Treatment of Hyperkalaemia

Both High potassium (hyperkalaemia) and Low potassium (hypokalaemia) levels can cause significant morbidity and mortality if left untreated.

Both problems have a wide number of causes, and treating the underlying problem will correct the disturbance once identified. Today, I will deal with hyperkalaemia.

Hyperkalaemia (K >5.0mmol/L)

Hyperkalaemia appears to become a problem for most patients when the level is >6.5mmol/L at which time the cardiomyocytes are most unstable and it is possible to develop life threatening dysrhythmias.

The typical ECG shows hyperacute T waves (Tall Tented T waves) and this should cause the doctor to act quickly-- this is a Medical Emergency. Other features include flat P-waves, increased PR interval. The QRS patten can eventually widen leading to a sinusoidal patterns and eventually VT/VF.

Causes of Hyperkalaemia

Dietary-- often forgotten! However, bananas, citrus fruits e.g. grapefruits, oranges have high levels of K. Salt substitutes, herb and nutritional preparations e.g. PEG feeds.

Drugs-- Lactulose (contains K), K supplements, ACEI / ARB / Aldosterone inhibitors can result in high K levels. Nephrotoxic drugs e.g. vancomycin, gentamicin can cause intrinsic renal dysfunction and the uraemia results in hyperkalaemia.

Other drugs known to raise K levels include:

Beta-blockers (reduced renin secretion and reduced cellular uptake of K), Heparin, Septrin / Bactrim (blocks apical membrane Na channels in distal nephron thereby inhibiting K secretion), Pentamidine, Penicillin G potassium, ketoconazole (impairs aldosterone metabolism, reduces aldosterone)

Aspirin overdose can result in a metabolic acidosis and hyperkalaemia. If an overdose of drugs is suspected and the patient has an acidosis, always check aspirin levels. In any case, aspirin lab levels should always be a routine tests in any overdose, including acetaminophen and tricyclic antidepressant levels.

Drinking de-icer Ethylene Glycol can also result in a metabolic acidosis and hyperkalaemia may result.

Infection- Sepsis resulting in renal injury from direct toxin effects to septicaemic shock can cause hyperkalaemia.

Endocrine-- Addison's disease ( low Na: High K), Diabetic Ketoacidosis, Hyperglycaemic Hyperosmotic Syndrome with renal failure can cause increased K.

Trauma-- Rhabdomyolysis from trauma, shock or infection results in release of large amounts of K which can result in cardiac arrest. Hypertonicity e.g. from a syndrome of hyperpyrexia related to anti-psychotic medication can result in rhabdomyolysis and raised K.

Haematological-- Haemolytic anaemia can result in intracellular release of K as can tumour lysis syndrome. Traumatic taking of blood can give a false reading of hyperkalaemia although most labs will report that the blood was haemolysed. Stored red blood cells release their K and hence, infusion of such cells might result in hyperkalaemia especially if the patient already has an underlying problem with raised K e.g. renal failure.

Metabolic-- metabolic acidosis of any cause can result in hyperkalaemia as a result of the competition for H/K release from the kidney into the urine. Hence, renal failure, hepatic failure, respiratory failure (type 2) and cardiac failure can all result in acidosis and hyperkalaemia.
Lactic acidosis from muscles hypoxia from hypoperfusion can result in raised K levels.

Type 4 Renal tubular acidosis (unresponsiveness to aldosterone) raises K levels too.

Familial Hyperkalaemic Paralysis and other rare genetic disorders.

Emergency Therapy

1) Calcium Gluconate 10ml 10% solution given over 2 mins- stabilises cardiac muscle cells

2) Glucose-Insulin infusion: 50ml of 50% glucose with 20 units of rapid insulin given to the patient over 1 hour

3) The above measures can be repeated if K level fails to decrease

4) Beta- stimulant drugs e.g. salbutamol, メプチン will cause a Temporary flux of K into cells thereby decreasing serum K levels. This can be given via a nebuliser in the ER department or on the ward

5) Furosemide (ラシクス） can sometimes be given provided that the cause is considered to respond to such therapy. However, it would be inappropriate to give such therapy if there is an element of dehydration as it would make that problem worse, whereas in fluid overload, it might be an appropriate therapy to use.

6) Ion Exchange Resins-- Calcium Resonium can be given orally or rectally and they will exchange one Ca ion for two K ions. They will cause a gradual decrease in K level over hours to days and so although they can be given during the emergency period, their effect will not be evident immediately. They can also cause constipation so make sure than a laxative is provided and not with Lactulose!!!

7) Infusion of bicarbonate-- can sometimes be considered but usually this is only given if the pH of the blood is very low e.g. pH<7.2, style="color: rgb(102, 51, 255);">8) Haemofiltration / Dialysis-- sometimes the patient will not respond to conservative less interventional therapies and so detoxifying the blood using haemofiltration / dialysis may be the only effective method for treating the high K levels. It is often best to speak to the nephrology services earlier rather than later so that preparations can be made to haemodialyse patients.

Clinical Gem: Insulin therapy is less likely to work if the patient is dehydrated or has a poor circulation as insulin needs blood to get to muscle!! Hence, always correct fluid balance status in your patients.

Assess fluid status by checking pulse, blood pressure, skin turgor, mucous membranes (is the tongue dry?), urine output (should be as a minimum 0.5ml/kg/hr; so in a 60 kg male = 30ml urine per hour) and consider CV line insertion and monitoring CV pressure.

Fever, Diarrhoea and Muscle Pain

This Case Has Been Anonymised to Safe Guard Patient Confidentiality

A 50 year old male patient who is a taxi driver who is normally fit and well who presented with a short 6 day history of:

1) Fever
2) Diarrhoea
3) Muscle pain
4) Dry cough

The fever was the initial symptom and was continuous rather than intermittent. The was no associated rigors (shivering) or sweats. The diarrhoea was non-painful, a dark colour but no visible blood or malaena (tarry stool).

The patient had been having diarrhoea once per day.

On the day prior to admission, he also had vomiting once although this became mixed with the diarrhoea so he was unable to describe the look of the vomitus.

The muscle pain was described more of a dyscomfort and was generalised. There was no associated joint pain or swelling and no skin rash. The cough was intermittent and dry. No sputum and no haemoptysis. No dyspnoea.

On further questioning, the patient had eaten sushi / sashimi one week ago ( one day before becoming unwell) but he could not remember what type of raw seafood as he had also been drinking alcohol on that day. He denied eating raw chicken or oysters. Being a taxi driver he usually bought an o-bento lunch box from the local convenience store and this was usually sushi.

He had no history of inflammatory bowel disease and no eye symptoms. He had never had any joint disease.

Previous medical history included 1) hypertension 2) renal glomerulosclerosis since a child and he took Olmesartan, Amlodipine and Allopurinol.

He otherwise drank alcohol occasionally and was an ex-smoker having at one time smoked 30 cigarettes per day.

On examination, he looked relatively well. Temp was 39 degrees C. No Cervical lymph nodes and no evidence of clubbing or splinter haemorrhages. Eyes showed conjunctival injection and mouth appeared appeared slightly red and the soft palate had white vesicular lesions that could not be scraped off. The tongue was coated and appeared to be candida albicans infection.

Blood pressure was 106/5o, pulse 72 bpm regular, JVP was not raised. There were no heaves or thrills and heart sounds 1 & 2 were present and there were no mumurs evident. Leg examination was normal with no oedema or DVT identified.

Respiratory rate was regular at 18/minute, normal percussion sounds and vesicular breath sounds. There was no wheeze or crepitations.

Abdominal examination revealed a soft, non-tender abdomen, with no evidence of hepatosplenomegally. There was no renal angle tenderness and bowel sounds were slightly increased. Rectal examination by the junior doctor revealed occult blood but there was no evidence of a mass and the examination was non-tender.

Skin was grossly normal.

Clinical Impression / differential diagnosis

Infective Diarrhoea

Bacterial diarrhoea e.g. Salmonella, E. coli, Shigella, Campylobacter, Yersinia enterocolitica, vibrio vulnificans, Clostridium difficile

Viral diarrhoea e.g. adenovirus (sore throat, red eyes, fever, diarrhoea-usually non-bloody)

Inflammatory

Inflammatory Bowel Disease e.g. Ulcerative colitis or Crohn's disease (bloody diarrhoea / fever / eye signs)

Vasculitic
Systemic Lupus Erythematosis (more a cause of abdominal pain than diarrhoea)
Polyarteritis nodosum

The Laboratory data revealed Hb 15.4 g/dl, low white cell count of 2.9, low platelets of 4.0, high fibrinogen level and normal INR/APTT. BUN was 26 and Creat 2.3 (normally 1.2), normal Na/K. Liver function was normal. CK normal. CRP was 9.

Blood smear showed no fragmented red cells. Stool examination revealed numerous white cells in the stool.

One concern was of a Haemolytic Uraemic Syndrome (HUS), but the history had been going on too long for this problem and the patient was well. Moreover, this clinical syndrome is predominantly seem in children. Another concern was DIC, but the blood smear was normal and the fibrinogen level was HIGH not low and one might see a MicroAngiopathic Haemoltic Anaemia (MAHA), raised INR and a low Haemoglobin is severe circumstances.

Another consideration was of Thrombotic Thrombocytopaenic Purpura (TTP) which is an adult problem associated with E. coli 0157:H7 infection just as is HUS, but there was no report of clumped platelets and the patient had no neuropsychiatric symtoms and no evidence of bleeding or haemolytic anaemia. TTP can also be found as a consequence of drug reactions particularly with Ticlopidine (which is used in Japan) where patients develop antibodies against the ADAMTS 13 protease that usually cleaves vonWillebrand Factor deactivating this enzyme. Familial cases of TTP show no activity of the above protease enzyme.

If this patient had an underlying immunodeficiency, for example AIDS, then other more innocuous infections could be a cause of bloody diarrhoea, fever, exudative sore throat and general systemic upset including: varicella zoster virus / Herpes Simplex Virus / Cytomegallovirus all of which can cause ulceration to the GI tract. Other immune deficient associated infections include the protozoal infections such as cryptosporidium, isospora belii although these do not cause a bloody diarrhoea.

In fact, the low white cells and platelets were likely related to a consumption from sepsis with the target of the sepsis being the bowel, which would explain the numerous white cells seen in the stool.

The patient was treated with intravenous antibiotics to cover the gram negative organisms and was rehydrated. By the next morning, the patient felt alot better and the diarrhoea and vomiting had stopped.

The patient had a colonoscopy to try and rule out inflammatory bowel disease.

The above example, however, shows you that fever, diarrhoea, cough, and myalgia do have a wide spectrum of possible diagnoses.

In view of his food history, which element is often left out of the medical history, it seems more than likely that he picked up a bacterial infection from contaminated food one week ago. In view of the relative bradycardia compared to his high temperature (which should have caused a higher pulse rate) and the dry cough and the invasive nature of this probable infection, this makes me consider invasive salmonella such as salmonella typhi or paratyphi as the cause of an Enteric Fever.

What is your opinion?? Please let me know.....

Great Case- Physical Examination of Heart Failure

This case has been anonymised to safe guard patient confidentiality.

This case is a typical General Internal Medicine (GIM) case, but it is important to get it correct.

The following case shows how a case should be written in the patient notes in the form of how to show pertinent positive and negative findings for each of the three main systems. The clinical diagnosis (assessment) and the plan for each problem is identified. Only by doing this can a logical way of dealing with complex and multiple problems be made easier to deal with, which improves on patient care and makes the problems easier to understand.

This patient was admitted with dyspnoea that gradually worsened over the day prior to her admission. The dyspnoea prevented her from lying flat and she was then admitted to hospital by ambulance. She apparently had no other symptoms.

She had a previous medical history including:

Acute MI x 3
Repeated admissions for Congestive Heart Failure (CHF)
Coronary artery stenting x2 last year
Chronic Renal Failure secondary to AMI last year

No Hx of diabetes.

Medications include 1) furosemide 20mg OD 2) aspirin 3) Amlodipine 10mg OD

She still continued to smoke 30 cigarettes per day and had done so for the last 70 years!
She drinks little or no alcohol.

On direct questioning, she denied any recent chest pain, no cough, sputum, haemoptysis or fever. She had chest pain during her last AMI but has had no recurrence on this admission or in the period before admission. Recently she had been thirsty and has produced darker coloured stool on defecation but she denied any constipation.

On examination, she looked well and was smiling.

BP 155/66 (wide pulse pressure), HR 90min regular, RR 30/min, Sats 86% on room air (94% on 5L oxygen), Afebrile (normal temperature)

No Jaundice. Anaemia- pale conjuctivae, No Clubbing, Cyanosis positive. Tar stained nails from cigarettes.

CV Examination: Waterhammer Pulse (Right Brachial pulse- high pressure felt under pulps of examiners fingers then collapses whilst arm elevated in the air), Quinke's sign Negative, Corrigan's Sign Positive (visible pulsations of carotid due to high output from heart), JVP raised about 6cm H2O. Apex not felt and no heave or thrills. Heart sounds 1 & 2 present and diastolic mumur at apex only with loudening on expiration. No radiation to left axilla. Patient unable to be sat forwards. Leg oedema present to 2/3 up both lower legs. No evidence of DVT.

Respiratory Examination: Tracheal Tug but central (reduced space between suprasternal notch and laryngeal cartilage consistent with chronic lung disease), percussion was dull at both lateral chest walls and at both bases of the lungs consistent with bilateral pleural effusions. 'Wet' crackles present 2/3 the way up both lungs. No wheeze. No Lymph nodes palpable.

Abdominal Examination: Soft, non-tender, semi-hard, smooth mass about 20cm x 20cm arising from the pelvis, but the examinaing hand could get below it and above the pelvic brim. Dull to percussion. Reduced bowel sounds over area of mass, but bowel sounds were present. No pelvic lymph nodes palpable. No hepatosplenomegally. Rectal examination was excluded due to difficulty lying patient on lateral side.

Basic Lab Data

Lab data showed anaemia of Hb 8.5 g/dl, MCV 104, BUN 35 Creat 2.36, normal Liver tests, BS 300, HbA1c 6.2%, CRP normal, WCC 14.4, Lymphocyte % raised 54%. LDH normal range. Troponin T Positive (between 0.06 and 0.1-- minor myocardial damage), CK normal.

ABG (on admission): pH 6.9, HCO3 14.1, PCO2 69, PO2 60, BE -12

Clinical Diagnosis based on History and Physical (plus some Lab data observations)

1) Heart Failure worsened- causes
i) Possible new MI
ii) Under medicated for heart failure (not on ACE-I / ARB)
iii) Hypothyroidism (raised MCV, anaemia)
iv) Systolic dysfunction due to metabolic acidosis
v) Worsening failure due to anaemia (high output HF)
vi) Worsening Aoartic Regurgitation
vii) Worsening failure due to Meig's Syndrome from Ovarian tumour

2) Aortic Regurgitation

3) Tricuspid Regurgitation

4) Abdominal Mass
i) Possible Benign Ovarian tumour
ii) Possible Malignant Ovarian / Bowel Tumour

5) Anaemia (with raised MCV)
i) Possible folate / B12 deficiency due to enlarging cancer
ii) Hypothyroidism
iii) Bleeding (imature reticulocytes enter blood stream)
iv) Bone Marrow invasion from tumour (immature blood cells enter blood stream})


6) Type 2 Diabetes Mellitus ( patient had 3 three random BS > 200mg/l and HbA1c 6.2%)

7) Mixed Metabolic and Respiratory Acidosis
i) From combination of Renal failure (metabolic component) and Heart Failure (respiratory acidosis and hypoxaemia)
ii) Diabetic Ketoacidosis (ketone bodies -- metabolic acidosis) and Heart failure (respiratory acisois)
iii) Lactic Acidosis from possible recent AMI plus heart failure


CXR revealed small bilateral effusions and upper lobe diversion and fluid in the right horizontal fissure. The LA shadow appeared enlarged. All features consistent with CHF.

ECG showed Left Bundle Branch Block-- consistent with previous MI (ECG normal prior to last MI)

Urine Analysis: Ketones Negative

Serum Lactate: Negative

CT was performed and revealed a large cystic mass arising from the pelvis. Awaiting formal diagnosis by the gynaecologists, but possible ovarian tumour.

Hence, in this case, the history and physical provide the physician with most of the answers. Careful cardiac examination showed not only probable ventricular dysfunction but also AR and TR just by looking at the neck and identifying carotid pulsations and the JVP. Waterhammer pulse and the diastolic murmur convinced me of the valvular problem.


The diabetes could be treated for symptomatic purposes to prevent thirst and polyuria rather than aiming to obtain perfect control. Metformin is contraindicated due to risks of lactic acidosis as a result of renal failure. The glitazones (e.g. rosiglitazone and pioglitazone) are contraindicated as CHF can worsen due to fluid retention effects from these drugs. The best oral medication in these circumstances would be a short acting sulphonulyurea such as Gliclazide. The renal failure prolongs the serum half life of SUs and the effects are for longer and hence, a short acting agent would be preferable. Glibenclamide and glimepiride would be dangerous and cause hypoglycaemia due to their long time of activity.

If this patient had had typical ischaemic chest pain and a troponin rise consistent with an AMI which could have been exactly calculated when it occurred, then IV insulin should be given consistent with the DIGAMI study (Diabetes and Insulin Glucose in Acute Myocardial Infarction), which study showed that tight glycaemic control improves mortality in the peri-AMI setting. Following this, the DIGAMI 2 study showed that there was no difference between using insulin or oral hypoglycaemic agents long term so long as tight control was maintained.

Should the aspirin have been stopped?? Well, there was no evidence of haemorrhage. The aspirin providing benefit for the patient's cardiac risks and new diagnosis of DM may still out weigh the risks. However, the patient has NHYA Stage IV heart failure and a malignancy which gives her a poor prognosis and hence, would it have been right to continue such treatment which might cause heamorrhage? Only further tests and observing the patient would provide the answers.

The heart failure was treated with 1) IV nitrates 2) Furosemide 60mg and this produced a marked diuresis and over the night of her admission, the patient's clinical condition and ABG improved.


CHF treatment

1) Fluid restricted to 500ml / day orally
2) Low salt / No added salt diet
3) Daily weighing of the patient to have exact measure of fluid loss
4) IV furosemide until fluid status is corrected and then increase the stable daily oral furosemide dose to 40mg/day OD
5) Consider adding in an ACE-I (which improves cardiac function and reduces hospital admissions from CHF and is also reno-protective in DM; hence dual beneficial functions but watch for worsening renal function. A 30% increase in creatinine is acceptable when starting ACE but if higher and / or K+>5.0mmol/L then consider stopping such therapy)

Anaemia and Raised MCV

6) Obtain thyroid studies, iron studies, folate, B12, blood smear

Cardiac Function Investigation

7) Order Echo to see current cardiac function and valve status

Investigation of possible Ovarian / Bowel tumour

8) Tumour markers esp CA-125 (raised with ovarian tumours), CEA

Diabetes Mellitus

9) Consider low dose Gliclazide / Insulin

As can be seen, this case is quite complex but it can and has been broken down in to smaller manageble pieces and there is a plan for every problem.

A Humane Death- the Role of the Palliative Care Team

In the UK and USA there are specialist teams that work both in the Community and Hospital referred to as the Palliative Care team.

These doctors and nurses deal soley with palliation and providing a painless, anxiety-controlled and humane death for terminally ill patients.

Terminally ill patients not only include those with cancer, but also those patients suffering with end-stage conditions such as COPD, Heart failure, Liver Disease and Chronically progressive debilitating neurological conditions.

They will review patients on a general ward and provide advice on stopping treatments that are not helping and commencing medications to help a whole host of different symptoms that the terminally ill may suffer such as pain, anxiety, constipation, ascites, respiratory secretions, etc...

Their role in the hospital setting is very important because when they are called in, a patient's treatment can be significantly altered from one of full active treatment to one which palliates, and the medical staff are then able to provide a different, more private and dignified standard of care, such as treatment in a side-room, less disturbance by medical personnel, less painful blood tests etc..

The palliative care team also run the Community Hospice care and in the UK, these small units are a cross between a hotel and hospital providing comfortable and relaxing surroundings for treatment. Not all patients are admitted in terminal stages; some are admitted for temporary treatments such as drainage of ascites (paracentesis) , respite care or even just to adjust pain relief under under a controlled environment.

In the UK, it is sometimes more important to provide the patient with a decent, humane and painless death rather than continuing to press on with aggressive pro-active medical therapy which is clearly futile. This sometimes involves stopping antibiotics, stopping drugs that are there to reduce risk factors of cardiovascular disease, such as stopping some blood pressure drugs, anti-platelets agents, statins as these may be unnecessary at their terminal stage of illness.

One could look at this type of medicine as 'giving up', but I do not see it as this, as usually the patient's condition reaches a point when it is clear that it is unfortunately not going to improve and therefore, it is better to alter therapy with the progression of their illness.

As far as I am aware, the Palliative Care services in Japan are not as developed as those in UK or America, and I truly believe that such services would make a wealth of difference to patients and it would also help patient's families to accept the inevitability and futility and also to enable them to make plans for the short-term future and allow for acceptance thereby making grieving easier to take.

Patients have a right to continue living but also the right to not have intolerable medical treatment, and as doctors, we must listen to our patients about what they want, rather than what we think is best for them. We are not special people with God-like powers and rules. We too are human and we must treat people equally as we ourselves would like to be treated.

The 'take home message' is Listen to, Respect and be Humane to your patients and do what is right for your patients at all times.

If you have any views on today's blog then please write me :) !!

Epocrates-- Drug Software for PDAs

Today's blog is a bit shorter than usual as I have a conference to host this evening.

I wanted to return to the importance of using drugs.

A good example of multiple drug interactions was in a patient who I saw recently with a pneumonia and long standing depression.

The pneumonia was consistent with an atypical organism being the cause and hence, a macrolide such as clarithromycin or a quinolone such as levofloxacin could have been used except for one very good reason:

This patient took a combination of 1) Two tricyclic antidepressants 2) a Noradrenaline uptake inhibitor drug.

The combination of the two classes is in fact quite problematic as it can cause hypertension but more importantly, the tricyclic levels can increase due to the presence of the latter drug.

The patient had been taking 3 anti-hypertensive drugs when the probable exacerbating factor of his blood pressure was the combination of anti-depressants!!

With my resident, we checked the possible drug interactions very speedily on a piece of software which is FREE called Epocrates (www.epocrates.com) and it enables you to do a comparison of any drug against another for interactions.

We were then able to check the two antibiotics clarithromycin and levofloxacin and unfortunately, they in combination with Tricyclic antidepressants, can cause a Long QT Syndrome and hence, Polymorphic Ventricular Tachycardia (Torsade de Pointes).

Hence, it was a very valuable way of checking potential drug interactions which allowed a modification of drug therapy to either Clindamycin or Doxycycline, both of which are alternatives and do not appear to interact with Tricyclics.

Thus, my advice is ALWAYS CHECK FOR POSSIBLE DRUG INTERACTIONS when considering adding in a new treatment of any kind. It can be life saving and using Epocrates software can save you time and it can tell you all the relevant drug information. However, it is not based on Japanese drug dosing but American drug doses which are higher, so you should, if you use this software, check the doses with a Japanese drug text instead.

Have you ever asked yourself the question why we do CT scanning?

Well, we get very sharp and accurate pictures that allow us to determine, in some instances, the possible cause of a particular medical or surgical problem.

I am not a surgeon and therefore, it would be inappropriate for me to comment on imaging studies for surgical problems in any detail other than generally accepted concepts and as a result , I shall mainly concentrate on imaging modalities for medicine.

CT HEAD SCAN

The CT head scan has revolutionised medicine in being able to see directly inside the cranium and to be able to identify a whole host of problems such as cerebral infarction/bleeding, tumours, raised intracranial pressure etc...

It is sometimes the only way to find out a problem.

I regularly hear of patients admitted with some type of confusion or reduced conscious level who, for example, may have a pneumonia or urinary tract infection, or an obvious acidosis / hypoxaemia or electrolyte disturbance. With the diagnosis being quite clear in most instances I have seen, on occasion, the patient is also put through the scanner to check their brain.

All patients with reduced consciousness should have a full physical examination first which includes a thorough neurological examination to see if the patient has any focal neurological impairment. If present, I would whole heartedly agree that a CT scan should be performed.

However, if there are no focal neurological signs and another causes of impaired conscious level can be identified, e.g. UTI causing an acute confusional state and with no signs of meningism, then performing a CT scan, in my experience, is usually normal and offers no additional value in diagnostic terms and the physician will have exposed the patient to radiation unnecessarily.

For example, hypercarbia as part of type 2 respiratory failure can result in cerebral oedema, but it also causes papilloedema. This is a physical sign that can be elucidated by fundoscopy which my provide the clue that there is cereberal oedema.

Moreover, I often hear that a patient needs a CT head scan prior to lumbar puncture. If there are no focal neurological signs and that includes NO PAPILLOEDEMA of the fundi (in the eye), then a CT head scan may not be required. This was confirmed in a paper in the New England Journal of Medicine several years ago (Hasbun et al, Computed tomography of the head before lumbar puncture in adults with suspected meningitis. NEJM 2001; 345: 1727-33)

However, as I understand it, fundoscopy is not routinely taught at medical school in Japan, which is quite different to the UK where it is taught. I also teach fundoscopy examination here in Japan, and when there is an emergency case in ER, on occasion, I am usually called to perform the fundoscopy examination. Hence, the only way to try and identify raised intracranial pressure (rather than ruling it out) is to perform a CT head at most institutions.

Fundoscopy is a dying art but it can potentially save a patient's life. A CT scan cannot always determine if there is raised intracranial pressure (false negative), and the same is true for an MRI scan. However, if fundoscopic papilloedema is present, then the patient has raised intracranial pressure until proven otherwise, and a lumbar puncture should not be performed as to do so might result in brain stem herniation( a good reference is Diederik et al, Community-Acquired Bacterial Meningitis in Adults. NEJM 2006. 354: 44-53).

The latter paper talks about repeated lumbar puncture or placement of a temporary lumbar drain to 'effectively reduce' intracranial pressure, although it does not allude to the mortality of such patients treated or the rate of cerebral herniation and as far as I am aware, this is not standard treatment.

I have personally seen a case of a patient with encephalitis whose only complaints were headache, fever and memory loss and papilloedema was identified by me, and when the CT was reviewed, there were indeed signs of raised intracranial pressure and cerebral oedema.

Hence, there must always be a good reason to do a CT head rather than just to screen the patient. If you suspect a brain tumour then a CT is reasonable, but if the cause of the confusion is due to a severe pneumonia, then performing a CT head scan with a normal neurological examination, might seem over intensive especially if there is no real clinical indication.

At the end of the day, the whole matter comes back to History and Physical Examination, as they are your guide to the cause of the problem (in most cases).

In order to consider doing any imaging, you have to consider what you are going to do with the result! For example, does every patient with a clinical catastrophic stroke with a GCS of 3/15 really require a CT head scan if the history and physical examination are consistent with the diagnosis? Most physicians would go ahead and scan such patients, if only for medical defence purposes, but a patient with a very low GCS usually portends a grave prognosis.


Some physicians would argue that to do a CT head scan in such circumstances could pick up an intracerebral problem that could be treated. However, in a terminal patient, it is sometimes far more humane to optimise their palliative therapy and make the patient as comfortable as possible in their last hours, days or weeks rather than putting them through perhaps unnecessary tests, treatments or surgery which the patient may not have wanted or in fact needed.

It is essentially, a case-by-case decision as no one patient is the same as the next, but the physician should always bear in mind 'am I going to gain anything from doing this test?'

So, when doing a scan, one has to take into account the social circumstances of a patient, their pre-morbid condition, their wishes, the severity of their present condition and whether by doing the scan, it will actually change your management of the patient.

CT Chest Scans

Pneumonia seems very common here in Japan. In the UK, most pneumonias are seen in the Winter/Spring months and very few are seen at other times. From my short experience here, the same is not true and pneumonia is common all year round with a higher number in Winter.

I have seen many chest x-rays (CXR) with old tuberculosis (TB) usually in the elderly age group. The vast majority have completely inactive disease. Without the usual symptoms of cough, fever, sweats, weight loss etc is unconvincing to me to perform a CT chest scan, unless there is CXR evidence of active disease.

Pneumonia can usually be diagnosed on CXR WITHOUT the need for a CT chest scan. However, again I have seen at various hospitals the acquisition of CT scans for uncomplicated and quite obvious pneumonias and I see this as unnecessary.

History and Physical should at the very least provide enough information to make a diagnosis of pneumonia (except perhaps atypical pneumonia, where chest sounds may appear normal) and CXR can usually suffice to confirm the diagnosis. If the suspicion is strong for an atypical pneumonia, with a normal CXR, then I would be the first to say 'get a CT'. However, the 'reflex' to always obtain a CT chest for pneumonias is not necessary as it usually does not change the management in the vast majority of cases I have experienced.

The patient is going to usually receive a Broad-spectrum antibiotic unless there is definite identification of the organism and sensitivities are known, in which case, a narrow spectrum antibiotic would be used. Basically, antibiotics are going to be given and hence, doing a CT in an uncomplicated pneumonia does not help treat the patient.

Blood cultures, sputum examination, urinary antigens may be far more helpful than a CT.

Repeat CXR after clinical resolution, normally at 4 weeks, is the usual way to detect any unusual features that come to light such as the hiding malignancy, and it is at that time that a CT should be done, if of course, there were no sinister signs of an underlying disorder on admission.

If on the other hand, the patient's hypoxaemia is out of keeping with a small area of consolidation on the CXR, then one must always consider a complicating Pulmonary Embolism, and the modality of imaging would be a SPIRAL CT or the new technique of MR pulmonary angiography, rather than a Plain CT. Hence, when thinking of imaging, one must always consider what one is looking to diagnose or exclude. Doing a Spiral CT will aide in the diagnosis of PE and hence, it would alter the patient's treatment, for example, the patient would need heparin added or thrombolysis or thromboembolectomy.

ABDOMINAL CT SCANS

The abdomen was once described by my best friend as a 'box of magic tricks', as was told to him by his General Practitioner. Clearly, the abdomen being only partially radiolucent to Xrays is difficult to image.

I think that formal imaging of the abdomen requires an even higher level of suspicion of a serious problem, because doing a CT exposes the patient to a higher level of radiation.

History and Physical Examination may be helpful, but an ultrasound performed by an experienced doctor or ultrasonographer specialist may provide the answer, thereby negating the need for a CT scan.

For example, I have been informed that at another hospital, a patient was admitted with a history of fresh rectal bleeding which was consistent with a clinical diagnosis of inflammatory bowel disease. Whereas the patient should have been prepared for a flexible sigmoidoscopy or colonoscopy, the patient was put in the CT scanner, and the report confirmed that it looked like inflammatory bowel disease. The patient still needed a colonoscopy in any case, which is the Gold Standard Test, so was the CT necessary? No.

The usual way of imaging is an abdominal X-ray to rule out Toxic Megacolon or perforation. Only if perforation is suspected, but not detected on Xray, would a CT be required, although a traditional decubitus abdominal film might also provide the answer. Thus, CT should not be routinely performed in such cases. In cases where there is straight forward peritonitis, a CT can be a very helpful tool.

If on the other hand, the physician was considering a bleeding divertiulum or an abscess, for the former problem, a colonoscopy may still provide an answer (bearing in mind not to perforate an diverticulum) or ultrasound scanning the area and then draining percutaneously. If colonoscopy was considered too dangerous, then a barium enema can also provide the answer and although several pictures of the abdomen are taken, it provides less radiation than with a CT.

Patients with an appendicitis normally have a good history and in advanced cases, a physical examination consistent with the diagnosis. Performing an ultrasound may reveal the swollen appendix or ' free fluid'. Watching the patient, the temperature, pulse, blood pressure should be the reason for surgical intervention or conservative management, and doing an abdominal CT, although producing very fine pictures, is exposing the patient to radiation, which in a young female patient is of great concern in respect of possible future reproductive problems.

Finally, you must be worn out reading today's blog, but fertile female patients requiring any abdominal imaging involving X-rays MUST be pregnancy tested. Although the patient may say that are not pregnant or there is no possibility of being pregnant, there are some cases when the patient IS pregnant, and proceeding with a scan in the absence of testing the patient is negligent. Pregnant women can shed some of their uterine lining in early pregnancy which may look like a period and so, it is always best to test anyway, with the patient's consent of course.

You should always explain to the patient the risk of exposure to, for example, a full body CT scan.

David Brenner and Carl Elliston of Columbia University for Radiologic Research have been able to calculate the life time risk of developing cancer due to radiation from a single body scan which is 0.08%. That is equal to one in every 1,250 people who has a full body CT will develop cancer as a result. That is quite a worrying figure!

Extrapolating this further, a 45 year old person having a full body CT every year for 30 years would cause one in 50 to develop a radiation-induced cancer.

If you are interested you can read the article for yourself: Brenner, J. J. and Elliston, C.D. Estimated radiation risks potentially associated with full body CT screening. Radiology. Vol 232 (September) P 735-738. 2004.

Medico-Legal Medicine: the Musts of Medicine

The following blog, is soley my opinion from what I have read in respect of medicolegal cases in the UK and I hope it is enlightening.

Medicolegal cases in the UK are on the rise, and the payouts for medical negligence are reaching mammoth amounts.

Why is taking a history and performing a detailed physical examination important?

Well, it protects the patient and the physician alike.

Taking a thorough history shows that the physician was trying his or her best to find the problem. It also identifies areas that the physician forgot to ask. Hence, having an armory of stock questions to cover all the possible life-threatening problems protects the patients, as the diagnosis will be made quickly, and this protects the physician as a result.

This is the purpose for the Review of Systems Questions. I always describe it as a 'safety net' as it will catch those problems that the patient or the doctor forgot to touch on in the earlier part of the interview. In doing so, problems that were previously unidentified come to the foreground, some of which might be serious e.g. prostate cancer, and the physician will be complemented for finding the problem that others have missed, rather than miss it and be scorned for failure.

Performing a rectal examination is a MUST do part of the abdominal examination as a way to identify the rectal cancer or prostate problem. It must always be performed in cases of anaemia, diarrhoea (it might be overflow diarrhoea from an obstructing cancer), constipation, change of bowel habit, fresh rectal bleeding, weight loss, jaundice (rectal tumour with mets to liver), groin lymphadenopathy (rectal tumours can spread to the groin as well!!), unusual utero-vaginal bleeding in case of the neoplastic fistula to bowel.... If you avoid the Rectal test, the patient fails to get diagnosed and the physician gets wrongly labeled as negligent by the lawyers!

Examining the external genitalia is ALSO part of the abdominal examination with a chaperone of course!

Pyrexia of unknown origin in a man, the physician MUST examine the testicles because testicular tumours can cause fever (and spread to the lungs), and the lump of the testicle may have gone unseen by the male patient.

Also, patients with congestive cardiac disease, liver disease, nephrotic syndrome or severe low protein states can develop genital swelling to the extent that their urethra cannot be identified and they may develop urinary obstruction. Failing to inspect the genitalia can be disastrous leading to suprapubic catheterisation, that might have been avoidable if diagnosed earlier, and again, the physician might be labeled as negligent.

Writing all the physical examination down and the vital signs is extremely important as it is your only proof that you did the job correctly.

Failing to write down the heart rate, blood pressure, temperature, respiratory rate and SpO2 and sometimes even the capillary blood sugar might be taken as negligence by a court.

For example, a patient who is severely unwell and who has shock vitals on admission and who subsequently dies due to their illness is not uncommon. However, if the doctor fails to write down the full set of vitals can be be accused of not treating the patient correctly even if they did their best.

Here is a good example:

Lawyer ' So, this patient had severe breathlessness in your ER department right?'

Doctor ' Yes, that is right.'

Lawyer ' So, where is your record of the respiratory rate and SpO2?'

Doctor ' I am sure I wrote it down'

Lawyer ' Where. There is no electronic record of it!'

Doctor ' But...'

Lawyer ' Is it not true, that the reason there is no respiratory rate and SpO2, is that the patient was already dead!'

Doctor 'No....'

Lawyer ' Well, doctor, we have no proof. You never wrote it down. The patient died in your ER department. How do we know that the patient was alive?!'

The above is a made-up example of just how important the vitals can be.

Vitals are important as they tell the senior doctors of how severe the patient's condition is and how quickly they need to act and where the patient should be located e.g. a normal ward or the ICU department !

Always documenting the important positive findings and the negative findings shows that the physician actually checked rather than saying everything was normal. My 'Everything' and the inexperienced junior doctor's 'Everything' are completely different, and what a junior may miss a senior would hopefully identify.

Hence, writing everything 'normal' without qualifying why it is normal is incomplete and not good enough for notes that might one day end up in the hands of lawyers who may not care about your career at all...just about winning their case and of course, getting paid!

Timing and dating notes and signing the entry (by signature or electronically) shows that the physician did attend their patient, for example, before their unexpected sudden death on the ward, which shows anyone looking, that the problem may have not been readily identifiable or that some other problem arose. It also shows that the physician did not neglect their patient.

Writing a summary and differential set of diagnoses also shows that the physician had made a diagnosis and that treatment was then initiated for the problems identified. Failing to make a diagnosis at all might be construed as incompetence by lawyers, but making a differential diagnosis shows that the physician thought of many problems rather than nothing being documented at all.

So, you may have been thinking that patient notes are there just to tell other doctors and the nurses what is going on with the patient. Think again!

Patient notes if kept poorly maybe the thorn in the doctor's side despite them being an excellent doctor, whereas perfect notes may show that the doctor did a superb job for the patient and that the end result was unavoidable.

Although the litigation in Japan is not as high as in Western countries, it should always be borne in mind that it will increase in time and that when you put 'pen to paper' or 'fingers to the keyboard', you may need to defend it in court one day and sometimes, many years later, when you can't even rememer the patient you saw at the beginning of the busy clinic this morning.

I hope this gives you something to ponder about.

All the best!

PLEASE FEEL FREE TO GIVE ME YOUR OPINIONS!!

Wallenberg Syndrome

This is an anonymised case of Wallenberg (Lateral Medullary) Syndrome, passed to me from another institution, in an elderly male patient whom had otherwise been of good health.

He had complained of sudden onset vertigo and nausea with vomiting. He described being unable to stand properly and he fell towards the right side. He also described double vision. He did not describe any subjective sensory abnormality or any limb weakness.

He had no previous medical history and took no regular medications.

He is a non-smoker and drinks occasional alcohol.

On examination, he was afebrile and looked well, pulse was regular and good volume, respiratory rate was 14 per minute and oxygen sats were 96% on room air.

His PNS examination was remarkable.

Tone was normal but he had a Left Pronator drift (consistent with an upper motor neurone defect). Power was 5/5 in the upper and lower Right limbs, but 4+/5 in the left upper and lower limbs albeit that his left side is the Non-Dominant side.

He was generally areflexic throughout.

However, the modality that had been alluded to was SENSORY testing and this revealed decreased sensation to light touch and painful stimuli (nociception) on the Left side.

His Right Plantar response was normal and the Left was Unresponsive.

Examination of his CNS revealed a Right sided Ptosis. Decreased sensation to both light touch and nociception of the RIGHT side of his face. His swallow reflex was normal.

Cerebellar examination revealed rotatory nystagmus on the Right side and some mild horizontal nystagmus to the left. The patient had past-pointing on the Right side and dysdiadochokinesis was negative.

In summary, the Clinical Findings showed:

1) Dissociated sensory deficit (loss of sensation on the right face and left body)

2) Positive Cerebellar signs suggestive of a Right Sided Cerebellar Insult

3) Horner's Syndrome on the Right

4) Areflexia

5) Mild left sided weakness (although, this may be a natural difference due to it being the non-dominant side)

6) Vestibular dysfunction (symptoms of vertigo/nystagmus)

These above symptoms and clinical signs were consistent with a diagnosis of Wallenberg Syndrome (this diagnosis had also been confirmed by a very astute neurologist) a somewhat rare diagnosis, and this case will forever be in my mind as a typical case.

His CT scan showed a small infarct in his lower medulla and the MRA was non-diagnostic, nor was the diffusion MRI.

It reinforces for me that history and physical are a superb way to find out the problem, and putting all the pieces of the jigsaw together one can form the diagnosis where a scan may be unhelpful or at least difficult to interpret. Physical examination can show the physician where the problem is likely to be, and even if the scan is negative, the physical signs cannot be ignored nor should they be, as they will tell the doctor that the problem is present. Repeated physical examination will also tell the doctor whether the patient is getting better or worse!!

This patient was commenced on anti-platelet therapy and underwent rehabilitation.

A really great case!!

An Interesting Case

Yesterday was very interesting for me and it reinforced to me how important history taking really is. This next case has been anonymised for confidentiality purposes.

At another hospital, I hosted a conference, and a junior resident presented a history of a 45 year old female who presented to hospital with a seizure before New Year.

The patient had developed a fever four days before admission and apparently had no other symptoms until the day of admission, at which point, the patient had a seizure in her home toilet.

The patient had complained of some apparent neck stiffness on the day of the fever but not on admission. The patient had no other medical ailments and took no regular medications. The patient is married, works as an airline hostess, smokes a box of cigarettes per day and consumes occasional alcohol in moderation.

At this point I stopped the Resident and asked for more history of the chief complaint before moving on with the previous medical history, but no more history was available, such as, had the patient had a recent cold, cough, sputum (and colour), any recent antibiotic therapy etc...

From here I heard the vitals which indicated a high temperature of 40 degrees C, SpO2 of 92%. Oxygen sats were too low for such a young patient. At this point, it was possible to form differential diagnoses including the following:

Seizure and Fever: possible meningitis, encephalitis, cerebral asbcess, cerebral vasculitis, cerebral tumour / metastatic disease as examples.

Hypoxaemia and Fever: pneumonia, other respiratory infections, aspiration pneumonitis post-seizure, pulmonary embolism.

Bloods showed a high CRP>10 and raised white cell count of 18, although having a raised white count is not uncommon following a seizure. Blood gas revealed a metabolic acidosis and hypoxaemia; urine analysis showed no sugar and 1+ ketones. Blood sugar was slightly raised at 187 but not diagnostic of DM on a random sample.

CT scan had revealed no abnormality, but lumbar puncture showed CSF pressure of 53cm water (normal <20),>

Hence, the diagnosis was confirmed to be meningitis, likely bacterial, from the CSF result, and I suggested from very little information and data at that time, that the patient had either a pneumonia causing meningitis, likely pneumococcal, or that the patient aspirated post-seizure.

I was then informed that the urinary pneumococcal antigen was POSITIVE. However, this does not itself rule out the possibility of a different organism having caused the meningitis, although it would seem highly likely that it was.

I considered that the acidosis and ketonuria could have been due to starvation or alcohol, but diabetic ketoacidosis was unlikely, as there was no sugar to be found in the urine and the serum glucose was not in the diabetic range.

Following this, we went to review the patient, and she had developed some retrograde amnesia from the illness and her husband was able provide an excellent history. She had developed a cough and green sputum before admission, and had seen her local doctor and a common cold had been diagnosed and antibiotics had probably been prescribed. The patient had only taken a few tablets, but she did not like to take medication and stopped it. The patient then drank alcohol following which she developed a seizure.

Examination yesterday was entirely normal in every respect except for a mild drug rash from antibiotics and some mild clubbing of her hands and feet.

The chest roentogen revealed some mild patchy alveolar change consistent with infection and the follow-on CT confirmed it was a pneumonia.

The acidosis was probably due to alcoholic ketoacidosis and / or starvation. The fact that the patient had taken antibiotics prior to presentation explains the inability to find the bacteria in the CSF, but only thorough history taking was able to elucidate this information.

Thus, the chief complaint and in this case, limited history and simple vital sign recording even without knowing the full examination allowed us to formulate a differential diagnosis based on:

1) Knowledge of common causes of fever and seizures
2) Common causes of fever and hypoxaemia
3) Causes of metabolic acidosis and ketones with absent urinary glucose

In such cases, taking a thorough detailed history from a relative can save on time, allow a better idea of what is going on, and they can fill in the gaps that this patient could not possibly know due to her amnesia!

The simplistic way is to formulate a differential set of diagnoses, then ask the pertinent diagnostic questions to aim to prove or disprove the idea. If elements do not fit, then ask questions to try and find out why they don't fit and keep asking questions until you are satisfied.

Remember, a CT scan cannot ask a history!

Effective communication provides for effective history, which provides effective understanding and hence, treatment and understanding of patient presentations in hospital improves.

Basically, keep asking WHY and never be satisfied until you have the answers !

Finally, this patient has clubbing which suggests that she may have an existing underlying problem. However, clubbing is beyond the scope of today's long article, but I will endeavour to cover it in the future.

Drug History, Side Effects and Interactions

Taking a comprehensive drug history can be very important in establishing a diagnosis.

Nearly all drugs have side effects and interactions with other drugs, which sometimes makes their use problematic and confusing.

In the UK, generic named drugs are used when the patient is admitted into hospital even if they take a Brand Named drug because the vast majority of doctors will immediately be able to identify the class of drug, its mode of action and the dose range.

Writing Brand Names on a drug chart is discouraged as some hospitals will not stock that Brand of drug with them only having the cheaper generic drug available.

It is always important to check that the doses are correct because it may have been previously prescribed wrongly. Simply continuing a drug because another doctor wrote it up is clearly incorrect without first considering if the patient needed it in the first place or whether they still continue to need it or whether there are better drugs available (with less side effects and better efficiacy) to take its place.

I know of some doctors who have seen patients admitted into hospital taking three or four different benzodiazepine drugs and two or three anti-psychotic drugs and they have had the associated side effects as a result. Why? Well perhaps, the drugs were not checked and new ones added in. Sometimes, the patient does not even know what they are taking and when they get home from hospital, they continue taking the previous drugs from another clinic plus the newly prescribed ones, which if not careful, leads to polypharmacy and potentials for side effects and toxicity.

The UK has a GP system where a patient is assigned a local General Practitioner. When the patient has an ailment, they go to see their GP. They do not have any choice of other facility although they may wish to see one of the several doctors working in such GP practises.

All the drugs are updated on computer and there is an automatic warning of side-effects and drug interactions alerting the GP in case of an error.

If a patient is admitted to hospital and the drugs are not known, then a quick call to the GP practise and hey presto, the drugs are available to the hospital doctor-- unless it is 2am!!

In Japan, there is perhaps too much choice with patients flitting from one hospital to another getting second, third or fourth opinions, with drugs being prescribed here and there, perhaps without knowledge of the patient visiting other institutions making such prescribing somewhat concerning.

Even if the patient is admitted, it can be impossible to find out where the patient has previously visited or to obtain proper information. There is no apparent interlinking between local clinics and hospitals to aide the patient care.

Hence, coming back to the point, it is evermore important to take a detailed and comprehensive drug history.

Checking drug levels such as digoxin, phenytoin etc may provide important clues.

For example, I recently saw a 75 year old male who was 'off legs' and falling over with double vision. He was taking phenytoin for seizures secondary to a previous cerebral infarction (stroke). Examination revealed cerebellar signs including horizontal sustained nystagmus and positive dysdiadochokinesis plus generalised absence of reflexes-- all consistent with chronic phenytoin toxicity.

I hope that by reading this blog, residents will give the drug history more emphasis and give consideration that the drugs may in fact, be causing the problem rather than some weird and wonderful obscure syndrome. Remember, common things are common and when you hear hooves it is usually horses rather than zebras!

If you would like further information / advice then please leave a message.

The Hidden Pneumonia

The following case has been anonymised to safe guard patient confidentiality which is the prime importance of all doctors for their patients. However, there are important points to be drawn from the following scenario, which is as follows:

A very elderly man was admitted to another hospital with a chief complaint of fever, breathing difficulty and reduced conscious level-- it was sad because he was so ill.

He had suffered from a right sided stroke last year and was nursed flat and fed by nasogastric tube at home.

He was unable to give the resident any history, so as is commonly the case, the family or carers are the only ones to give a history if any at all.

In this case, the family mentioned that the patient had developed 'breathing difficulty' and his conscious level had decreased.

On admission, the patient was febrile (40 degrees C), shocked with a low blood pressure, tachycardia and his consciousness was decreased. His skin was very dry, JVP was not raised. Heart sounds were normal. His oxygen sats were 96% on nasal cannula oxygen, respiratory rate 24/min. Auscaultation revealed some fine right sided crackles, but left sided examination revealed course 'wet' crackles at the base and mid zone.

ABG revealed a compensated respiratory alkalosis and hypoxaemia on room air.

Clinically, this patient had a left sided pneumonia and dehydration.

Bloods revealed severe dehydration (Na 165, BUN 70, Creat 0.67), a normal white cell count but a high CRP >13. Urine analysis showed 3+ bacteria.

Such severe dehydration can occur due to the sweating phase component of fever, raised metabolic rate from infection, and also NG feeds can add to the problem as they contain standardised solutes which do not take into account the changes in body requirements, as in this case when water replenishment would have been of better advantage.

The junior resident rightly considered a urinary tract infection as a cause of infection and therapy was commenced for that. However, on first inspection, the Chest Roentogen (CXR) looks relatively normal for an elderly patient-- until you take a second look.

However, there was consolidation BEHIND the heart shadow-- a hidden pneumonia. In any case, the history from his family and his physical examination provided the salient diagnostic clues. The Chest Roetogen is not there to make the diagnosis, it is taken to aide in the formation of a diagnosis.

If at first you do not see, look again, and stand back from the Xray. Unfortunately, on the above picture, the streaky consolidation which is evident on the CXR has not shown up particularly well.

When inspecting a CXR always look in areas that your eye would normally ignore, such as behind the heart, below the diaphragms, as pneumonias can be lurking in those places. Things that are usually missed on Xray are inspection of the ribs (looking for fractures / destruction from cancer), the clavicles, shoulder joints and scapulae-- all important structures. Moreover, the thoracic spine is also very important on a chest Xray, which is usually missed as well.

Don't just look at the lungs and the heart borders-- that is not inspecting an Xray in detail-- it is just the beginning. Also, don't forget to check the patient name!!

One final note of warning, patients being fed with an NG tube in a recumbent position may be predisposed to aspiration of their feed and hence, these 'at risk' patients should be nursed at an incline such that gravity will not allow for feed to regurgitate up the oesophagus and cause aspiration-- of course, never say never, it can still occur despite these measures.

Instructing the nursing staff to nurse these patients at an incline is a MUST and not to lie them flat and this also goes for patients with Cardiac failure and Respiratory Disease, in which patients, can become easily short of breath....but that is for another blog entirely, and I shall touch upon this area again in the future.

Endocarditis

Since being in Japan on this occasion, I have seen at least 4 cases of endocarditis and heard of at least one other.

One case I picked up myself in my first week, and the only complaint was a fever in a very well looking patient sitting in his bed in front of me. The look of his poor dentition and a loud systolic murmur led me to the diagnosis, whereas the 'full body CT' performed on admission, had failed to elucidate the cause. Goal directed testing e.g. echocardiography picked up the vegetation and the patient received valve-saving reconstruction surgery.

More recently, two young female patients developed IE and one was found to have a 'floppy mitral valve' with regurgitation and blood cultures growing streptococcus salivarius (alpha-haemolytic strep) with the only contributing cause being dental work performed several months before; a classical case of subacute bacterial endocarditis. But for the experience and expertise of my colleague in the outpatient clinic, this diagnosis could have been missed- well done to him!

The second female patient presented with a rapidly progressive multifocal pneumonia and it was initially considered, by myself and others, to be a post-influenzal staphylococcal pneumonia on clinical grounds alone before any microbiological data were available. It was unsurprising to find all 4 blood culture bottles had grown S. aureus. However, an echocardiogram was performed and this revealed a Ventricular Septal Defect (VSD) with a large vegetation (2cm!!).

Another case of suspected IE was found on a patient with terminal cardiac failure who presented to ER with a fever. He had been developing worsening dyspnoea at rest and rapidly progressive renal failure. The fact that his fingers and toenails had the most splinter haemorrhages I have ever seen (plus Beau's line: arrest of nail growth), a loud cardiac murmur and blood in the urine convinced me he also had IE.

He was transferred to another hospital and so it was not possible to get confirmation of the suspected diagnosis.

Where is all this leading?? Well, in the UK, the diagnosis of infective endocarditis is extremely uncommon. I have personally only seen two cases in seven years and hence, to hear of at least 4-5 cases in under a year has been an eye opener to me.

A patient with a fever, young or old, should always have their finger nails examined for splinter haemorrhages, finger pulps for Osler's nodes, the palms forJaneway Lesions, and if you can do retinal fundoscopy, Roth's spots.

A cardiac murmur may be absent, but in most cases I have seen, they have been present and usually are consistent with regurgitation (systolic or diastolic) from an incompetent destroyed valve. Finding blood in the urine should alert the physician to possible renal infarcts from septic thromboemboli derived from the vegetation. The usual 3 sets of blood cultures must be taken even in the absence of a fever and an high ESR e.g. 80mm/hour, can provide useful clues for making the diagnosis.

A transthoracic echo can sometimes reveal the vegetation, if large enough, but for the small millimeter size vegetations, only an oesophageal echo will do.

The junior doctors need to bear this diagnosis in mind for causes of fever, because if missed, the results can be catastrophic. Examining the hands (particularly the nails) can give the doctor the clue they need to make the diagnosis on physical examination alone, which a CT scan would never see.