Long Case - A Teenager With Lower Limb Weakness

Sharing one case we encountered in ward recently and is possible to encounter a similar scenario in the exams. 

An 18 year old male was returning from a feast after the Eid celebrations and found it difficult to get himself out of the car upon reaching home. He found it to occur suddenly. He was already feeling unwell (he could not describe how he was feeling unwell) since departing the feast. He had difficulty moving both his legs and he was also very lethargic. He had similar problems affecting his arms and he needed to be carried down from the car. He remained conscious throughout the indicent. 

Further history revealed no preceding or accompanying fever, no vomiting or diarrhoea, no bowel or bladder issues, no back pains. He had no headaches, no blurred vision, no dysphagia or speech abnormalities, no facial asymmetry. He also reported no palpitations or chest pains.

He did however report some numbness or tingling sensation affecting his extremities. 

In the past medical history section, he reported experiencing similar lower limb weakness occurring 4 months earlier in Jan 2023 for several hours. However at that time the weakness was not as bad as current presentation as he was still able to bear weight and walk although he needed assistance. He did not seek treatment at that time as he attributed it to being over tired after a game of soccer. His lower limb weakness gradually improved with leg massages and drinking "100-PLUS". Otherwise there was no other significant history with no previous hospital admissions or health issues. 

Family history was unremarkable as well with no similar occurrences affecting other members of his family. 

He had no significant drug history and he is not taking any medications or supplements. He did not consume herbal or traditional remedies either. 

Systemic review was also normal and he reported no significant weight loss or anorexia. 

Social history revealed he is studying at a local community college and is active is sports. He is a teetotaler and does not smoke. He is single and is not sexually active. He has not been involved in any illicit substances or recreational drugs. 

Physical examination showed him to be alert, calm with good hydration. There were no neurocutanoeus stigmata. He was afebrile with normal blood pressure.

However he was tachycardic. Manual heart rate was 120 beats per minute with regular rhythm and normal pulse volume. Capillary refill was normal. 

Neurological examination noted normal muscle bulk with no fasciculations noted. He had normal sensation in both upper and lower limbs as well. However he had proximal muscle weakness whereby hip flexion was only 3/5 bilaterally whereas shoulder abduction was also only 3/5 bilaterally. Ankle plantar and dorsiflexion was normal with power 5/5 and wrist dorsiflexion was also strong with power 5/5 bilaterally. 

There were fine tremors affecting both upper limbs. However muscle tone was normal for both upper and lower limbs. 

Reflexes were brisk in both upper and lower limbs but Babinski response was flexor (downgoing). There was no clonus elicited. 

There were no spinal cord abnormalities or tenderness found on examination of the spine.

Examination of the other systems revealed no heart murmurs or displaced apex beat, clear lung fields to auscultation and no goitre. Cranial nerves were normal and there was no proptosis and ophthalmoplegia.

A provisional diagnosis of periodic hypokalemic paralysis was made with a differential diagnosis of renal tubular acidosis and hyperthyroidism. 

12 lead ECG showed sinus tachycardia with a rate of 100 beats per minute with normal axis and no ST-T abnormalities. 

A bedside glucometer finger prick test revealed capillary blood sugar of 7.5 (random) which was normal. 

Blood tests were sent for blood gas analysis, kidney profile with electrolytes and also thyroid function testing. Urine tests were sent for any proteinuria or glycosuria. 

Blood gas results returned normal with no metabolic acidosis. 

His blood electrolytes showed hypokalemia at a level on 2.5 mmol/L. He received multiple intravenous potassium corrections on top of oral potassium replacements. 

Additional urine test for potassium excretion was ordered but unable to be tested due to lack of reagent (budget constraints). 

His hypokalemia proved difficult to correct and he required frequent and multiple intravenous potassium corrections on top of maintenance potassium in normal saline drip. 

Serum Magnesium was normal. 

Eventually, we discovered the actual diagnosis when the thyroid function test results returned after several days. His TSH was markedly suppressed at < 0.001 and his T4 was elevated at 58. 

He was commended on carbimazole and propranolol and soon after we found it easier to correct his hypokalemia. His tachycardia also improved and stabilised at 60-70 beats per minute. 

His lower limb and upper limb musle strength gradually improved and he was eventually able to self ambulate without assistance after 2 days of initiating anti thyroid therapy. 

Further history regarding autoimmune symptoms did not yield any positive history. Nevertheless, we decided to send thyroid autoantibodies. Ultrasound neck showed a slightly but diffusely enlarged thyroid gland with increased vascularity.

His final diagnosis was revised to Grave's Disease. 

The odd thing about this case was the absence of thyroid eye signs and a clinically palpable goitre. Perhaps we caught the disease in its early stages. He probably had hyperthyroidism for quite some time, perhaps preceding Jan 2023. As a result, his hypokalemia may already be there but he was compensating well. When he sweat a lot while playing soccer back in Jan 2023, his potassium levels probably plunged and he manifested as bilateral lower limb weakness.  His potassium levels were replaced partially after he consumed "100 PLUS" and thus resulting in gradual improvement in muscle weakness. Also important to take note is that Grave's disease is relatively uncommon among males and if the diagnosis is confirmed, overall prognosis wont be as good for male patients compared to female patients with Grave's disease. 

He was discharged well on Day 5 of anti thyroid treatment with oral potassium replacement. He was able to walk home unaided. There was no more hand tremors, his vitals have returned to normal levels and he is no longer tachycardic. 

CCE.

Long Case - Approach to a case with Left Lumbar Pain

This patient presented with a history of left flank pains for 1 week associated with fever. The patient has history of Type 2 Diabetes Mellitus and Hypertension both of which were uncontrolled. 

This scenario is a common occurrence in the medical ward. And likelihood of it appearing for the MBBS Final Exams are also high. And the diagnosis is pretty straightforward, if tackled systematically. 

Based on the above information alone, students should be able to draw up a list of differentials. In order to form a sensible list of differential diagnoses, I would suggest the student to use the patient's anatomy as a source of inspiration. 

Potential causes of the left flank pain (in anatomical order from superficial to deep):

Skin: Herpes zoster

Subcutaneous tissue and Muscle: Hematoma or abscess/ cellulitis

Colon: Colitis

Kidney: Pyelonephritis, Renal colic, Obstructive uropathy, Renal abscess, Renal tumours

Adrenal: Adrenal tumours 

Lymph Nodes: Lymphadenitis

Muscle: Psoas muscle abscess or intramuscular hematomas

Spine: Prolapsed intervertebral disc with nerve impingement

Based on the differentials above, the student can sit down to exclude each differential by taking a thorough history as well as examine the patient in detail.

In real life, the case above was diagnosed by the Emergency Doctor as having left sided pyelonephritis based on the symptom of fever and left flank pain. This is not wrong as patient has Uncontrolled Type 2 Diabetes Mellitus which predisposes the patient to ascending urinary tract infection. 

From history taking done by Medical Officer from Internal Medicine unit, there was no chills or rigors accompanying the fever and there was no vomiting that usually accompany pyelonephritis. There was also no dysuria/ hematuria/ incomplete voiding sensation. Patient had no diarrhoea or hematochezia to suggest colitis. There was no injury to the abdomen to suggest hematoma. Patient had no history of fall and no limb weakness to suggest a spinal cord or sciatica issue. Patient did report numbness affecting BOTH lower limbs particularly the feet in stocking distribution, up to both shins. This is likely due to diabetic peripheral neuropathy rather than related to spine issue. 

During systemic review, patient mentioned having rash over the left side of abdomen which appeared 2 days prior to presentation to the Emergency Department. The rash was not itchy but painful to touch. 

The patient did not have any abdominal distension, no significant anorexia and no unexplained weight loss to suggest a malignant pathology. 

After taking the above history to rule in and rule out the possible differentials, the next step was to do a complete physical examination to confirm the findings as what is usually required in the final MBBS examination. 

However, take a look at the photo below which was taken by the Internal Medicine Physician attending the patient. 

Multiple vesicles with crusting over the left lumbar region...lateral view

Similar lesions were also seen at the left loin region extending all the way to the midline posteriorly

The photos show herpes zoster of the left T8 or T9 dermatome. This diagnosis can easily be made if the patient has been adequately exposed. Therefore it can only be concluded that the diagnosis of left pyelonephritis was made without exposing the patient properly. In this patient, the left renal punch was "positive" because it was tender over the herpes zoster site at the left loin region. Deeper palpation revealed no kidney enlargement and no tenderness. 

Urine analysis also did not show features of urinary tract infection.

Thus the diagnosis of left pyelonephritis was changed to left T8/ T9 dermatome herpes zoster.

IV antibiotics that was started for pyelonephritis was stopped and oral acyclovir was started as the rash onset was just 2 days old. Analgesics was started as well to help reduce the pain.

This is how a student is expected to approach any long case. Based on the chief or presenting complaint, the student should draw up a list of differentials (preferably according to anatomical distribution to avoid missing any possibilities). Then go ahead with taking a complete history (history of presenting illness, past medical history, past surgical history, drug history, obstetric or gynae history for females, family history, allergy history, social history and last but not least, the systemic review). And then proceed with physical examination to further narrow down the differential list and verify the provisional diagnosis. I cannot help but re-emphasize the importance of adequate exposure when performing the physical examination. Without adequate or proper exposure, the student risks missing out on important signs and making an accurate diagnosis. Worse still, the student may be penalized by the examiner for improper examination technique (adequate exposure is important part of physical examination technique).

CCE. 

Lower Motor Neuron CN 7 Palsy

CN 7 aka Facial Nerve Palsies are one of the most favourite topics to appear in the MBBS final exams. Take a look at the photo below. 

What is striking is that this man has facial asymmetry. The first challenge for the student is to decide which side is the abnormal side and which side is normal.

The photo above shows a flattened or loss of right nasolabial fold indicating the facial abnormality is on the right. 

If you look closely enough, there is also loss of wrinkles over the right forehead. This is an important clue to show that this is a lower motor neuron (LMN) lesion involving the facial nerve (CN 7).

Once you suspect the diagnosis of CN 7 LMN lesion, then you'll need to quickly identify the possible causes. I would like highlight 5 common causes of LMN CN 7 which may appear for the exams.

1. Mononeuritis - connective tissue disorders/ diabetes

2. Parotid gland swelling

3. Ramsay Hunt Syndrome

4. Cerebellopontine angle tumours

5. Bell's palsy (idiopathy)

If you look closely at the photo above, you may be able to appreciate a bump protruding outwards (red arrow) from the right angle of mandible (compared to the left angle which is concave).

This patient has a right parotid gland tumour, which has compressed on the right facial nerve resulting in lower motor neuron right facial nerve palsy.

Once the diagnosis is established and the cause identified, next and last step is to try identify possible complications of the diagnosis. A common problem with people suffering from LMN facial nerve palsy is the inability to close the ipsilateral eye lids completely. This can result in excessive drying of the conjunctiva and cornea leading to red and irritated eyes, a condition called exposure keratitis. Prolonged irritation and drying can cause corneal scarring which may impair vision. So whenever students encounter a LMN facial nerve palsy case, always look out for exposure keratitis after the aetiology of the LMN facial nerve has been identified. 

Always keep this triad in mind when approaching any case: Diagnosis - Aetiology - Complication....This will ensure your assessment of the patient is complete. 

CCE.  

Gout and Cushing....how are they related?

This was a case of a gentleman I saw in MOPD few years ago. He had these changes to his hands. 

From this picture we can see multiple tophi over the dorsum of the hands particularly over the extensor tendons as well as extensor surface of the wrists and distal forearms. There is a particularly large tophi overlying the 2nd metacarpophalangeal joint. 

You will be able to make the diagnosis of gouty arthritis just based on the above photo. However do not stop there. Go further by looking for other clues to suggest a possible aetiology of the gouty arthritis. Look for psoriatic rashes over the dorsum of hands and extensor surfaces of the limbs, also look for nail changes suggestive of psoriasis e.g. pitting nails. And also take the opportunity to look at the forearms for any arteriovenous fistulas to suggest chronic kidney disease that has progressed to end stage disease requiring hemodialysis. CKD can be associated with worsening of gout due to reduced renal clearance. 

This photo further illustrates the extent of gouty tophi deposition over the extensor surfaces and also over the elbows. 

This photo shows tophi on the ear pinna. Tophi formation tend to occur not only on the extensors but also at areas of the body where temperatures are cooler. Cooler temperatures make uric acid deposition easier. That is one reason why tophi is often seen over the distal extremities like the toes (especially the first metatarsophalangeal joint in podagra) and also the pinna. 

But take a look at the next photo. 

Take note that this patient has a body habitus suggestive of Cushing's syndrome. There is central obesity noted. There are also multiple striations over the anterior abdomen due to excessive stretching (the classical purplish or pinkish striae is not clearly seen in this photograph). And in the second photo above, the patient has a thick neck. If seen laterally, this patient also has a dorsocervical hump due to excess fat deposition (not in photo). 

The last photo above also shows multiple hyperpigmented marks on both sides of the umbilicus. Those scars are indicative of recurring injections likely from insulin therapy. Meaning this patient can be suspected to have concomitant diabetes mellitus, a diagnosis which is not surprising considering his physical appearance. This also further strengthens the diagnosis of Cushing's syndrome, of which diabetes mellitus is a feature. 

So now we have two diagnoses:

1. Chronic tophaceous gout

2. Cushing's syndrome 

So how do we tie both the diagnoses? The answer is steroids. If you are able to take one history, I would suggest you to ask about the drug history...the patient would tell you he has been visiting many clinics over the years for joint pains due to gouty attacks. During each visit he will receive a common cocktail of painkillers which often include steroids. On top of that, he also visits retail pharmacies and self medicate his joint pains by purchasing painkillers and steroids over the counter. As a result of the chronic steroid exposure, he has developed secondary Cushing's syndrome which is a complication of trying to treat his gout. Unfortunately, because of no proper follow up, he was not started on uric acid lowering treatment e.g. allopurinol. He will definitely benefit from it. 

CCE. 

The Hiatus Explained

Dear students,

First and foremost, I would like to extend my heartfelt congratulations to those who have made it through the recent MBBS Finals for Class of 2022. To those who did not make it, keep pressing on. Cross that hurdle and earn your title. 

Secondly, I would like to extend my apologies for the prolonged silence in this blog. There have been no new posts since Dec 2022. This is because I have been distracted since Jan 2023 by many issues, some of which include myself being posted to a new Specialist Hospital i.e. Hospital Pendang. With this move, I am no longer able to conduct direct clinical teachings with Final Year students. 

On top of that, I have also been busy with my new role as a visiting consultant physician in a private medical centre in Alor Setar city. 

However, teaching is a passion I have and I would still go back to teaching whenever the opportunity arises. 

Therefore, following this post, I will begin to continue updating this blog and posting relevant clinical cases and sharings to assist students in preparing for their final professional exams. 

May I request everyone who have been following this blog, to share with your juniors and encourage them to share with their juniors as well so that the knowledge imparted here will be passed on continuously.

 And also feel free to update or comment if there are any new information regarding clinical medicine or examination techniques which I may miss out. I try to keep up with the latest developments in clinical medicine, but I may fall short in certain areas. Appreciate it if we can keep each other updated whenever needed. 

If there are any requests for certain topics to be discussed, feel free to post in the comment below this post. 

To the new batch of final year students, good luck and enjoy the process. Internal Medicine is fun. 

Happy learning. 

CCE. 

JUGULAR VENOUS PRESSURE (JVP)

The JVP is an important sign to look out for especially for the CVS station.

The JVP will indicate if there is presence of fluid overload. 

Students are expected to know how to measure the JVP and to identify the characteristic features of a JVP. The height of the JVP is measured from the manubriosternal angle (Angle of Louis) until the top of the JVP pulsation. 

An abnormal JVP is a measurement of > 3cm above the manubriosternal angle. 

The JVP is best assessed in good lighting so ensure that you have your pen torch ready for extra illumination.

JVP characteristics:

1. Visible but not palpable

2. Presence of double waveform

3. It is occludable at the base of the neck

4. There is hepatojugular reflux 

CCE.

HOW NOT TO SCREW UP YOUR ABDOMINAL SHORT CASE EXAM

When you hear the bell ring and you are directed to enter the examination room, do remember your manners and greet the examiners with a brief “Good morning” or “Good afternoon”. Never before in the history of the university was there a need for a “Good night sir”. In the excitement of the exams, time can be hazy and you may lose track of it. But stay grounded and always stay in touch with reality. That is why a good night sleep the day before is essential. You don’t want to be making a fool of yourself even before the examination begins.

Upon entering the room and after you have greeted the examiners, your name will be read out and you are supposed to verify that the candidate name read is indeed your name. After which, automatically proceed to the examination bed where the patient is seated or lying down. You will find the examination instructions pasted on the table. Read it carefully and take note of the patient’s designated name and also the exam question. 

For example, the question may read “Madam A has abdominal discomfort. Please examine her abdominal system.”

A short reminder on refraining from addressing patients with “aunty”, “uncle”, “pakcik” or “makcik’. We have been doing this habitually during our day to day practice and it is customary for us as this is a respectful way of addressing our senior patients. But for the purpose of major examinations, please use the patients’ designated names instead, to sound more formal.

After reading the instructions, proceed with positioning the patient to prepare for abdominal examination. Patients should be placed in full supine position whenever possible. The head can only be supported by one pillow (maximum) but if the patient is able to tolerate without any pillow, that would be best. Remember to expose the patient adequately as well. For male patients, if they are consenting, request the patient to remove the shirt completely. For female patients, perhaps it would be better to just expose the abdomen from xiphisternum all the way down to the suprapubic or pubic symphisis region for the sake of the patient’s modesty. For the purpose of this post, I will begin the examination from general inspection, then the peripheries before the abdomen itself.

General inspection, look for:

1. Overall patient condition i.e. restless, in discomfort or comfortable. Take note of any obvious dysmorphism e.g. Cushingoid appearance etc. and last but not least any obvious skin discolorations e.g. bronze skin (hemochromatosis or iron overload conditions e.g. thalassemia), sallow skin (chronic kidney disease may suggest polycystic kidney disease or obstructive uropathy or failed renal transplant case) or jaundiced skin.

2. Look at IV drips – blood product transfusion, antibiotics, dextrose infusion etc that may give a clue to the underlying abdominal diagnosis

3. Look at CBD bag at the bedside if any – pay attention to urine colour: tea coloured urine may suggest a liver or hematological disorder, hematuria may suggest an underlying coagulopathy (possible liver disorder related)

4. Look at temperature charts at bedside if any (may indicate an infective diagnosis)

 

Hand examination (as far as possible ask the patient to lift their own hands up, you may support the hands once they have done so). Pay particular attention to the following details:

1. Finger clubbing – lower your eyes to the nail fold or Lovibond’s angle to look for loss of angle, you may also do the Schamroth window test by opposing both thumbs or index fingers together to look for loss of diamond shaped window.

2. Leuconychia – this will indicate hypoalbuminemia which may be related to the patient’s nutritional status or underlying chronic liver disease (to differentiate this from pallor, in leuconychia, the nail bed blanching will not be visible through the nails as the nails are opacified in leuconychia)

3. Nail bed colour – may hint at anemia if there is pallor

4. Capillary refill time – indicator of adequate perfusion

5. Splinter hemorrhages – stigmata of endocarditis (relevant for the abdominal station as endocarditis may be associated with splenomegaly)

6. Koilonychia – suggestive of iron deficiency – indicates underlying chronic blood loss or gastrointestinal malignancy

7. Symmetrical deforming polyarthropathies (suggestive of Rheumatoid arthritis) – may be related to the abdominal station as RA may be associated with splenomegaly in a condition called Felty syndrome

8. Tendon xanthomas – suggestive of dyslipidemia (may be associated with Non Alcoholic Fatty Liver Disease (NAFLD) or Primary Biliary Cirrhosis (PBC))

9. Intrinsic muscle wasting – indicative of nutritional status (relevant to malabsorption or chronic disease e.g. GI malignancy)

10. Hepatic flaps – hepatic encephalopathy (a sign unlikely to be seen in the exams as patients are usually well and stable). Remember to ask the patient for any pain over the wrists before performing dorsiflexion of the hands and jerking the fingers backwards to stimulate the flapping movements. 

 

Upper Limbs:

1. Bruises/ petechiea – will suggest an underlying coagulopathy or thrombocytopenia

2. Scratch marks – elevated bilirubin levels or uremia may cause itching leading to scratch marks

3. Tattoos – may indicate a risk for viral hepatitis infection

4. Multiple needle prick marks – may suggest underlying abuse of intravenous substances (risk for viral hepatitis or retroviral infection)

5. BCG scar – tuberculosis is a differential for any chronic infection in our part of the world

6. Axillary hair – look for loss of axillary hair by abducting the shoulders a little (loss of axillary hair is seen in chronic liver disease, but need to differentiate from patient’s who regularly shave their armpits)

7. Tendon xanthomas over the elbows (may indicate underlying severe dyslipidemia)

8. Arteriovenous fistulas – indicate underlying end stage kidney disease. Need to consider polycystic kidney disease in the abdominal exam station. And also look out for renal transplantation scars later on during the examination.

 

Head and neck:

1. Eyes – look for conjunctiva pallor and sclera icterus. Also observe for xanthelasma (please do not mention Kayser- Fleishcer rings as those are only seen using slit lamp examination) and arcus senilis which may indicate underlying hyperlipidemia. 

2. Mouth – angular stomatitis (indicate iron deficiency or vitamin B deficiency), glossitis (B12 deficiency), oral thrush (immunocompromised state), gingitis and caries (predisposes to endocarditis which may be associated with splenomegaly, thus making it relevant for the abdominal station), gum hyperplasia (may indicate underlying exposure to drugs like cyclosporine – an immunosuppressant that is used for renal transplant patients (relevant to the abdomen station), phenytoin (anti epileptic drug which may also be relevant to the abdomen station) or acute myeloid leukemia)

3. Neck – look for dialysis catheters, enlarged cervical lymph nodes (I would suggest examining the cervical nodes after completing the abdominal examination when you are able to sit the patient up).

Chest:

1. Spider naevi – bear in mind it can also be found in normal persons. But if there are more than 3 spider naevi found, then chronic liver disease should be suspected first.

2. Gynecomastia – look for a disc like tissue swelling in the retro-areolar region in males. It is usually tender so be gentle while palpating for it. It may indicate underlying chronic liver disease but also indicate that the patient may be on certain drugs like spironolactone. Spironolactone is a common diuretic used for patients with decompensated liver cirrhosis with ascites.

 

Abdomen:

1. Symmetry of movement with respiration – for this step I would take a step or two back and inspect the anterior abdominal wall while asking the patient to take a deep breath in and then exhaling. This movement will enable me to look for any asymmetry of abdominal wall movements. This may indicate or suggest an underlying mass.

2. Peristaltic movements – this may indicate an underlying bowel obstruction; which is unusual for the medical examination (so do not look too hard for this sign)

3. Pulsations – visible pulsations may be relevant for the abdominal examination. A pulsatile mass adjacent to the midline will alert you of a possible underlying abdominal aortic aneurysm. You will need to palpate with caution to prevent rupturing the aneurysm.

4. Surgical scars – pay attention to midline laparotomy scars, laparoscopic scars (most often at the umbilicus region and at the left or right upper quadrants), peritoneal tapping scars and appendicectomy scars. Pay close attention to subcutaneous injection scars over the periumbilical regions which may hint at regular insulin use or iron chelation therapy use (both of which are relevant to the abdominal system).

5. Visible and dilated veins – usually caput medusa (may suggest underlying liver cirrhosis with portal hypertension)

6. Cough impulse – this maneuver is to examine for possible inguinal hernias. Although this step is included in the abdominal examination, this may not be so practical for the medical station.

7. Superficial palpation – this step is to elicit any abdominal tenderness or guarding which may indicate underlying peritonism. It is highly unlikely for students to encounter such a condition in the exams, therefore, I would suggest performing this step by palpating the abdomen in 4 quadrants instead of 9 quadrants.

8. Deep palpation – this step is more important as it is intended to identify abdominal masses. Therefore it is better to perform this step by palpating the abdomen in 9 quadrants.

9. Liver palpation – begin from the right iliac fossa (RIF) and progress superiorly toward the right subcostal margin. I would recommend taking control of the patient’s breathing by asking the patient to breathe in and breathe out on your command at a pace that is suited to the student. This will allow the student to better appreciate the movement of any liver that are moving with respiration. When the patient is inspiring (breathing in), the palpating hand should be kept still awaiting the inferior liver edge to hit the hand. When the patient is expiring (breathing out), the palpating hand should move superiorly towards the right subcostal margin if no liver edge is felt. Once the liver edge is felt, the palpating hand should keep still to mark the position of the liver edge. Using the left hand, the student can feel the surface of the liver and its consistency. Remember to try to get above the mass as well to verify that the mass is indeed the enlarged liver. After that, the measuring tape should be brought out and measurements taken from the inferior liver edge to the right subcostal margin along the right mid clavicular line. Once done, the right hand can feel along the inferior liver edge to determine if its regular or irregular margins and ill- or well-defined. This is followed by percussion beginning from the right iliac fossa, gradually moving superiorly until the position of the palpable liver mass earlier. The student should take note of the change in percussion note from resonant to dull over the liver mass. Remember to also percuss the upper right hemithorax and progress inferiorly towards the right subcostal margin to identify the superior margin of the liver. Once the percussion note is dull, that is the superior margin and the measuring tape is brought out again and measurement taken from the dull point towards the right subcostal margin along the right midclavicular line. The entire liver span would be a summation of the distance from the upper margin of liver to the right subcostal margin and the distance from the right subcostal margin to the inferior margin of the liver. 

10. Spleen palpation – begin from the RIF and move diagonally towards the left hypochondrium. As per liver palpation, advance towards the left hypochondrium every time the patient expires until you feel the splenic tip hitting your fingertips. Once you’ve felt the splenic tip contacting your fingertips, stop moving your palpating hand and remain still. Use your left hand to begin feeling the surface and consistency of the spleen and attempt to get above it. Following which, draw the measuring tape again and measure the spleen size starting from the left subcostal margin along the left midclavicular line extending diagonally towards the splenic tip. Then percuss from the right iliac fossa towards the splenic mass to appreciate the change in percussion note from resonant to dull upon reaching the splenic mass. To further verify the splenic mass, percuss also the Traube’s space. In the event the spleen is not palpable, then percuss the Traube’s space. If the Traube’s space is resonant, then it is unnecessary to palpate for the spleen in right lateral position. If the Traube’s space is dull, then should proceed with turning the patient to right lateral position and then re-palpate the spleen from the umbilicus towards the left hypochondrium. Bear in mind, other causes may contribute to a dull Traube’s space on percussion i.e. left pleural effusion or a stomach mass.

11. Kidney palpation – the kidneys are balloted to determine if they are enlarged. If there is a mass arising from the right or left lumbar, the student would be required to approach it like any lump and bump i.e. palpation of the edges, surface, consistency, measurement of size in two dimensions, attempting to get above and below the mass and also percussion. A kidney mass would have overlying resonant percussion note as it is a retroperitoneal structure and the bowel loops are lying anterior to it.

12. Ascites – if the abdomen is grossly distended, it is adequate to perform fluid thrill. If the abdomen is not distended or mildly distended only, then shifting dullness percussion should be performed to identify any underlying ascites. During shifting dullness, while the patient is on right lateral position, can take this opportunity to examine the sacral area for sacral oedema and also inspect the posterior superior iliac crests bilaterally for bone marrow aspiration scars. After completing the shifting dullness percussion, it is also possible to palpate for the spleen in right lateral position if the spleen was not palpable in supine position (if Traube’s space was dull to percussion note).

13. Inguinal lymphadenopathy – I would suggest taking the opportunity to examine the inguinal nodes for any nodal enlargement after turning the patient back to supine position upon completing the examination for ascites.

 

Neck:

After completing inguinal node examination, sit the patient up to examine the cervical nodes. Avoid palpating the jugular chain nodes on both sides at the same time. This is to avoid compressing the carotid sinus simultaneously which may cause vagal syncope. 

 

Respi:

While the patient is sitting up, take the opportunity to auscultate the lungs if time permits – look for crepitation to suggest pulmonary oedema or reduced breath sounds to suggest pleural effusion. These indicate the patient may be fluid overloaded as a result of hypoalbuminemia or as a complication of underlying chronic liver disease or end stage kidney failure.

Back:

While the patient is still sitting, move inferiorly to the sacral area after auscultating the lungs. Examine the sacral area for sacral oedema as well as look for bone marrow aspiration scars over the posterior superior iliac crest region. If this step has been performed earlier, then this step need not be repeated.

 

Lower limbs:

Lastly, move to the legs and while looking at the patient, compress the bony prominences over both ankles to look for pitting pedal oedema.

 

After completing all the above, offer to complete your examination by offering to perform:

1. Rectal examination – not every patient will require this unless indicated. Per rectal examination would definitely be required if the patient is pale, and the examination is to look for melena to suggest gastrointestinal hemorrhage.

2. External genitalia examination – offer to perform this examination if chronic liver disease is in your differential diagnoses. This examination is basically to look for loss of secondary sexual characteristics e.g. testicular atrophy or loss of pubic hair which may be a manifestation of chronic liver disease or in cases of iron overload (transfusion dependent thalassemias or hemochromatosis) resulting in pituitary dysfunction.

3. The student may also offer to perform any steps which the student thinks may contribute to the diagnosis that was not done during the examination due to time constraints.

Having completed the physical examination, the next step would be to SUMMARISE the relevant findings that will lead to the provisional or main diagnosis. After which, remember to offer several relevant differential diagnoses.

Without a proper set of provisional and differential diagnoses, it will be difficult to proceed with a proper discussion on investigations and treatment plan.

Good luck and keep practicing.

 

CCE.

MBBS Finals 2022 - The End is Near

It is Nov 22, a few more weeks to your MBBS finals. You have already amassed a vast amount of knowledge and hopefully, clinical experience, in the past 10 months or so since your Year 5 program started and soon, all those will be put to the test.

It is even more important now to consolidate your learnings and begin to filter those extra knowledge from those essential knowledge. Take note that not everything you have learned in your daily clinical exposure will be tested in the finals. Understandably so because the spectrum of coverage for everything in medicine is so broad and there is only so much time allocated for each student during the examinations.

This is the time when the study list handed out by your faculty at the start of Year 5 will be most valuable. Use that as a guide for your revision. Narrow down your focus to make revision more effective. Time is of the essence. You wont have time to digest and absorb the entire Harrison’s or Guyton’s medical textbooks.

And with all that knowledge on hand (in brain, actually), it is also equally important to know how to apply those on the exam day itself when faced with the patient in the examination room.

For those who are easily anxious, it would be good to learn relaxation techniques to keep your mind clear. Drawing a comparison with our recently concluded GE15 on Nov 19, 2022 which resulted in a hung parliament, you wont want to have a hung mind during the exam day. Keep your nervousness in check, stay focused with a clear mind, speak the right things (and not everything you see), and god willing (regardless whether you are religious or an atheist, you need some amount of divine blessing during the finals) you will clear the finals and graduate.

Over the next few weeks prior to the final exam date, I will find time to post summaries of approaches to the short case examinations for the major medical station systems and hopefully some spot diagnoses cases.

Do read on and make this blog your revision companion.

All the best.

 

CCE.

Tendon Xanthomas

Dear students,

Sharing with you a case I encountered in the cardiology ward some years ago. It was a case of a young patient in her 20s. She suffered an extensive myocardial infarction few months before I met her in the cardiology ward. She was admitted for coronary angioplasty plus stenting.

She had several siblings who were all myocardial infarction survivors and if I recall correctly, her parents were also cardiovascular patients. She has familial hyperlipidemia. 

I recalled her blood lipid levels were shockingly high and blood samples were very lipemic (oily). She was already on several high dose statins and fibrates. My colleagues in the cardiology team were even discussing plans for a lipid dialysis as they were desperately trying to solve her resistantly high blood lipid levels. The challenge was that the treatment was very limited and only very few centres were offering such treatment options, not to mention the high cost of such treatment as well. 

Below are pictures of tendon xanthomas found on the patient.

For those who have yet to see tendon xanthomas, the above photos depict how one looks like. Good luck.

CCE.

Parkinsonism

Parkinsonism is when there is a triad of bradykinesia, resting tremors and rigidity. There are many causes of parkinsonism. The most commonly seen parkinsonism in the  undergraduate medical final examinations would be Idiopathic Parkinson's disease. 

However, not everyone presenting with Parkinsonism signs have Idiopathic Parkinson's Disease. Therefore students should be wary and mindful about offering the diagnosis of Idiopathic Parkinson's disease upon encountering patients with the above triad. Remember, Idiopathic Parkinson's is a clinical diagnosis and its aetiology is idiopathic i.e. cause is uncertain. Although it is a clinical diagnosis and lab and radiological workup is not required to make the diagnosis, it is also important to consider other differentials causing Parkinsonism signs especially if the patient has risk factors. 

One key feature of Idiopathic Parkinson's Disease is that it is asymmetrical. In the early stages of the disease, parkinsonism can be seen affecting one side of the body. As shown in the video above, this patient has resting tremors affecting his right hand. 

The video below shows bradykinesia affecting the right hand of the same patient. 

As the disease progresses over the years, it may affect the contralateral side of the body as well. However, the key feature remains and Parkinsonism signs would still be asymmetrical. As shown in the next video below, this elderly gentleman has advanced Idiopathic Parkinson's disease as well but take note that the frequency of tremors affecting one arm is different from the other arm. 

Anything that causes damage to the basal ganglia can result in Parkinsonism. For example stroke (vascular), demyelinating diseases, brain tumors, drugs or even metabolic disorders like Wilson's disease. It is good to revise about Parkinsonism as it is a common appearance for the medical examinations. 

CCE.