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.