A Minor Gripe - Work Up Of Constipation

Dear Bloggers

Today I would like to have a minor gripe. My gripe is about the overuse of abdominal X-rays to rule in / rule out constipation.

Patients with constipation may present with various symptoms including:

• Nausea
• Vomiting
• Anorexia
• Difficulty passing stool (straining)
  
• Passage of hard stools
• Abdominal pain

A rectal examination provides far more information than an abdominal X-ray when working up a patient with constipation. Feeling for hard stool, determining if there is occult blood, malaena or frank hemorrhage and determining if there is malignancy e.g. colorectal / prostate cancer is all possible and essential, something that a plain X-ray cannot do.

To perform an abdominal X-ray in order to avoid the rectal exam is in my opinion a neglection of duty to the patient. Patients may indeed have a full colon with stool and an X-ray may reveal that constipation is present, but it does not provide the mechanism which caused the constipation. For example, is the constipation due to sluggish bowel movement or a rectal cancer!?? A plain film will not always show you the cancer hiding in the rectum --- only the examining finger can do that or more advanced radiological studies.

In this technological age, aren't we forgetting our basic examination skills that have been tried and tested by the ingenious physicians of the past only to be replaced by fine CT pictures that cannot always provide the diagnosis that we are seeking. Without the background of thorough physical examination skills, soley relying on a machine to make a diagnosis is like building a brick house on sand --- it is destined to sink when we need shelter from the storm. We need a good foundation on which to build and that foundation is the physical examination.

Performing a rectal examination is free and does not cause radiation exposure whereas an X-ray does cost money (albeit pennies / yen) and there is significant radiation exposure. This latter point is something that many physicians forget. Never do harm to your patients and do not expose them to unnecessary procedures which might be harmful (immediately or long term) when another method might provide the same or better information with less harm.

Hence, when it comes to constipation please remember to do the rectal examination. If you are concerned about bowel obstruction then that would be an indication for an AXR but it cannot really be justified to take a plain film to rule out / rule in constipation when your finger can give the same information.

If you want to investigate further (after a rectal exam), then I would suggest utilising an ultrasound scan which is non-invasive and provides no radiation exposure.

X-rays and CT scans should be reserved for those patients in whom the diagnosis is unclear after the basic physical examination and ultrasound and in whom you want to rule out serious pathology. They should not be utilised as a first measure unless there is evidence of an acute pathology e.g. acute surgical abdomen, and by which other tests cannot provide the diagnosis. Remember that radiation from CT scans increases the risk of cancer -- please see a previous blog article from 2007 which explains this in more detail on the following link.

Please Consider......

Hypertension and Spinal Cord Injury

Dear Bloggers

I wanted to impart to you a rather rare case of a patient who had a history of spinal cord injury and who developed accelerated hypertension and cold upper extremities.

This male patient had a C-spine fracture and transection of the spinal cord 5 yrs before following a fall and he was left with quadriplegia and reliant on mechanical ventilation to breath.

He was normally otherwise well albeit fully dependent.

On the evening of admission, the patient developed a low grade fever but otherwise had no new symptoms.

The blood pressure was noted to be 220/110 mmHg and his carer noticed that his hands and arms were very cold to the touch.

He was admitted to the hospital via the emergency medical services.

There was no other other relevant medical history and the patient was taking no regular medications.

There was no relevant family history.

The patient was cared for at home and was nursed 24 hours a day on a pressure bed and had home mechanical ventilation. The patient was fed via PEG tube and required full help with toileting.

On examination

The patient was fully alert and was able to speak albeit softly. Temp 37.5 degrees C.

HEENT examination was grossly intact.

Cardiac: pulse 74/min, BP 220/110 mmHg, JVP not elevated, Heart Sounds 1 + 2. No added sounds and no murmurs.

Resp: RR= 14/min (ventilator setting), tracheostomy in vivo, spO2 98%, expansion equal, percussion resonant, chest sounds clear.

Abdomen: Soft, flat, non-tender (remember patient has spinal cord transection), no obvious masses, normal bowel sounds. Rectal examination not performed.

Extremties - DVT prevention stockings on both legs. No oedema, redness or pain.

Cranial Nerves: II - normal, pupils equal and reactive to light and accommodation. III, IV, VI - normal extra-ocular movements, V- normal motor and sensory modalities. VII - normal. VIII- normal, IX, X, XI - no gross abnormalities, XII - normal tongue movement.

PNS - Power 0/5 throughout all limbs, absent sensation up to C3 level, Babinski bilaterally extensor.

Laboratory

Lab studies were generally normal except for a slight rise in the WBC count of 12 x 10-9/L Urine analysis revealed turbid urine. WBC >100 / hpf, RBC 5-10 / hpf, nitrites +, protein 2+, bacteria 4+ (gram stain: Gram Negative Bacilli).

Urinary catheterisation revealed 1 L of urine in the bladder.

CXR - NAD

ECG - 74/min, no focal abnormality.

Diagnosis

The diagnosis here is obviously a urinary tract infection with urinary retention.

However, why did the patient develop hypertension and peripheral vasoconstriction?

The answer is unique to spinal cord injury patients and it is termed Autonomic Dysreflexia.

Certain noxious stimuli such as Urinary Retention (associated with UTI), impaction of stool within the bowel, pressure sores, fractures or intra-abdominal disease lead to a dysfunction of the autonomic responses of the heart and vascular contractility. This lack of control of the sympathetic nervous system leads to vasoconstriction and hypertension. Interestingly, a parasympathetic response occurs above the level of the lesion albeit that it is not sufficient to offset the adverse actions of the sympathetic response.

This can occur in patients with spinal cord lesions above the T6 cord level and the frequency of those affected is variable. It is unusual in the immediate aftermath of injury but usually occurs within the first year.

Patients can present with various symptoms and signs and include:

• headache
• nausea
  
• bradycardia or tachycardia
• sweating
• hypertension
• nasal congestion
• altered mental state e.g. anxious
  

Patients may exhibit no symptoms at all whereas others may develop profound bradycardia leading to cardiac arrest or hypertensive crisis causing intracerebral bleeding and convulsions.

Patients can be managed in several ways and include sitting them up to cause the BP to drop, searching for inciting stimuli (e.g. urinary outflow obstruction / UTI), acute reduction of BP (nitrates, peripheral calcium channel blocker, ACE-I, hydralazine, IV labetolol).

In this case, the history of spinal cord injury and the symptoms of peripheral vasoconstriction plus profound hypertension made the diagnosis of autonomic dysreflexia a certain diagnosis at the bedside and after the hunt for the inciting cause, a UTI and urinary outflow obstruction were found.

Treatment with urinary catheter insertion to relieve the obstruction and antibiotics caused the BP to drop within several hours, with a resting BP of 100/60 mmHg without the need for acute anti-hypertensive therapy. The perfusion to the upper limbs normalised spontaneously.

For more in-depth reading concerning patients with spinal cord injuries, please read UpToDate 16.2

Have a great day.... :-)

The Meningitis Quandry

Dear Bloggers

Today, I would like to discuss an area of medical uncertainty - the partially treated meningitis!

Sometimes a patient will present to the doctor with the classical features of meningitis and antibiotics are started before the lumbar puncture can be performed because for example, of the potential delay in obtaining a cranial CT scan or that the patient is too far from the nearest hospital and a delay in giving antibiotics might be deleterious. Note that GPs in the UK have traditionally administered i.m. or i.v. benzylpenicillin to patients with suspected meningitis before they are taken to hospital.

This of course is the correct management because a significant delay can result in adverse outcomes in meningitis.

However, partially treated bacterial meningitis can cause the conversion from a predominantly neutrophil predominant CSF cell count to a predominantly lymphocytic cell count. Therefore, on initial examination, it may look as if the patient has a viral meningitis!

How do we differentiate between viral and partially treated bacterial meningitis? Now that can be almost impossible ! However, there are some features of the CSF that can guide us although none are absolutes.

Bacterial meningitis has CSF that tends to appear turbid on gross visual examination and upon analysis, the glucose is usually <50%>

Conversely, viral meningitis fluid appears macroscopically clear, has lymphocyte predominant cells (early infection may show neutrophils!!), the CSF glucose >50% of the level of the serum glucose in most cases and the protein is usually raised only mildly (by <1.5mg/dl)

Protein levels are usually only mildly raised in viral infections (as above) whereas they can be >1.5mg/dl in bacterial infections.

Of course, gram stain can be negative in partially treated meningitis and so this cannot be relied up.

There is evidence to suggest that CSF can still remain positive for organisms up to approximately 4 hours after the administration of antibiotics, so this can be helpful to still look for the organisms within this time frame.

Blood cultures should always be taken in meningitis patients as bacteraemia can give positive results allowing isolation of a potential organism with a subsequent tailoring of therapy.

Remember that certain bacterial infections can present with a lymphocyte predominant cell count and they include listeria monocytogenes infection (consider in the over 50s age group) and tuberculosis. TB meningitis can produce a macroscopic fibrin web.

Fungal infection with cryptococcus neoformans can also produce lymphocyte predominant CSF and this should be considered in patients with severe liver disease and not just HIV patients. In HIV patients, the rest of the CSF can appear normal and hence, the CRAG testing and Indian Ink stain are the mainstay of confirming the diagnosis.

Hence, it is not as clear cut to make a diagnosis between viral and bacterial meningitis when antibiotic treatment has muddied the waters, as the vast majority of handbooks and textbooks out in the world arena would suggest-- I know as I have reviewed several recently and they all differ markedly in respect of the analysis of CSF. Most texts simply differentiate between how to make the diagnosis of viral versus bacterial meningitis and very few actually discuss partially treated meningitis.

One such book that does address this important point is the Oxford Textbook of Medicine and please consider reviewing this for more in-depth reading. Another good book has been written by Dr Makoto Aoki, Specialist in Infectious Disease medicine in Japan. This text is currently written in Japanese -- an English version is however a must please! :-)

So, when faced with the viral meningitis versus partially treated meningitis patient what do you do?

Firstly, still take the blood cultures even whilst on antibiotics - they may still prove to be positive.

Secondly, examine the CSF for bacteria, and if microscopically negative ( as in partial treatment meningitis ), send fluid for culture and rapid analysis e.g. meningococcus (PCR), pneumococcus (latex agglutination), HSV (PCR), TB (PCR) depending upon the clinical scenario and what you consider are the likely causes in your patient.

CSF can be stained for Acid Fast Bacilli and if in doubt, repeat CSF samples should be taken separately over several days (total of 3 samples) and fluid should also be sent for long term culturing. 90% of patients with TB meningitis also have a positive tuberculin skin test and it is still worthwhile performing. A negative skin test does not rule out TB.

Thirdly, continue the antibiotics until such time that it can be established (if possible) that it is or is not a bacterial infection e.g. PCR and cultures results (CSF and blood).

In the under 50s, adults should receive cetriaxone plus vancomycin [current UK guidelines 2005 suggest only using Cefotaxime] whereas over 50s require additional ampicillin therapy to cover listeria infection.

I would hope that future handbooks and textbooks fully address the problem of partial treatment meningitis.

It just goes to show that patients do not write the textbooks and that nothing is ever fixed in stone.

Have a great week....!

Missing AMI.....Oh, My, My

Dear Bloggers

Acute myocardial infarction, as part of the Acute Coronary Syndrome spectrum, is a common problem and in patients who are alert, the diagnosis can often be considered based on the symptoms alone which include:

• Severe central 'crushing' chest pain
• Radiation of pain to the neck, jaw or arms
  
• Dyspnoea
• Nausea and vomiting
• Cold sweating

The diagnosis can often be established by performing a 12-lead ECG to look for ST elevation or for more subtle features such as T-wave inversion, sinusoidal ST segment, poor R wave progression, deep ST depression, Q-waves and new onset left bundle branch block, etc

However, in the patient who is unconscious lying on a bed in the ICU, how is it possible to even know if they have developed an AMI?

Most patients are usually linked up to a bedside monitor and that can often provide a clear picture of the situation by seeing a rhythm change and abnormal ECG features as described above. The other additional method is to check for cardiac enzymes.

Remember that there are several enzymes released during muscle damage which include:

• Creatinine Kinase and the MB fraction (positive for up to 48 hours)
  
• Aspartate Transaminase
• Lactate Dehydrogenase
• Myoglobin
• Troponin T and Troponin-I (positive for up to 10 days)
  

Any good textbook of acute medicine will show you the rise and fall of the various enzymes which may be able to guide the physician to make the diagnosis of AMI. However, currently, the most specific, sensitive and prognostic measure is to check the Troponin level.

By failing to check the Troponin, it is possible to miss an AMI. Sometimes, the CK and AST can be normal (especially after several days; the AST may not rise at all !!) and the physician is fooled into a false sense of confidence that an AMI has not occurred. However, the AST and CK can soon fall after an AMI whereas the Troponin can stay elevated for over a week.

For example, in the UK, I experienced one such case in a patients who presented with typical chest pain but who's ECGs were completely normal in addition to the CK and AST. He was treated with aspirin and LMW heparin as was the protocol for 'atypical' chest pain. His Troponin T was positive at 12 hours. The patient had no evidence of renal failure. This patient was transferred for percutaneous intervention (PCI) treatment. In this case, the history was all important and the usual ECG and CK /AST were unrevealing. Only the Troponin-T being positive confirmed our worst thoughts.

Renal failure has been cited as a reason not to do a Troponin test in some institutions because it can be falsely raised. One should not be fooled into thinking that a Troponin should not be measured just because the patient has renal failure - quite the contrary. Remember that patients with renal failure are at high risk of coronary disease and hence, these two problems go hand in hand. It is better to over investigate such patients by performing a troponin test to include or exclude an AMI rather than assuming it is just because of renal failure.

In respect of a patient on an ICU, a rise in the CK, a change in the ECG, blood pressure instability, dysrhythmias etc should alert the physician to the possibility of an undiagnosed acute coronary event. In such cases, a 12 lead ECG is mandatory as is a Troponin test. If the latter test is negative initially, it does not exclude an AMI !

It can take a minimum of 6 hours for the Troponin to become positive and most authorities state that 12 hours post-event is when Troponin can be truly said to be positive or negative [>9 hours after onset of symptoms and negative Troponins indicates low probability of myocardial damage / infarction]. Hence, the Troponin should be rechecked at least 6-9 hours after onset of symptoms with an initial negative test.

One group [Hamm, CW. Cardiac biomarkers for rapid evaluation of chest pain. Circulation 2001; 104:1454], investigated if AMI diagnosis could be made rapidly within 90 minutes by measuring serum CK-MB, troponin I, and myoglobin in the event that an ECG was non-diagnostic. Their results were interesting with sensitivity and specificity over 95% for diagnosing AMI. However, the test needs to be validated and therefore, this triple cardiac enzyme test is not currently advocated. The problem in using myoglobin is that it is a non-specific marker.

Currently, recommendations for investigation of acute coronary syndrome state that if ACS is suspected, the Troponin T or I should be performed and only in centres where it is not available should the CK-MB be performed. The measurement of total CK is again, non-specific, and should not be used to make the diagnosis of an AMI.

However, the total CK being raised can certainly provide a clue that an ACS might have occurred especially in the unconscious patient, and hence, performing a Troponin-T or I would be the Gold Standard for diagnosis taking into account ECG +/- Echo findings.

A cardiac echo is also important. An echo may reveal regional wall motion abnormalities which may become evident even before then onset of pain in AMI patients. Such abnormalities were seen in patients undergoing PCI treatment when their coronary arteries were reversibly occluded by the angioplasty balloon. It is said that having no obvious echocardiographic abnormalities excludes an AMI although the reverse is not true i.e. a hypokinetic echo result does not always equal AMI. Hence, it can be difficult to sometimes know if an abnormality is truly due to an AMI. Hence, performing a 12-lead ECG and comparing it to a previous ECG (if available) plus cardiac biomarkers are necessary to absolutely identify if an AMI has taken place.

Currently, the European Guidelines from the European Resuscitation Council 2005 do not mention about the use of echocardiography to sustain a diagnosis of AMI. However, the 2003 task force of the American College of Cardiology recommend using echocardiography to aid in the diagnosis of AMI unless it has been proven by other means [history / ECG / Cardiac markers].

Remember that cardiac markers can also be raised in other conditions. For example, myocarditis, PE, cardiac intervention etc, can cause positive Troponins. A diagnosis that is common in Japan is 'Octopus Trap Heart' - also termed Takotsubo, a form of localised myocardial stunning with the absence of significant coronary artery disease whereby the heart chamber changes shape and takes on the form of an octopus trap. Please visit the following website for an excellent review of the topic. Note that takotsubo can only truly be diagnosed once ACS has been ruled out by coronary angiography. Treatment for takotsubo is considered supportive although UpToDate 16.2 suggests use of aspirin, ACE-I / ARB and beta-blockers as for heart failure, whereas ACS requires the addition of:

• Clopidogrel
• Statin
  
• Low Molecular Weight Heparin
• Coronary stenting / Revascularisation surgery

However, in patients who present with features supportive of an AMI, you must fully exclude an AMI before making the diagnosis of takotsubo which means having the patient on full AMI treatment and proceeding with angiographic intervention until proven otherwise.

So be careful in making a rare diagnosis such as takotsubo when the more common diagnosis of ACS is likely to be present.

In order to differentiate non-ACS causes from ACS, percutaneous intervention e.g. coronary angiography, is helpful. PE workup would involve D-Dimer testing, use of a PE scoring system e.g. Modified Well's Score / Modified Geneva Score, leg dopplers, echocardiography and ultimately, spiral CT.

Hence, in summary, when dealing with an unconscious patient on an ICU with the concern about an AMI, it is important to rely on the combination of tests as described above, and not one test alone. Remember that common things are common, such as AMI, and to thoroughly investigate is the correct management in addition to starting cardiac medications [as outlined above] before a final diagnosis of AMI is determined or excluded, as delaying treatment can result in muscle damage and hence I quote the famous words of 'Time is Muscle'. If the final diagnosis turns out to be the rare takotsubo then so be it, but if not and it is the common ACS, then at least the patient would have been treated rather than waiting to make a perfect diagnosis at the expense of the patient's heart muscle.

Please consider.....

Corticosteroids-- Our Friend and Foe

Dear Bloggers

Today I would like to discuss about the use of corticosteroids.

Such drugs have been used for many years as immunosuppressants in a whole host of conditions including autoimmune disorders, connective tissue diseases, haematological malignancies, skin disorders etc.... and the list goes on.

However, although there can be many beneficial effects of 'steroids', the side effect profile both acutely and chronically is a major concern including diabetes, osteoporosis, hypertension, development of a Cushingoid body habitus, immune suppression, adrenal suppression etc...

So, when as doctors we consider about starting systemic steroids, we must be absolutely certain of the diagnosis because if we make an error in judgment, the outcome can be catastrophic.

Systemic steroids are not typically used for just a few days, except perhaps in acute asthma or an exacerbation of COPD, but usually for many months to years and so when committing a patient to a necessary poison we must be certain we have done all that is possible to investigate the condition and to ensure that it is indeed the correct diagnosis in order to warrant the use steroids.

It is often easy to assume that a patient with fever, joint pain and a vasculitic rash has a connective tissue disease and to then dash in with systemic steroids. Infective endocarditis can also present in this way and without a thorough work up of the cause of all these elements there may be a misdiagnosis, the wrong treatment and fulminant infection.

Remember, steroids can mask a fever and can attenuate pain e.g. patient with an acute abdomen on steroids may not experience the severity of pain as would a patient not using steroids in an acute peritonitis.

Hence, starting systemic steroids can result in a drop in fever and a temporary improvement. However, be warned, the immune suppression by high dose steroids can allow undiagnosed infection to flourish and this can result in detrimental sequelae.

So when a patient has a fever one should consider all possibilities of what might be causing it e.g. infection, drugs, endocrine, CTD, neoplastic, granulomatous, metabolic etc....

However, common things being common, the likely cause is usually infection, at least if the onset is acute.

One must exclude infection first when considering fever, as untreated infection is a serious problem for the patient.

When considering the focus of infection ask the patient where they have a problem. They can sometimes pin-point the problem for you.

Don't ignore their complaints because they may be telling you the diagnosis e.g. cheek pain with sinus tenderness / percussion tenderness on examination may signify sinusitis.

Consider Body Systems when considering infection. For example:

• HEENT - sinus infection, ear infection, throat infection e.g. quincy etc
• Cardiac - pericarditis, endocarditis, myocarditis
• Respiratory - pneumonia, abscess, bronchiectasis, etc
• Abdomen - cholecystitis, cholangitis, liver abscess, diverticulitis, appendicitis etc
• Musculoskeletal - septic arthritis, discitis, fasciitis, abscess e.g. psoas
• Urogenital - UTI, pyelonephritis, perinephric abscess, PID etc
• CNS- meningitis, encephalitis, abscess etc
• Endocrine - viral / bacterial thyroiditis
• Skin - cellulitis, abscess, furunculosis

Then with the general basic list of body systems and potential causes as above borne in mind, ask questions with regards to each body systems to see if there are any symptoms which might uncover the focus of an infection. This is also a kind of infection-centric review of systems.

Without considering a thorough list of causes, sites of infection can and will be missed by the physician.

If infection has been excluded, then non-infective causes should be considered e.g. drug fever, DVT-PE, connective tissue diseases etc...

Hence, rushing in with steroids may make the patient feel momentarily better and make the physician feel joyous at how the patient has been miraculously fixed, but be warned - steroids do not fix all ailments.

There is a famous quote by Alexander Pope which goes as follows 'Fools rush in where angels fear to tread' which means that the unaccustomed are often reckless attempting things that the wise would otherwise avoid.

Of course, there are very few indications for absolutely needing to start steroids immediately except in cases such as temporal arteritis or acute severe bronchospasm from asthma or COPD. Hence, ruling out infection first is an absolute necessity in most cases.

If steroids need to be used e.g. Temporal arteritis, but the patient has for example a high risk of concomitant TB or a pneumonia etc, then treatment for that infection must be started at the same time.

Hence, next time you are asked to start steroids or you yourself consider starting steroids, please review the patient history and re-examine whether your diagnosis is the correct one and if so, has infection been completely ruled out first.

Please consider....

A Case of Fever and Headache- The Answer

Dear Bloggers

Below are the answers to the recently published case.

Questions:

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

• Recent Travel to Thailand
• Insect bite (s)
  
• Fever
• Headache
  
• Chills
• Malaise
• Generalised Arthralgia and Myalgia
• Weight loss
• Retro-orbital pain
• Mild petechial rash
• Mild splenomegaly
• Mild muscle pain
• Neutropenia and mild thrombocytopenia
• Elevated CK, AST and LDH
  

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

This history is consistent with an infective aetiology although other causes should also be considered such as drug induced, connective tissue disease, neoplastic, and haematologic diseases.

Infective causes from this area of the world include:

• Malaria
• Dengue (haemorrhagic) fever
• Leptospirosis
• HIV
• Typhoid fever
• Scrub Typhus
• Rickettsia
  

However, other infective causes that could result in similar features include:

• Parvovirus B19
• Infectious mononucleosis
• Cytomegalovirus
• Hep A, B, C
  
• Infective Endocarditis

However, the fact that the patient received an insect bite it is mostly likely to be a mosquito and hence, mosquito-blood-borne diseases should be highly suspected. The history is very important here. The patient did not go through jungle areas on foot and this makes tick bites unlikely and with no exposure to contaminated water e.g. swimming in rivers, also makes Leptospirosis less likely. The fact that a sexual history was not obtained is a pity as there is a high level of HIV in Thailand and the above features could be consistent with an acute HIV seroconversion illness. Being of advancing age does not preclude sexual intercourse and a sexual history should be taken when appropriate.

Drug-induced causes: This patient takes Lansoprazole and Allopurinol. Both drugs can affect the bone marrow resulting in blood dyscrasias. Always consider drugs as an actual cause or a contributory cause and if in doubt the drugs should be discontinued either temporarily or permanently.

Connective Tissue Disease (CTD): This problem should be considered although I do not think it is very likely. Vasculitis can present with headaches, fever, weight loss, arthralgia, myalgia, petechial bleeding, splenomegaly etc. Even the neutropaenia and thrombocytopaenia could be accounted for by a CTD. Such examples might include SLE, Adult Still's disease, Rheumatoid vasculitis and Temporal arteritis with PMR [blood dyscrasias as outlined above are not consistent with this diagnosis].

Adult Still's disease usually presents in adolescents and young adults although it has been described in older patients and has a bimodal age distribution. It is a cause of the haemophagocytic syndrome. It is very unlikely in this case.

Rheumatoid vasculitis usually presents after many years of chronic RA and hence, in the absence of this history, it makes such a diagnosis very unlikely.

Neoplastic: The fact that this patient had a previous tumour is important. One would want to know the previous Duke's staging to consider whether metastatic disease was a possibility. However, in view of the abrupt onset and history of foreign travel, the consideration of malignancy as the cause is very unlikely here.

Haematologic: Other haematological disease that could account in part for the symptoms include the acute leukaemias with secondary infection from neutropaenia. Lymphoma with autoantibody production against neutrophils and platelets is a possibility too although again, as I have mentioned, with the history of travel and abrupt onset of symptoms, it would seem that a primary haematological cause is less likely.

3) What tests need to be done?

In this case an infective aetiology is likely. Tests should include:

• Thick and Thin Blood Smears to investigate Malaria. The Thick film of blood is used to make the diagnosis of malaria and is positive on the first smear in 95% of cases. However, they should be repeated every 6-12 hours if initially negative for up to 48 hours to rule out this infection. The Thin films are used to determine the malaria spp and the extent of parasitic load in the blood.
• Falciparum antigen testing / HRP-2 / parasite LDH / PCR (if available)
• Antibody / Antigen / PCR testing for Dengue, Typhus, Rickettsia, Leptospirosis, HIV (if there is a high risk history), EBV, CMV, Parvovirus B19, Hepatitis A, B, C
  
• Blood cultures x 3 and cardiac echo- infective endocarditis can present as a 'vascilitis' and the murmur may not initially be appreciated.
• Urine analysis and culture to exclude infection
• Stool culture e.g. salmonella
  

Other tests to consider include:

• Checking the blood smear for a primary blood dyscrasia
• Bone Marrow Examination
• Autoimmune profile plus anti-platelet antibodies
  

4) What is the likeliest diagnosis in this patient?

In view of the recent history of travel to Thailand, a mosqito bite and the various symptoms including retro-orbital pain and a mild petechial rash, in addition to the neutropenia and thrombocytopaenia, the dengue haemorrhagic fever should be considered highly likely.

However, the other above cited differential diagnoses need to be considered and appropriately investigated and excluded because the respective treatments are different.

For example, scrub typhus is due to infection from Orientia tsutsugamushi which is similar to but also distinct from usual Rickettsial spp. It can also produce retro-orbital pain, myalgia and a rash (sometimes petechial). It has been described for such infections to be transmitted in suburban Bankok.

Leptospirosis is a predominatly water borne infection and has classically been caused from exposure to water contaminated with leptospira from infected rats urine. The organism usually gains entry from an abrasion in the skin and causes similar features as in this case. However, one usually develops a leukocytosis rather than a leukopaenia which goes some way against this being the cause. However, 90% of leptospira infections are self-limiting (not Weil's disease) and the organisms are cleared within a week. Hence, this diagnosis would need to be ruled out.

Malaria is one of those diagnoses that should always be investigated and ruled out. This patient did not use malaria prophylaxis putting her at potential risk for malaria infection. Malaria can present similarly to the above patient and hence, doing the appropriate exclusion tests is a necessity.

The current guidance for tourists going to Thailand as per UpToDate 16.2 suggest that urban transmission and daytime rural exposure to malaria are very low and that prophylaxis is not necessary. One needs to however avoid insect bites [this patient did not avoid such bites!]

However, if there is going to be potential exposure e.g. travel to rural areas with exposure during the evenings (when mosquitos are most active) then prophylaxis is recommended. There is a high level of chloroquin, mefloquin and Fansidar resistance in Thailand and hence, prophylactic regimens should include doxicycline or Malarone prophylaxis.

Hence, a patient with a history of possible exposure to malaria e.g. mosquito bite with the above symptoms e.g. fever, headache etc, should have malaria excluded. Please see the detailed UK guidance on the following link

5) What is the treatment?

For Dengue (haemorrhagic) fever of this severity, the patient was isolated in a positive pressure room. The malaria screen was negative. Several of the above tests could not be investigated e.g. the test for Dengue was not available, although the bone marrow examination excluded a leukaemia / lymphoma and an autoimmune profile was within normal limits.

The patient was considered to have a virally induced haemophagocytic syndrome which was seem on the bone marrow examination and she was started on high dose steroids and immune globulin infusions. The above therapy is not usually necessary for treatment of typical uncomplicated Dengue as it is usually self-limiting and supportive treatment is the norm. Before starting high dose steroids in such a patient, one should always try to rule out other serious infectious aetiologies first e.g. TB.

There have only been a handful of cases of the reactive haemophagocytic syndrome being described in Dengue Fever [medline - hemophagocytic & dengue as search criteria] and such an occurrence appears to be unusual.

Reviewing the latest UpToDate 16.2, for such a reactive viral aetiology, treating the underlying cause is the first measure (if of course there is a treatment available) and failing that, it is advocated to start Dexamethasone plus Cyclosporin. However, there have been case reports of intravenous immunoglobulins showing some effect. High dose steroids are usually of limited benefit.

The causes and pathophysiology of the Viral Haemophagocytic Syndrome is complex and I would refer you to a more detailed text such as UpToDate.

Dr Stein, University of Florida, has kindly provided his answers to the case below:

1. Problem list

• Fever
• HA/retro-orbital pain
• Chills
• Malaise
• arthralgias/myalgias
• foreign travel
• weight loss
• drug adverse reaction potential
• petichial rash
• splenomegaly
• leukopenia
• borderline thrombocytopenia
• elevated CK, AST

2. a. Viral infection: adenovirus, coxsackie, enterovirus, dengue, HBV, EBV, parvovirus B19, HIV, typhoid fever, rickettsia, malaria, chikungunya- were RBC's in urine? where is U/A?

2b Allopurinol hypersentivity syndrome

3. Viral Ab tests, Salmonella, shigella Ab/blood cultures, wet blood smears

4. Dengue fever

5. Supportive

Many thanks to Dr Stein for the concise answers to the questions.

In the end, this patient made a superb recovery over a 5-day period. The neutrophil and platelet counts recovered and the patient's symptoms dissipated. Whether the recovery of the blood abnormality was as a result of the therapy or the natural course of the viral illness is not certain.

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.