Respiratory Examination (OSCE Guide)

1/03/2020

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. 

EXAMINATION PROPER

RESPIRATORY SYSTEM EXAMINATION – INSPECTION

1. CHEST DEFORMITIES

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
2. SURGICAL SCARS

Look for surgical scars. Never miss it! If you detect the lobectomy or pneumonectomy scar, you have your case there.

3. RESPIRATORY PATTERN

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.

4. RESPIRATORY RATE

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.

5. CHEST WALL MOVEMENTS

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”.

RESPIRATORY SYSTEM EXAMINATION – PALPATION

1. CHEST EXPANSION

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.
2. TRACHEAL DEVIATION

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!
3. APEX BEAT

Look for deviation of the apex beat indicative of a “mediastinal shift” when there is a tracheal deviation.

4. VOCAL FREMITUS

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

RESPIRATORY SYSTEM EXAMINATION – PERCUSSION

1. PERCUSSION TECHNIQUE

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

2. PERCUSSION NOTES
  • Hyper-resonant – Pneumothorax
  • Resonant – Normal Lung
  • Dull – Consolidation, Lung Fibrosis
  • Stony Dull – Pleural Effusion
3. TIDAL PERCUSSION

This is done to “exclude elevated hemidiaphragm causing basal dullness” from other causes like Lung Fibrosis, Basal Pneumonia, Lung Collapse or even Pleural effusion.

Percuss along the midclavicular line from the 2nd intercostal space downwards. Normally upper level of the liver dullness is met at 5th intercostal space in right side. If you encounter basal dullness, ask the patient to take a deep breath in, and percuss again. If the percussion note becomes resonant (being dull previously), it is due to elevated hemidiaphragm.

RESPIRATORY SYSTEM EXAMINATION – AUSCULTATION

1. HOW TO AUSCULTATE?

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).

2. WHAT TO AUSCULTATE?

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)
3. VOCAL RESONANCE

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).

4. BREATH SOUNDS & ADDED SOUNDS
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
5. SECOND HEART SOUND (P2)

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.

SAMPLE PRESENTATION – RESPIRATORY EXAMINATION

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.

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

1/03/2020

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.

BELL’S PALSY – EXAMINATION

DIAGNOSE BELL’S PALSY

  • 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)

LOCALIZE THE LEISON

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.


FREQUENTLY ASKED QUESTIONS

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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Chronic Liver Cell Disease (OSCE Guide)

1/03/2020

Chronic Liver Cell Disease (OSCE Guide)

You do not have to be an expert in order to diagnose a patient with Chronic Liver Cell Disease (CLCD), as it is too obvious even with inspection alone. But you might be under-prepared for this case, just because you would not expect such easy cases at the exam settings.

So, try to memorize all the key features suggestive of CLCD and organize your presentation mentioning the important positives as well as the negatives. Always try your best to assess the aetiology and the complications of CLCD during your examination.

CHRONIC LIVER CELL DISEASE – EXAMINATION

GENERAL EXAMINATION

The general examination of CLCD is vital and you can get many important positive and negative findings for the diagnosis, aetiology & complications. There are two ways you can look into this step of examination. Easier way for a beginner would be, examining region by region remembering the clinical features you have to look for in each region.


But the smarter (and more advanced) way is mind mapping the clinical findings into diagnosis, aetiology & complications (Refer the Flashcard).

BIRD’S EYE EXAMINATION
  • Generalized Oedema & Ascites – Due to Hypoalbunaemia
  • Cachexia – Chronic Disease & Poor Nutrition
  • Running Fever – Spontaneous Bacterial Peritonitis (SBP) – (Complication)
  • Skin Pigmentation – Suspect Haemochromatosis – (Aetiology)
  • Petechiae & Ecchymosis – Due to coagulopathy & Thrombocytopenia (Complications)
  • Tattoos – Hepatitis B & C (Aetiology)
FACE
  • Jaundice (Sclera, Palms) – Suggestive of Decompensation of CLCD – (Complication)
  • Pallor (Conjunctiva, Tongue) – Anemia (Multifactorial: Blood loss, BM suppression, Poor Nutrition) – (Complication)
  • KF rings – Suspect Wilson’s Disease – (Aetiology)
  • Xanthelasma – Suspect Primary Biliary Cirrhosis (PBC) – (Aetiology)
  • Parotid Swelling – Alcoholic CLCD – (Aetiology)
CHEST & BACK
  • Gynaecomastia – Altered sex hormone metabolism (Palpate & Confirm)
  • Spider Navi – Number & size correlates with the severity. (Palpate & Confirm)
  • Body Hair Loss – Altered sex hormone metabolism
HAND & FOOT
  • Asterixis – Hepatic Encephalopathy
  • Finger Clubbing – Hypoalbunaemia
  • White nails – Hypoalbunaemia
  • Palmar Erythema – Vasodilatation in CLCD
  • Dupuytren’s Contracture – Alcoholic CLCD (Aetiology)
  • Ankle Oedema – Hypoalbunaemia

ABDOMINAL EXAMINATION

INSPECTION
  • Abdominal Distention (Ascites)
  • Smiling Umbilicus (Ascites)
  • Surgical Scars (Previous Hepatobiliary Surgery, Peritoneal Aspiration Marks, Liver Biopsy Marks)
  • Distended Superficial Abdominal Veins – Caput Medusa (Portal Hypertension – Complications)
PALPATION
  1. Superficial Palpation – Tender? Suspect SBP.
  2. Hepatomegaly
    • How many centimetres?
    • Is it tender? – Suspect Hepatoma (Complication of CLCD), Hepatitis (Alcoholic / Infective)
    • Is it hard in consistency with irregular margins? – Suspect Hepatoma (Complication)
    • Hepatic Bruit? – favours Hepatoma
  3. Splenomegaly – Indicates evidence of portal hypertension.

In patients with Cirrhosis liver is usually shrunken. So, you won’t be expecting the liver to be enlarged. But what if the liver is palpable? Then suspect Hepatoma, Alcoholic CLCD & NAFLD.

IMPORTANT FACT TO BE REMEMBERED
PERCUSSION
  • Assess the volume status of the patient. Grade the ascites. Elicit “Shifting flank dullness” in a patient with moderate ascites OR “Fluid thrill” in case of a large ascites.
AUSCULTATION
  • Liver and Splenic bruits (over the enlarged liver & spleen)
  • Hepatic Venous Hum (over the epigastrium)

CLCD – CASE PRESENTATION

This patient has generalized body swelling with gross abdominal distention and does not appear to be drowsy. He is icteric and anaemic. He has got no Xanthelasma or KF rings. The patient is having parotid swelling, gynaecomastia and there are multiple spider navei located on upper chest and the back. He has got palmar erythema, finger clubbing, leukonychia and there is Dupuytren’s contracture in the right hand. He has bilateral pitting ankle oedema and there is no asterixis.

The abdomen is distended and the umbilicus is slightly inverted & retracted (smiling umbilicus). There are no surgical scars or distended superficial veins of the abdomen. There is no tenderness on superficial palpation. Liver is not palpable. There is a left hypochondrial mass 3cm from the costal margin, which moves diagonally with respiration. Its superior border is not palpable and its not ballotable. There is a notch in its anterior border. It is dull to percussion and its dullness continues with the splenic dullness with no evidence of band of resonance in between. There is moderate ascites as evidenced by shifting flank dullness; no fluid thrill. There is no splenic or liver bruits.

My diagnosis is Decompensated Chronic Liver Cell Disease (CLCD) complicated with portal hypertension probably due to heavy alcoholic abuse. He has got no evidence of SBP or Hepatic Encephalopathy


FREQUENTLY ASKED QUESTIONS

1. Generalized Oedema & Ascites 2. Finger Clubbing 3. Dupuytren’s Contracture 4. White Nails 5. Palmar Erythema 6. Gynaecomastia 7. Body Hair Loss 8. Parotid Swelling 9. Ankle Oedema 10. Spider Navei
1. Portal Hypertensive Gastropathy - Blood loss 2. Poor Nutrition 3. Bone Marrow Suppression - Due to Alcohol
1. Palmar erythema 2. Gynaecomastia 3. Loss of body hair 4. Spider navei
Its due to recanalization of the umbilical vein secondary to portal hypertension. In portal hypertension, the direction of the flow is away from the umbilicus whereas in Inferior Vena cava obstruction, it is towards the umbilicus.
1. Hypoalbunaemia (Decreased production & intake) 2. Activation of Renin-Angiotensin Axis
1. Intraabdominal Malignancy 2. Congestive Heart Failure 3. TB peritonitis 4. Pancreatitis
1. Alcohol 2. Viral - Hepatitis B & C 3. Autoimmune - Autoimmune hepatitis, Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis 4. Metabolic - NASH, Wilson’s Disease, Haemochromatosis 5. Drugs - Methotrexate, Amiodarone
1. Infection 2. Spontaneous Bacterial Peritonitis (SBP) 3. GI Bleeding 4. Hypokalaemia 5. Sedatives 6. Hepatocellular Carcinoma
1. Ascites & Spontaneous Bacterial Peritonitis 2. Oesophageal varices & Hematemesis 3. Hypersplenism & Thrombocytopenia 4. Coagulopathy 5. Hepatic Encephalopathy 6. Hepatocellular Carcinoma
1. Running fever 2. Abdomen is tender to superficial palpation 3. Percussion tenderness
It is the reversible neurological dysfunction or coma due to liver failure.
Grade 1 - Insomnia / Day-night sleep pattern reversal Grade 2 - Disorientation Grade 3 - Confusion Grade 4 - Coma
1. Omit offending drugs - Omit Frusemide & Spironolactone 2. Find & Treat the cause - Treat constipation (Enema, Lactulose) 3. Antibiotics - IV Ceftriaxone & Oral Metronidazole 4. Supportive Care - NG feeding, IV fluids
• Resuscitate the patient - A B C approach • Correct Hypovolemia - IV fluid until blood is available • Prevent bleeding - IV infusion of Tranexamic acid & Octreotide • GI Tamponades - Temporary measure until definitive treatment carried out • UGIE & Banding - Definitive treatment option
1. FBC 2. Liver Function Test (Albumin, Total Protein, AST, ALT, GGT, ALP) 3. PT/INR 4. Serum Electrolytes 5. USS abdomen
1. To confirm the diagnosis (Assess the size & echotexture) 2. To detect Portal Hypertension & Splenomegaly 3. To detect any focal lesions
1. Hepatitis B Surface Antigen 2. Hepatitis C Antibodies 3. Serum Fe and Ferritin 4. Serum Ceruloplasmin 5. Liver biopsy
1. Slowing / Reversing the cause - Stopping Alcohol, Immunosuppressive therapy 2. Relieving Symptoms - Diuretics, Ursodeoxycholic acid (for itching) 3. Minimizing Acute decompensation - Treating infection & Constipation, Prophylactic Antibiotics 4. Treating Complications - Hepatic Encephalopathy, SBP 5. Liver transplant - Final resort
It is also known as Primary Biliary Cholangitis which is a autoimmune disorder of the liver. It results from a slow and progressive destruction of biliary canaliculi causing accumulation of bile and other toxins in the liver (Cholestasis). Eventually this results in scarring, fibrosis and cirrhosis.
1. Bilirubin 2. Ascites 3. Encephalopathy 4. Prothrombin Time 5. Albumin
1. Liver resection 2. TACE (Transarterial Chemo-embolization) 3. Liver transplant

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Mitral Stenosis (OSCE Guide)

1/03/2020

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”.

MITRAL STENOSIS – EXAMINATION

GENERAL EXAMINATION

GENERAL EXAMINATION
  • 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)
PULSE
  • Irregularly Irregular – Underlying Atrial Fibrillation (Complication)
  • Volume – Low volume in severe MS (Severity Marker)
  • Rate – may vary (Slow or Fast AF)
BLOOD PRESSURE
  • Narrow Pulse Pressure (PP) in Sever MS due to low cardiac output (Severity Marker).
JUGULAR VENOUS PRESSURE (JVP)

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.

PRECORDIAL EXAMINATION

INSPECTION
  • Midline Sternotomy Scars (Previous Mitral Valve replacement)
  • Mitral Valvotomy Scars in the lateral chest wall (Previous Mitral Valvotomy)
PALPATION
  • 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)
AUSCULTATION
  • 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).

EXTENDED EXAMINATION

  • 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)

MITRAL STENOSIS – CASE PRESENTATION 01

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.

MITRAL STENOSIS – CASE PRESENTATION 02

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.


FREQUENTLY ASKED QUESTIONS

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

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Thyroid Examination (OSCE Guide)

1/03/2020

Thyroid Examination (OSCE Guide)

Thyroid examination or the examination of a goiter commonly encountered at Surgical OSCE stations.


THYROID EXAMINATION

Firstly, greet the patient and take consent. Make sure you have enough space behind the patient’s chair before proceeding with the examination.

Examine from front
  1. Inspect – Offer a glass of water and ask to swallow on command & look for the lump moving upwards with deglutition. Observe from the side.
  2. Only if the lump is small and in the midline, ask the patient to put the tongue out while stabilizing the jaw and look for the lump moving upwards.
  3. Look for scars (previous lobectomy scar) and dilated neck veins.
  4. Only if the lump is a large one, elicit Pemberton’s sign.
Then go to back of the patient,
  1. Palpate the thyroid gland from behind. Examine using one hand at a time while stabilizing the gland from the other. Feel for the consistency and nodularity of the gland.
  2. Examine for cervical lymphadenopathy.
After that, come back to front of the patient and look for,
  1. Tracheal deviation – Feel along the trachea downwards.
  2. Retrosternal extension – Check whether you can feel the lower border of the gland while the patient is asked to swallow. If cannot percuss to elicit retrosternal dullness.
  3. Displaced carotid pulsation – Check both carotid pulses, one at a time.
  4. Thyroid bruit – Auscultate over the right upper lobe.
Finally, examine for eye signs and hands to complete the thyroid examination
  1. Eye Signs – Look for Exophthalmos (See from behind), Lid retraction, Lid lag, and Ophthalmoplegia.
  2. Hand signs – Look for sweaty hands, tachycardia (radial pulse), fine tremors.

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THYROID EXAMINATION – PRESENTATION

This patient is having a lump in the anteroinferior aspect of the neck which moves up with deglutition. There are no visible surgical scars in the neck or dilated neck veins and Pemberton’s sign is negative.

The lump is firm in consistency and its surface is nodular with a prominent nodule in the right upper lobe. There is no cervical lymphadenopathy. Its lower border can be felt, trachea is deviated to the left side and the right carotid pulse is deviated posterolaterally. There is no bruit. She is clinically euthyroid and there are no thyroid eye signs.

So, my probable diagnosis is a clinically euthyroid longstanding multinodular goiter (MNG) without retrosternal extension. I would like to investigate her with a thyroid profile, USS neck and FNAC of the prominent nodule to decide on further management



FREQUENTLY ASKED QUESTIONS

1. What are the causes of diffuse thyroid enlargement?

1. Simple colloid goiter.
2. Thyroiditis.
3. Grave’s disease.

2. What are the differential diagnosis for a solitary nodule of the thyroid (SNT)?

1. Prominent nodule of an MNG.
2. Hemorrhage into a colloid cyst.
3. Thyroid adenoma.
4. Thyroid carcinoma.
5. Foci of thyroiditis.

3. What would be the next management option, if the histology of an SNT comes as follicular neoplasm?

Thyroid lobectomy and look for the histology to decide on further management. If the histology is malignant, the other lobe is also removed later.

4. Where would you auscultate for a bruit?

Over the right upper lobe laterally while the patient is holding the breath.

5. What is the significance of a thyroid bruit?

It indicates the increased vascularity of the gland (hyperdynamic circulation) – seen in Grave’s disease.

6. What are the compressive features?

1. Nocturnal dyspnea and cough.
2. Recent onset dysphagia.
3. Deviated trachea.
4. Displaced carotid pulse.

7. What are the features of retrosternal extension?

1. Distended neck veins.
2. Positive Pemberton’s sign.
3. The lower border of the goiter cannot be felt.
4. Retrosternal dullness.

8. What are the malignant features?

1. Recent rapid enlargement.
2. Recent voice change (Hoarseness).
3. Hard in consistency.
4. Cervical lymphadenopathy.
5. Irregular margins.
6. Multiple attachments.

9. What are thyroid eye signs?

1. Lid lag.
2. Lid retraction.
3. Exophthalmos.
4. Proptosis.
5. Ophthalmoplegia.

10. How do you identify a thyroglossal cyst?

It moves upward with deglutition as well as with the protrusion of the tongue when the jaw is fixed. Being in midline differentiates it from goiters.

11. Why do we have to excise thyroglossal cysts?

1. Cosmetically unacceptable.
2. Prone to get infected.
3. May undergo malignant transformation.

12. What is the surgical procedure for a thyroglossal cyst?

Sistrunk procedure (Complete excision of the cyst and its tract together with the middle part of the body of the hyoid bone).

13. What are the indications for thyroidectomy for a multinodular goiter (MNG)?

1. Cosmetically unacceptable (Patient’s wish).
2. Compressive symptoms.
3. Secondary thyrotoxicosis.
4. Suspected or proven malignancy.

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Ulnar Nerve Palsy (OSCE Guide)

ulnar_nerve_palsy
1/03/2020

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.


ULNAR NERVE PALSY – EXAMINATION

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.

PRESENTATION

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.



FREQUENTLY ASKED QUESTIONS

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.

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Carpal Tunnel Syndrome (OSCE Guide)

1/03/2020

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.


CARPAL TUNNEL SYNDROME – EXAMINATION

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).

PRESENTATION

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.



FREQUENTLY ASKED QUESTIONS

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.
Fig

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Inguinal Hernia (OSCE Guide)

1/03/2020

Inguinal Hernia (OSCE Guide)

Examination of an inguinal hernia is a vital part of surgical examination methods. It is one of the most basics skills that every medical student and doctor should be aware of.

More importantly, differentiating between a femoral and inguinal hernia plays a major role here.

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


INGUINAL HERNIA EXAMINATION

You will be asked to examine the groin area of a patient who is lying supine, but always remember to examine the patient in the erect position as well, at some point in your examination.

  1. Get the Consent, cover the area and expose adequately.
  2. Look carefully for surgical scars in the groin (Recurrent hernia?).
  3. See the shape of the lump in the groin. A direct inguinal hernia is usually globular in shape and an indirect one may be sausage-shaped (inguinoscrotal swellings).
  4. Ask the patient to cough,
    • To elicit expansile cough impulse.
    • Inorder to visualize a hernia that cannot be seen.
    • To see the full extent of an already visible hernia.
  5. ONLY IF the hernia still cannot be seen, ask the patient where the lump is (It may be a scrotal swelling!!) and ask him to stand up at this point & look for a bulge appearing on the groin area on coughing (Very rare to give invisible ones in an exam setting).
  6. Once the hernia is visible, demonstrate the palpable expansile cough impulse.
  7. ONLY IF there is no past surgical scar indicating a previous repair, differentiate whether it is direct or indirect hernia.
    • Ask the patient himself to reduce the hernia fully for you.
    • If the patient is unable to do so, ask the examiner whether you may try to reduce it (DO NOT try to reduce without the consent of the examiner)
    • ONLY IF the hernia is reduced,
      1. Locate the deep inguinal ring (2methods can be used).
        • 1 cm above the femoral pulse (Easy way).
        • 1 cm above the mid inguinal point (midpoint between the anterior superior iliac spine and pubic tubercle).
      2. Ask to cough while you are applying firm pressure on deep inguinal ring with your index finger.
      3. If the lump can be controlled by digital pressure over the deep ring, it is an “Indirect inguinal hernia”, if not it is a “Direct inguinal hernia”.
  8. Examine the external genitalia to exclude phimosis and coexisting scrotal lump which is very common.
  9. If the patient was supine throughout your examination, ask him to stand up before you finish and look for,
    • A coexisting small hernia on the other groin.
    • A coexisting varicocele.

PRESENTATION

This patient has got a globular shaped lump in the right groin region. It has visible and expansile cough impulse. The hernia can be completely reduced and cannot be controlled by applying firm pressure over the deep inguinal ring. He has got no phimosis and there are no coexisting scrotal lumps. The contralateral groin is normal. So my probable diagnosis is uncomplicated right-sided direct inguinal hernia and I would like to offer him inguinal hernia repair under spinal anesthesia.



FREQUENTLY ASKED QUESTIONS

1. How do you locate the deep inguinal ring?

Method One – 1 cm above the femoral pulse (Easy way).
Method Two – 1 cm above the mid inguinal point (midpoint between the anterior superior iliac spine and pubic symphysis).

2. If you see a scar of a previous repair, do you still want to locate the deep inguinal ring?

No. Once a hernia is repaired, its anatomy is disturbed. So a recurrence of a hernia arises from the weakest part of it. Hence it is neither direct nor indirect.

3. If you cannot control the hernia by applying firm pressure over the deep inguinal ring, can it still be an indirect hernia? Why?

Yes, it can be.
1. Not enough pressure applied.
2. Finger is not on the deep inguinal ring.
Anyway, this method is just for crude assessment. The direct or indirect nature of a hernia is best identified during the surgery.

4. From where does an indirect inguinal hernia appear?

It comes from deep inguinal ring, passes obliquely through the inguinal canal and may continue through the superficial inguinal ring to the scrotum. It arises lateral to the inferior epigastric artery. Commonly due to persistent processes vaginalis.

5. From where does a direct inguinal hernia appear?

It occurs as a result of weakened posterior wall of the inguinal canal and arise medial to the inferior epigastric artery. So a direct inguinal hernia is not within the spermatic code. It may descend to the scrotum though.

6. What is the importance of differentiating direct and indirect inguinal hernia?

No importance! Management is the same for both.

7. What is the landmark to differentiate direct from indirect inguinal hernia during the surgery?

Inferior epigastric artery.

8. At what age, inguinal hernia are operated on children?

As early as possible due to the high risk of strangulation.

9. What are the treatment options?

1. Mesh repair (Gold standard).
2. Darning repair.
3. Bassini repair.
4. Shouldice repair.

10. What is the difference in surgical steps of managing inguinal herniae?

Indirect inguinal herniae require both herniotomy (excision of the hernia sac) & herniorrhaphy (hernial repair) while direct inguinal herniae usually only necessitate herniorrhaphy.

11. What are the aetiological factors?

1. Chronic cough.
2. Constipation.
3. Cigarette smoking.
4. Bladder outflow obstruction (BOO)

12. What are the complications of inguinal herniae?

1. Irreducibility.
2. Obstruction.
3. Strangulation.
4. Incarceration

13. What are the complications of the surgery?

1. Acute urine retention.
2. Hematoma formation.
3. Pain.
4. Infection.
5. Ischemic orchitis.
6. Recurrence.

14. What is the risk of recurrence after a Mesh repair?

Less than 1%.

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