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]

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.



Pleural Effusion (OSCE Guide)


Pleural Effusion (OSCE Guide)

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.


  • Respiratory Distress – In large effusions
  • Cachexia – Malignant effusion, Hypoalbuminemic effusion, TB effusion
  • Running Fever – Suggestive of Synpneumonic effusion
  • Sputum Cup – Bloodstained in Malignant, Tuberculous effusions
  • Ankle Oedema – Organ (Liver, Heart, Kidney) failure & Hypoalbunaemia
  • Malignancy – Distended neck veins, Horner’s Syndrome, Small Muscle Wasting of hand, Finger Clubbing, Tar staining, Lymphadenopathy (cervical, axillary, supraclavicular, epitrochlear)
  • Rheumatological Disease – Rheumatic nodules, Deforming arthritis, Rash
  • CLCD – Gynaecomastia, Spider naevi, Parotid swelling, Jaundice
  • Heart Failure – Elevated pulsatile JVP


  • Tachypnoea, Decreased movements in affected site, Look for aspiration marks, Radiotherapy marks.
  • Reduced chest expansion, Reduced vocal fremitus, Trachea is deviated to the opposite side (in large effusions), may be central if the effusion is associated with Lung collapse.
  • Stony Dull (Percuss for the upper margin of the effusion).
  • Reduced or absent breath sounds with decreased vocal resonance, Bronchial breathing can be heard above the effusion.


  • Hepatomegaly & Splenomegaly – If Lymphoma is likely.
  • Apex beat & 3rd heart sound – If heart failure is likely.


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. What are the causes of dullness at the base of the lungs other than pleural effusion?

1. Lung Collapse 2. Lung Consolidation (Pneumonia, Pulmonary Infarction) 3. Pleural Thickening 4. Lower Lobectomy 5. Raised Hemidiaphragm

2. How do you rule out raised hemidiaphragm from other causes?

Using Tidal Percussion.

3. How do you differentiate each of the other four cases from a pleural effusion?

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

4. What are the two types of pleural effusions?

1. Exudate Effusion. 2. Transudate Effusion.

5. How would you differentiate those two types?

Analyzing pleural fluid protein level. When proteins < 30 g/L – “Transudate”. When proteins > 30 g/L – “Exudate”.

6. What are the causes of transudative effusions?

1. Cardiac Failure 2. Liver Failure 3. Renal Failure 4. Hypothyroidism 5. Nephrotic Syndrome (Hypoalbuminemia)

7. What are the causes of exudative effusions?

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

8. What are the basic investigations you would do?

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)

9. What are the second line investigations you would do?

1. Pleural Biopsy 2. CECT Chest 3. Bronchoscopy

10. What is the normal volume of pleural fluid in pleural space?

1 mL.

11. What is the minimum volume of Pleural fluid that can be detected clinically?

500 mL.

12. What is the minimum volume of Pleural fluid that can be seen on Chest Radiograph PA?

180 mL.

13. How can you detect smaller pleural effusions?

1. Lateral decubitus X-ray 2. Ultrasound Chest

14. What is the use of ultrasonography in Pleural effusions?

1. Detect smaller effusions 2. Detect loculated effusions 3. Guided aspiration of pleural fluid & pleural biopsy 4. Differentiate pleural thickening from effusions

15. What is the normal composition of pleural fluid?

• pH – 7.6 to 7.64 • Proteins < 1-2g/L • WBC < 1000/mm3 • LDH < 50% of Plasma • Glucose = Plasma Glucose level

16. What are the basic investigations you would do from pleural fluid following aspiration?

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)

17. What is the investigation you must do immediately after the aspiration?

Post aspiration Chest X-ray.

18. What is the condition you are looking for in post aspiration Chest X-ray?

Acquired Pneumothorax.

19. What is Light’s Criteria for exudative effusions?

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

20. What is Pyothorax?

Presence of inflammatory fluid or pus within the pleural space.

21. What is the management of a Pyothorax?

Urgent IC tube insertion.

22. What is Chylothorax?

Milky white pleural fluid, when fluid cholesterol >4 g/L. Occurs due to lymphatic obstruction and Nephrotic syndrome.

23. What are the causes of haemorrhagic Pleural effusions?

1. Malignancy 2. Tuberculosis 3. Trauma

24. What are the causes of high LDH in Pleural fluid?

1. Empyema 2. Malignant Effusions 3. Rheumatoid Effusions

25. What are the causes of low glucose in Pleural fluid (same as causes for low pH)?

1. Empyema 2. Malignant Effusions 3. Rheumatoid Effusions 4. Tuberculosis 5. SLE

26. What is pleurodesis?

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.

27. What are the indications for pleurodesis?

1. Recurrent malignant effusions 2. Recurrent pneumothorax

28. What are the chemicals used for pleurodesis?

1. Talc 2. Doxycycline 3. Bleomycin

29. What is Meigs Syndrome?

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 Palsy (OSCE Guide)


Oculomotor Nerve Palsy (OSCE Guide)

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 palsiesIn 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.



1. Unilateral Ptosis (Often Complete Ptosis)

This is obvious! You have to manually and gently elevate the upper eyelid when you carry on your examination to look for ophthalmoplegia.

2. Divergent Strabismus

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.

3. Ophthalmoplegia

Impaired adduction of eye due to paralysis of Medial Rectus.

4. Mydriasis (Dilated Pupil)

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.

  • Surgical Third Nerve palsy – When Pupil is affected (dilated)
  • Medical Third Nerve palsy – When pupil is spared.
5. Loss of Accommodation Reflex

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.

1. At Midbrain – Contralateral Hemiplegia (Weber Syndrome)

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.

2. After emerging from Midbrain – Isolated Surgical Third Nerve Palsy

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.

3. At Cavernous Sinus – Associated IV & VI Nerve Palsies and Sensory Loss in V1 & V2.

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.

4. At Orbit – Associated IV & VI Nerve Palsies and Sensory Loss in V1 (NOT V2).

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.


1. From where the Oculomotor nerve originate?

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.

2. Describe the anatomical pathway of the Oculomotor nerve?

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.

3. What are the structures supplied by the Oculomotor nerve?

◦ 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)

4. What are the eponymous syndromes associated with oculomotor nerve palsy?

1. Weber Syndrome – Third nerve palsy + Contralateral Hemiplegia 2. Benedikt Syndrome – Third nerve palsy + Contralateral Involuntary Movements

5. What are the causes of oculomotor nerve palsy?

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 (OSCE Guide)


Lung Fibrosis (OSCE Guide)

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).


  • Shortness of breath – due to fibrosis itself
  • Peripheral Cyanosis (in advanced disease)
  • Probable Aetiology (mainly try to find any evidence of underlying rheumatological disease)Rheumatoid Arthritis – Rheumatoid nodules, Rheumatoid arthropathy
    1. SLE – Petechial rash, Butterfly rash, Alopecia
    2. Systemic Sclerosis – Tight & shiny skin, Atrophic nails
    3. Psoriasis – Psoriatic arthropathy (Nail pitting, subungual onycholysis)
    4. Ankylosing Spondylitis – Loss of lumbar lordosis
    5. Tuberculosis – Cachectic, Lymphadenopathy, Apical flattening
    6. Drug (steroid) Side effects – Cushingoid features (Steroid purpura, Moonlike face, Buffalo hump)

Out of above mentioned ones, 1-3 causes predominantly “Basal fibrosis” and 4-6 causes “Apical fibrosis”.

Basal Fibrosis Vs Apical Fibrosis


  • Decreased chest movements are seen bilaterally.
  • In case of asymmetrical involvement, movement reduction will be seen localized.
  • Symmetrical reduction in chest expansion usually in both lower zones.
  • Reduced vocal fremitus.
  • Trachea is not deviated in symmetrical bilateral involvement (but may be deviated to the affected side in cases fibrosis is localized “Unilateral apical fibrosis seen in TB”).
  • Dull.
  • Reduced Vocal Resonance.
  • Reduced-intensity of breath sounds.
  • Fine-end inspiratory basal crepitations in both lung fields is the classical finding of IPF. You have to listen very carefully, as these crackles (crepitations) are “very fine” at times.
  • If you hear “Rhonchi”, think of an alternative diagnosis, since it is not usually not associated with Lung fibrosis.


  • Look for loud second heart sound in Pulmonic area (Indicative of Pulmonary Hypertension)
  • Elevated JVP
  • Right ventricular heave (Cor Pulmonale)
  • Proximal Myopathy – (if steroid overuse is suspected)


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. What are the causes of interstitial lung disease?

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

2. What is Cryptogenic Fibrosing Alveolitis?

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.

3. What are the subtypes of Idiopathic Lung Fibrosis (IPF)?

1. Acute Interstitial Pneumonia (AIP) 2. Usual Interstitial Pneumonitis (UIP) 3. Non-Specific Interstitial Pneumonia (NSIP)

4. What are the rheumatological diseases associated with interstitial lung disease?

1. SLE 2. Rheumatoid Arthritis 3. Systemic Sclerosis 4. Ankylosing Spondylitis 5. Psoriasis

5. What are the vasculitic conditions associated with interstitial lung disease?

1. Polyarteritis Nodosa 2. Wegner’s Granulomatosis 3. Chrug-Strauss Syndrome 4. Goodpasture’s Syndrome

6. What are the drugs associated with interstitial lung disease?

. Methotrexate (MTX) 2. Amiodarone 3. Gold 4. Nitrofurantoin

7. What are the conditions causing a predominant apical fibrosis?

1. Tuberculosis 2. Allergic Bronchopulmonary Aspergillosis (ABPA) 3. Ankylosing Spondylitis 4. Psoriasis 5. Sarcoidosis 6. Radiation 7. Langerhans Cell Histiocytosis

8. What are the conditions causing a predominant basal fibrosis?

1. Idiopathic Pulmonary Fibrosis (IPF) 2. Rheumatic Arthritis 3. Drugs 4. Asbestosis

9. What are the respiratory causes of clubbing?

1. Interstitial Lung Disease 2. Lung CA 3. Bronchiectasis 4. Mesothelioma 5. Lung Abscess 6. Cystic Fibrosis

10. What are the radiological features seen in Chest X-ray in idiopathic pulmonary fibrosis?

• Bi-basal reticulonodular infiltrates • “Honeycomb” appearance in advanced cases

11. How would you investigate a patient with lung fibrosis?

• FBC, CRP, ESR • Chest X-ray, HRCT, MRI • Arterial Blood Gas (ABG) • Rheumatoid Factor, ANA, ANCA • Immunoglobulin levels

12. What are the complications of interstitial lung disease?

1. Respiratory Failure 2. Recurrent Pneumonia 3. Pulmonary Hypertension 4. Cor pulmonale 5. Lung CA

13. What type of respiratory failure will it cause?

Type 1 Respiratory Failure.

14. What are the basic principles of management in this patient?

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)

15. What are the immunosuppressive agents commonly used in these patients?

1. Prednisolone 2. Azathioprine 3. Methotrexate 4. Cyclophosphamide

16. What are the antifibrotic agents available?

1. Colchicine 2. D-Penicillamine

17. What are the surgical options available?

Lung transplantation.



Hepatomegaly (OSCE Guide)


Hepatomegaly (OSCE Guide)

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.



  • Generalized Oedema & Abdominal Distention – Background CLCD
  • Cachexia – Malignancy (Liver secondaries)
  • Stigmata of CLCD – Parotid swelling, Gynaecomastia, Body hair loss, Spider navei, Palmar erythema, Dupuytren’s contracture, White nails.
    Background CLCD & Hepatomegaly favors the diagnosis of Hepatocellular Carcinoma.
  • Jaundice (Sclera, Palms) – Malignancy (Liver secondaries), CLCD
  • Pallor (Conjunctiva, Tongue) – Hematological malignancy, CLCD
  • Finger Clubbing – GI Lymphoma, CLCD4
  • Asterixis – Hepatic encephalopathy
  • Ankle Oedema
  • Lymphadenopathy – Cervical, Axillary, Epitrochlear (Malignancy)


  • Abdominal Distention (Ascites seen in malignancy & portal hypertension)
  • Right hypochondrial Fullness – (Large hepatomegaly)
  • Surgical Scars (Peritoneal aspiration marks, Liver biopsy marks)
  • Sister-Mary-Joseph Nodule – Metastatic deposits from bowel CA, hepatocellular CA, and lymphoma
  • Superficial Palpation – Routine
  • Organomegaly (Hepatomegaly)
    1. Palpate for the lower margin & estimate the size
    2. Feel the tenderness, nodularity, regularity and consistency
    3. Percuss for the lower margin from below upwards
    4. Percuss for upper margin from above downwards
    5. Exclude coexisting Splenomegaly
  • Percuss for the liver
  • Percuss for free fluid
  • Look for Hepatic bruit (Hepatocellular CA, Hepatic metastasis, Alcoholic hepatitis)


Sometimes hepatomegaly may be due to venous congestion secondary to right heart failure. Look for,

  • Elevated JVP
  • Loud second heart sound
  • Third heart Sound


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.


1. Hepatocellular Carcinoma (Hepatoma) 2. Malignant Deposits in Liver 3. Alcoholic Liver Disease 4. Nonalcoholic Fatty Liver Disease (NAFLD) 5. Primary Biliary Cirrhosis 6. Alcoholic Hepatitis 7. Hepatic Congestion 8. Infectious Disease 9. Hepatic Infiltration 10. Vascular Diseases of Liver 11. Polycystic Liver Disease
1. Focal Nodal Hyperplasia 2. Nodular Regenerative Hyperplasia 3. Hepatic Adenoma 4. Cavernous Haemangioma
1. Colorectal carcinoma 2. Oesophageal carcinoma 3. Gastric carcinoma 4. Lung carcinoma 5. Breast carcinoma 6. Renal carcinoma 7. Bone tumours
1. Constrictive Pericarditis 2. Congestive Cardiac Failure 3. Right Heart Failure 4. Restrictive Cardiomyopathy 5. Budd-Chiari Syndrome
1. Viral - Hepatitis A, B, C, E, EBV, CMV, Herpes Simplex 2. Toxoplasmosis 3. Amoebiasis
1. Amyloidosis 2. Glycogen storage diseases
1. Bud-Chiari Syndrome 2. Sickle Cell Disease
It is caused by obstruction to hepatic venous outflow. It can occur at any level from Hepatic venules, Hepatic Vein or IVC and the most common cause is venous thrombosis. It is diagnosed by USS Abdomen and thrombolysis & angioplasty are the treatment options.
It indicates a recent enlargement of the liver.
It is due to the stretching of the liver capsule (Pain sensitive) due to the enlargement of the liver.
1. Infective Hepatitis 2. Alcoholic Hepatitis 3. Hepatic Congestion 4. Malignancy
It is associated with Alcoholic Hepatitis & Liver Malignancy (Primary or Metastatic).
It is almost diagnostic of Portal Hypertension.
Usually heard in hepatic neoplasm with inflammatory changes.
A patient who had cirrhosis with portal hypertension has developed hepatocellular carcinoma.



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.



Bell’s Palsy [Facial Nerve Palsy] (OSCE Guide)


Bell’s Palsy [Facial Nerve Palsy] (OSCE Guide)

Facial nerve palsy can be either UMN type or LMN type. It can be unilateral or bilateral. The most common scenario would be LMN type unilateral facial nerve palsy (Bell’s Palsy) you would encounter at the exam. LMN lesions affect both upper & lower parts of the face in contrast to the UMN lesions.

You should be thanking your destiny if you got Bell’s palsy as one of your cases at the exam because it is one of the easiest short cases you would ever get at the neurology station. Though it is a pretty straightforward case, just diagnosing Lower Motor Neuron (LMN) type of facial nerve palsy may not be enough for you to acquire higher marks. Always think about the possible aetiology & try to localize the site of the lesion whenever possible once you detect LMN type of facial nerve palsy.

The general instruction would be to “Examine the lower motor crannial erves” or “Examine the motor cranial nerves”. Always follow the instruction of the examiner.



  • Facial asymmetry (involving affected half of the face – both upper & lower parts)
  • Delayed / Absent Blinking of one eye (affected side)
  • Loss of facial expressions
  • Drooping of the corner of the mouth (affected side)
  • Deviation of the mouth to the opposite side when the patient is asked to clench teeth.
  • Widened palpebral fissure (affected side)
  • Flattened nasolabial fold (affected side)


1. At Parotid gland (Parotid Neoplasm)
  • Palpate the gland enlargement (Neoplasia).
  • Elicit parotid tenderness (Parotitis).
  • Look for surgical scars on the parotid gland (Previous Surgery).
2. At External Acoustic Meatus (Ramsey Hunt Syndrome, Infection)
  • Look for vesicles in external auditory canal & soft palate.
  • Look for pus discharge from the ear.
3. At Middle Ear (CSOM, Cholesteatoma)
  • Look for hyperacusis – A tuning fork would sound louder in the affected ear.
4. At Internal Acoustic Meatus (Acoustic Neuroma)
  • Look for hearing impairment (Associated 8th nerve palsy when entering together with the facial nerve at internal acoustic meatus).
5. At Cerebellopontine Angle (CP angle tumour)
  • Associated 5th nerve palsy – Look for ipsilateral facial numbness along with hearing impairment (8th nerve palsy), 6th nerve may also be involved.
  • Ipsilateral Cerebellar Signs.
6. At pons (Pontine infarction / Hemorrhage)
  • Associated 6th nerve palsy (Lateral Rectus Palsy) of the affected side. Check eye movements.

Facial Nerve Palsy (Bell’s Palsy) – CASE PRESENTATION

This patient is having left side facial asymmetry involving both upper and lower parts of the face. There is absent blinking of the left eye. The mouth is deviated to the right side when an attempt to clench the teeth. There is reduced facial expressions with widened palpebral fissure and flattened nasolabial fold on the left side.

The parotid gland is not enlarged or tender. There is a vesicular rash involving the left external auditory meatus and soft palate. Other cranial nerve examination is unremarkable.

He is having left LMN type Facial nerve palsy secondary to reactivation of Varicella-Zoster Virus; that is Ramsay-Hunt Syndrome.


In UMN lesions of Facial nerve (“Central Seven”) only the lower part of the face on the contralateral side is affected whereas in LMN lesions of Facial nerve (“Bell’s Palsy”) both upper and lower parts of the face on the ipsilateral side are affected.
Intracranial Branches • Greater Petrosal nerve • Communicating branch to Otic ganglion • Nerve to Stapedius • Chorda Tympani Extracranial Branches • Posterior auricular nerve • Nerve to Digastric muscle • Nerve to Stylohyoid muscle • Five major facial branches (Temporal, Zygomatic, Buccal, Marginal mandibular & Cervical)
1. Corneal Reflex - efferent arc. 2. Palmomental reflex
1. Bell’s Palsy (Idiopathic) 2. Parotid Tumours 3. Ramsy-Hunt Syndrome 4. Otitis Media 5. Cerebellopontine Angle Tumours 6. Acoustic Neuroma 7. Mononeuritis Multiplex 8. Basal Skull Fractures
1. Guillain Barre Syndrome 2. Sarcoidosis
It indicates involvement of nerve to Stapedius muscle in inner ear and suggests the lesion is proximal to this level.
It is upward and outward movement of the eye when an attempt to close the eyes. It is a normal defense reflex and becomes noticeable when the orbicularis oculi muscle is weak as in Bell’s palsy.
It is the idiopathic LMN type facial nerve palsy.
Diabetes accounts for 10% of Bell’s palsy.
1. FBC, ESR, CRP 2. Nerve Conduction Studies (if GBS suspected) 3. MRI brain (if SOL suspected)
• Physiotherapy • Corneal Protection (Eye lubricant and covers) • Oral Acyclovir • High Dose Oral Prednisolone (5 days)
1. Persistent facial weakness 2. Corneal abrasions 3. Pain 4. Hemifacial Spasms
It is the LMN type facial nerve palsy caused by reactivation of VZV (Herpes Zoster) affecting the facial nerve.


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