Sexual History

Dear Bloggers

I am on my vacation this week, but it will not prevent me for writing to you all.

Today I want to mention about taking a sexual history This is an essential part of the history taking especially when considering patients with unexplained systemic symptoms and signs, genitourinary symptoms, neurological diseases, fertility problems etc.

When asking a sexual history, try to be tactful. Speak ideally in a private room off the main ward, but if not possible speak in a low voice to the patient or even write down the questions on paper and ask the patient to answer in writing so that those around do not hear the conversation. This of course depends on the literacy of the patient. Remember that such answers, verbal or written, are CONFIDENTIAL and should not be divulged to persons unrelated to the care of the patient. Written responses should be filed in the confidential patient notes.

Most patients are normallyseen in an outpatient setting and ideally, patients should be interviewed in a clinic room without others being able to overhear. A specialist STI clinic may be more preferable to the patient in some circumstances which usually have tailored facilities.

Questions to ask include:

-Are you sexually active? If so, how frequently ?

-Do you have sex with men or women or both ?

-Are you currently in a monogomous relationship? When was the last time you had sex with someone else? (Remember that being married does not preclude polygamy)

-What type of sex do you engage in? Oral, vaginal, anal etc? Any unusual sexual practises e.g. Group sex?

-Do you engage in safe sex? What do you think it means ?

-Do you use condoms / cervical cap / female condom / spermicide / contraceptive steroids / coitus interruptus (withdrawal before ejaculation) ??

-If you / your partner use a condom, is it worn strictly before insertion or just before ejaculation?

-Have you ever had a sexually transmitted infection (STI)? If so, when ? What type? Where was it diagnosed? How was it treated and for how long?

-Do you worry that you might be at risk of a current STI or HIV infection? Have you ever wanted or been tested for HIV? What was the result?

-(Female) How are your periods ? Regular? How many days between your periods? How many days do you bleed? Are they heavy or light? Do you think you might be pregnant? Have you ever been pregnant? Have you ever had a loss or pregnancy or a termination ?

-Have you had any unusual vaginal discharge e.g. yellow or fishy smell, or an itchiness? [trichomonas, gonorrhoea / chlamydia, candida]

-Does your penis itch inside during erection? Any milky discharge? [gonorrhoea / chlamydia]

-Do you get pains during sexual intercourse (female)? Painful during deep thrusting (female)? Pain on ejaculation (male)? [PID / Prostatitis-- gonorrhoea / chlamydia / mixed infection]

-Have you ever had penile / vulval /anal warts? [HPV]

-Have you ever had a rash in your groin / anal region ? Was it painful? Has it recurred from time to time? [HSV infection]

-Any recent / previous scabs on your penis / vulva / any unusual rash on the palms of your hands or the soles of your feet? Any generalised rash? Any mouth ulcers? [syphilis]

Other questions that could be asked include asking about the patient's occupation e.g. sex worker; exposure to contaminated blood or blood products e.g. tattooing, IV drug misuse, blood transfusion, haemophiliac [not a strict sexual history question]

What's the use of a sexual history at all?

The above questions are useful to determine if the patient is high risk for acquiring / transmitting STIs.

It determines the locations of the body that might be at risk from infection e.g. mouth, anus, vagina-cervix, and hence, which areas need to be tested e.g. cervical swabs.

It determines if an STI has ever been diagnosed and how it was treated and whether it was treated adequately.

Painful sex might indicate Pelvic Inflammatory Disease (PID) and painful ejaculation can signify prostatitis (as can painful defecation and bloody ejaculate).

Basically, the string of questions above can give a clue about the likely cause of an STI e.g. penile itching can be from gonorrhoea, chlamydia trachomatis etc..

Asking about 'safe sex' is important as patients ideas vs doctors ideas are sometimes different. Some people consider that STI transmission only comes from ejaculate exposure and only put on a condom just before ejaculation. This is NOT protected sex. Semen can still leak from the urethra even before ejaculation. Moreover, it does not prevent exposure to HSV, HPV, chlamydia, gonorrhoea, syphilis or HIV. Only condom use prior to insertion can decrease such exposure.

Remember that PID can also cause spontaneous abortion or reduced / loss of fertility. Hence, a pregnancy history is important.

Always consider asking about current pregnancy. Always consider doing a pregnancy test if even the patient thinks they are not pregnant. Early pregnancy can cause bleeding simulating a period. Missing a pregnancy in a person with an STI should be avoided as it changes what kinds of treatments can be provided e.g. Doxycyline should be avoided in pregnancy, and puts the foetus at increased risk e.g. HIV transmission during delivery.

Remember that odd rashes that involve the hands and feet can signify secondary syphilis. An influenza-type illness with headache, sore throat, disseminated morbilliform rash, fatigue, malaise etc may signify an acute HIV seroconversion illness. Remember too, that those patients with viral meningitis should also have a sexual history taken as HIV can present in this way. An HIV test with prior consent from the patient should be considered in such circumstances.

Please remember to ask about this important part of the history. It can sometimes give you the answer unexpectedly.

As doctors, it is your responsibility to find out the patient problems to make a competent diagnosis. Ignoring the sexual history from feeling embarrassed will only lead to further problems. If you miss an important diagnosis such as this, the embarrassment will come back on you for certain.

For a good easy reading text on STIs I would advocate the ABC of Sexually Transmitted Infections by Adler et al, fifth edition. BMJ Books.

Please consider.

An International Flavour

Dear Bloggers

Yesterday saw a group of international medical students visit this institution. Although their visit was only 2 hours, it was still possible in that time to do a short problem based learning [PBL] case and some bedside examination.

It was very impressive to see medical students of all different years of training trying to contribute to the PBL case in order to work out potential problems. One thing I found interesting was the fact that people from other countries do not mind making mistakes in the classroom. By making mistakes and learning where they might have gone wrong allows the whole group to understand. There is no embarrassment in making mistakes and nobody really minds.

As part of my training of doctors in Japan, I make it clear that I want to hear the opinions and answers from the junior doctors, whether they are right or wrong-- that is an important point. It is better to make the mistakes in the classroom setting and learn the best / correct / EBM way to then avoid potentially making a mistake on a real patient. At my institution, I have been able to propogate an environment whereby doctors can speak openly and freely in my teaching sessions and moreover, they are requested to answer questions rather than passively absorbing a lecture. The beauty of Problem Based Learning is that it requires interaction not only from the teacher to the audience but vice versa.


From the 18 members who joined this session, the vast majority have been taught the Review of Systems questioning methodology which is used as a screening tool to define new or existing symptoms or conditions.
Such medical students came from Indonesia, Australia, Hong Kong, Malaysia, Taiwan, Thailand, the Ukraine, South Korea and the UK. The Review of Systems teaching is an integral part of history taking and allows the physician the better understand all the problems that the patient has. By asking all the questions and getting 'no' replies is better than just saying that 'the patient did not say'. The latter relies on the patient having a good memory and thinking that they understand what is medically relevant. That situation would be in a perfect world and diagnoses could be made very quickly. Sadly, it is not the case and hence, screening questions from the ROS must be utilised. Of course, positive replies to questions can lead to the uncovering of a new disease that had been otherwise previously missed or not appreciated.


Finally, at the bedside I was immensely impressed with a young lady student from Malaysia who in her 3rd year of medical school could identify that the patient being examined, had heart failure just by inspection alone, and when she listened to the heart, she defined a 2/6 Levine systolic mitral regurgitant murmur and a gallop rhythm. I say again, she was a 3rd year medical student-- not yet a doctor.
The junior doctors at this institution also receive such high level training in physical examination allowing them to make daily assessments, for example, of patients with heart failure without the need to keep taking chest Xrays. The physical examination is a learned skill that can be taken anywhere and diagnoses at the bedside can be made in the absence of lab data and radiology. It is quick, very cheap (free) and highly effective.

Although such training was just a short snap-shot of what can be taught at this institution, the students seemed very pleased and impressed.

Always remember that every problem that is identified needs an Assessment and every Assessment needs a Plan. There can be no Plan [i.e. radiology / labs / therapeutics] without an adequate Assessment [as taught by Professor Stein, Florida, USA]. It is akin to driving in the dark without headlights.

Finally, I would like to thank Professor Masami Matsumura of Kanazawa University for attending this institution to join my teaching rounds yesterday in addition to the above international medical student teaching session.

Professor Matsumura's comments and opinions were precise and very helpful.

Also, thanks to all the other doctors at my institution who took their time to help out during the day to make it the success that it was.

A Case of Fever and Headache-- A NEW QUIZ !!

Dear Bloggers

Here is a really great case supplied to me from a distant hospital in Japan. It is anonymised as usual to safeguard patient confidentiality.

A 63 year old female was admitted with a four-day history of

• Fever
• Headaches
• Chills
• Malaise
• Generalised arthralgia and mylagia
  

These symptoms began quite abruptly during a trip in Thailand. The patient had visited several places including cities and countryside areas in Bankok and Chenmai over the period of a week.

Fever: The fever was initially high up to 40 degrees C and fluctuated over several days. At the onset of the fever there was one episode of a chilly feeling but no overt rigors.

Headache: This was occipital in origin but not severe. In was dull in nature and the patient did not complain of neck stiffness or photophobia. There was no nausea, vomiting or overt rash.

Arthralgia: This affected the larger joints such as the elbows, knees and shoulders. There was no complaint of joint swelling or redness. The arthralgia symptoms worsened during the rising fever. The myalgia was described as generalised and mild.

On further questioning, the patient denied eating raw or under cooked food, she drank bottled water. There was also weight loss of 4 kilos during the period of travelling abroad.

Importantly, the patient admitted to receiving a mosquito bite on her right ankle at dusk within the hotel which she stayed. The bite predated the onset of her symptoms.

There was no confusion, vomiting, diarrhoea, abdominal pain, cough, chest pain, dyspnoea, rash, and no UTI symptoms.

The patient also admitted to retro-orbital pain at the onset of the illness (pain behind the eyes).

No malaria prohphylaxis was taken.

Previous Medical History included

• Sick Sinus Syndrome (permanent pacemaker inserted)
• Colonic carcinoma 5 years ago (cured)
• Gout
• Gastritis
  

Medication

1. Lansoprazole 30mg O.D.
2. Ferrous sulphate 200mg T.D.S
3. Digoxin 125mcg O.D.
4. Allopurinol 100mg O.D.

NKDA

Family History

Father- gastric cancer
Mother - stroke disease

Habits

Never smoked, Alcohol 1 beer per week.
Otherwise fit and independent.

No Sexual History was Taken.


Physical Examination

On admission the patient looked slightly unwell. GCS 15/15; fully alert and conversant.

General: mild petechial type rash on the left anterior abdominal wall. No JACCOL.

HEENT: - nothing particular of note. No conjuctival pallor or jaundice.

CVS: Pulse 70 regular, BP 110/61mHg, JVP not raised, no heaves or thrills. Heart sounds 1 & 2 present. No added sounds or murmurs.

RESP: RR 12 / min, SpO2 94% breathing ambient room air. Percussion resonant, Auscaultation normal vesicular breath sounds.

ABDO: Soft, flat, non-tender, no hepatomegaly, mild splenomegaly. Normal bowel sounds. No bruits.

MUSC-SKEL- Normal range of movement of the joints. Non-tender, no swelling or erythema. Slight muscle pain.

Abbreviated Neuro Exam- No neck stiffness, Brudzinski and Kernig Signs negative. Normal movement of the upper and lower limbs. Gross power intact. Babinski sign negative.
Pupils equal and reactive to light. Normal extra-ocular movements. Otherwise intact cranial nerve. Fundoscopy revealed no bleeding and no papilloedema.

Laboratory Data

Total White Cell Count 1.4 x 10-9/L (decreased); neutrophils 25%.
Hb 13.4 g/dl
MCV 89.1 fl
Platelets 129 x 10-9/L (decreased)

Creatinine Kinase (CK) 816 IU/L (elevated)
AST 82 IU/L (elevated)
ALT 41 IU/L
LDH 331 IU/L (elevated)
ALP 151 IU/L
gamma GT 13 IU/L

Bilirubin (total) 1.0 mg/dl
Amylase 94 IU/L

Questions:

1) Bearing in mind the history, physical examination, and basic laboratory data, please make a problem list.

2) Taking into account the geographic location please list the possible differential diagnoses that could result in the above features.

3) What tests need to be done?

4) What is the likeliest diagnosis in this patient?

5) What is the treatment?

I would like all the readers to have a go at answering this question. Please post your answers on this blog and I will publish those answers that are submitted with the actual answer in the near future. GOOD LUCK !!!!

Have a great weekend..... :-)

Prostration Equals Intubation

Dear Bloggers

Today I want to touch on the topic of aspiration. This is a common medical problem in Japan and the aspiration of food or gastric contents can be due to a whole host of medical and surgical problems which predispose for these substances to enter the respiratory tract to cause both chemical induced inflammation and polymicrobial infection.

All the famous textbooks can tell you the history, physical, examination x-ray findings, bacterial culture results and treatment modalities.

I want to concentrate on a simple thing-- patient positioning.

Take for example, a patient with a small bowel obstruction 小腸の閉塞. Such patients have frequent vomiting and are at significant risk of aspiration of bowel contents which include gastric acid and organisms. Such patients normally require nasogastric tube suction to prevent the contents from regurgitating leading to aspiration. Moreover, intravenous fluid administration and a strict nil by mouth regimen should be adhered to until the problem is resolved.

Patient positioning is extremely important. If a patient is lying flat at 180 degrees (prostrate) and if there is incomplete closure of the functional valve at the lower oesophageal sphincter, there is a real risk of regurgitation / vomiting with secondary aspiration. Having visited many hospitals in Japan, it is very variable whether patients are nursed flat or at an incline.

If patients are nursed at an incline, gravity helps the patient to reduce the likelihood of the regurgitation effect. It is not at all fool proof as patients nursed at an incline can still vomit and aspirate, but the 'head up' incline certainly reduces the risk of aspiration although, I would also advocate additional NG tube suction, intravenous fluid and nil per oral regimen otherwise known in the UK as 'drip and suck'.

If the patient has contraindications to being nursed at an incline e.g. shock, trauma, then the patient should ideally be nursed in the 'recovery position' or if not possible, to protect the airway with an endotracheal tube still with concomittant NG drainage of the gastric contents. The tracheal intubation is a drastic move but may be necessary if the other approaches are not feasible.

However, if the patient has no obvious contraindications, please consider raising the head of the bed e.g. 30 degrees or higher if need be, to ensure that the head of the patient is at an safe incline rather than flat, in order to reduce the risk of aspiration.

Although patients in Japan are commonly nursed in the flat / prostrate position, there is no evidence that there is any need for them to be nursed in such a position.

Moreover, as I have eluded to in previous blogs, patients with chronic lung disease, heart failure, acute myocardial infarction, etc should all be nursed at an incline e.g. 45, 90 degrees depending on the severity of their disease in order to aid respiration. Lying such patients flat is not helpful for their conditions and aspiration can occur here to worsen the scenario.

UpToDate 16.1 also advocates nursing patients at an incline. Please check out their website.

Professor Alan Lefor, Resident Professor of Surgery, Jichi Medical University (previously Prof of Surgery and Oncology at Cedars-Sinai Medical Center, USA) has kindly commented on the aspect of aspiration per se and ventilated patients.

In the USA, all patients on ventilators are expected to have the “ventilator bundle” which is defined as

The key components of the Ventilator Bundle are:

· Elevation of the Head of the Bed

· Daily "Sedation Vacations" and Assessment of Readiness to Extubate

· Peptic Ulcer Disease Prophylaxis

· Deep Venous Thrombosis Prophylaxis

This is an important quality measure in the USA, and by doing all 4 things, complication rates are significantly lower. Please note the inclusion of elevation of the head of the bed, as you emphasize.

By using anti-acid meds, if there is aspiration, it is not as serious.

I agree that positioning is critical, and that patients should have the head of the bed elevated.

Furthermore, it is critical to understand that nasogastric suction does NOT prevent aspiration, in fact by stenting open the LES [Lower Esophageal Sphincter], it may increase the rate of aspiration. Therefore, meticulous care is needed to assure that the tube is functioning well and emptying the stomach.

Also, aspiration is possible with endotracheal intubation. Thus, good clinical care and elevation of the head of the bed is required as well. Too many people think that once there is an NG or intubation that they don’t have to worry about aspiration. This is simply wrong.

Thank you as always Professor Lefor for such helpful comments.

As has been raised above, patients should be receiving thromboprophylaxis. This is indeed the case in the UK for any patient who is immobile and peri- /post- surgery. In fact, patients who are immobile >3 days or post-surgery are at increased risk of DVT-PE and to signify just how important it is, this is incorporated into the Modified Well's Score for PE prediction. Such patients, unless contraindicated, should receive Clexane (enoxaparin LMW heparin).

This may, however, not be possible in Japan as such therapy is not covered by the health insurance system. However, it is possible to provide subcutaneous unfractionated heparin twice daily e.g. 5000 U bd. Nevertheless, there is always the concern by physicians that patients may bleed on heparin. One has to measure the risk to benefit ratio of giving prophylactic heparin. The risk of bleeding with patients using LMWH is about 3-4% and such bleeds are usually non-life threatening. However, mortality from PE i.e. undiagnosed or untreated ranges from 30-40% (treated PE mortality is about 5%) . Hence, the numbers of risk to benefit are in favour of prophylaxis. Immobile patients are at risk of DVT and PE and there have been several cases of patients at various hospitals in Japan developing DVT-PE who were not receiving prior prophylaxis.

Moreover, in the UK, ICU patients are generally nursed with the head up with NG tube on free drainage / suction and IV proton pump inhibitors are given. Intravenous H2 blockers e.g. ranitidine, soon develop a reduced efficacy and are inferior compared to PPI therapy e.g. omeprazole / pantoprazole, the latter drugs which have the most evidence base. Again, as mentioned to by Prof Lefor, lying intubated patients flat is not helpful as it does not prevent aspiration and may also impair respiration.

Prof Lefor raised an extrememly important point with regards to attempting to extubate the patient. The longer the patient is maintained on pressure ventilation, which reduces the work of breathing in most instances, there is soon respiratory muscle wasting making it more difficult to eventually wean the patient off the ventilator. Of course, patients should be weaned as soon as is clinically safe to do so, but prolonged periods of intubation should be avoided at all costs to prevent the horror scenario of ventilator dependence.

I hope the above clinical discussion is helpful to all physicians...please consider....

Have a great day.....

Teaching the Nurses Abdominal Examination

Dear Bloggers

Last night was the second in my series of lectures of teaching the various elements of clinical examination to the nursing staff.

The topic of last night's meeting was the abdominal examination.

It was necessary to explain that much of what leads to differential diagnosis of abdominal disease is based on the history.

For example, with abdominal pain, was the onset acute or slow onset, the location, the quality, the severity, radiation of the pain, relieving factors, precipitating factors and exacerbating factors, etc... All these elements can be important to give a particular diagnosis more weight than other disease processes.

One of the nurses raised an excellent question with regards to why acute appendicitis typically begins as central abdominal pain and then becomes localised in the right iliac fossa. It was then necessary to explain about the difference of the nerve supply to the bowel compared to that of the abdominal wall and distension of a viscus resulting in poorly localised pain compared to direct stimulation of the parietal peritoneum resulting in localising pain respectively.

In this 2-hour session, it was not possible to cover all the elements of the history and physical examination of the abdomen, but a number of serious conditions and their clinical manifestations were covered e.g. pancreatitis with Cullen's and Grey-Turner's signs, bowel obstruction, acute cholecystitis and so on.

From the photo above, it can be seen that the 'simulated patient' and other nursing staff were asked to perform the clinical examination for encephalopathy, known as hepatic flapping tremor or asterixis.

Thanks to Yuka-san for such great translating to the nursing staff !

Have a good day.... :-)

Ways to Identify Jugular Venous Distension

Dear Bloggers

I often get asked the question about how to identify the internal jugular vein for measuring the Jugular Venous Distension (pressure).

It is sometimes not so easy to be able to identify by just positioning the patient.

Interestingly, in some US based examination texts, they mention that the patient should be positioned at 30 degrees. This concept is contrary to the traditonal way of checking the JVP which is at 45 degrees-- the UK standard.

Hence, with the patient at 45 degrees, they should turn their head to the left hand side thereby exposing the two heads of the sternocleidomastoid muscles (sternal head and clavicular head). The internal jugular vein should be seen to run between these two heads in an upward and anteroposterior incline.

The normal JVP is no more than 4cm H2O. This is measured in a vertical direction from the manubriosternal joint to the maximum height of the jugular venous pulse.

An estimated height is adequate because the most important thing is to identify if it is raised or normal i.e. just visible.

There are several different wave forms to the JVP, which although are described in the traditional physical examination textbooks, in everyday practise, only a few of them are clinically helpful.

If one is unable to idenfity the JVP by position at 45 degrees alone, then if the patient has no abdominal pain, try pressing on the liver and watch for a rise in the JVP. This is the hepatojugular reflex.

Moreover, the JVP has a double pulse compared to the carotid that has just one.

By positioning the patient vertically, the JVP should disappear (unless severe venous obstruction) whereas the carotid pulse does not. Conversely, by lying the patient flat, the JVP should then increase.

The JVP may sometimes be missed by the inexperienced eye particularly if the patient has a large neck with subcutaneous fascia. One other sign is to look for movement of the earlobe. With severely elevated JVP, with the large upstroke of blood in the internal jugular vein, it causes the earlobe, beneath which it runs, to move!

Why is the JVP important at all??

JVP is important because with the right clinical history, it may aid in the diagnosis of heart failure, atrial fibrillation, tricuspid regurgitation, cor pulmonale, PE, tamponade, iatrogenic fluid overload etc... Although it is relatively non-specific for the above conditions, it nevertheless gives the physician some idea that there is pathology occuring that requires further investigation.

For example, in a patient with slowly increasing breathlessness, dyspnoea on exertion and at rest, plus the complaint of bilateral leg swelling, the physical examination looking for the raised JVP and lung crackles would make one consider at least the common diagnosis of heart failure.

Conversely, sudden on onset of dypnoea, chest pain, haemoptysis, unilateral leg pain with an examination of a tachycardia, raised JVP and a clear chest would make most competent physicians consider a large pulmonary embolism.

I hope this helps!

Why Are The Hands So Important?

Dear Bloggers

Today I want to go over why I think the physical examination of the hands is such an important part of the general physical examination.

Without a good look at the hands, one can sometimes miss the diagnosis that might otherwise take a long time to make via other means.

After standing at the end of the bed to observe the general appearance of the patient, I advise to then look at the hands.

Check the nails-- these are like the looking glass into the body. Digital Clubbing is a great sign to find and can help to narrow your differential diagnosis significantly. Please see my previous posting on this topic of clubbing here.

One can also see the arrest of nail growth referred to a Beau's Lines, which are horizontal indentations in the nails. One can accurately date the onset of serious illness by measuring the distance in millimeters from the Beau line to the edge of the nail fold. The nail grows approximately 0.1 mm / day. Hence, for example, a distance of 5mm would equate to onset of illness dating back 50 days or just under 2 months.

Muehrcke's Lines are paired white lines without indentation that are seen in the nail in patients with hypoalbuminaemia, post-chemotherapy etc.

Splinter haemorrhages, which are outlined in my previous blog entry linked above, are a fascinating phenomenon which may indicate infective endocarditis. They are not a pathognomic feature because they can also be caused by trauma to the nail. Hence, if you see them, don't just consider I.E. Ask the patient if they do gardening or some other hobby or employment that exposes them to nail trauma. However, more than 6 is significant for considering I.E.

Koilonychia (spoon nails) is the famous sign of iron deficiency anemia. However, never forget to look at the corners of the mouth for red, painful areas which is known as angular cheilosis. The tongue may be affected by atrophic glossitis (inflamed). Problems with swallowing should alert you to the rare post-cricoid web which can become cancerous. The presence of the latter with IDA is referred to in the UK as the Plummer-Vinson Syndrome and in the USA as the Patterson-Kelly-Brown Syndrome. Both identical syndromes were described at approximately the same time in the two English speaking continents!

Looking at the nail folds is very important. Sometimes, nail fold infarcts can be visualised as is the case in rheumatiod vasculitis and several other vasculitic disorders. Moreover, if one looks closely at the nailfold proper, seeing capillary loops may signify systemic lupus erythematosis (SLE)! Yes, just from looking at the nailfold!

As I documented last week, Quinke sign can be found in the nail in the area of the interface between the white and red areas of the nail. It can also be found in the skin-- ? B−sign :-)

Nails can also be affected by psoriasis and take on several features including:

• Subungual hyperkeratosis (thickening of the nail)
• Onycholysis (lifting off of the nail)
• Nail pitting (looks like the indentations on the surface of a thimble)
• Nail ridging

In the UK exams, they may sometimes just show the doctor the patient's finger nails and ask for the diagnosis without showing the patient's skin. Psoriasis would be the right answer.

Looking at the tips of the fingers can reveal the tender Osler Nodes (small lymph nodes) of I.E.

One might also be able to identify the skin colour changes of Raynaud's Phenomenon.

Tightening of the skin of the fingers is a sign of possible systemic sclerosis.

Of course checking for diffuse synovial swelling, joint swelling, joint pain and deformation is important and part of the rheumatological examination and diagnoses of RA, osteoarthritis, gout, etc, can be made in addition to the unusual Complex Regional Pain Syndrome which can mimick rheumatic disease.

Looking at the palm of the hand may reveal thickening and shortening of the 4th and 5th tendons that one sees with Dupytren's contracture, the cause of which is usually due to alcoholic liver disease, although other causes include

• Use of heavy, vibrating machinery e.g. drilling tools
• Peyronie's disease
• AIDS
• Epilepsy (due to drug treatment)
  

The palm may also reveal Janeway lesions of I.E., and hence, this is another very important place to observe for signs of this serious infection.

Palmar erythema (red palms) is another helpful sign as it may signify one for the following

• Liver disease
• Thyrotoxicosis
• Rheumatoid arthritiis
• Pregnancy (the distended abdomen usually gives you a better idea :-) )

Checking the lines in the palms may reveal hyperpigmentation which is consistent with increased output of ACTH e.g. Addison's disease, ACTH secreting tumour; obviously, this depends upon the race of the patient as it is easier to identify in lighter skinned individuals.

Ask the patient extend their arms and fully extend the palms with open fingers to look for the sign of asterixis (flapping tremor) that one can observe in

• Hepatic encephalopathy
• CO2 retention
• Uraemia

Checking for muscle loss in the hand e.g. thenar eminence, may give you a clue about median nerve impairment whether it be an entrapment in the carpal tunnel (check Phalen's and Tinel's tests for that) or higher up in the arm / cervical area.

Checking the muscles on the dorsum of the hand (Dorsal interossei) can signify a motor neuropathy, myopathy, or malnutrition if bilateral and diffuse. However, be warned, unilateral dorsal interosseus muscle wasting in a smoker can signify the presence of a Pancoast tumour.

Other neurological signs can be found in the hand which include the fine tremor of thyrotoxicosis, the pill-rolling tremor and cog-wheel rigidity of the wrist in Parkinson's disease. Hoffman's Sign, flicking the nail of the middle finger in a downward motion leads to the flexion of the index finger and thumb, which signifies an upper motor neurone lesion.

The last and widely neglected part of the physical examination is taking the radial pulse. This is truly essential. One must assess the heart rate, rhythm, and volume quality. The first two are relatively easy to understand. The third essential element requires experience in understanding the normal pulse and being able to understand the abnormal.

The patient with a high bounding pulse which collapses may well have aortic regurgitation or a vascular shunt e.g. portocaval anastomosis in liver failure, dialysis shunt. On the other hand, the pulse may be slow to rise which signifies advanced aortic stenosis.
A jerky pulse may signify hypertrophic cardiomyopathy.
The low volume pulse can be found in patients with poor cardiac output, hypovolaemia e.g. vascoconstriction, and is described as thready.

Hence, as can be appreciated, there is a vast amount of information that can be gleaned from examining the hands.

For a more in depth explanation and to see pictures of the examples I have given above, please see a good physical examination book. I would highly recommend MacLeod's Clinical Examination, which has 424 pages with detailed colour illustrations and is published by Churchill-Livingston which is obtainable from Amazon or other good book sellers. I used an earlier edition for aiding my learning of physical examination as a student, and I consider it as an excellent book for this medical art. In my opinion, it is better than the various 'famous' USA physical examination books that are promoted in Japan.

Hence, please start looking at the hands. You will be amazed what you may find.

Hokkaido and beverages to boot!

Dear Bloggers

I recently returned to Hokkaido to teach the junior residents in an excellent local hospital.

Most of the residents I have worked closely with previously and it was a delight to be able to impart some further knowledge based on hearing the histories and seeing the physical examination of various patients.

Below are some photos of the residents and nursing staff attending the rounds.

Later in the evening, the hospital team and myself dined out locally to try some cuisine in an old converted red brick warehouse which housed a famous German-style beer restaurant. You can see the red brick behind ! Ahhh, reminds me of England..... As can be seen, when drinking from a glass boot, when one wants to get the last drop of beer, it can prove quite a challenge.

Here is the original boot of beer. It was my first time to see such a glass....!

One the other hand, for nostalgia purposes, I was duty bound to have my own country's brew of the famous Guiness, otherwise known as Black Gold :-) or Genius!

Following such a lovely gathering of like minded doctors and the free flow of beverages, we went to a famous Mountain to observe what is regarded as one of the most beautiful night views in the world. I would agree whole heartedly. What a great night !

The next day, up bright and breezy, albeit slightly worse for wear, it was time to teach the residents about how to use the traditional opthalomoscope.

Here, the 1st year doctor is looking for the 'red reflex'

Here the doctor is trying to identify the position of the optic disc.

Opthalmoscopy is best performed in a darkened room with the patient's pupils dilated with tropicamide

In this patient, the doctor was able to identify bilateral dense opacities in the lenses consistent with cataracts.

I am looking forwards to going back again.... :-)

Quinke Sign in the Skin !!!!

Dear Bloggers

Sorry for keeping you waiting for new updates this week.

Here is a patient from with ankylosing spondylitis who was noticed to have pulsating carotid arteries in the neck.

Examination revealed a high upstroke volume of the radial pulse followed by a collapsing quality. The carotid pulsation was the classical Corrigan Sign.

Cardiac examination revealed a low grade systolic murmur at the aortic area with radiation to the carotid arteries in the neck. There was no audible diastolic murmur.

Femoral bruits were heard and the popliteal arteries were also palpable (in normal individuals it is unusual to feel the popliteal arteries unless hyperdynamic circulation or popliteal aneurysms are present).

As can be seen from the video below, Quinke Sign is strongly positive. Usually, one sees Quinke sign in the nail bed as a change in the redness that surrounds the white part of the nail near to the nail fold. It is a bit like watching the 'tide come in and out' in the nail. However, in this patient, the regurgitation was so strong, this change in blood flow pattern could be seen in the skin !!!

This patient had suspected Aortic Regurgitation. 

Ankylosing spondylitis is associated with aortic root dilatation and may precipitate aortic regurgitation. Other causes of aortic dilatation include:

• Marfan's Syndrome
• Reiter's Syndrome
• Atherosclerosis
• Syphilis (aortitis)
• Hypertension

Causes of Aortic Regurgitation not associated with dilatation include:

• Rheumatic heart disease
• Infective Endocarditis
• Trauma
• Bicuspid valves
• Disproportionate cusps

As a first year doctor in the UK, I first found Quinke sign in an elderly lady with accelerated hypertension who had a wide-pulse pressure. On the ward round the next morning I mentioned to the consultant that the patient had Quinke sign. The consultant boastfully said that he had never seen it-- until he indeed checked the patient and confirmed that it was indeed Quinke sign!!

Just because you may have not seen a sign does not mean that it does not exist anymore or is somehow obsolete. I have seen Quinke sign over a dozen times or more in my career by just spending the time to look for the sign when considering the diagnosis of Aortic Regurgitation.

Things to think about at the bedside to suspect the diagnosis include:

1. Wide Pulse Pressure
2. Collapsing pulse and Water Hammer pulse
3. Quinke Sign
4. Corrigan Sign 
5. De Mussett's Sign (head nodding with the cardiac cycle)
6. Femoral Bruits 'Pistol Shot'-type
7. Popliteal pulses being palpable
8. Aortic ejection systolic flow murmur
9. Diastolic flow murmur

Have a good day!

Headache and Sensory Changes - History Reveals All !!

Dear Bloggers

This next case has been anonymised for safeguarding patient confidentiality.

In a recent case at a distant hospital in Japan, a young patient was admitted with a headache and sensory changes down the left side of her body.

The headache had occurred in the morning and had woken the patient from sleep. She had severe pain and was unable to stand. She then noticed that she had sensory changes down the left side of her body although her limb movements appeared to be unimpaired. 

She mentioned to the junior resident that she had no previous medical history of note and was taking no regular medications.

There was no history of thrombotic diathesis, no symptoms of SLE, no pregnancy or consumption of oestrogens and no smoking history. She had no subjective fever and had no preceding infective symptoms. She complained of no neck stiffness or photophobia. She had not had any preceding sexual intercourse prior to the onset of symptoms (n.b. sexual intercourse is a classic history before SAH). There was  no chest pain or interscapular pain. She complained of no bone / vertebral pain and the headache was not worsened by subjective head or neck movement.

On examination (when seen by the resident), there were focal problems on general physical examination.

Neurological examination revealed left sided cerebellar signs of slowed irregular movement when performing finger-to-nose examination, mild nystagmus to the left side and dysarthria. There was sensory loss including modalities of light touch and nociception on the same side.

There was no sensory loss involving the face, and cranial nerves were otherwise normal.

The differential diagnoses before cranial imaging included:

1. Stroke (infarction or bleed) causing a Wallenberg Syndrome (Lateral Medullary Infarction)
   
2. Encephalitis
   
3. Meningitis
   
4. Transverse Myelitis
   

After several hours, the patient had had several studies including CSF examination and a cranial MRI scan.

The patient was then seen by a senior physician who wanted more history!!

The patient first mentioned the headache. The senior physician asked the patient to explain the quality of the pain. The patient replied that it was a throbbing type pain. Such throbbing is generally inconsistent with any of the above causes. 

The next question was whether the pain was unilateral or bilateral. The patient mentioned that it was predominantly unilateral.

The physician then asked if the patient had a 'history of migraines'. The patient said-- YES!

The next question was- 'Is this the same pain as with previous migraine attacks?' -- YES!

Why the patient had not mentioned migraine to the resident doctor is anyone's guess, but it is clear that the diagnosis of migraine had not be entertained because the quality of the headache had not initially been appreciated. Pain in the head is not simply pain. Pain has many different qualities e.g throbbing, lancinating, pressure-type, superficial, deep etc. However, in a young patient, throbbing pain would make one consider migraine whereas in an elderly patient, temporal arteritis might be the cause.

Some patients do not remember their medical history in detail and may have infrequent migraine episodes such that they do not think to mention it to the doctor. The fact that the patient had a headache should always make the physician consider whether migraine is a possible cause. 

Basilar-Type Migraine can cause headache and peripheral sensory problems such as this.

The patient recanted the previous migrainous episodes and there had always be a visual aura. However, on this occasion the patient had awoken with the symptoms and hence, no aura had occurred. However, migraines classically can occur upon waking and may even wake the patient from sleep!

On physical examination, the cerebellar signs were still mildly present but the sensory deficits had completely resolved which was not consistent with an infarction (unless it was TIA) , bleed or infective cause, but it was more consistent with basilar type migraine.

The MRI scan was normal as was the CSF examination.

The patient was given simple pain relief (acetaminophen) but not anti-migraine treatment, as in basilar-type migraine such abortive therapies can be associated with infarction and are best omitted. Symptoms entirely resolved and the patient was discharged home on the same day.

When asking about pain one needs to know several things which include:

• Location
  
• Quality
  
• Severity
  
• Onset (sudden or slow onset)
  
• Causative, relieving or exacerbating factors
  
• Radiation
  
• Duration
• Associated symptoms
  

There is a medical mnemonic to help with this as follows:

COLD RAP TAPE

•C- Character e.g. What is it like?

•O- Onset e.g. When did it start?

•L- Location e.g. Where did you notice it?

•D- Duration e.g. How long does it last?

•R- Relieving factor e.g. What makes it better?

•A- Aggravating factors e.g. What makes it worse?

•P- Precipitating factors e.g. What brings it on?

•T- Therapy e.g. What have you tried to make it better?

•A- Associated symptoms e.g. Do you have any other symptoms along with this?

•P- Past medical history e.g. Have you ever had anything like this before?

•E- Emotional impact e.g. what concerns do you have about this and how it may affect your life

The work up of the patient by the resident was entirely correct to rule out severe pathologies and I fully support that approach. If the patient were to have further episodes of Basilar-Type Migraine, the patient should not have further investigations unless there are unusual features e.g. neck stiffness, fever, persistent symptoms i.e. failure to resolve, because such investigations are unlikely to be revealing.

For further reading on this neurological condition, please see UpToDate or any good medical text.

As for the actual diagnosis, this was reached within 4 questions by taking more history.

Please consider asking about migraine when you see a patient. Enquire about visual symptoms, cluster-type headaches, worsening of headaches with neck movement, laterality of pain, pain quality, severity, associated symptoms etc, as listed above. These features will help you discriminate the likely cause and guide you with further tests and therapeutics.

Please consider....

Bedside Better Than MRI

Dear Bloggers

There is too much reliance on machinery to try and help us as physicians make a diagnosis. 

The next case, which as always has been anonymised, demonstrates that a simple history and bedside examination was all that was needed to establish a firm diagnosis.

A 70 year old female was admitted to a hospital in North Japan with dizziness on standing, weakness of her legs and blurring of her vision.

She had been otherwise well one week before admission and had been started on hypertensive medication by a local doctor for newly diagnosed hypertension. The patient had been taking the drug according to directions. However, she began to experience dizziness on standing and leg weakness. All symptoms resolved when she was lying flat at night time. She denied collapse or loss of consciousness and there was no history of chest pain. However, when she stood up, she did experience a rapid heart beat but without chest discomfort.

There was no previous medical history of note.

She was a non-smoker and only drank occasional alcohol. She lived with her husband in a ground floor apartment.

On examination the patient looked well and was alert and fully conversant.

General: Afebrile. No jaundice, anaemia, clubbing, cyanosis, oedema or lymphadenopathy (JACCOL)

CVS: Pulse 72 regular, BP 190/90 (lying), JVP not elevated, Heart sounds S1 normal, loud S2. No added sounds or murmurs. No carotid bruits. No peripheral oedema.

RESP: RR 16/min, Sats 98% breathing ambient room air, trachea central, expansion  normal, percussion resonant bilaterally, auscaultation normal vesicular breath sounds.

ABDO: Soft, flat, non-tender, no rebound or guarding. No organomegaly or masses. Bowel sounds normal. Rectal exam normal and no faecal occult blood.

CNS- Cranial nerves II-XII within normal limits.

PNS- tone, power, reflexes, coordination, sensation all within normal limits.

The resident was uncertain of the cause of the symptoms and the patient underwent several tests.

ECG- revealed slight sinusoidal T wave abnormalities in the lateral chest leads but there was no ST elevation or depression.

Lab Data- revealed elevated liver function with AST and ALT being 3x normal. The bilirubin and ALP were normal. All other blood results were normal including the CBC, Renal function and Cardiac enzymes (CK and Troponin-T).

CXR- was within normal limits.

CT head scan was performed which revealed only age-related cerebral atrophy.

MRI head scan again revealed no pathological problem.

In this case, the history is extremely important. The patient had started a new anti-hypertensive drug and had begun to develop what appeared to be postural-related symptoms which resolved on lying flat.

Unfortunately, the history had not been fully appreciated by the resident. Despite a normal neurological examination, the patient still underwent cranial scanning, twice, which was unnecessary.

An astute physician reviewed the patient at the bedside and obtained further history which again supported the likely diagnosis of postural hypotension. A simple bedside test was performed which gave the diagnosis.

Initially, the patient was laid flat and the blood pressure was 193/92mmHg. The patient was then elevated to about 50 degrees sitting and at one minute the blood pressure was rechecked and was 189/87mmHg and there were no symptoms. At two minutes with still no symptoms present, the blood pressure was 180/79mmHg. By three minutes, the patient was developing blurred vision and the blood pressure was 178/77mmHg. It was decided to stand the patient with her being held on either side by a physician and with a third physician checking the blood pressure. Full resuscitation equipment was available in case of collapse.

On standing, the patient developed the full set of dizziness symptoms but was fully conversant with no loss of consciousness. The blood pressure at one minute was 150/69mmHg. Pulse rate had not risen appreciably.

On lying the patient flat, the symptoms completely resolved.

Hence, this patient had confirmed postural (orthostatic) hypotension likely to be drug-induced.

A blood pressure drop of more than 20 mmHg of the systolic and / or 10 mmHg of the diastolic (20/10 mmHg) are consistent with the diagnosis of postural hypotension.

Other problems to consider are autonomic failure (pure autonomic failure, diabetes, multisystem atrophy, Parkinson's disease), hypovolaemia (e.g. dehydration, haemorrhage etc), adrenal failure, pituitary failure, baroreceptor dysfunction etc.

However, with such a strong history of starting a new drug and developing postural hypotension, the drug was the likely offender and in addition, it may well have been the cause of the mild liver dysfunction.

In this case, a simple bedside test would have sufficed to make the diagnosis. Cranial scanning was not necessary especially as the thorough neurological examination was within normal parameters.

You may be saying to yourself, 'Hang on a minute, the blood pressure is still high but the patient has hypotensive symptoms?!' Yes, that is correct. This patient despite not having what we would all regard as true hypotension nevertheless has a sufficient drop in both systolic and diastolic blood pressure on standing to cause symptoms. This is a relative hypotension and is still relevant and should not be ignored just because the systolic blood pressure remains above 100mmHg !

Normal Blood Pressure Homeostasis

When initially standing up, approximately 0.5-1.0 litres of venous blood pools in the capacitance vessels. Baroreceptors sense a drop in blood pressure and result in reflex vasoconstriction, increased heart rate and return of venous blood to the heart. These effects are immediate and without appreciable symptoms to a normal individual. Longer  term changes include increased renin output to increase angiotensin II and aldosterone to increase vessel tone and sodium reabsorption respectively. Other changes include the increased output of ADH which leads to vasoconstriction and increased water absorption from the kidneys.

Pathological Causes

Hypovolaemia- in states of severe hypovolaemia e.g. bleeding, approximately 3o% of the blood volume can be lost before postural blood pressure drops can be seen. This is especially relevant in young patients. Hence, asking questions about bleeding and searching for possible unseen causes e.g. abrutio placenta, GI haemorrhage are mandatory.

Drugs- the elderly are very sensitive to drugs. Even seemingly innocuous drugs can have adverse side effects such thiazide diuretics, tricyclic antidepressants, beta-blockers, neuroleptic medications. As I always say, take a decent drug history and look up the side-effects (if you don't already know them) and check for drug-drug interactions!

Adrenal Failure- steroids are required to allow the vascular smooth muscle to be responsive to circulating catecholamines to maintain vascular tone. Hypocortisolaemia leads to vascular collapse and hence, patients with no obvious hypovolaemia and no offending drugs, should have this easily treatable condition ruled out. Other possible signs might be a low sodium and high potassium in addition to fasting hypoglycaemia. However, patients with a normal K level can still have hypocortisolaemia.

Pituitary Failure- Absence of ACTH leads to a similar problem of hypocortisolaemia. Whereas adrenal failure is associated with raised ACTH levels and hyperpigmentation, panhypopituitarism, and hence low ACTH output, is not. Checking anterior pituitary hormones would be advisable and should be part of the work-up for patients in whom the immediate cause of postural hypotension is not clear.

Other conditions are associated with autonomic failure and include diabetes mellitus, and hence, checking a fasting glucose and a 75 gram oral glucose tolerance test would be appropriate. HbA1c is not part of the British or American Diabetes Association guidelines for making the diagnosis of diabetes as it can be misleading.

Multi-System Atrophy (MSA) which includes the famous Shy-Drager and Parkinsonism etc should be considered but such abnormalities of cerebellar dysfunction, tremor, bradykinesia and cog-wheel rigidity should be unmasked during the physical examination (if performed correctly!) 

Autonomic failure can be examined for by doing the postural blood pressure testing and checking compensatory changes in heart rate. If the heart rate fails to increase by more than 10  beats per minute during the postural test, then this suggests autonomic failure. Heart rate increase > 100 / min suggests hypovolaemia. If symptoms develop without hypotension, then this suggests Postural Orthostatic Tachycardia Syndrome (POTS); this is usually evident in younger patients.

Investigations for autonomic failure include the measuring of the R-R interval on ECG with the patient doing slow breathing. The ratio of the R-R interval of expiration to inspiration should be more than 1.15. If less, it suggests autonomic failure.

Baroreceptor dysfunction paradoxically occurs in patients with hypertension which thereby predisposes elderly patients to orthostatic hypotension. The commonest cause in the elderly is decreased baroreceptor responsiveness plus impaired arterial constriction.

Treatment

1. This involved removing / treating the underlying cause
2. Postural manoeuvres such as getting out of bed slowly in the morning, taking sufficient fluid and salt in the diet (as long as their is no hypertension or heart failure), using compression stockings to improve venous return, addition of fludrocortisone to mimimise symptoms in those individuals with sufficient salt intake, midodrine to cause vasoconstriction and non-selective beta-blocker Propranolol which leads to uninhibited alpha-vasoconstrictive effects.

Lessons to be Learned

• Avoid cranial scanning unless it is absolutely necessary; just because you can scan someone does not mean that you have to or that you should. A thorough history and examination may be sufficient to give all the necessary information. Only if there is a neurological abnormality e.g. upper motor neurone signs, should the patient be scanned.

• Patients with a history of postural related symptoms should have a bedside measurement of blood pressure. An initial lying blood pressure should be performed and then repeating the measurements at 1, 2 and 3 minutes in the sitting position (if the patient cannot stand) or standing. If the patient is stood up, they should be supported in case of potential collapse with full resuscitation equipment being available. Blood pressure measurements should then be performed at 1, 2 and 3 minutes.  

• A blood pressure drop of more than 20 mmHg of the systolic and / or 10 mmHg of the diastolic (20/10 mmHg) is consistent with the diagnosis of postural hypotension.

 In this case, there was a hint of dropping blood pressure at 3 minutes when sitting and this  was confirmed after just 1 minutes of standing.

• Patients without a supportive drug history and in whom there is no clear cut cause, should have a rectal examination to check for gastrointestinal haemorrhage. Consider other potential causes in the elderly as listed above.

Have a great week !