Right Eye Horner's Syndrome

This elderly male patient presented with chronic coughing associated with dyspnoea and weight loss. 

Examination noted partial ptosis of the right eye but no ophthalmoplegia.

Further examination of the eyes noted reduced pupil size over the right eye compared to the left eye. 

The left eye pupil size was normal.

A diagnosis of right Horner's syndrome was made. 

Respiratory examination noted bronchial breathing over the right lung apex with tracheal deviation to the contralateral side suggestive of a right pancoast tumour. 

Therefore the unifying diagnosis was Right pancoast tumour causing Right eye Horner's syndrome. 

CCE. 

Cranial Nerve 3 Palsy - Surgical CN3

The picture below shows a young girl with complete ptosis of the left eye. She presented with progressive and worsening ptosis affecting her left eyelid. At the same time, she reported having diplopia as well. 

Upon elevating her left upper eyelid, her left eyeball is displaced inferolaterally in neutral position. This finding is consistent with a left CN 3 (occulomotor) palsy. The eyeball is deviated in such a manner due to unopposed action of the left lateral rectus and left superior oblique muscles which are innervated by the left CN 6 (abducens) and left CN 4 (trochlear) nerves respectively. 

It is also important to take the opportunity to assess the left pupil size to determine the possible cause of her left CN 3 palsy. In this picture, it can be seen that her left pupil is dilated compared to the right pupil. This suggests that she may have a space occupying lesion compressing the CN3. In most cases, a cerebral aneurysm (particularly from the posterior communicating (PCOM) artery) need to be looked for. The pathogenesis of a dilated pupil in such a scenario is that an aneurysm arising from the PCOM artery compresses on the CN 3 putting pressure on, and damaging the parasympathetic nerve fibres that innervate the constrictor pupillae muscle that is responsible for pupillary constriction. These parasympathetic nerve fibres run on the surface of the CN 3, therefore when there is an external compression onto the CN3, the parasympathetic nerve fibres would be affected as well.

Once a surgical cause i.e. an aneurysm has been excluded, then a medical cause can still be possible. Bear in mind, the parasympathetic nerve fibres that innervate the constrictor pupillae muscle that is responsible for pupillary constriction is also supplied by tiny blood vessels called vasa nervorum. The vasa nervorum are equally susceptible to damage from medical diseases e.g. connective tissue disorders, diabetes mellitus, atherosclerosis etc like other arteries elsewhere in the body. Once the blood supply to the parasympathetic nerve fibres are disrupted, there will be ischemic damage followed by impaired parasympathetic nerve function resulting in a dilated pupil.

CCE.

Koilonychia

Dear students, welcome back. 

This image shows koilonychia i.e. spoon shaped nail deformities. The typical description is that such nail changes will be able to hold a drop of water. Such abnormal nail changes are usually seen in chronic iron deficiency anemia.

This photo was taken from the hand of a patient diagnosed with Hereditary Hemorrhagic Telangiectasis. As a result of chronic occult bleeding, he was admitted for symptomatic anemia and required blood transfusions. 

It is important to look out for koilonychia when encountering a patient with chronic anemia. Remember to get a complete history regarding chronic blood loss e.g. menorrhagia or bleeding per rectum etc. A complete dietary history confirming reduced iron intake is also important.

CCE.

Dyspnoea - Approach to a patient with dyspnoea for the long case examination

Dyspnoea is a common complaint encountered both in the exams and real clinical practice. 

To approach a patient with dyspnoea, you need to have a list of possible differentials in your mind to enable you to start off the interview smoothly without wasting much time. It is advisable to conduct your long case examination in a "hybrid" manner, whereby after clerking the patient for several minutes, you may proceed with physical examination while taking more relevant history concurrently. This will save you lots of time when comparing to compartmentalising your long case session into history taking, followed by physical examination, then drafting out your management plan.

The causes of dyspnoea are numerous and can be broadly categorized into the systems. This way, it will be easier to draw out a longer list of differentials which you may tackle during history taking and physical examination:

1. Respiratory 

- Asthma:

• Enquire about diurnal variation of symptoms (worse at night or early mornings, symptoms less during afternoons)
• Enquire about atopy: eczema, allergic rhinitis
• Enquire about triggers: dustmites, pollen, animal dander, environmental pollutants (smoke, dust, chemical aerosols etc), respiratory tract infections
• Enquire about family history of asthma or atopy
• Important to enquire about asthma control - frequency of symptoms and exacerbations (will impact treatment plan)
• Look for triggers causing exacerbations in current setting: respiratory tract infections, recent exposure to allergens, non compliance to inhalers or oral medications
  
• Examine for atopy: eczema at the joint flexures (commonly at antecubital fossa or popliteal fossa), nasal turbinate hypertrophy (allergic rhinitis)
• Examine the lungs for ongoing bronchospasm: signs of respiratory distress (tachypnoea, tripod positioning, tracheal tug, intercostal and subcostal recessions), expiratory wheezing or prolonged expiratory phase.  
• Remember to examine the sputum pot if provided in the exams. Look for purulent  sputum to suggest pneumonia 

- Chronic lung disease (Chronic obstructive airways disease/ interstitial lung disease):

• Enquire about symptoms without diurnal variation
• Enquire about history of cigarette smoking
• Enquire about occupation: shipyard workers/ painters (asbestos), sawmill workers, quarry workers, clearners, farmers
• Enquire about previous lung infections e.g. pulmonary tuberculosis, recurrent lung infections that may lead to pulmonary fibrosis/ bronchiectasis due to scarred lung tissue
• If the patient has fertility issues with bronchiectasis, consider Kartagener's syndrome
• Examine for barrel shaped or hyperinflated chest wall, clubbing, asterixis (Co2 toxicity), palmar erythema (chronic Co2 retention), nicotine staining (cigarrete smoking)
• Examine the lungs for ongoing bronchospasm: signs of respiratory distress (tachypnoea, tripod positioning, tracheal tug, intercostal and subcostal recessions), expiratory wheezing or prolonged expiratory phase.
  
• Remember to examine the sputum pot if provided in the exams. Look for purulent or blood stained sputum to suggest bronchiectasis 
  

- Pneumothorax:

• Enquire about chest trauma
• Enquire regarding previous pneumothorax
• Enquire about any thoracic procedures e.g. chest tube, decortication, pleurodesis
• Enquire about family history
• Enquire about patient's height and proceed to examine height and arm span if there is a clinical suspicion of Marfan's. 
• Enquire about history of chronic lung disease or connective tissue disorders
• Enquire about ongoing current lung infection: fever, cough, pleuritic chest pains
• Examine for tension pneumothorax which can be life threatening (unlikely to appear in exams but it is good practice in clinical setting): tracheal shift to contralateral side, displaced cardiac apex beat, reduced chest expansion with increased percussion resonance over the affected side, cyanosis, tachypnoea
  

- Pleural effusion:

• Enquire about lung infection: fever, cough, pleuritic chest pains (parapneumonic effusions)
• Enquire about lung malignancy: anorexia, weight loss
• Enquire about pulmonary TB symptoms: chronic coughing, hemoptysis, drenching night sweats, anorexia, weight loss, PTB contact
• Enquire about heart failure symptoms: reduced effort tolerance, pedal oedema, orthopnoea, paroxysmal nocturnal dyspnoea, cough with frothy pinkish sputum 
• Enquire about chronic liver disease symptoms: yellow discoloration of the eyes, generalised itching, easy bruising, hemoptysis, epistaxis, abdominal distension, pedal oedema, alcohol consumption, sharing of intravenous syringes, multiple sexual partners
• Enquire about kidney disease: frothy urine, hematuria, facial puffiness, scrotal swelling, pedal oedema, nausea/ vomiting, generalised itching

- Airway obstruction/ restriction

• Enquire about foreign body aspiration/ choking episodes prior to onset of dyspnoea
• Examine for stridor 
• Enquire about oral cavity or upper airway swellings: allergic reaction, chemical burns, smoke inhalation, trauma
• Enquire about neck compression: large goitre, large tumour/ hematoma/ subcutaneous emphysema
• Enquire about fatigability: ptosis/ diplopia more prominent towards the evening or night, proximal upper/ lower limb weakness (all these suggestive of Myasthenia gravis)
• Enquire about lower limb paralysis as well; if ascending pattern, suspect Gullain-Barre syndrome (need to check precipitating factors e.g. recent viral infection) and examine for absent reflexes. 

2. Cardiovascular

- Congestive heart failure

• Enquire about reduced effort tolerance, its best to classify severity using the NYHA classification
• Enquire about orthopnoea, paroxysmal nocturnal dyspnoea, leg swelling, cough with frothy pinkish sputum to suggest pulmonary oedema
• History of myocardial infarctions or coronary artery intervention procedures e.g. stenting or bypass grafting surgery
• History of valvular heart diseases or any valvular surgeries
• History of endocarditis or rheumatic fever/ heart disease
• History of congenital heart disease (usually the uncorrected ones will likely progress to decompensated heart failure at a later age)
• Clarify with the patient regarding instruction by health provider concerning fluid restriction and whether patient is compliant to fluid restriction advice
• Any precipitating factor to suggest cardiac decompensation: look for infection, anemia, new myocardial ischemia

 

 

- Myocardial ischemia/ angina

• Enquire about crushing retrosternal chest pains or left sided chest pains with typical radiation to left shoulder/ arm, jaw/ neck and associated nausea/ vomiting/ diaphoresis
  
• Expect atypical presentation in special groups e.g. elderly, diabetic patients
• Enquire about reduced effort tolerance, exertional angina, try classify according to Canadian Cardiovascular Society (CCS) classification. 

- Venous thromboembolism

• Usually dyspnoea will be sudden onset
• May be associated with pleuritic chest pains (as a result of pulmonary infarction)
• Enquire about precipitating conditions e.g. prolonged immobilisation (long haul flights), recent pelvic or lower limb /trauma or surgeries, on combined oral contraceptive pills, history of thrombophilia (unprovoked venous thrombosis, arterial thrombosis, early pregnancy loss, connective tissue disease)
• Examine for pulmonary hypertension (loud P2, left parasternal heaving, tricuspid regurgitation)
• Examine for pleural rubs (pulmonary infarction)
• Examine abdomen for pelvic masses or intra-abdominal tumours
• Examine the lower limbs for any painful calf swellings to suggest deep vein thrombosis
• Look for recent surgical scars over the abdomen and lower limbs
• Look for signs of connective tissue disease: malar rash, discoid rash, peripheral joint deformities, alopecia, Raynaud's phenomenon, sclerodactyly etc. 

3. Hematological

- Anemia

• Enquire about dizziness, headaches, pale look, palpitations, reduced effort tolerance
• Enquire about blood loss: gastrointestinal bleeding, menorrhagia, hematuria, bleeding wounds
• Enquire about fever, bleeding tendencies (may suggest reduced leucocytes or platelets as well, thus pointing towards a hematological or connective tissue disorder)
• Enquire about dietary habits: pure vegetarian, lack of iron in diet etc
  
• Examine for pallor, bruises, hepatomegaly, splenomegaly, lymphadenopathies
• Look at the nails for koilonychia (chronic iron deficiency)
  
• May offer to do rectal examination to look for melena
  

- Hyperviscosity - polycythemia, thrombocytosis, leucocytosis

• On the other hand, excessive blood cells can also cause dyspnoea when there is hyperviscosity
• Ask about headaches, blurred vision, thrombotic episodes e.g. stroke, angina, claudication pains etc
• Ask about bleeding tendencies as well (thrombocytosis can manifest as bleeding) 
• Examine the patient for plethora (polycythemia), hepatomegaly, splenomegaly (may be massive in Myelofibrosis or any of the other Myeloproliferative neoplasms)
• Examine for enlarged lymphadenopathies as well (to suggest a hematological disorder)
• Examine for gum hypertrophy (may suggest acute myeloid leukemia)

4. Endocrine

- Diabetic ketoacidosis

• The severe metabolic acidosis usually seen in DKA can manifest as dyspnoea. The patient may be tachypnoiec as a compensatory mechanism to the metabolic acidosis. Acidotic breathing also known as Kussmaul breathing is different compared to the usual hyperventilation or tachypnoea. You will need to see several or multiple such presentations to be able to appreciate Kussmaul breathing. However, rest assured, such a case will not appear in your exams. 
• Get history about diabetes mellitus and any osmotic symptoms (weight loss, polydipsia, polyuria).
• Enquire about any precipitating factors: infection, trauma, fasting (dehydration), surgery, angina etc
• Do bear in mind that any condition that causes organ failure resulting in metabolic acidosis can also manifest as dyspnoea

- Thyroid disorders

• Paarticularly hypothyroidism. Hypothyroidism causes reduced muscle strength (including respiratory muscle weakness), fatigue and reduced effort tolerance. 
• Hypothyroidism can also cause weight gain and is also associated with obstructive sleep apnoea which can cause dyspnoea as well

5. Drugs

- Drug overdoses - 

• Certain drugs like salicylates (common example is aspirin) can cause high anion gap metabolic acidosis which may result in Kussmaul breathing. 
• Opioid toxicity can suppress the respiratory drive and lead to dyspnoea in toxicity. However opioids if used appropriately can reduce dyspnoea (commonly used by palliative teams everywhere). 
• Therefore it is important to get a proper drug history and explore regarding possible drug toxicity. If there is suspicion of toxicity, it is also prudent to explore regarding possible deliberate self harm. 

6. Psychiatry

- Anxiety:

• The anxious patient may have palpitations, sweating, hand tremors, feeling fearful constantly together with dyspnea 
• In a panic attack, patients may be hyperventilating which may result in carpopedal spasms, so ask about muscle spasms or cramps usually affecting the hands and feet. 
• Patients may complaint of perioral numbness with or without numbness affecting their extremities. If present, this may further suggest an anxiety aetiology. 
• Try to enquire about concomitant major depression symptoms, which may accompany patients suffering from anxiety. 

It may seem like so much to do when seeing a patient with dyspnoea. This is where practice is important and it helps you to go through your differentials more effectively. Also, tailor the differentials to the patient in front of you. Not every differential will be applicable. For example, a young patient who is lean without a barrel shaped chest is unlikely to have chronic lung disease (therefore you need not dwell too long in excluding this differential). A reminder also to examine the patient while taking the patient's history concurrently to save time. You cannot afford to be too compartmentalized in the exams due to time constraint. 

Happy practising. 

CCE.

Apex Beat Missing - What to do?

Looking for the cardiac apex is an important part in the cardiovascular examination, be it the long case or short case examination.

If the cardiac apex is not palpable in the supine position (patient propped up at 45 degrees of course), then the next step is to request the patient to raise the left arm above his or her head and turn to the left lateral position. This enables the cardiac apex to be closer to the thoracic wall thus easier to be palpated.

However, in some situations, the cardiac apex remain elusive in its usual expected anatomical location. Some possible causes are:

1. Thick chest wall

- the thick subcutaneous tissue makes it difficult to feel the apex 

2. Emphysema

- the overlying hyperinflated lung tissue masks the cardiac apex and makes it more difficult to detect

- a hyperinflated chest wall can be suspected when the antero-posterior chest thickness is similar or greater than the distance between the nipples (this is an informal tip, and I do not think it is verified or supported in any medical textbook to my knowledge). 

3. Pericardial effusion

- Increased fluid accumulation in the pericardial layers may "muffle" the cardiac apex making it less easy to detect by palpation over the precordium. 

- However, a significant pericardial effusion may be required to be present before causing "loss" of apex beat. Thus there may be other signs to suggest a significant pericardial effusion e.g. reduced pulse volume, elevated jugular venous pressure and muffled heart sounds. 

4. Dextrocardia

- After satisfying yourself that the cardiac apex is not located within the left hemithorax, try looking for it on the right side instead. 

5. Is the patient "alive"?

- This possibility is unlikely in the exam setting, but of course, just to be sure, ensure there is spontaneous breathing and peripheral pulses are also palpable (especially the carotid pulse) at the same time. 😆

- However this scenario may be possible in the regular medical ward, particularly in the acute cubicle where there are critically ill patients. Some years ago, I have come across a house officer (HO) trying to palpate for the apex beat during morning ward rounds and the poor HO requested for assistance as he was unable to find the apex despite numerous attempts. Upon attending by the senior medical officer, the patient was found to have no spontaneous circulation and immediate resuscitative attempts were started. 😅

CCE. 

Atrial Fibrillation

Atrial fibrillation is a common occurrence in the medical examination. It can appear either as a short case examination or part of the long case examination.

Atrial fibrillation can be easily missed especially if there is bradycardia or tachycardia. However with practice, it can be detected rather easily. 

The 3 key features of atrial fibrillation that a student should be able to identify are:

1. Irregularly irregular rhythm

2. Variable pulse volume

3 Pulse deficit*

* A pulse deficit is when there is discrepancy between the peripheral pulse rate and the heart rate. Depending on which medical article you refer to, pulse deficit can vary between 5 to 10 beats per minute to be considered significant. 

Once atrial fibrillation is detected, a good student will go on to try to determine its cause or associated features:

1. Thyrotoxicosis

- look for signs of hyperthyroidism: exophthalmos, hand tremors, proximal myopathy, goitre with bruit

2. Elderly

- Elderly patients are more prone to have atrial fibrillation

3. Valvular heart disorders

- Examine the heart for any murmurs; commonly mitral stenosis or even mitral regurgitation

4. Heart failure

- Chronic atrial fibrillation may progress to heart failure especially if the heart rate is inadequately controlled. Conversely, patients with heart failure are also prone to develop atrial fibrillation. 

CCE. 

The Lifelong Learner - Foreword

Dear life students,

This blog is created with the main intention to provide guidance to students pursuing medical education either at the undergraduate level or higher, particularly in the subject of Internal Medicine. This avenue is an added measure to reach out to students due to my limited contact time for teaching in the clinical setting.

Being a clinician in Internal Medicine and part time educator affiliated with a local centre for higher medical education, my time is mostly occupied by clinical work and other associated duties in the clinical centre where I am currently serving. The number of hours allocated for each student group is limited as determined by the university and does not commensurate with the vast number of topics in Internal Medicine. Granted that students have already been handed a list of examination topics and syllabus by the medical faculty to narrow down the study scope as well as faciliate revision. 

However, in my opinion, medical education is not, and should not be about passing exams only. Medical education should be focused on producing medical graduates who will be safe and competent practitioners. And the basics in Internal Medicine is already a lengthy list making it a challenging task to emphasize every aspect of the it for the final MBBS or MD exit exams.  

Throughout my more than 15 years of clinical experience, I have come to appreciate the importance of adequate exposure and training for our junior doctors and medical graduates. Having a competent junior colleague on the medical team is crucial and would make patient management more comprehensive and smooth. 

Therefore it is my hope that this avenue will provide students with more exposure to practical medical knowledge especially those relevant to clinical practice and at the same time, assist them in their preparations for their professional examinations.

Let this platform be a medium for exchange of medical knowledge as I believe in two way exchanges. One can never be too old to learn or re-learn. Some information can be forgotten along the way and it is always good to have a reminder every now and then. Feel free to raise a question or add on to the information posted in the comment section. And please do point out any errors on my part that you may come across in your reading of my content. 

Thank you and happy learning. 

CCE.