Answer To Recent Case- Acute Weakness and Sensory Impairment

Dear Bloggers

Here is the answer to the recent case.


Question 1: From history and examination, list the problems with this patient

• Rapidly progressive weakness of the lower limbs with numbness
• Ascending sensory level to T10
• Bowel and bladder disturbance
• Loss of muscle power, deep tendon reflexes and Babinski absent in lower limbs
• Incomplete presence of light touch and vibratory sense; absent nociception and thermoreception
  
• Loss of anal tone and 'wink' sign
• Hypertension
• Smoker
• Mildly expansile aorta
  

Question 2: What immediate test or tests would you perform and why?

From the acute history of weakness and numbness progressing over minutes, loss of bowel and bladder function with progression over several more hours is consistent with a acute spinal cord condition either from external compression or impairment of blood supply or a transverse myelitis.
The patient was otherwise well and was afebrile on admission, making a viral infection less likely. Moreover, there was no history of previous back problems e.g. disc herniation. The fact that the patient is a smoker and hypertension are cardiovascular risk factors and with this history, it is consistent with an acute spinal cord infarction.

The immediate test would be do perform an MRI to rule in or out a spinal cord compression. An abdominal ultrasound or CT to look for an aortic aneurysm would also be prudent if there was a history of abdominal pain and/or an abdominal aorta consistent with aneurysmal change. An ECG should be performed to look for atrial fibrillation which might contribute to systemic embolisation. Echocardiogram would also be worthwhile to rule out a cardiac source of embolism e.g. intra-atrial thrombus, vegetation from endocarditis.

Question 3: What anatomical problem is this from the history and physical examination?

The anatomical problem is two-fold. Firstly, the blood supply to the spinal cord has been impaired and this has led to infarction. However, from the physical examination, the nociception and thermoreception plus motor are predominantly impaired whereas a modicum of light touch and vibratory sense are maintained.

In view that the anterolateral cord contains the descending long tracts (corticospinal tracts) and the ascending spinothalamic tracts (pain and temperature), it would appear that the anterolateral cord is most affected with less of the dorsal cord affected which convey senses such as light touch and vibratory sense. However, strangely, the joint position sense was impaired which also runs up the dorsal columns. This cannot be easily explained unless the patient already had an existing peripheral neuropathy prior to the onset of this disorder e.g. diabetes mellitus.

In view that there is a single anterior spinal artery supplying the anterior cord and two posterior spinal arteries, this problem is consistent with an anterior spinal artery occlusion and anterolateral cord infarction.

Question 4: What is the current evidence based treatment for such a condition?

There have been many proposed therapies including anti-platelet treatment, anti-coagulation, thrombolytic therapy. This condition is relatively rare and so being able to perform a randomised control trial is difficult. Hence, most treatments are based on a case by case basis.
However, therapy is similar to that of cerebral infarction.

To date, there has been only one published case of using thrombolysis in a patient with this problem, although I have heard of another case of spinal cord infarction where thrombolysis was also used [unpublished] with good results.


Tex Heart Inst J. 2007;34(1):134-5.

Acute spinal cord ischemia during aortography treated with intravenous thrombolytic therapy.
Restrepo L, Guttin JF.

In the above case, the infarction occurred after aortography rather than de novo without an inciting cause.

In this case, anti-platelet therapy was commenced without modification of the patient symptoms and following this, heparin was commenced. The patient did not receive rTPA.

There was a minimal response to therapy with only a slight improvement in sensation but no improvement in motor response. It is therefore not certain whether the mild improvement was related to the treatment or just the natural course of the condition.

The intial MRI scan showed some osteoarthritis high up in the neck but not considered to be the cause of the symptoms when reviewed by the neurosurgeons. The cord proper looked normal.
A repeat MRI taken after several days again looked normal.

CSF examination was not performed.

ECG showed sinus rhythm and the echocardiogram revealed no thrombus. Abdominal echo revealed no evidence of an abdominal aortic aneurysm.

Arteritis was also considered but the ESR was within the normal range for age and sex.

Several doctors have kindly responded to the case and include Professor Alan Lefor, Professor of Surgery, Jichi medical school, Japan gives a surgeons view of the history and physical followed by the kind Dr Masami Matsumura of Kanazawa University School of Medicine with an indepth and excellent break down of the case into its essential elements. Thanks to both these esteemed doctors for their opinions here.

Professor Alan Lefor:

To me, a case of acute paralysis and anal sphincter loss of tone, is an acute spinal cord problem such as trauma (no history here), spinal cord ischemia (like a dissection, but in the absence of pain might not be as high on the list, although she does have hypertension) or spinal cord compression (like a tumor, hematoma).

My workup would start with a CT scan to evaluate the aorta and spinal canal looking for dissection, aneurysm, and spinal canal mass.

Rx for a dissection would be htn control.

Dr Masami Matsumura:

Questions
1) From history and examination, list the problems with this patient.

Problem list:
#1 Numbness of the buttocks
#2 Rapid onset lower limb weakness, then paralysis of the lower limbs
#3 Reduced muscle tone
#4 Reflexes knee (L2-4) absent, ankle (S1) absent
#5 Light touch- decreased in lower limbs up to the umbilicus (Th10) region
#6 Vibratory sense (posterior column) was intact on the pelvic brim (S3) and right knee (L4) but absent further down
#7 Nociception and thermoreception were absent.
#8 Reduced anal tone (S2-4)
#9 Bowel and bladder disturbance.
#10 Absence of joint position sense (posterior column)
#11 Hypertension
#12 Smoking history
#13 Aorta mildly expansile

Assessment:
At the beginning, this patient is 70 years old woman who has history of HTN and smoking. I would use following system for thinking differential diagnosis in view of weakness. I would differentiate neoplastic or degenerative diseases first.

Vascular: possible, infarction of spinal cord, arterio-venous malformation
Infection: less likely,spinal epidural abscess,Lyme disease, syphilis
Neoplastic: possible, vertebral or spinal cord tumor, metastasis ofbreast cancer, lung cancer,gastrointestinal cancers,or renal cell carcinoma, non-Hodgkin's lymphoma, plasmacytoma, multiple myeloma, orparaneoplastic syndrome
Collagen: possible, sarcoidosis, polymyositis, vasculitis, Guillan-Barre syndrome, SLE (very rare)
Toxic/Metabolic: less likely, periodic paralysis, hypokalemia
Trauma/Degenerative: possible,intervertebral disk disease or spinal stenosis,
Congenital: less likely
Iatrogenic: less likely
Idiopathic: less likely,amyloidosis

Cauda equina syndrome is likely in this case from problem #1 to #10.
#1 Numbness of the buttocks
#2 Rapid onset lower limb weakness, then paralysis of the lower limbs
#3 Reduced muscle tone
#4 Reflexes knee (L2-4) absent, ankle (S1) absent
#5 Light touch- decreased in lower limbs up to the umbilicus (Th10) region
#6 Vibratory sense was intact on the pelvic brim (S3) and right knee (L4) but absent further down
#7 Nociception and thermoreception were absent.
#8 Reduced anal tone (S2-4)
#9 Bowel and bladder disturbance
#10 Absence of joint position sense (posterior column)

Cauda equina syndrome is included in concept of epidural spinal cord compression (ESCC).

UpToDate 16.1 describes as follows:
Neopalastic ESCC is a common complication of cancer that causes pain and sometimes irreversible loss of neurologic function. In adults, the tip of the spinal cord usually lies at the L1 vertebral level; below this level, the lumbosacral nerve roots form the cauda equina, which floats in cerebrospinal fluid. With cauda equina lesions, the weakness is associated with depressed deep tendon reflexes in the legs.

My first question is as follows:
Can we interpret problem #5 Light touch- decreased in lower limbs up to the umbilicus (Th10) region as a finding of cauda equina syndrome?
UpToDate 16.1 describes as follows:
When a spinal sensory level is present, it is typically one to five levels below the actual level of cord compression. Saddle sensory loss is commonly present in cauda equina lesions, while lesions above the cauda equina frequently result in sparing of sacral dermatomes to pinprick.

Cauda equina syndrome can cause decreased light touch in lower limbs up to the umbilicus (Th10) region.

My second question is as follows:
Why she doesn't have back pain?

UpToDate 16.1 describes as follows:
Pain is usually the first symptom of ESCC, being present in 83 to 95 percent of patients at the time of diagnosis.
This patient didn’t complain back pain. But 5 to 17 percent of ESCC cases don’t disclose back pain.

Third my question is as follows:
What is the cause of her cauda equina syndrome?

UpToDate 16.1 describes as follows:
The three most common are prostate cancer, breast cancer, and lung cancer, each of which accounts for about 20 percent of cases.

This patient is woman and smoker.Vertebral or spinal cord tumor, metastasis of breast cancer, lung cancer, gastrointestinal cancers, or renal cell carcinoma, non-Hodgkin's lymphoma, plasmacytoma, or multiple myeloma must be differentiated.

Problem #13 Aorta mildly expansile is probably caused by #11 Hypertension.

Questions
2) What immediate test or tests would you perform and why?
MR imaging

UpToDate 16.1 describes as follows:
MR imaging offers several potential advantages over myelography.
It produces anatomically faithful images of the spinal cord and intramedullary pathology and is even more sensitive than radionuclide bone scans at identifying bony metastases. It can image the entire thecal sac regardless of whether a spinal subarachnoid block is present. It is not contraindicated with large brain metastases, thrombocytopenia, or coagulopathy. It spares the patient a lumbar puncture.

Questions
3) What anatomical problem is this from the history and physical examination?
From the history and physical examination, cauda equina syndrome is likely. Neoplastic disease or degenerative disease including spinal canal stenosis might be the cause of L1 or L2 vertebral level compression.

Questions
4) What is the current evidence based treatment for such a condition?
Administration of corticosteroids is first strategy. Next surgical management with anterior decompression should be considered. If diagnosis is neplastic, radiotherapy or chemotherapy should be planned.

UpToDate 16.1 describes as follows:
Management include the administration ofcorticosteroids(dexamethasone ), followed either by surgery and/or radiotherapy (RT). Aggressive surgical management with anterior decompression appears to give better results than RT alone in patients who are candidates for surgical intervention. Compared to RT alone, surgery followed by RT is associated with better neurologic outcomes. Chemotherapy may be beneficial in patients with chemosensitive tumors.

Interestingly, both Dr Matsumura and Professor Lefor listed spinal cord ischaemia / infarction as part of their differential diagnoses from the history and physical examinations. This is the most important thing.

The case by itself without the advanced imaging studies is very difficult to make an accurate diagnosis and in this case, MRI did not show an obvious mass lesion or even the usual cord infarction pattern. However, with the history of rapid onset, paralysis and sensory loss affecting specific sensory modalities, and a non-diagnostic MRI scan, spinal cord infarction was still considered the most likely.

This was later confirmed by a most excellent neurologist.

Summary

In summary, spinal cord ischaemia is rare accounting for <1% of all strokes. Most spinal cord ishaemia occurs due to abdominal surgery. The spinal cord is supplied by one anterior spinal artery and two posterior spinal arteries. Superiorly the vessels originate from the vertebral arteries and they receive feeding radicular arteries from many levels with many coming from the intercostal arteries.
The Adamkiewicz artery is most commonly affected. Studies have shown that the most probable cause of infarcts is related to mechanical stress affecting the radicular arteries which can extend for several levels. Vertebral body infarcts can also occur and are associated with cord infarction and can be another sign of radicular artery occlusion.

There is an association of spinal cord ischaemia and spinal disease and in such chronic compressive diseases there is impairment of blood flow which can impair collateral blood supplies putting at risk the compensatory mechanisms in the event of ischaemia.

Transient ischaemic attacks affecting the spinal cord can also occur.

Clinical Features Associated with Various Types of Spinal Cord Ischaemia

Anterior spinal artery territory- bilateral motor impairment with spinothalamic impairment

Posterior Spinal artery territory- bilateral motor impairment with dorsal column sensory impairment

Complete [transverse] infarct- Bilateral motor impairment with total sensory loss at and below the area of the ischaemia.

Unilateral infarcts produce a hemiparesis, in the case of anterior impairment, a contralateral spinothalamic deficit and with a posterior impairment, a unilateral dorsal column impairment.

[please review the neuroanatomy of the various sensory pathways-- spinothalamic neurones cross over at the level of entry and traverse to the contralateral side and ascend in the lateral spinothalamic tracts whereas the dorsal column input ascends directly from the site of entry and cross over in the brainstem region. The routes of these two pathways explain why there is a difference in the sensory impairment within the spinal cord and different findings on physical examination].

There are no clear guidelines for treatment as there have been no prospective clinical studies and various anti-thrombotic / anti-coagulation measures have been tried in previous cases. In my opinion, a prospective study seems unlikely to be able provide a clear answer because of the paucity of such strokes.

A Classic Sign-- the Spider Naevus

Dear Bloggers

I apologise for not writing this week. I have been very busy indeed!! I was in Hokkaido teaching junior doctors the art of history taking and physical examination.

Here is a video that was taken some time ago of a patient with chronic liver disease from alcohol excess, which shows the classical sign of a spider naevus / vascular spider.

As can be seen, when the lesion is pressed, the blood is pushed out and when the finger pressure is released, the vascular lesion fills from the centre and spreads outwards. There is a central red area which is the feeding vessel. This is classical !!

Spider naeva are commonly found in chronic liver disease, pregnancy and in patients using oestrogen steroids. They are induced by the high level of oestrogens.

As for the answer to the recent case, I have deferred this until next week. Sorry ! :-0

Have a great weekend!

A Helpful Way to Identify Patient Deterioration Early!

Dear Bloggers

As physicians, we have all been called urgently to attend the patient who has been deteriorating over several days and who is peri-arrest.

An imaginary example of a typical patient vignette includes the orthopaedic patient with a hip fracture, recently operated and with worsening urine output, low fluid intake, increasingly rapid pulse and onset of confusion. Nursing staff have been charting the deterioration in parameters but were unaware of when to tell the surgical doctor because the doctor is always in the operating theatre treating trauma patients.

Another case vignette might be the patient admitted with general deterioration and weight loss with worsening breathlessness, but the junior doctor is on-call in the Emergency Department and has no time to come and see the patient and the nursing staff are unable to pinpoint the problem and have no idea how to help the patient except to give more oxygen.

These types of patient problems do occur in real life and unfortunately more often than one would perhaps envisage. From the two case vignettes, the underlying problem is not initially acute. There has been a chronic or subacute progression leading to deterioration in parameters of the patient thereby leading to a worsening state and hence, peri-arrest.

Sometimes the doctor does not pick up the problem either because of inexperience, infrequent visits to the patient, failure to adequately examine the patient rather than just the area of their specialty interest e.g. the broken hip, failure to ask the patient about new problems and symptoms, failure by nursing staff to adequately measure the daily observations, failure to report problems to medical staff because of inexperience or over work.

However, such problems cannot always be avoided in hospitals although it is possible to measure patient observations and enter them into a Scoring System which involves the patient's pulse, blood pressure, temperature, respiratory rate and AVPU score. The number generated by the parameters provides a total score which can then determine if the patient is at increased risk of deterioration and death.

Such a scoring system is referred to as an Early Warning System (EWS) and nursing staff can calculate this at the bedside and call the doctor in charge of the patient to attend the patient immediately for reassessment to see if changes are required to the patient's therapy to prevent further deterioration.

Many UK hospitals use such a system and it can lead to very appropriate changes in treatment.

Some hospitals have Intensive Therapy Unit 'Out-Reach' teams of highly experienced nurses that patrol the wards for such patients who are deteriorating with high EWS scores and they can make assessments and call the ITU specialists physicians for further help in addition to the Attending Physician so that an appropriate plan of action can be instituted such as moving the patient to the HCU / ICU for further treatment or the decision of appropriateness of active treatment versus palliative treatment, etc.

An interesting study using this EWS scoring system was published by the Oxford University Press several years ago in respect of all new acute admission on a Medical Assessment Unit with validation of a modified EWS. The results are interesting and show how changes were made to patients treatment in an attempt to reduce mortality and provide more appropriate care. The link to paper is here. Please read it and make up your own minds.

In several hospitals I have visited in Japan, I have not seen any equivalence to an EWS scoring system or an Out-Reach team. With many hospitals in Japan having an electronic patient system [Denshi Kalte], such a scoring system could be entered by the nurses with an immediate score produced for the patient with advice to the nurse whether a call to the doctor is warranted.

Such an idea is not new and not labour intensive and can help with patient management.

In the UK and USA amongst other western countries, there has been increasing training of specialist nurses in all specialties who can perform various important functions to aide patient care e.g. gastroenterology nurses, rheumatology nurses, dermatology nurses, Emergency specialist nurses, ITU specialist nurses etc... Such a common place nurse specialist is not so common place in Japan with there still being over-reliance on doctors to carry out almost all assessments and interventions when there is an unfortunate lack of doctors in various hospitals who cannot plug all the leaking holes in the wall.

With increased nursing and physician training, awareness of an Early Warning System and provision of a modicum of responsibility for nurses to intervene in patient treatment decisions, the care of acutely ill patients and deteriorating patients could in my opinion be improved and this is borne out by the evidence from several UK studies, one reference that I have also provided above.

If such a system could be implemented in all hospitals in Japan, there might conceivably be a reduction in sudden cardiac arrests and overall mortality as problems could be dealt with that much earlier.

This would certainly make an interesting study in Japan if anyone is interested by this idea!

Please consider!!!

Another interesting problem!

Dear Bloggers

This anonymised case is a warning for all of you out there when you see someone with leg weakness and numbness to appreciate how rapidly problems can progress. Please try and answer the case as best you can and you are welcome to leave your answers anonymously.

A 70 year old female who was otherwise well was admitted following a short history of

• numbness of the buttocks
• rapid onset lower limb weakness
  

The patient had got up for breakfast normally and was sitting eating her breakfast. She suddenly began to notice numbness of her buttock region and a 'heavy' feeling in her lower back. She decided to visit the toilet as she thought she might pass stool. In the toilet the sensation continued and after several minutes, the patient was unable to stable from the toilet seat because of leg weakness. Her family were concerned and called an ambulance and the patient was taken to the local hospital.

The patient denied any back pain. There was no history of vertebral disc problems, no chest pain or abdominal pain. There were no palpitations. The patient denied symptoms of diabetes such as excessive thirst, blurred vision etc. There was no history of being previously unwell and there were no symptoms consistent with infection or bleeding.

The patient was a known hypertensive and took atenolol 25mg once daily.

She had no drug allergies. She smoked 15 cigarettes per day for 40 years and she consumed small quantities of alcohol occasionally.

On examination

The patient seemed otherwise well. She was afebrile. Pulse 64/min regular. BP 140/80. RR- 16/min. Sats 98% on room air.

CVS: Heart sounds normal. Regular rhythm. No added sounds or murmurs. No peripheral oedema.

RESP: trachea central. Percussion resonant. Breath sounds vesicular.

ABDO: soft, non-tender, no hepatosplenomegaly, bowel sounds normal. No bruits. Aorta mildly expansile

CNS: Cranial nerves 2-12 normal.

PNS:

RUL LUL RLL LLL

Tone Normal Normal Normal Normal
Power 5/5 5/5 4+/5 4+/5
Reflexes
Biceps Normal Normal
Supinat Normal Normal
Triceps Normal Normal
Knee Normal Normal
Ankle Normal Normal

Sensation
Light touch- normal in upper limbs, decreased in lower limbs around ankles and buttocks.

Babinski sign was normal bilaterally.

Coordination of the lower limbs was not performed.

Vertebral examination was non-tender.

Over several hours the neurology worsened:

RUL LUL RLL LLL

Tone Normal Normal Reduced Reduced
Power 5/5 5/5 3/5 3/5
Reflexes
Biceps Normal Normal
Supinat Normal Normal
Triceps Normal Normal
Knee Absent Absent
Ankle Absent Absent

Babinski sign became negative bilaterally.

Sensation
Light touch- normal in upper limbs, decreased in lower limbs up to the umbilicus (T10) region. Vibratory sense was intact on the pelvic brim and right knee but absent further down. Nociception and thermoreception were absent. Joint position sense was not performed.

Anal tone was reduced with an absent anal 'wink' sign.

In fact, the weakness progressed further resulting in paralysis of the lower limbs and bowel and bladder disturbance. However, light touch and vibratory sense were maintained although nociception and thermoreception remained absent. Joint position sense was interestingly absent.

Questions

1) From history and examination, list the problems with this patient.

2) What immediate test or tests would you perform and why?

3) What anatomical problem is this from the history and physical examination?

4) What is the current evidence based treatment for such a condition?

The answer to this fascinating case will be published in the near future.

The Patient Discharge Plan

Dear Bloggers

Patient home discharges are as important as admitting the patient and getting the diagnosis and treatment correct.

As a medical student I was never taught how to assess a patient to plan for a discharge home. I assumed that it would be up to the decision from the senior doctor to decide whether the discharge home was appropriate. As I did my house officer years (residency) in the UK, through the many, many and sometimes tiring ward rounds, I was able to understand how the Consultants decided on how best to plan for a home discharge.

Young patients could usually be discharged on the day the Consultant gave them permission to leave hospital whereas with the elderly patients with mobility and social problems, I learned that a multi-disciplinary team was necessary to provide a safe transfer out of hospital to avoid re-admission because of failure to provide adequate supportive care. For example, elderly patients sometimes need a home visit with an Occupational Therapist to decide whether in fact the accommodation is safe or whether modifications need to be made to make the place more safe. Moreover, some patients who have no home support e.g. no family, need social worker advice to plan for home helpers or new accommodation.

Patients who have become weak after illness need rehabilitation to improve their activities. Sometimes, nutritionalists need to assess the patient to ascertain if calorific intake is sufficient.

All of these other modalities need to be considered in the elderly patients or those patients with special needs.

Hence, when the patient is admitted, it is worth considering when you are thinking of discharge home and what special services the patient is going to require. Hence, a plan can be organised early to engage such services so that the time can be used optimally. It is no good to just sort out the patient's pneumonia and at the end of it say that the patient can go home if they live in bad accommodation, have no support and can't walk properly.

However, patients who have no pre-morbid or social problems can usually be safely discharged as soon as possible.

I have heard of somewhat unusual examples as reasons for keeping patients in hospital and they include

• waiting for the the CRP or ESR to become normal
• waiting for liver function to completely normalise
• waiting for dose of prednisolone to become less than 30mg/day

I previously based my discharge of patients particularly on how they felt and how they looked by physical examination with of course taking into account investigative data. A patient with a recent pneumonia who has entered the recovery phase and is feeling well should not be kept in hospital just for the sake of watching the CRP. That is not a cost-effective reason and blocks an acute bed costing the patient and medical services more money with no particular evidence basis for keeping such patients in hospital.
The CRP in such patient is of course going to be raised, but it is the patient's clinical condition that is most important.

A patient with a raised ESR for polymyalgia make take several weeks or even months to decreased to an acceptably 'normal' level on steroids. Most PMR patient feel well within 48-72 hours of starting steroids and by keeping 'well' patients in hospital again serves no purpose.

Doses of steroids e.g. prednisolone >30mg/day is not a good reason for keeping patients in hospital. Yes, steroids are associated with many adverse side effects. However, if patients are well on their treatment and they have a good social structure and can attend regular outpatient appointments for assessment, then there is absolutely no reason to keep patients in hospital even on high dose therapy.

Patients mostly want to get back to some sort of normal home life, and the longer they remain in hospital the more institutionalised they will become. Moreover, the more they are kept in hospital, the more expensive it will be for them.

In addition, the more patients that you acquire on your medical service without discharging them, despite the fact that they are well, it will lead to the system becoming clogged up with well patients!

Well patients should not be kept in the hospital a second longer than is necessary.

Please consider....

Answers to Case: Patient with Fever, Headache and Sore Throat

Dear Bloggers

Here are the answers to the case from last week.

Question:

1) From just the history and physical examination, list the problems with this patient.

• Fever- low grade
  
• Headache- temporal and occipital location
• Sore Throat
• Tongue pain
• Restricted Jaw opening - TRISMUS
• Shoulder pain
• Fatigue / lethargy
• Lymphadenopathy
• Weight loss of 2kg
• Change in sense of taste and coated tongue
• Hepatitis C infection
• Raised AST & ALT + INR
• Normocytic Anaemia

2) Was there any indication to do a lumbar puncture in this case? Were there any contraindications? What is your interpretation of the result?

• Apart from the fever, there was no obvious indication to perform a lumbar puncture in this case. The patient despite having some headache said it was made worse when combing his hair. Meningeal pain does not worsen by touching the skull. There were also no meningeal signs from symptoms or physical examination. Moreover, there was an obvious relative contraindication that being the raised INR. In fact, an INR >1.4 is a relative contra-indication against LP until the coagulopathy has been corrected (see UpToDate 16.1-Lumbar puncture: Technique; indications; contraindications; and complications in adults).
  
• There is a real risk of puncturing a blood vessel leading to uncontrolled haemorrhage with the potential of causing spinal cord compression leading to paresis, from an extradural haematoma. However, if the need for a lumbar puncture is high, an experienced practitioner should perform the lumbar puncture with the aim of obtaining CSF on the first pass of the needle to avoid unnecessary trauma. Some practitioners recommend fluoroscopic examination to avoid puncturing small blood vessels.
  
• The LP results show that indeed there was trauma making the result somewhat difficult to intepret. However, in view that there are generally 1 white cells for every 1000 red cells, by scaling down the figures one would obtain a mildly raised neutrophil count. However, the LP was in fact repeated, which was again slightly traumatic and this revealed an otherwise normal white cell differential. Gram stain was again negative.

3) What other tests would you like to perform on the day of admission?

• In view of the above history, the diagnosis of Giant Cell Arteritis with Polymylagia Rheumatica is highly likely. Therefore, an Urgent ESR should be obtained. The patient also requires an Urgent Opthalmological Consult to look for retinal vessel occlusion which might be asymptomatic.
  
• Moreover, in view of the sore throat, throat swabs for streptococcus, adenovirus should be obtained. EBV and CMV levels would also be useful here in view of the lymphadenopathy, abnormal liver function and anaemia.
• Three sets of blood cultures should be obtained and and a cardiac echo performed.
• In view of the Hepatitis C infection, a mixed cryoglobulinaemia is a possibility although there are no skin ulcers, so obtaining cryoglobuilin levels would be useful for purposes of exclusion.
• Autommune Profile including ANCA, Rheumatoid Factor, ANA, etc
• TB PPD skin test could be performed and a chest Xray to look for typical TB shadows (there was no such problem in this case). Aiming to rule out TB should not delay the start of steroids in this severe vasculitic condition because of the risk of blindness and stroke. If TB is also considered likely and cannot be ruled out, then treatment for this should also be commenced empirically with the steroids until such tests rule in or rule out the infection, if indeed that is possible (See UpToDate 16.1- Major side effects of systemic glucocorticoids).
• Although this patient has Hepatitis C infection, starting steroids should not be delayed.
  

4) What is your diagnosis? What one test will provide the definitive diagnosis here?

• Suspected diagnosis was:

Giant Cell Arteritis with Polymylagia Rheumatica.

• An urgent temporal artery biopsy should be obtained.
  

5) What treatment would you start and when? How long do you continue such therapy and what other considerations are necessary?

• Oral prednisolone 40-60mg/day should be started immediately even before biopsy is taken because of the high risk of visual loss, stroke and dissection (please see UpToDate 16.1)
  
• Steroids should be kept at high dose for 2-4 weeks monitoring symptoms and ESR. Then slow tapering over 1-1.5 years
• Aspirin should also be given as it reduces the risk of stroke and other vascular events when compared to steroids alone.
• In view of high dose steroids plus aspirin, a proton pump inhibitor (PPI) should also be given to reduce the risk of gastric haemorrhage.
• Steroids can cause osteoporosis and consideration should be given to commencing a bisphosphonate on a weekly basis e.g. Alendronate 70mg. These drugs can also cause gastric irritation and so once a week dosing should be considered. This is yet another reason to provide PPI treatment.
• The patient should be monitored for diabetes and on discharge should be kept under regular outpatient follow-up and the patient should monitor their glucose by use of urinary test strips.
• Opportunistic infection should be considered in patients who are imunosuppressed by corticosteroids especially with doses >10mg /day or a cumulative dose > 700mg. Patients have a higher risk of pneumonia and infection with pneumocystis jiroveci. However, the risk is still small and hence, there is no current recommendation for use of Pneumocystis prophylaxis in patients on steroids alone (see UpToDate 16.1-Major side effects of systemic glucocorticoids )
  

Here is an excellent comment on the case from Dr Masami Matumura of Kanazawa University Medical School.

This case is difficult to diagnose, but challenging case.

Questions
1) From just the history and physical examination, list the problems with this patient.

I listed problems as follows;

1 Fever
2 Headache (which was worse when he combed his hair, suspect scalp pain)
3 Sore throat
4 Fatigue
5 Weight loss
6 Shoulder discomfort
7 Inability to open mouth
8 Impaired taste
9 Tongue pain
10 History of Hep C infection
11 Redness of throat
12 Lymphadenopathy
13 Anemia
14 Tachycardia
15 Tender temporal and occipital areas on the cranium
16 Tender in the neck

2) Was there any indication to do a lumbar puncture in this case? Were there any contraindications? What is your interpretation of the result?

I think there was no indication of lumbar puncture in this case. Because physical examination didn't disclose meningisumus. No neck stiffness, Kernig's and Brudzinski's signs were negative.
I think there were no contraindications for lumbar puncture. PT-INR was 1.52, slightly high. If meningitis is highly suspected, lumbar puncture should be performed.
Considering of the result of cerebrospinal fluid (CSF), traumatic tap is highly suspected. Because count of RCC in CFS was 1600. In this situation, I would order Indian ink stain. We can rule out cryptococcal meningitis.

3) What other tests would you like to perform on the day of admission?

I will order ESR and ALP in this case first. ESR must be high, approximately 100 mm/hour.

4) What is your diagnosis? What one test will provide the definitive diagnosis here?

My diagnosis is polymyalgia rheumatica (PMR) associated with giant cell arteritis (GCA)

Again my problem list is as follows;
1 Fever
2 Headache (which was worse when he combed his hair,
suspect scalp pain)
3 Sore throat
4 Fatigue
5 Weight loss
6 Shoulder discomfort
7 Inability to open mouth
8 Impaired taste
9 Tongue pain
10 History of Hep C infection
11 Redness of throat
12 Lymphadenopathy
13 Anemia
14 Tachycardia
15 Tender temporal and occipital areas on the cranium
16 Tender in the neck

Chronic inflammatory process is highly suspected by problem No. 1, 4, 5, 13, and 14. Collagen disease, infection, and malignancy should be differentiated. I would think problem No. 2, 3, 6, 7, 8, 9, 11, 12, 15, and16 are consistent with manifestations of PMR/GCA.
Another differential diagnosis is Sjogren’s syndrome associated with vasculitis. Problem No. 3, 8, 9, 11, and12 are manifestations of Sjogren’s syndrome. I have never seen a patient with Sjogren’s syndrome associated with vasculitis. But it is my one of differential diagnosis.
Another differential diagnosis is cryptococcal meningitis. This is less likely. I mentioned above.

I listed differential diagnoses as follows:

• PMR/GCA
• Sjogren’s syndrome associated with vasculitis
• Microscopic polyangiitis
• TB
• Cryptococcal meningitis
• Infective endocarditis
• Lymphoma

In this case, PMR/GCA is most likely. This patient is 70 years old man and discloses fever, headache (scalp pain), sore throat, fatigue, weight loss, shoulder discomfort, inability to open mouth (suspect claudication), tongue pain, anemia, tachycardia, tender in the neck, and tender
temporal and occipital areas on the cranium. Patient history and physical examination tell us the chronic inflammatory condition and characteristics of PMR/GCA. ESR is usually greatly increased in PMR/GCA. ALP is also increased in PMR/GCA.

Biopsy of the temporal artery is needed.

Criteria for the diagnosis of PMR/GCA is as follows;
(Bird, 1979)
1 Age > 65
2 Onset <>
3 Morning stiffness > 1 hour
4 Depression or weight loss, or both
5 Bilateral shoulder pain and stiffness
6 Upper arm tenderness
7 ESR > 40 mm/hour

If any three features, Sensitivity 92% Specificity 80%

5) What treatment would you start and when? How long do you continue such therapy and what other considerations are necessary?

I would want to confirm the existence of vasculitis and rule out TB. The possibility of TB is low, because the patient doesn’t have respiratory symptoms and abnormal findings in chest X-p.
Involvement of vessel may be segmental in patients with GCA, the diagnosis may be missed on routine biopsy. Serial sectioning of biopsy specimen is recommended. After the biopsy, glucocorticoid therapy should be started. Treatment should begin with prednisolone, 40 to
60 mg per day for four weeks, followed by tapering to a maintenance dose of 7.5 to 10 mg per day. This treatment should be continued for at least 1 to 2 years because of the possibility of relapse. If my diagnosis is correct, we can expect dramatic clinical response to prednisolone
therapy in this case.

The patient is 70 years old man. We should be careful of side effects of prednisolone therapy, especially opportunistic infection including pneumocystis pneumonia or cytomelgalovirus infection. Osteoporosis is another important side effect of prednisolone therapy in high aged patients. I would prescribe bisphosphonate to him when I start prednisolone therapy.

He has Hep C infection too. The existence of Hep C infection is not contraindicated for prednisolone therapy, however, we should monitor his liver function closely in steroid tapering phase.

Thank you very much for showing me interesting case presentation.

Thank you for such an excellent case commentary Dr Matsumura.

The result of this case indeed revealed the diagnosis of Giant Cell Arteritis with Polymyalgia Rheumatica. This was confirmed by a positive biopsy result.

Echocardiogram revealed no vegetation and blood cultures were negative.
Autoimmune screen was unhelpful with all major antibodies being negative e.g. ANA, ANCA

There was an unfortunate delay in starting the steroid therapy and the patient experienced some partial visual loss and unilateral numbness of his fingers and toes.
Opthalmological examination revealed occlusion of some of the retinal vessels.

Steroids were commenced immediately following this deterioration at a dose of 40mg prednisolone / day, and the patient's symptoms resolved before the result of the biopsy was known.

Moral of This Story

History and Physical Examination can give you the diagnosis to a case despite the difficulty of putting together the symptoms and signs. If GCA is suspected, steroids must be started immediately and not delayed because of the real problem of visual loss, as occurred in this case.

Delay potentially occurring to confirm the diagnosis by biopsy or the concerns about other diseases such as TB should not deter you from starting empirical steroid treatment for GCA. If there are concerns about other diseases such as TB, then empirical treatment should also be commenced for these until they are ruled in or ruled out.
GCA is one of those diagnoses where there are no 100% accurate tests and even the temporal artery biopsy can be negative.

Hence, you have to rely on what the patient says to you and what you find by examination and trust in yourself to have the confidence to start a treatment that can have many adverse side-effects by can also be not only sight saving but also life saving.

Please consider....

A Patient with Fever, Headache and Sore Throat

Dear Bloggers

Today, I bring you another most exciting case.

It is up to you to try and work out the diagnosis here.

A 70 year old male was see in another hospital's outpatient clinic with the following symptoms:

1. Fever
2. Headache
3. Sore Throat

Fever: The above symptoms had started gradually three weeks before. The fever was observed by the patient to be about 37.5 degrees and with slight increase above this in the evenings. There were no rigors associated with the fevers.

Headache: The headache had also come on gradually and was located in the sides of the patient's head and also at the base of the skull at the back. The headache was worse when the patient combed his hair. There was no associated nausea, vomiting, neck stiffness or photophobia. The patient denied visual disturbance and there was no limb weakness described. There was no history of a 'thunder clap' severe headache and no visual aura's.

Sore throat: The sore throat also started at the same time. The patient had been to see a local doctor and inspection of the throat revealed redness but no exudate. No throat swab examination was taken. An upper respiratory infection was favoured, and a 3rd generation cephalosporin was prescribed on that basis but no resolution of symptoms was observed.
The patient's symptoms were becoming progressively worse and he was feeling increasingly tired and had observed a loss of 2kg in body weight.

On further questioning, the patient was also experiencing shoulder discomfort and had in fact been feeling tired for almost 6 months. Moreover, the patient also complained of a recent inability to fully open his mouth. Also, his taste had become impaired. There was also confirmation that there was some tongue pain whilst eating food.

Body Systems Review

The patient denied joint and muscle pain and she described no swelling, no skin rashes, no cough / sputum / dyspnoea / haemoptysis / night sweats. There were no cardiac symptoms such as chest pain or palpitations. There were no other gastrointestinal symptoms such as epigastric pain / vomiting / constipation / diarrhoea / jaundice / change in colour of stool + urine / haematemesis / haematochezia. The patient had no obvious neurological symptoms.

The patient was a non-smoker and there was no history of contact with tuberculosis.

Previous medical history included Hep C infection following vaccination as a child.
There were no other medical problems.

The patient was taking no medications and there were no known drug allergies.

The patient was retired and lived with his wife in a 3rd floor apartment. There was a working elevator which had never had problems. However, when asked, he considered that it might take him several minutes to walk up the several flights of stairs if the elevator was to break because of fatigue.

On examination

The patient looked chronically ill but was fully alert and conversant.

HEENT: His tongue was coated with a thick white covering which was confluent rather than patchy. The oral mucosa was not coated. The throat was mildly red with no exudate. The thyroid was normal size and non-tender. There were several lymph nodes below the mandible bilaterally which were mildly tender, smooth and mobile. They were <1cm>
There was conjunctival pallor but no scleral jaundice.

Hands revealed no peripheral signs of systemic disease.

CVS: pulses were all present. There was a tachycardia of 100/min regular. JVP was not raised.
Heart sounds were normal with no murmur and no added sounds. There was no leg oedema and no evidence of deep vein thrombosis.

RESP: RR- 18/min, Sats 98% on room air, trachea central, no tracheal tug, normal percussion note and normal breath sounds.

ABDO: Soft, non-tender, no masses, no organomegaly, normal bowel sounds. Rectal examination was normal and revealed no faecal occult blood.
There was no jaundice and no signs of chronic liver disease.

CNS: Cranial Nerves 2-12 were normal. Taste sensation was not checked. Fundoscopy was not performed.

PNS: No neck stiffness, Kernig's and Brudzinski's signs were negative. Jolt accentuatuation was negative. Tone, power, reflexes, coordination and sensation were within normal limits.

Musculoskeletal Examination revealed tender temporal and occipital areas on the cranium. There was full range of movement of the neck but generally tender. There was no joint pain or swelling and muscles were non-tender.

Skin Examination: There was no obvious skin abnormality.

Bloods: revealed a normocytic anaemia with a haemoglobin of 8g/dl. Platelets were slightly raised. White cell count was slightly elevated at 12.1 x10^9/L. Liver function tests were three times normal for AST and ALT. HCV PCR was positive. INR was 1.52. Renal function was normal.

Urine: normal.

Lumbar Puncture was performed revealing RCC 1600, WBC 23 (neutrophils 15, Lymphocytes 8), normal protein and glucose. Gram stain negative.

CXR: Normal

ECG: sinus tachycardia.

Questions

1) From just the history and physical examination, list the problems with this patient.

2) Was there any indication to do a lumbar puncture in this case? Were there any contraindications? What is your interpretation of the result?

3) What other tests would you like to perform on the day of admission?

4) What is your diagnosis? What one test will provide the definitive diagnosis here?

5) What treatment would you start and when? How long do you continue such therapy and what other considerations are necessary?

The answers to this fascinating case will be provide in the near future. Please send me your answers so that they can be placed on the answer page.

Happy sleuthing.... :-)

Answer To Recent Case

Dear Bloggers

Here are the answers to the recent case.

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

The other abnormal feature is the platelet count. In fact, she had only 3,000 per microlitre of platelets hence, Severe thrombocytopaenia. Her WBC count was normal, as was her haemoglobin and other coagulation studies.

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Her legs were most affected because of the effect of gravity and venous pooling. The blood being under a column of pressure and with low platelets resulted in severe petechial haemorrhage.

In view of the recent infection, and no other sinister findings being found on examination such as lymphadenopathy, the suspected diagnosis was a viral induced thrombocytopaenia. ITP was also considered strongly in view of the patient's presentation, her female gender, a normal sized spleen and absence of other symptoms.

Of course, malignancy e.g. MDS, leukaemia, other autoimmune diseases e.g. SLE, were considered, but in view of an otherwise normal blood differential and no other features consistent with these pathologies, they were not really considered to be likely as the cause.

Question 3: Why might the BUN be raised?

The BUN may have been raised because of asymptomatic gastric haemorrhage.

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

This patient is high risk for parenchymal haemorrhage. Initially, low platelets results in cutaneous petechiae. If the platelet count worsens, then mucosal bleeding occurs. At this point, one should be highly suspicious of potential severe bleeding ensuing e.g. intracranial haemorrhage, GI bleeding.

Hence, the patient should not be sent home and should be admitted to hospital for investigation and prompt treatment.

Question 5: What other tests would you like to perform?

• The patient should have viral titres taken e.g. Adenovirus, Parvo Virus, Hep C, CMV, EBV, Mumps, Rubella Autoimmune profile e.g. Anti-DS DNA, ANA Abs for SLE
• Blood smear to look for abnormal cell morphology
• Anti-platelet antibodies (if available)
• Bone Marrow Examination-- essential to aid in the diagnosis
• Ultrasound of the abdomen to look for splenomegaly
• Ultrasound of the knee to look for haemarthrosis-- aspiration is not safe with profoundly low platelet counts.
• Rectal examination for occult bleeding (easy to do and often avoided!!)
  
• Gastroscopy and colonoscopy
  
• Treatment here would be to transfuse platelets and treat the underlying cause (if known)

The bone marrow examination revealed: increased numbers of megakaryocytes of normal morphology. There was also a slight increase in the erythroid precursors.

The serology revealed: a normal panel autoimmune profile e.g. normal levels of ANA.

Her viral serology showed past infection with CMV and EBV and Parvovirus and HCV were negative. Other viral serology was unfortunately no performed.

Abdominal ultrasound revealed a normal spleen.

Anti-platelet antibodies were positive with a level of 75 (normal <5).

Hence, in view of the clinical history, physical examination, the bone marrow examination and positive anti-platelet antibodies, it was considered that the diagnosis was:

Immune Thrombocytopaenic Purpura.

She received prednisolone at a dose of 1mg/kg/day -- 50mg in total, and her platelet count increased to 30,000 within 3 days with no new bleeding problems. However, despite high dose steroids, the platelet count did not increase much beyond this level thereby prompting the use of other treatment modalities (see description and treatment of ITP below)

Here is a most excellent response from Professor Masami Matsumura of Kanazawa University School of Medicine with his opinion on the case.

This is interesting case for approaching the diagnosis.

ID/CC: 50-year-old woman with a diffuse skin eruption

Problem list:

1. Episodes of URTI
2. Diffuse skin eruption, suspect petechiae
3. Oral mucosal bleeding
4. Left knee acute monoarthritis without trauma history
5. Oedema of both ankles
6. Mildly raised BUN (20.1)
7. Mild monocytosis
8. Mildly raised CRP

Assessment:

After episodes of URTI, she had left knee acute monoarthritis, diffuse skin eruption, and oral mucosal bleeding. These issues are consistent with Immune Thrombocytopenic Purpura (ITP). Another differential diagnosis is Henoch-Schonlein purpura. Acute polyarthritis is observed in this disorder. However, oral mucosal bleeding is not observed in Henoch-Schonlein purpura. Moreover, palpable purpura is characteristic of this disease. I think ITP is most likely in this case.

Another differential diagnoses are follows:

• Hematologic malignancies including CLL
• MDS
• SLE
• Viral infection including hepatitis C and HIV
• Evans’s syndrome

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

This patient has mucosal bleeding. I think her platelet count is under 10,000/m(micro)L.

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Her physical examination revealed acute monoarthritis in left knee. When we see acute monoarthritis, Gout, Pseudogout, Infectious arthritis, Bleeding, and Trauma (PIG TB is my mnemonics) must be differentiated. She denied trauma episode. Bleeding is most likely in this case.

Question 3: Why might the BUN be raised?

I suspect GI tract bleeding. GI tract bleeding can cause elevated BUN.

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

This patient must be admitted into hospital for close examination and treatment!!

Question 5: What other tests would you like to perform?

• Fundoscopy for examination retinal bleeding
• Peripheral blood cell morphology for detecting large platelets
• Coagulation studies including PT and APTT
• ANA, HCV antibody assay
• Abdominal echo for evaluate spleen size
• Bone marrow aspiration

An anonymous response was received as follows:

1.? Platelets>low; stool occult blood +
2. Henoch Schoelein, Behcet [pathergy from your History], Parvo 19, R/O DVT, anti-phospholipid syndrome
3. ^ BUN from GI bleed
4. In Japan, admit; in North America follow-up in clinic
5. Skin Bx, Fiber Colon/gastro filber if stool blood +; L knee OA

Immune Thrombocytopenic Purpura (ITP)

This is a bleeding disorder resulting from low platelets not associated with another systemic disease. For the diagnosis to be made, other disorders should be excluded through other tests. Autoantibodies are usually produced against the platelet resulting in the low platelet level. In children, a viral infection can also result in ITP.

The spleen is usually normal size except if there is co-existent viral infection.

The symptoms and signs are of petechiae and mucosal bleeding e.g. in the mouth, GI tract etc. Examination of the blood reveals an isolated reduction in platelets but an other normal morphology and differential of white cells and red levels.

Bone Marrow examination reveals normal or increased numbers of megakaryocytes with other bone marrow elements being normal. Other pathologies should be excluded as described above and HIV testing should be performed in those individuals considered to be at risk because this infection can appear in an identical way to ITP.

Treatment consists of corticosteroids e.g. Prednisolone 1mg/kg/day. In those patients who respond to treatment, the platelet count should increase to normal in 2-6 weeks. The steroid dose is then tapered accordingly. In patients who do not respond to treatment and in who have a high risk of haemorrhage, splenectomy is considered.

Other immunomodulatory treatments are sometimes used such as immune globulin transfusions, cyclophosphamide, azathioprine and the anti-CD20 antibody (Rituximab).


Many thanks for all those doctors who contributed to give their opinions on this case.

There will be more great cases coming....stay tuned!!! :-)

A Case For You To Answer

Dear Bloggers

This case was provided to me by another physician and it has been anonymised for purposes of confidentiality.

A 50 year old female was seen in another hospital's out patient clinic because of a diffuse skin eruption.

She had been mildly unwell for 2 months with symptoms of an upper respiratory tract infection, the symptoms that included sore throat, mild fever, chills and nasal congestion. He was initially seen and given acetaminophen and multivitamins. Her throat examination at that time was red but with no exudate. No antibiotics were prescribed. No throat swabs were taken.

Her symptoms initially improved but there was a recrudescence of the same symptoms prompting a return to the hospital outpatient clinic. Again, medications for control of symptoms were prescribed and no antibiotics.

Two weeks before her current presentation, the URTI symptoms had completely resolved and she was feeling otherwise well.

However, after several days, her left knee began to hurt and she found it difficult to walk properly. There was no apparent swelling of the joint or preceding injury as mentioned by the patient.

A reddish-blue eruption began to emerge on her arms, legs and trunk. The eruption was composed of apparently very small areas of haemorrhage which were non-blanching and over approx 1-2m in diameter. The worse affected areas were her lower limbs. She also described other areas erupting after scratching her skin.

She denied visual disturbance, headaches, rectal bleeding or haematuria. Her other joints were non-painful.

She had described noticing blood in her mouth when cleaning her teeth and recent nose bleeds when blowing her nose hard several days before admission.

Previous medical history was nothing in particular apart from seasonal rhinitis.

She was taking no medications

She had no relevant family history and was a non-drinker and non-smoker.

On further questioning, she had no weight loss, a good appetite, no night sweats. No abdominal pains or other GI symptoms. In fact, she was otherwise feeling well.

On examination

Temp 36 C, Pulse 80 regular, BP 120/80, RR- 12, Sats 98% on RA. No Jaundice, Anaemia, Clubbing, Cyanosis, or Lymphadenopathy (JACCL)

She looked well but had a diffuse rash (as described above). Mouth- blue-black raised vesicle on the right lateral border of the tongue and on the buccal mucosa bilaterally. Elevation of the tongue revealed fresh blood in the lateral gutter at the junction of the floor of the mouth and the medial aspect of the gums.

CVS: JVP not raised. Heart sounds were normal. No evidence of DVT.

RESP: Percussion resonant, breath sounds vesicular.

ABDO: Soft, non-tender, no hepatosplenomegally. No ascites. Bowel sounds increased. Rectal examination not performed.

Left knee- mildly swollen. Not warm or tender. Bruising over infra-patella region. No patella tap. Crepitus on extending knee joint.

Oedema of both ankles.

Initial screening bloods were entirely normal except for a mild monocytosis, mildly raised CRP and BUN (20.1) but normal creatinine PLUS one other feature.

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Question 3: Why might the BUN be raised?

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

Question 5: What other tests would you like to perform?

PLEASE SEND IN YOUR ANSWERS BY POSTING THEM ON THIS BLOG ANONYMOUSLY AND THE CASE RESULT WILL BE AVAILABLE IN THE NEAR FUTURE.

Clinical Skills

Dear Bloggers

Now is the season when medical students visit various hospitals around Japan for a 3-day period to see what each institution has to offer for the purposes of future training in the respective residency programmes.

In Japan, most medical students do not have any clinical 'hands on' experience until the beginning of the 4th or 5th year of medical school.

From my previous interactions with several students and residents at different institutions, the general consensus is that the teaching of clinical skills at university is not optimal for what they need to examine patients. Of course, some medical schools have many sessions for teaching on real patients and there is the newly introduced OSCE system to ensure that there is a basic minimum standard. Hence, training can be variable depending on the institution in question.

Some UK medical schools have the medical students learning clinical skills from their very first year by placing them with a community general practitioner who can select for them well patients with chronic illness, who attend the clinic to have their history taken in full in addition to examination by the student. The general practitioner then listens to the history and demonstrates the examination to reinforce good practical skills and to advise on additional history which can help to make a bedside diagnosis.

My medical school was one of the first to do this in the UK and that was nearly two decades ago.

Although the basic knowledge of medicine was still to be learnt, by intercalating the learning from each system, over time it was then possible to gain deeper understanding plus having the background knowledge of how to examine for signs.

Hence, when it comes to the official clinical years, which start from the third or fourth year in the UK system, the medical student already knows the basics such as percussion, auscaultation etc...

One method that is very informative is the ward round system and listening to the consultants taking extra history and examining the patient. The UK medical system is somewhat adversarial in its way towards medical students because invariably they get picked on to be asked the various causes of XYZ disease or how to examine for ABC sign. Although this can sometimes be a stressful process, it forces the medical student to read about the patients they see. Moreover, the consultants invariably ask the medical students again at various stages of their attachment to a firm. Knowing the answer shows that medical student has taken the time to find out what the consultant wants to know.

By joining ward rounds and seeing the patients 'hands on' is the best way to learn clinical skills rather than just from a book in the class room. Patients do not write the books and there can be any number of possible combinations of acute and chronic diseases to provide a challenge to the doctor. This cannot be found in detail to any great extent in a book.

To really understand clinical medicine, you have to do clinical medicine.

Although these 3-day snap shot visits by medical students provide a mere glimpse of how hospital life operates, it is in my opinion, insufficient to learn new clinical skills.

At this hospital, there is the opportunity to do short term externships of several weeks to a month whereby the medical student can be exposed to the daily rigors of clinical medicine and how to treat the common acute problems and the difference of how to treat chronic diseases.

They get the opportunity to take histories from patients and to learn clinical examination in depth.

Such students who have done this in the past with me have learned a lot and their experiences have been very positive.

If you are interested in such an externship at this institution, then please contact me at the email address at the bottom of the blog page.