Sever MS due to low cardiac output (Severity Marker).

Elevated JVP – Indicative of Pulmonary Hypertension and RHF (Complication).
If JVP elevated, you should carefully look for other signs of PHTN & RHF later on your examination & mention them in your presentation.


  • Midline Sternotomy Scars (Previous Mitral Valve replacement)
  • Mitral Valvotomy Scars in the lateral chest wall (Previous Mitral Valvotomy)
  • Tapping Apex – (Palpable First heart sound) – Underlying Loud S1 (Mobile & pliable Mitral valve leaflets)
  • Parasternal Heave – RVH due to RV pressure overload (Complication)
  • Diastolic Thrill at Apex – Underlying loud diastolic murmur (For Diagnosis)
  • Palpable Second heart Sound (P2) – Pulmonary HTN (Complication)
  • Loud S1 – Mobile & pliable Mitral valve leaflets.
  • Or else Soft S1? – Calcified & Immobile Mitral valve leaflets. (Not Necessarily a Complication)
  • Loud P2 – Pulmonary Hypertension (Complication)
  • Opening Snap – Mobile & pliable Mitral valve leaflets (Refer FAQs).
  • Rumbling Type, Low pitched, Mid-diastolic Murmur at Mitral area – Best heard with the Bell in left lateral position. Presystolic accentuation of the murmur is heard if the patient is in sinus rhythm.
  • Functional Tricuspid Regurgitation – You should actively look for this murmur if you found any features to suggest the patient is having PHTN or RHF (e.g. Elevated JVP, Parasternal heave, Loud p2). There will be a “systolic murmur at Tricuspid area which is louder in inspiration”. This is due to increased resistance in pulmonary vasculature secondary to MS, causing backflow via the tricuspid valve (Severity Marker).
  • Graham-Steel Murmur – This is also an additional murmur hear in severe MS due to increased pulmonary vasculature resistance causing backflow via Pulmonary valve in diastole. It is, in fact, the “Pulmonary Regurgitation murmur heard”. There will be an early diastolic murmur at the pulmonary area (Severity Marker).


  • Lung Bases – Bibasal fine crepitations would indicate left heart failure secondary to MS. But these are rarely heard if the patient is on diuretics. (Complication)
  • Tender Hepatomegaly – Would indicate RHF following PHTN secondary to MS (Complication)


This patient is not having peripheral stigmata of infective endocarditis. There is no malar flush or ankle edema. The pulse irregularly irregular, the volume is normal and normal in character. His BP is (Valve) & JVP is not elevated.

On precordial examination, there are no surgical scars suggestive of previous valve replacement or mitral valvotomy. The apex beat is undisplaced & tapping in character. P2 is not palpable and there are no thrills or parasternal heave. The first heart sound is loud whereas the pulmonary component of the second heart sound is of normal intensity. There is an opening snap in early diastole followed by a grade 2 mid-diastolic rumbling type murmur best heard at the apex which increases in intensity with expiration while patient is in left lateral position. Bilateral lung bases are clear & there is no tender hepatomegaly.


This patient is not having peripheral stigmata of infective endocarditis. There is malar flush and ankle oedema. The pulse irregularly irregular, volume is low and normal in character. His BP is 110/90 mmHg & JVP is elevated.

On precordial examination, there is a lateral thoracotomy scar. The apex beat is undisplaced & tapping in character. P2 is palpable and there is a parasternal heave, but no diastolic thrills palpable. The first heart sound is loud as well as the pulmonary component of the second heart sound. There is grade 2 mid-diastolic rumbling type murmur best heard at the apex which increases in intensity with expiration while the patient is in the left lateral position. Opening snap is not heard. In addition, there is a pansystolic murmur best heard at LLSB (tricuspid area) and an early diastolic murmur best heard at the Pulmonary area, both are louder in inspiration. There are fine crepitations on both lung fields & tender hepatomegaly.

So, this patient has undergone mitral valvotomy in the past and now having severe Mitral restenosis and associated Atrial Fibrillation with evidence of Pulmonary Hypertension leading to congestive cardiac failure. There is functional tricuspid regurgitation & Graham-Steel murmur of Pulmonary regurgitation due to the pressure overload secondary to severe PHTN. The mitral valve leaflets are clinically immobile & calcified.


1. Rheumatoid Arthritis 2. Systemic Lupus Erythematosus (SLE) 3. Congenital MS 4. Carcinoid Syndrome 5. Whipple's Disease
1. Atrial Septal Defect (ASD)0 2. Mitral Valve Prolapse 3. Tricuspid Stenosis
1. Left atrial myxoma 2. Austin flint murmur (in Aortic Regurgitation) 3. Carey Coombs murmur (in acute rheumatic carditis)
A murmur heard in between second heart sound and the first heart sound.
It is the accentuated and palpable first heart sound which is best felt at the apex.
Because the valve cusps are widely apart at the onset of systole and suddenly shut with the forceful ventricular contractions.
It is caused by the sudden opening of stenosed mitral valve with left atrial contraction. Usually opening of valves does not cause any sound. But in MS, an opening snap is heard due to increased atrial pressure.
It indicates the valves are still pliable and the patient is suitable for percutaneous transeptal mitral commissurotomy (PTMC). When they are diffusely calcified, the opening snap disappears.
1. The turbulence of flow occurs when it is < 2 square centimeters. 2. Clinically significant MS is when it is < 1.5 square centimeters. 3. Severe mitral stenosis is when it is < 1 square centimeters.
Thickening of valve leaflets, nodularity and ultimately commissural fusion resulting in a “fish-mouth” like valve.
1. Long murmur 2. Narrow gap between S2 and OS
1. Malar Flush (Low cardiac output) 2. Narrow Pulse Pressure (Low cardiac output) 3. Irregularly irregular pulse (Atrial fibrillation) 4. Loud P2 (Pulmonary hypertension) 5. Functional Tricuspid Regurgitation (Severe Pulmonary Hypertension) 6. Graham-Steel Murmur (Pulmonary Regurgitation due to severe PHTN) 7. Paraventricular heave (Right ventricular hypertrophy) 8. Distended neck veins (Increased JVP) 9. Tender hepatomegaly (RHF) 10. Bilateral pitting oedema (RHF)
It is due to development of severe Pulmonary HTN leading to low cardiac output.
1. ECG P mitrale - bifid P waves (due to left atrial enlargement) Irregularly irregular QRS complexes (if AF present) 2. Chest X-ray Double silhouette sign (due to enlarged left atrium) Features of RHF (Upper lobe diversion, Kerly B lines) 3. 2D Echocardiography To confirm the diagnosis
1. Antitussive medication - for bronchitis 2. Low dose diuretics - for dyspnoea 3. Beta-blockers & Calcium channel blockers - to increase exercise tolerance 4. Management of AF - Rate control, Rhythm control, Anticoagulant therapy
1. Symptomatic patients with significant mitral stenosis 2. Patients with pulmonary hypertension regardless of the severity 3. Recurrent thromboembolism despite anticoagulation
1. Balloon valvuloplasty 2. Percutaneous transeptal mitral commissurotomy (PTMC) 3. Open commissurotomy 4. Mitral valve replacement



Ulnar Nerve Palsy (OSCE Guide)


Ulnar Nerve Palsy (OSCE Guide)

The examination of hand for neuropathies is commonly encountered at OSCE stations. Ulnar Claw-hand is a very characteristic finding in Ulnar nerve palsy.

Firstly, introduce yourself and get consent before you proceed to examine the patient.


Given below is a targeted examination for Ulnar nerve palsy. But remember to examine other nerves (Median & Radial) to exclude multiple nerve involvement.

  1. Ask the patient to spread out the hands for you and try to spot diagnose the “Ulnar claw hand” (Clawing of the medial two fingers of the hand).
  2. Inspect carefully both the palmar and dorsal aspect of the hands and look for,
    • Wasting of hypothenar eminence (compare with the other side).
    • Dorsal guttering (due to wasted Interossei muscles) – Palpate the 1st finger web where the wasting is often obvious.
  3. Examine the functions of the muscles supplied by the Ulnar nerve.
    • Palmar Interossei – Ask the patient hold a card between two fingers while you attempt to pull it away using the same two fingers.
    • Dorsal Interossei – Ask the patient to keep the hand on a flat surface and spread out the fingers against resistance.
    • Adductor Pollicis – Ask the patient hold a paper between the thumb and the radial aspect of the index fingers while you attempting to pull it away. Flexion of the terminal phalanx of the thumb to hold the paper indicates a positive Froment’s sign.
  4. Examine the sensory distribution.
    • High lesions – There is an area of sensory loss over both palmar & dorsal aspects of the medial side of the hand and medial one and half fingers.
    • Low lesions – There is an area of sensory loss only over the palmar aspect of the medial side of the hand and medial one and half fingers.
  5. Try to identify a probable aetiology.
    • Look for depigmented anaesthetic patches and Ulnar nerve thickening at the elbow (Leprosy).
    • Look for scars on the forearm (trauma).
  6. Offer to assess the patient’s quality of life.


There is marked clawing of the ring and little fingers of the right hand and there is wasting of hypothenar eminence with dorsal guttering, but the thenar eminence is not affected. The actions of palmar and dorsal interossei are impaired and Froment’s sign is positive.

The opposition of the thumb and finger extension is intact. There is an area of sensory loss over the palmar aspect of the medial side of the hand and medial one and half fingers. There is no hypopigmented patches or ulnar nerve thickening and there are no visible scars on the forearm.

So my tentative diagnosis is right-sided Ulnar nerve palsy, probably a lower lesion.


1. What is “Clawing”?

It is the hyperextension of the metacarpophalangeal joints and flexion of proximal and distal interphalangeal joints.

2. Why does it occur?

It is due to paralyzed Interossei and Lumbricals with unopposed action of long flexors and extensors.

3. What is “Ulnar claw hand”?

The clawing is only obvious in medial two fingers (Because lateral two Lumbricals which are supplied by the median nerve are spared).

4. What is the “Ulnar paradox”?

Surprisingly, high division of the ulnar nerve (anywhere hand’s breadth above the wrist) causes less clawing than the lower lesions.

5. What is the anatomical basis of the Ulnar paradox?

In higher lesions the innervation to the medial half of Flexor Digitorum Profundus is also lost, causing less intense flexion of the fingers.

6. How do you differentiate?

From the degree of clawing and the area of sensory involvement (see examination).

7. What are the muscles that are innervated by the Ulnar nerve?

1. Flexor Carpi Ulnaris.
2. Medial half of Flexor Digitorum Profundus.
3. All Palmar Interossei.
4. All dorsal Interossei.
5. 3rd & 4th Lumbricals.
6. Adductor Pollicis

8. What is the basis of Forment’s sign?

The patient tries to compensate for the ‘lost’ adduction of the thumb by flexion of it (with Flexor Pollicis Longus which is supplied by the Median nerve).

9. What are the causes of Ulnar nerve palsy?

1. Leprosy (often bilateral).
2. Laceration over the wrist or anywhere along its course.
3. Fracture medial epicondyle.
4. Dislocation of elbow.
5. Cubital tunnel syndrome.
6. Degenerative arthritis.
7. Malunion of fractures of the lower end of the humerus (Tardae Ulna nerve palsy).

10. What are the surgical options for Ulnar nerve palsy you know of?

1. Ulnar nerve decompression.
2. Ulnar nerve anterior transposition.
3. Medial epicondylectomy.



Carpal Tunnel Syndrome (OSCE Guide)


Carpal Tunnel Syndrome (OSCE Guide)

The examination of hand for neuropathies is commonly encountered at OSCE stations. One of the most common scenarios would be carpal tunnel syndrome.

Firstly, introduce yourself and get consent before you proceed to examine the patient.


Usually, the command is to examine the hands of the patient, but sometimes you might be given a clue like “This lady presented with tingling sensation in her hands”. The disease is often bilateral.

  1. Ask the patient to spread out the hands for you.
  2. Look for,
    • Wasting of thenar muscles.
    • Scar of a previous carpal tunnel decompression surgery.
  3. Examine the functions of the muscles supplied by the Median nerve.
    • Abductor Pollicis Brevis – Ask the patient to place the dorsum of the hand on a flat surface and lift the thumb towards the ceiling against resistance (Pen touch test).
    • b. Opponens Pollicis – This muscle is usually not tested as it may also be supplied by the ulnar nerve ( an anatomical variation).
  4. Examine the sensory distribution.
    • There is an area of sensory loss over the palmar aspect of the lateral three and a half fingers.
    • However, the sensation over the thenar eminence is preserved.
  5. Special Signs to elicit,
    • Tinel’s Test – Tap over the flexor aspect of the wrist over the midline. If the patient feels a tingling sensation over the distribution of the median nerve, the test is positive.
    • Phalen’s Test – Ask the patient to flex the wrists maximally and keep for one minute. If the patient feels pain in the hands, the test is considered positive.
  6. Try to identify a probable aetiology.
    • Obesity.
    • Hypothyroidism – Goiter? Facial puffiness? Loss of lateral third of eyebrows?
    • Rheumatoid arthritis – Shawn neck deformity? Boutnier’s deformity? Z thumb?
  7. Offer assessment of the patient’s quality of life (QOL).
    • Nocturnal and early morning worsening of symptoms.
    • Effects on occupation or activities of daily living (eg: Washing clothes).


This patient who presented with tingling sensation of hands has bilateral thenar muscle wasting but there is no wasting of hypothenar eminence or dorsal guttering. There are no visible surgical scars, suggestive of previous carpal tunnel decompression surgery. Her opposition of the thumbs is weak and the pen touch test is positive, but there is no weakness in finger adduction or extension. There is an area of sensory loss over the palmar aspect of the lateral three and a half fingers and no other areas of sensory loss. Tinel’s test and Phalen’s test are positive. So my tentative diagnosis is bilateral Carpal Tunnel Syndrome (CTS) and I would like to assess her functional disability and probable aetiology.


1. What is Carpal Tunnel Syndrome?

It is the symptomatic compression of the median nerve at the carpal tunnel where it runs deep to the flexor retinaculum (Commonest entrapment neuropathy).

2. What are the boundaries of the carpal tunnel?

Roof – Flexor retinaculum. Medial (Ulnar) – Pisiform & Hook of Hamate. Lateral (Radial) – Scaphoid and Trapezius. Palmar aspect – Transverse carpal ligament.

3. What are the structures that pass through the carpal tunnel?

1. Median nerve.
2. Four tendons of Flexor Digitorum Superficialis.
3. Four tendons of Flexor Digitorum Profundus.
4. Tendon of Flexor Pollicis Longus.
5. Tendon of Flexor Carpi Ulnaris (in a separate compartment).

4. What are the structures that pass over the carpal tunnel?

1. Palmar cutaneous branch of the Median nerve.
2. Ulnar nerve.
3. Ulnar artery.
4. Tendon of Palmaris Longus.

5. Why not the sensation over the radial aspect of the palm is affected?

Because the palmar cutaneous branch of the Median nerve is given away proximal to the flexor retinaculum and which passes over it.

6. What are the muscles in hand which are innervated by the Median nerve?

1. All thenar muscles except Adductor Pollicis.
2. Radial two Lumbricals.

7. Name one investigation to confirm your clinical diagnosis?

Nerve conduction studies (NCS).

8. What are the known causes of carpal tunnel syndrome?

1. Obesity.
2. Pregnancy.
3. Hypothyroidism.
4. Diabetes Mellitus.
5. Rheumatoid Arthritis.

9. What are the differential diagnosis?

1. Cervical rib.
2. Cervical spondylosis.
3. Pancoast’s syndrome.

10. What is the surgery?

Carpal tunnel decompression by longitudinally dividing the flexor retinaculum in full length in a bloodless field under local anesthesia.

11. What are other non-surgical treatment options?

1. Local steroid injection.
2. Splinting of the wrist at night.
3. Treating the underlying cause.


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