Abuse Of My Blog

Dear Readers

I am occassionally getting anonymous comments that are an abuse of this blog and as moderator, I must choose whether such comments should be published.

In the main, most polite and reasonable comments are published.

I should stipulate that only clinically related comments in respect of this site will be published and not advertisements for peoples books!!

However, I feel it is now necessary to restrict all comments by asking all those who wish to leave a comment to do so by signing into Gmail.

I trust that you will understand reasons for this decision as I hope it will ensure that the quality of legitimate comments is maintained.

WOW!!! What A Case For Differential Diagnosis !!!!

I have another GREAT CASE here which comes from a distant hospital.

The case is anonymised as always.

The patient was an elderly female who was referred to the hospital after an emergency call out for Chest Pain.

The patient had awoken at 10:30pm when she got up to visit the toilet. She developed sudden onset of chest pain that was severe and continuous and sharp in nature. The pain was also described as radiating to the patient's back. After 1.5 hours the patient arrived at the hospital and quickly underwent emergency examination.

Further history was taken and it became apparent that the pain was situated to the left of the epigastrium (so called the left hypochondrium). It was unrelated to movement or respiration. The patient denied being breathless, and it was apparent that this was the first time this pain had occurred. There was no associated cough, sputum, haemoptysis, radiation to the neck/jaw/arms, no nausea, no vomiting, no report of recent tarry stools (malaena). There was no history of GERD and no history of flatulence. The patient denied weight loss, constipation or diarrhoea. There was no description that the radiating pain was tearing or not.

The only previous medical history was of hypertension which the patient had for 10 years. She had decided to stop her anti-hypertensive medications 3 months previously without medical advice.

The patient smoked 60 cigarettes per day and liked to drink sake.

On examination, the patient was afebrile, BP 200/120, heart rate of 68/min, respiration rate was 16/min with an Sp2 of 96% on room air.

Physical examination was unrevealing except for signs of liver disease (palmar erythema and spider naevae on the upper chest).

Chest and abdomen revealed no localising signs for the cause of the pain and the abdomen was not distended and apparently non-tender.

However, the ECG revealed ST depression and T wave inversion in V5 and V6 suggestive of ischaemia.

Blood results revealed a normal initial CPK 86 (61-265) but the CK-MB was raised 17 (4-16) but Troponin T was <0.05.>3.3, AST 75 (13-37), gamma GT 467 (12-49), CRP 1.13 (<0.30) style="font-weight: bold;">pH 7.485, pCO2 38.5, PO2 64.9 (74-108), HCO3 29 (21-29), BE 6.2.

The top differential diagnoses included:

• Acute MI
• Pulmonary embolism
  
• Unstable Angina
• Aortic Dissection

The chest roentogen looked normal.

The CT abdomen was revealing as it showed a very abnormal aorta. See below:

On seeing the patient by a senior doctor, it became apparent that the history was slightly different. In fact, the patient had described ABDOMINAL PAIN, rather than chest pain as relayed by the paramedics to the hospital staff, and it was described as 'PULSATILE', not sharp, meaning for every heart beat the pain recurred i.e. pulses of pain. It was also asked whether the patient had been experiencing back pains in the SAME LOCATION sometime before the severe pain to which the answer was YES.

The patient denied symptoms of intermittent claudication (ASO).

The patient had undergone emergency surgery and the diagnosis was described as a pre-rupture of an Abdominal Aortic Aneurysm (AAA). The surgeon described it as pre-rupture as there was no bleeding into the retroperitoneal space. The location was infrarenal and involved the iliac arteries as well. The patient had a graft placed and achieved good haemostasis and pulses to both limbs.

However, it was also of concern about the aorta higher up in the patient's chest as on initial inspection of the Contrast CT, it looked like there was a proximal dissection that had migrated to the lower abdominal aorta. On more detailed inspection it appeared that there were two separate vascular luminal dissections, one in the thorax and one in the abdomen, the latter being the bigger of the two.

It was of concern that the more proximal dissection had been overlooked in the emergency situation because of the large possible impending rupture of the large abdominal aortic aneurysm.

Hence, it was requested that the doctors have the radiological films formally reviewed by a Radiologist and the result is below:

Thoracic lesion: dissecting aortic aneurysm (thrombus closing type) is seen from the bifurcation of the left subclavian artery to the upper surface of the diaphragm .

Lower abdominal dissecting aortic aneurysm (New pathologic lesion) is seen. At least TWO dissected cavities are overlapped. They are not enhanced, but the density is comparatively high.

Upper abdominal lesion, there is no dissected area but some enlarged lesion can be seen.

Radiology confirmed a total of THREE dissecting aneurysms in this patient.

This is an extremely interesting case, and it is rare to see three dissections in a single patient.

Obviously, the surgeons were concerned about impending aortic rupture as a result of continuing oozing of blood into the aortic wall, and hence, the patient underwent emergency surgery, but in the main, uncomplicated distal dissecting aortic aneurysms are treated conservatively with blood pressure control.

The more proximal dissections involving the aortic root and arch DO require surgical intervention on an emergency basis as complications such as stroke, aortic insufficiency, coronary ischaemia, tamponade and haemothorax (left sided) can occur, all of which may be fatal.

However, by far the commonest cause of dissections is vascular injury by high blood pressure and in the main, hypertension is associated with distal dissections rather than proximal ones, as in this case.

Other causes include:

• Trauma/iatrogenic- cardiological investigations / procedures e.g. coronary angiography, CABG, Previous aortic valve replacement
  

• Inflammatory disease causing vasculitis e.g. syphilitic aortitis, Takayasu's arteritis, RA etc
• Collagen Disease: Marfan's Syndrome (approx 50% cases of dissection aged <40 style="font-weight: bold;">Ehlers-Danlos syndrome, annuloaortic ectasia
• Congenital: Biscupid aortic valve- dissection always involves the ascending aorta, Coarctation of the Aorta, Turner's Syndrome (associated with coarctation)
• Drugs: Cocaine; transient rise in blood pressure from surge in catecholamines
  

Finally, to recap, most dissections occur in the 60-80 age group and more in males than females.

The pain of dissection is SEVERE and can be Sharp or classically 'tearing' in nature in the rear of the chest or produce back pain. Pain can also be in the anterior chest. The pain can radiate to the chest or abdomen.

Proximal dissections are more associated with chest pain and distal dissections with abdominal and back pain respectively as a general rule.

Examination should include examining all the peripheral pulses. Typically, if dissection is present one may see a 20mmHg difference in blood pressure in the upper limbs.

Examine the JVP, as may be elevated in Tamponade.

Examine for Pulsus Paradoxus-- drop of >10mmHg BP during inspiration; associated with Tamponade.

Listen for reduced heart sounds and listen for the diastolic murmur of Aortic Regurgitation (proximal dissection).

Percuss the chest for effusion (might be a haemothorax)-- however, patients typically will have internally exsanguinated if this is present.

Listen for bruits or absence of bowel sounds-- suggestive of vascular compromise.

Check neurological examination if evidence of weakness as it implies vascular occlusion by the migrating dissection (proximal dissections).

ECG can be normal, especially in Distal dissections, but in proximal type, it may cause coronary ischaemia.

Chest Xray can be normal in dissection and does not exclude the diagnosis.

Once dissection has been considered, it must be excluded, and scanning modalities such as CT are quick and provide a degree of accuracy to reach the diagnosis.

Finally, well done to the doctors who got the diagnosis and treated the patient quickly !!!

Have a Great Golden Week!!!!!!!!!

UpToDate Keeping Me UpToDate

Dear Readers

It would seem that although I am reading UpToDate for some of the best EMB and references around, UpToDate USA and Japan are reading this blog too!!

I recently had contact from their Japanese Office Director, and I very much welcome the review of this blogsite as they will only find complimentary words for such a great product.

I have been kindly advised that the UpToDate software should work on Japanese Windows Pocket PCs, for example, the Willcom PPC made by Sharp.

If any of you have UTD which has been having any problems on your Japanese PPC then please contact the UTD Japan Office and I would hope that they will be able to sort them out as soon as possible :)

UpToDate, Inc. Japan Office
Sumitomo Shinbashi Bldg.7F
1-8-3 Shinbashi Minato-ku
Tokyo 105-0004
Japan
japan@uptodate.com
Tel 81-3-3572-5002
Fax 81-3-3572-5003

Best wishes.............

Sherlock Nose

This case has been anonymised for patient confidentiality.

An elderly patient was originally admitted several weeks ago with a fever and after investigations, a urinary tract infection was diagnosed. The urine grew a drug resistant Proteus mirabilis that was probably acquired at the nursing home where the patient normally resides.

It was not initially know what the organism was and so a broad spectrum antibiotic cover was used (cetriaxone).

Initially, the patient made good progress until one week ago when fever recurred. After work-up, it was established that the patient had acquired a hospital infection from Pseudomonas aeruginosa and Group B streptococcus, with infiltration being noted at the lingula of the left upper lobe. Quite rightly, antibiotics were changed and the patient was started on piperacillin and tobramycin to which the organisms were sensitive.


However, the patient continued to deteriorate with no change in the spiking fever and with raised white cells and CRP.

A senior doctor was asked to consult for the patient because despite good antibiotic cover for the identified organisms, the chest xray was worsening.

Before seeing the patient the senior doctor was shown a recent Xray and it revealed a well circumscribed lesion in the right upper zone, not typical of a pneumonia.

Most importantly, going to see the patient gave a potential diagnosis.

On entering behind the curtain there was a very strong smell of anaerobic organisms, a similar smell of most hospital laboratories !! Knowing that the patient was diabetic, the feet were initially examined for infected diabetic foot ulcers. However, although there was some pressure areas, there was no ulceration.

The feet were smelt closely, but no smell was emminating from them. The smell was followed upwards and it became extremely strong from the patients MOUTH !!!!

A torch was shon in the mouth and it revealed a green exudate on the top of the right gum area consistent with an anaerobic infection. This patient's mouth was also extremely dry because of mouth breathing only.

Listening to the chest, there were reduced breath sounds at the right upper zone and crackles at the right base and left mid zone consistent with some of the Xray findings.

At this point, the diagnosis pointing to being a Lung Abscess from anaerobic infection until proven otherwise with possible aspiration pneumonia at the right base as well, although the Xray does not show obvious right basal changes, and hence, this shows just how important good clinical examination is.



It was advised that the patient see an oral specialist to ascertain if there was any evidence of oral abscess and to detail the dentition.

Moroever, this patient underwent CT scanning and it revealed an unusual but well circumscribed pneumonia rather than an abscess.

However, with an obvious oral anaerobic infection plus evidence of oral aspiration in addition to markers of infection, being unresponsive to aerobic cover antibiotic therapy and a well circumscribed right upper lobe lesion, the differential diagnosis should always include an anaerobic abscess.

The patient responded well to piperacillin and clindamycin and the infection resolved rapidly.

However, the oral anaerobic infection still persisted despite antibiotic therapy and good mouth cleansing.

The patient later developed a further pneumonia and this time it was diagnosed as a severe fungal pneumonia which was refractory to therapy and this was an indicator of severely impaired immunity.

The commonest cause of lung abscess is from anaerobic organisms and often the patient has poor dentition and aspirates the bacterial during respiration to predispose to the infection.

Moreover, this patient was immunocompromised due to diabetes and in addition, the patient had already had two other infections in recent weeks. Most significantly, the patient had Parkinson's disease and Lewy Body Dementia and had previously aspirated and thus, he was always at significant risk for this problem.

Of course, in this case, the presence of Psuedomonas may have been the cause of the abscess but certainly coverage of anaerobic organisms was warranted here.

Remember to always look at the FEVER CHART and a good indication of an abscess is the classical Spiking Fever. Try and keep things simple, like trusting your sense of smell, and often the diagnosis makes itself known to the doctor.

Hence, all that was needed was a nose, a stethoscope, an Xray and of course, Sherlock Holmes.

Today's story is thus Sherlock Nose !!

Have a great Golden Week !!!!

Having passed this case on to Professor Tierney he made a number of observations:

Firstly, only 60% of bacteroides produce the typical anaerobic smell and hence, the absence of such as smell does not exclude the diagnosis of an anaerobic infection.

Secondly, in the patient without teeth, the presence of a lung abscess is lung cancer until proven otherwise. Original quote was: A lung abscess without teeth is cancer of the lung until proven otherwise- Prof Tierney

Thirdly, lung abscess treatment should include rigid bronchoscopic drainage with antibiotic therapy.

Many Thanks to Professor Tierney on these points, and I am sure the Blog Readers fully appreciate his expert contribution.

TB Alive and Well In Japan

Todays blog is just a quick reminder to ALL doctors to consider Tuberculosis infection in any patient of any age presenting with chest symptoms.

Recently, a young patient presented to a northern Japanese hospital with a two week history of cough, sputum and a mild fever.

She had been seen 3 years previously with a similar episode and Mycoplasma infection had been diagnosed and subsequently treated.

She had no current risk factors for tuberculosis and denied risky sexual exposures. Her grandmother had had TB earlier in her life.

The patient was otherwise healthy and was taking no medications.

Her examination was otherwise unrevealing including chest examination.

The clinic doctor considered this to be an atypical pneumonia due to the history of the current illness and previous atypical pneumonia.

However, the chest radiograph revealed a right apical lesion which was highly suspicious of Tuberculosis.

Sputum examination with the Ziel-Nielson stain revealed two acid-fast bacilli.

Hence, these results were very suggestive of active tuberculosis primary infection.

Interestingly, she had only a mild fever and cough but none of the typical features in her history such as:

• night sweats
• weight loss
• chronic cough
• bloody sputum

Of course, it is useful to obtain a formal bacteriological diagnosis through growth on Lowenstein-Jensson media, but this should never delay treatment for TB.

Always think TB !!

Do you have any current figures for the background prevalence of TB in Japan and know why Japan has such levels of TB?? If you know, then please let us all know by leaving a message on my blog!

Wow What A Case!!!!

This anonymised case concerns a middle-aged male patient who presented to another hospital with a five day history of:

• Pleuritic chest pain
• Cough
• Fever

The pleuritic chest pain was associated with breathing and was sharp in nature. In did not occur on moving. There was no central cardiac chest pain of ischaemic origin. The pain was also described to be in his back but it was not tearing in nature.

The cough was non-productive and intermittent.

The fever was low grade in its characteristic. He denied rigors and sweats.

The patient had been initially seen five days previously at our ER department and it had been considered that he had pleurisy and he was given acetaminophen and allowed home. However, these symptoms got worse and the patient was seen at the outpatients with the new symptom of Haematuria which was non-painful with there being no urological symptoms.

On examination she was stable but appeared in pain.

Pulse was 90/min, JVP was raised, BP normotensive but there was a drop of approximately 10mmHg in blood pressure during respiration. Temp 38 degrees and RR was 14/min. Sats 89% on room air.

Lymph nodes were not paplable.

The patient had dullness at both bases. With the patient sat forwards there was a loud sharp murmur in the tricuspid area on Inspiration which disappeared on Expiration. On lying flat, there were some audible crackles over the lower left parasternal border.

Whereas the initial chest Xray had been normal, then second one, just a few days later, revealed bilateral mild effusions and a globular heart. Her initial ECG when performed in the ER was normal, but the second revealed 1mm ST elevation in V5 and V6 with no reciprocal changes and no ST saddling or P-R depression. The voltage was also reduced.

Bloods revealed a raised white cell count, CRP 3o, slightly raised bilirubin but normal AST and ALT. ALP was slightly raised but no isoenzyme was taken. The haemoglobin was within normal limits. Renal function was normal. CK and CK-MB were not raised.

The suspected diagnosis was an acute pericarditis.

A cardiac echo was performed which revealed a rim of pericardial fluid with there being no RV collapse. There was no evidence of a vegetation either.

CT scan was performed which revealed the same pericardial effusion plus bibasal pleural effusions.

It was suggested that the effusions should be examined and the fluid obtained was yellow 'straw' coloured but slightly turbid. The white cell count was >3,000 and the pH 7.3. The sample was sent for Rheumatoid factor, culture, LDH, Glucose and TB examination.

Possible causes of acute pericarditis include:

Drugs and Toxins

• procainamide
• hydralazine
• phenytoin
• isoniazid
  

(Produce a Lupus-Like Syndrome)

Infection

• Viral: Echovirus, Coxsackie

• Bacterial: Streptococcus spp (particularly pneumococcus), Staphylococcus, Mycoplasma, TB, Haemophilus
• Fungus: Histoplasmosis, candida, aspergillus, coccidioides
  

Trauma

• Recent cardiac surgery / intervention e.g PTCA

Inflammatory

• Post-AMI
• Dressler's Syndrome
• Post-Radiation therapy
• SLE, RA, MCTD, systemic scleorsis
  

Neoplasia

• Infiltrative neoplastic diseases e.g. primary or secondary tumors
• Lymphoma /Leukaemia

Metabolic

• Uraemia, Hypothyroidism
  

Interpretation

Well, this is a very interesting case as the patient had clearly developed a percarditis and a rapidly enlarging effusion with signs of tamponade e.g. drop in BP and raised JVP. The murmur on sitting which disappeared on lying may be due to haemodynamic changes with venous flow changes. The typical scratching pericardial rub is also usually found with the patient sitting forwards BUT it is classically heard on Expiration not Inspiration.

The rapidly enlarging pericardial effusion with ensuing tamponade should prompt for the patient to be considered for pericardiocentesis. In this case, the pericardial effusion stopped enlarging and thus far, he has avoided requiring this procedure.

In respect of the haematuria and raised bilirubin level of which both direct and indirect bilirubin were raised, may be consistent with an intravascular haemolysis although typically the indirect level is raised.

Consideration should be given to Mycoplasma as the cause, as this can produce Cold Haemagglutinins which can produce such manifestations of haematuria. However, patients tend to develop a low grade anaemia which this patient did not have. Moreover, one should not rule out infective endocarditis here either.

Due to the rapidity of her symptoms, TB was considered unlikely, but it was still tested for.

There were two considerations here:

• Pain relief
• Anti-microbial therapy

This patient had been taking long-term aspirin although she had no cardiovascular history. One concern was of a haemopericardium from a haemorrhagic pericarditis. The usual therapy for pericarditic pain is NSAID therapy, but all anticoagulants should be avoided if there a rapidly enlarging pericardial effusion.

Hence, one suggestion was to use opioid pain relief instead. However, haemorrhagic transformation of pericardial effusion is a theoretical risk. The patient did eventually receive NSAID therapy.

Secondly, despite the vast majority of cases of acute pericarditis revealing a viral origin, it still needed to be considered as a bacterial cause especially as the pleural fluid contained such a high amount of white cells.

Hence, it was suggested adding a third generation cephalosporin (Ceftriaxone) which would cover the vast majority of organisms explained above plus continuing the clarithromycin to cover mycoplasma.

Blood cultures revealed Gram Positive Cocci and later identified as a fully sensitive streptococcus pneumoniae organism.

Acute Bacterial Pericarditis is the likely diagnosis here although a Purulent Pericarditis had not been confirmed as a pericardiocentesis has not been performed. For that diagnosis a pericardial effusion should either be macroscopically or microscopically purulent. However, some infections such as viral and bacterial, particularly Mycoplasma hominis, do not produce a purulent effusion (UptoDate 15.1)

Infectious aetiologies resulting in a purulent pericarditis include pneumonia, endocarditis or even meningitis.

Ultimately, if this patient's pericardial effusion had failed to improve and / or her clinical condition worsens, then she would have needed a formal pericardiocentesis which has the advantage of being both therapeutic and diagnostic.

Typically, analysis of fluid in purulent pericarditis shows cells ranging from 6,000 to 250,000 per microL, low glucose of <35mg/dl style="font-weight: bold; font-style: italic;">UpToDate 15.1)

Antibiotic regimens depend on local resistance levels, the immunocompetency of the patient and whether the patient has developed the problem in the community or in hospital.

Most regimens include either a 3rd or 4th Generation cephalosporins and Vancomycin needs to be considered in view of the problems of MRSA in this era and this was later recommended in this patient.

Non- infectious aetiologies can also present with a purulent pericardial effusion such as malignancy, uraemia and recent surgery.

Finally, a transthoracic echocardiogram may miss an endocarditis and hence, a trans-oesophageal echo which has a higher yield would be advisable.

However, the modified Duke's Criteria does not require for a vegetation to be present to make the diagnosis of endocarditis, but please refer to my earlier blog on endocarditis for those details.

For a fuller explanation please see UpToDate 15.1.

The patient made an uneventful recovery and was left with a mild pericardial rub and no chest pain.

Rheumatological Case- V. Interesting

I have a very interesting rheumatological patient to tell you about.

Firstly, as always, the patient has been anonymised to safe guard confidentiality.

The patient was a middle-aged female and who presented to another hospital with a history of muscle pain in the proximal lower limbs, some upper limb-shoulder discomfort and pain in the occipital-neck area. The patient also had a low grade fever. The patient complained of no eye problem, no temporal tenderness, no jaw or tongue claudication (symptoms for Giant Cell Arteritis). The patient had no symptoms suggestive of infection. Patient had a normal appetite but had complained of some weight loss. There was no complaint of changes in bowel habit.

The was no joint pain or swelling. No skin rashes. No respiratory symptoms.

The patient had no other significant history and was taking no regular medications.
The patient had occasional alcohol and cigarettes.

Physical examination revealed a low-grade fever. Vital signs were otherwise normal. Eyes revealed a slight purple discolouration to the upper eye-lids.

The was no lymphadenopathy and cardiovascular, respiratory and abdominal examinations were normal.

Occipital tenderness was present one week previously but only seemed to be a problem when the fever was present. There was no temporal artery tenderness.

Neurological examination revealed proximal muscle wasting, some lower limb muscle discomfort on palpation. Power and Reflexes were maintained.

Clinical Impression from history and examination:

• Polymalgia Rheumatica (PMR)
  
• Possible Dermatomyositis

However, ESR >100 and CK was low NOT RAISED. Auto-antibody tests were all NORMAL although anti-JO-1 antibody is still awaited.

In view of the history, physical and blood results, the diagnosis is very likely to be PMR.

However, infection needed to be ruled out. CXR was normal. Urine examination was normal. Blood cultures were normal.

Cardiac ECHO was normal. CT scan of abdomen was again normal.

Despite this data, the doctors were advised to start antibiotic therapy with there being no evidence of a bacterial infection and a negative infection screen.

Following this therapy, steroids were advised to be commenced.

It was considered that this diagnosis was PMR in view of the history, symptoms, ESR >100 and with a negative auto-antibody and infection screen.

The concern here was the occipital pain experienced by this patient. This could represent Giant Cell Arteritis which has a significant overlap association with PMR (approx 25-30%). Patients with GCA are at risk of visual loss and arterial infarcts and need to be treated on an expedited basis with steroids and aspirin. Usually, an arterial biopsy is taken to confirm the diagnosis but even if the biopsy appears normal the diagnosis of GCA cannot be excluded as vessel changes can be multifocal.

Patients with PMR typically experience proximal muscles pain and weakness, but on physical examination, the power appears almost normal. The CK is normal although the ALP may be raised due to peri-portal inflammation. The ESR is usually high but even normal ESR can be consistent with PMR.

Dermatomyositis on the other hand can present with weakness, wasting but the CK is high as is anti-Jo-1 antibody. Other manifestations include purple skin changes around the eyes, on the dorsum of the fingers, elbows etc and are Heliotrope as so named. Patients may also have fibrotic lung changes and there is an association with malignancy (10% in patients aged >40yrs) although this is disputed. Such malignancy tends to be gastrointestinal in origin.

In this case, it was advised that the steroids be started on an expedited basis and one would have hopefully seen a response with 48 hours.

Steroids usually need to be continued for about 2 years and they are slowly tapered over that time mindful of the patient's symptoms and ESR.

This patient's blood sugars would also need to be monitored as steroids can induced Type2 Diabetes mellitus due to their multiple blood glucose elevating effects and insulin resistance.

In the long term this patient would have needed to have bone density scanning to look for osteoporosis with the treatment there being once weekly alendronate (fosamax).

Consideration should have been given to using a Proton Pump Inhibitor to reduce the risk of upper gastrointestinal bleeding especially as the patient would have been potentially taking several problematic gastric agents in the future including steroids, aspirin and fosamax.

Ways to Improve Treatment in Emergencies

There have been a few cases I would briefly like to discuss where I consider the use of evidence based medicine and protocol guidance could have made a difference.

A young male was seen with an influenzal illness and then wheezing. The patient had a back ground of severe asthma having been previously ventilated. It would appear that this patient continued to smoke cigarettes and took aminophylline and inhaled therapy, although at the time of admission, the inhaler therapy was unknown.

The patient had severe-life threatening asthma-- he could not speak, respiratory rate was 25, pulse 120 although BP was high rather than low. The patient was using accessory muscles and had severe diffuse wheeze.

ABG- revealed a respiratory acidosis and hypoxaemia, and it was decided to intubate and ventilate the patient under propofol sedation.

The problem began a few days earlier when he was seen at a clinic and where he was given iv steroids and sent home. The next day he went to another hospital and was given aminophylline and steroids and discharged after just 24 hours. He worsened at his home which precipitated his admission to a different hospital.

Firstly, the only safe way to discharge patient is to know that their Peak Flow measurements are stable and not less than 25% of the normal predicted value for the patient's age and sex. If Peak Flow is not measured, the doctor has no formal means of assessing the severity of asthma and whether it is getting better or worse. Asthma patients can only be switched to inhalers once Peak Flow is stable and they still need to be hospitalised for at least another 24 hours and be stable on inhaler therapy before allowed to go home. Moreover, patients usually need several days of steroid therapy orally to reduce bronchial oedema associated with asthma and this cannot be cured by a 'one-off' shot of methylprednisolone.

Secondly, he was quite rightly intubated and ventilated, but when the patient was seen by a senior doctor, although the ABG had significantly improved, the patient was poorly sedated, respiratory rate was higher at 32/min, pulse was 150 (sinus tachycardia) and the patient had severe wheeze, on the left more than the right.

Clearly the therapy needed maximisation and this was a case of severe-life threatening asthma as a result of a viral infection and smoking.

The advice obtained, based on evidence and guidance from UpToDate 15.1 and British Thoracic Guidelines was to:

• Add beta-stimulant
  
• Provide a high dose of steroid using a traditional steroid for asthma treatment such as methylprednisolone or hydrocortisone; not betamethasone that had been given.
  
• Magnesium sulphate therapy (used to stabilise histamine containing cells)
• Paralyze and formal mechanical ventilation (with a general anaesthetic) as this would reduce the work of breathing, and GA can have a bronchodilator effect e.g. isofluorane. I have also seen this effected with high dose propofol under mechanical ventilation.
  

In the UK, where intravenous salbutamol is available, I would advocate its use in this severe form of asthma and in addition, the use of nebulised atrovent with salbutamol (beta-stimulant) which together have a better effect on control of asthma than beta-stimulant alone. As I understand it, and cannot quite fathom why, ipratropium (atrovent) is not available in nebulised form in Japan, when this is a life-saving and relatively innocuous therapy useful in asthma and COPD.

I have talked of asthma before on this blog, but I have found that its management in Japan is not in keeping with other international guidance and there needs to be standardisation for provision of effective evidence based therapy.

Peak Flow measurement is extremely important and this patient could have possibly avoided this episode if he had been keep in the previous hospital on appropriate therapies and under close observation.

If you wish to know more, please check the British Thoracic Guidelines for asthma plus UpToDate 15.1.

Another problem I have encountered is the wrongful belief that it is correct not to treat atrial fibrillation and by treating the underlying cause it will somehow spontaneously resolve itself.

This kind of advice is NOT consistent with international therapy for AF.

Arrhythmias are not a normal occurrence and AF amongst other rhythm disturbances, can precipitate coronary ischaemia and make heart failure or underlying ischaemia far worse. Moreover, the longer that AF is left untreated, the more difficult it becomes to cardiovert the patient. Elderly patients who are affected by AF the most, may have other underlying diseases and a drop in perfusion due to fast AF can cause compromise to other organs.

Hence, it is important to treat AF promptly and not leave it to somehow get better by itself.

Dehydration in itself, is not an established cause of AF.

Patients should also receive some form of anticoagulation, unless contraindicated, to reduce the risk of stroke events which are approximately 2% per year but higher in cases where there is underlying mitral stenosis.

Fast AF with low BP should be treated by DC Cardioversion but if normotensive, it can be slowed with effective drugs such as Amiodarone, beta-blockers or Ca channel blockers or Class 1c drugs such as flecainide or propafenone acutely.

If there is heart failure and if it is not safe to give beta-blockers or calcium channel blockers e.g. with a low ejection fraction, then amiodarone or digoxin can be given.

Flecainide cannot be given if there is underlying ischaemic heart disease as it can be made worse by this drug and hence, is probably inadvisable in most instances as one of the commonest causes of chronic AF is ischaemic heart disease.

Flecainide and propafenone should not be given chronically as ironically they increase the risk of death from dysrrhythmias.

Even mild to moderate AF should be treated to slow the rate to less than 100 as the ventricles have more time to fill and hence, the ejection fraction and cardiac output can improve.

Of course, trying to establish the underlying cause of AF and treating that may help the AF to resolve e.g. thyroxicosis, sepsis, AMI, but rate-slowing therapy should NOT BE WITHHELD unless somehow contra-indicated.

I appreciate that this may be the view of some cardiologists to take the 'wait and see approach', but this is not consistent with international guidance.

Hence, in Japan, although the diagnosis can readily be established, the emergency treatment still needs to be effectively provided and based on current evidence and through step-by-step protocols that any level of doctor can follow.

Senior doctors need to maintain their knowledge base through paper reviews and using the most up-to-date of medical texts, as these days, therapeutics are rapidly changing and hence, so should the medical practices in Japan.

Teaching the junior doctors the right way through evidence based medicine is the only way to improve acute and continuing therapy and having seniors available who know how to effectively treat the patient by putting this knowledge into practise and guiding their junior physicians.

I reiterate again, that it is best to carry a PDA where quick access to electronic books can be effected such that stardardised medical therapy can be provided at the bed side with confidence that the junior doctor is doing the job correctly.

Fluid Balance, Drugs and Heart Failure

I have recently heard of some cases of worsening heart failure that have resulted from the underlying disease of heart failure but also due to under treatment with diuretics and over administration of fluid.

For example, a young female admitted to another hospital with acute oliguric renal failure from sepsis was being provided over 2.5 litres per day in IV fluid and she was unable to be extubated due to acute heart failure, bilateral effusions and type 1 respiratory failure.

She required daily haemofiltration to remove the excessive fluid but this was still insufficient to treat the problem. It was clear that fluid balance needed to be controlled. In a usual healthy patient, daily 'insensible losses' e.g. fluid loss from breathing, sweating and loss in faeces is approximately 500ml in a stable condition. This will increase in pathological conditions e.g. fever, hot conditions, diarrhoea etc.

In the absence of urine production such as in acute oliguric renal failure, in order to attain the status quo, fluid input should match fluid output through considering insensible losses once euvolaemic. This may be quite difficult to acieve especially when intravenous drugs need to be given plus nutrition. However, it is of importance to help control acute heart failure and hypertension which are obvious problems.

Furosemide was also given by the attending physician in this setting but proved ineffective in stimulating urine output and this is in keeping with the observations that Furosemide is not associated with any significant clinical benefit in the prevention and treatment of acute renal failure in adults and with high doses being associated with ototoxicity. BMJ 2006;333:420-3.

After taking advice, the attending physician in reducing the fluid input and continuing daily haemofiltration, the acute heart failure with effusions reduced so that the patient could come off the ventilator.

An example at the other end of the spectrum, was in an elderly patient at another hospital with heart failure who had presented with 'asthma'. She had a history of heart failure and had been treated for asthma with steroids for one month but she developed recent worsening respiratory function which suggested that the cause was perhaps 'cardiac asthma' from her underlying heart failure.

She was using BIPAP and the Xray showed a mixture of CHF and infection. MRSA had been identified in 3 out of six blood cultures. One concern was she was also receiving over 1 litre of intravenous fluid per day and daily furosemide dose was just 20mg/day with only an additional furosemide dose if the urine output decreased below 100ml/hour.

This is not standard treatment for heart failure as you either diurese a patient to reduce fluid or if dehydrated, given judicious fluids to maintain kidney function, but not both at the same time otherwise there will never be an accurate and continued fluid loss.

This is a bit like filling a container from the top but opening the tap from below and hoping to keep the fluid level the same. In other words, the heart failure will not be effectively treated.

When a patient is fluid overloaded with a background of cardiac failure, such patients need fluid restriction to approximately 500ml orally (see insensible losses above) per day to ensure that they go into a NEGATIVE fluid balance through diuresis, that we commonly refer to as 'drying out the patient'.

Patients should be weighed daily to ensure sustained weight loss and a general rule is to lose approximately 1kg per day in excess fluid unless renal dysfunction occurs in which case a slower diuresis can be effected.

Patients should also have no added salt in their diet. If IV fluids are to be given, they should not contain sodium, and hence, dextrose should be provided. ACE inhibitor or ARB therapy should started and Spironolactone considered (to treat secondary hyperaldosteronism) if the patient has excess oedema and the CHF does not respond to the ACE-I/ARB alone.

Moreover, it is somewhat dangerous to have ACE-I/ARB plus Spironolactone used together as it may cause worsening renal dysfunction and HYPERKALAEMIA especially in the elderly who tend to suffer with heart failure the most. However, close monitoring of renal function should be instituted. Spironolactone reduces mortality from CHF so its use should be considered.

Patients commonly need intravenous furosemide at much higher doses than 20mg/day, and I am used to giving at least 40 to 160mg of furosemide per day to patients on a case-by-case basis to establish a controlled cardiac state. As oral bioavailability of furosemide is only about 50% and that this may be reduced further from gastric oedema in heart failure, it is always preferable to give intravenous furosemide in advanced heart failure.

A very good question was 'What about the patient having low blood pressure'.

Well, if one considers why the patient has low blood pressure, the answer can be simply made. In heart failure with systolic compromise (rather than the diastolic compromise), the more the ventricle is over stretched, the less the muscle can contract (Starling Effect) and hence blood pressure may decrease despite rises in heart rate and central venous pressure. As there is a high output of aldosterone and catecholamines, a low blood pressure in the absence of another cause, suggests poor cardiac function.

Renal failure in CHF is contributed from the vasoconstrictive effect, and hence by reducing the ventricular filling and improving the ejection fraction in theory, the vasoconstrictive effect should be reduced leading to better renal perfusion and better diuresis.

In advanced heart failure, injection of furosemide causes a greater release of renin and plasma norepinephrine resulting in vasoconstriction but with an acute initial drop in ventricular function and rising filling pressures. However, blood pressure increases. This is an acute effect of furosemide injection seen in the first hour. Ann Intern Med 1985 Jul;103(1):1-6

In such cases of low blood pressure, counter-intuitively, furosemide causing diuresis, can aid in raising the blood pressure. However, furosemide can also cause venodilatation, similar to the venous morphine-effect, and can drop the blood pressure further especially if blood pressure is dependent on heart rate and raised central venous pressure when there is poor ventricular function, and so using it alone may be problematic especially when it is not known which are the greater contributors to maintaining the blood pressure.

It is likely that there is an interplay between venodilatation, vasconstriction (from secondary hyperaldosteronism), diuresis and reduction in circulatory volume thereby reducing pre-load and after-load with the use of furosemide.

However, if patients have severe cardiac failure and low blood pressure (shock) they essentially have cardiogenic shock, and ionotropes can be used to support such patients in the short term such as Noradrenaline, Dobutamine or High Dose Dopamine.

It should be mentioned at this juncture that despite the beneficial blood pressure elevating effects of inotropes, they have not been shown to improve survival.

CPAP is also a good short term measure of aiding heart failure and improving oxygenation, BUT if patients have low blood pressure, such non-invasive ventilation can worsen BP control and hence such therapy may be relatively contra-indicated.

Providing renal dose dopamine to ensure continued renal perfusion is of unproven benefit (Lancet 2000; 356: 2139-43) and the general opinion based on current evidence is not to use renal-dose dopamine in renal failure (UpToDate 15.1: Use of vasopressors and inotropes; Intensive Care Med 1996 Mar;22(3):213-9)

Hence, in this patient, the suggestion was to reduce daily fluid administration and to increase the daily amount of furosemide with the consideration to curtail unproven therapies such as renal-dose dopamine.

The Pain Relief Pyramid

In my career so far, I have noticed that patients on occasion have their pain relief poorly managed by junior physicians.

Patients in the UK and Japan all experience pain of some sort, depending upon their underlying condition. However, the expression of the pain can be different.

I have noticed that when patients complain of pain, the pain relief provided may sometimes be inadequate either because the pain is simply not appreciated by the doctor, the patient expresses their pain and their treatment wishes poorly and the doctor's knowledge and experience in treating pain may be limited.

In order to treat pain effectively, it must be understood what is actually causing the pain.

Is the pain organic or functional? Is it inflammatory (Sharp)? Is it bone pain (deep and aching)? Is it cardiac pain (central chest, severe and heavy)? Is the pain muscular? Is the pain like a lightning bolt? Does it come on at night and feel like burning and associated with 'pins and needles' (neuropathic)? Is the pain the result of a problem elsewhere (radiating pain)?

For example, inflammatory pains such as pleuritis and tenosynovitis are effectively treated with acetaminophen and NSAIDs.

However, ischaemic chest pain from an acute myocardial infarction is not going to be treated effectively from these mild analgesic agents and morphine is required in this setting.

I recently was teaching residents that pain relief must be given to patients suffering from an acute myocardial infarction rather than just calling the cardiologists and hoping the pain will just go away as the patient leaves the ER department (and out of your sight and responsibility) as they go to the catheter lab for PTCA and stenting ! When I mentioned using morphine or diamorphine, the residents looked astounded and said that this was only used in terminal disease. Well, the UK guidance for treating AMI is pain relief with morphine/diamorphine and from my experience, it is extremely effective and calms patients down as well, in an otherwise very painful and stressful situation.

Pain from cancer is again effectively treated with opioid or opiate therapy but some pains are also helped in combination with acetaminophen and / or NSAIDs and even neuropathic pain therapies (detailed later). Radiotherapy and bisphosphate use in bone pain conditions can also be very useful.

There are less strong opiate therapies such as codeine phosphate, which is an effective analgesic agent used in situations when acetaminophen and / or NSAIDs are still providing ineffective to suppress pain. However, they can cause constipation so are generally given with lactulose / senna or magnesium hydroxide.

In the UK, we generally use an analgesic pyramid for treating pain such that pain can be effectively treated. Hence, in severe pain of any type we use oral morphine or even intravenous diamorphine, unless contra-indicated, and not just for terminal cancer patients.

For example, a patient with pericarditis may have a sharp-type pain. Acetaminophen should be given first and if ineffective, a non-steroidal drug (NSAID) can be added or substituted. If however, the pain gets worse despite treatment, an opioid such as codeine phosphate can be added to the above regimen.

Another example is in myeloma with bone pain; if the pain got worse despite the above three drugs, the codeine could be stopped and oral morphine liquid could be given instead. The advantage of using morphine orally is that a total daily amount can be estimated which controls pain, and following this a dose of Morphine Sulfate (MST) can be estimated and given instead of the oral morphine. Lets say a patient requires 20mg of oral morphine per day to control their severe chronic back pain, an estimated daily dose of long acting MST can be given at 10mg twice daily as an initial starting dose and increased if the pain is still problematic.

Morphine naive patients can safely be given 5-10mg every 3-4 hours and those on long term doses may require larger amounts to control their pain (UpToDate 15.1)

Of course, if morphine sulfate doses escalate further, transdermal opiod patches can be used such as Fentanyl which provides a much smoother delivery of the drug and avoid having to take lots of MST tablets and are changes after 72 hours.

Pethidine which is a tablet, intramuscular and intravenous opioid therapy, can sometime be given for pain relief. Its main advantage is that it is not supposed to cause contraction of the duodenal papilla (Ampulla of Vater / Sphincter of Oddi) unlike morphine, and it is therefore useful in conditions such as biliary colic and pancreatitis.

The downside of such therapy in the long term is addiction and 'professional' patients in the UK sometimes ask specifically for pethidine if they get a return of their 'pain'. I have experienced such patients who do not have clinical pain but manufacture their condition in order to obtain pethidine or morphine like compounds to feed their physical and psychological addiction.

However, short term use (days) of opiate/opioid use, for example, in an acute MI will not lead to addiction, and chronic pain syndromes are likely to need such therapies in any case.

Buprenorphine is a partial agonist with a high binding affinity for opiate receptors and it is used in acute pain. It is excreted mainly in the faeces and some in the urine unchanged.

Non-Traditional Analgesic Therapies

Sometimes, Tricyclic antidepressant therapy can be used for chronic headache or neuropathic pain. Traditionally, amitryptilline 10mg as a starting dose has been used and incrementally increased until effective pain relief is achieved. However, tricyclic agents although having antidepressant properties, are fraught with side effects from their anti-histamine, anti-muscarinic blocking properties. These agents cannot treat acute pain as they are pain modulators and in fact, take several weeks before the patients experience a reduction in their pain.

Perhaps better therapies are Gabapentin or Pregabalin, which are effective therapies for neuropathic pain syndromes, and in the UK are typically used in Diabetic patients who can develop severe nocturnal pain due to diabetic neuropathy.

Another very new development is with the drug Duloxetine which is a dual SNRI anti-depressant which is effective in neuropathic pain syndromes and is also used in diabetic patients. In is approved in more than 70 countries for use in severe depression, but as I understand it, Japan will be marketing the drug for use in incontinence.

Of course, non-drug treatment of pain can be with TENS (Transcutaneous Electrical Nerve Stimulation) which can be effective for 'gating' pain and is used in pregnant patients and chronic back pain conditions in the UK. Basically, this consists of stick-on pads that deliver an electrical current onto the skin of the affected area thereby stimulating the local nerves and making them refractory to the conduction of painful stimuli from the area downstream causing the painful condition.

Salmon Calcitonin is an effective therapy used in the UK and USA for treating osteoporotic fractures. It is given subcutaneously until the pain level is reduced by approximately 50%. It is usually given for a week or thereabouts, but it is frequently associated with nausea and vomiting. However, it is an effective therapy for such bony conditions and is combined with oral bisphosphonate treatment and traditional analgesic agents.

Protecting Your Patients When Giving Analgesia

Always be very careful when prescribing NSAIDs. Adverse side effects include asthma in susceptible individuals, GI bleeding and renal failure to name but a few.

Always take a careful drug and allergy history to ensure that patients have not experienced adverse effects from these drugs in the past.

In the elderly, if you do consider NSAID therapy, please consider adding a Proton Pump Inhibitor (not H2 blocker) especially in the elderly as this is the most effective acid-suppressant therapy and this may prevent a patient developing an ulcer with prevention being better than cure!

Check BUN and Creatinine a few times a week to ensure that the patient does not develop renal failure. If the patient has underlying renal disease and / or is taking diuretic therapy or other potentially nephrotoxic agents, then be warned as NSAIDs reduce renal blood flow through abolition of vasodilatory prostaglandins and renal failure can ensue.

NSAIDs can be substituted by using the above combination of acetaminophen and codeine phosphate but please be careful in patients with liver dysfunction as codeine / morphine compounds require the liver ( and kidneys) to be eliminated. Remember, morphine has the addition of two glucuronic acid side chains (morphine diglucuronide) to be excreted in the bile / urine. Renal failure can slow the excretion of morphine as well, dependent on the creatinine clearance, so dose reductions for opioid/opiates may be necessary.

The elderly are also very sensitive to opiates / opioids in who may benefit the most from having their pain controlled and hence, a smaller starting dose may be necessary.

Specific major side effects include reduced respiratory rate, pin-point pupils, confusion, unconsciousness, hallucinations and the classical 'opiate twitch' seen in opiate toxicity. Luckily, the reversal agent is Naloxone (Narcan), given intravenously and intramuscularly or as a constant infusion and I have personally seen over-treated and unrousable patients suddenly start breathing and open their eyes after seconds of an injection of the anti-dote. Unfortunately, NSAID side effects cannot be reversed as easily! However, please remember that naloxone's effects are short lived and sometimes an infusion is necessary and hence, in patients with hepatic and/or renal failure this may need to be prolonged.

ALWAYS REMEMBER, IF YOU DO NOT KNOW THE ANSWER OR WHAT TO DO, THEN ASK YOUR SENIOR FOR HELP AND NEVER GUESS!

For a full analgesic explanation, side effect profile and indications and contra-indications, please refer to a pharmacology text before prescribing. Some major information on drugs can also be found in UpToDate 15.1

So, I hope that the above gives you a better idea of how to treat pain, and your patients will feel better as a result.

Please let me have your feedback.

End of Life Decisions

As physicians, how do we manage End of Life Decisions?

We are all taught to treat conditions to make people better and then as doctors, we will have tried our best at all costs.

However, although this kind of thinking is respectable and usually appropriate, in some cases it may be inappropriate for the patient or in fact, even inhumane.

Sometimes as doctors, by keeping patients tied to a bed, on a ventilator with TPN dripping into their neck when they have an End Stage/ Terminal disease and will not recover and when the patient has had a poor quality of life, this kind of therapy makes the doctors feel better for trying but certainly not always the patient who is receiving it.

In such cases, it may be more humane to treat symptoms and to withdraw unnecessary therapies which are not helping the patient and which may be prolonging their agony or discomfort.

I hear of many cases where family members wish for their relative to have active treatment such as antibiotics and feeding whilst at the same time, they do not want Cardiopulmonary Resuscitation (CPR). I think in some circumstances this is sometimes an appropriate way but it is of course, on a case by case basis.

However, for example, in the patient who has had a Cardiopulmonary Arrest (CPA) with extensive hypoxic-ischaemic brain damage and who is otherwise 'Brain Dead' in the sense of no higher cerebral functioning, should we be treating infections and maintaining fluids when the chances of restoring the patient to a functional and meaningful life are negligible?

This decision is not an easy one to make.

However, patients deserve to be treated humanely and not be exposed to procedures and therapies that are not going to be effectively life prolonging or improve their quality of life.

In such cases, it is sometimes better to complete antibiotic therapies, if justified, and then not to restart if further infection occurs. Fluids may prolong life by preventing renal failure, but in patients who are at the end of life and moribund, fluids are unlikely to be necessary either.

Sometimes, rather than giving intravenous fluids, subcutaneous fluids can be given, thereby avoiding the painful procedure of trying to find and puncture a vein which can be quite painful especially in oedematous patients with no visible blood vessels! Subcutaneous fluid with normal saline (no potassium) can maintain a level of hydration and nursing staff can resite the fluids easily.

Ventilated patients can sometimes be transferred to non-invasive ventilation or even mask and oxygen therapy in order to reduce the uncomfortable therapy that intubation and ventilation can represent.

Basically, change therapies that would be used to treat patients actively to ones that are more conservative but at the same time, more humane by being less invasive and uncomfortable.

When patients reach the End of Life stage, it is perhaps better to give symptomatic, palliative therapy than continuing active, invasive therapies that are clearly not working and inhumane to the patient.

Although families have a big input to what happens with their relative, they should understand through the physician's explanations, that therapies change dependent upon the patient's condition. Moreover, continuing some therapies is at the request of the family, but you as doctors have responsibility for overseeing the care of the patient, not the family.

Through effective and honest communication with the family and stating why treatments would be inappropriate, for example, due to poor prognosis and being inhumane, the family members might have a different perspective with regards to using palliative therapies rather than inappropriate active therapies.

Remember to always put your patients first and not subject them to inhumane treatment even if it makes you feel uncomfortable.

Although as doctors you can do many treatments, it does not always mean that it is appropriate to do so and it is not for us to feel good that we did something when the patient is then put through inhumane treatment.

Please consider.

How to spot acute liver failure

Acute liver failure is quite a rare occurrence whilst chronic liver disease is relatively more common.

The two conditions can sometimes be confused in the jaundiced patient and even missed entirely if a careful history and physical examination is not taken.

Patients with acute liver failure do not usually have a history of liver disease and in fact, they may have no unusual history at all.

Nevertheless, a careful history should be taken concerning the causes of liver failure e.g. viral hepatitis, drugs, alcohol etc...

So, how do you spot a patient with acute liver failure with no pathognomonic signs?

Well, conscious level is important.

Always score the Glasgow Coma Scale and aim to use a mini mental test scoring system of up to ten questions to see if the patient can remember immediate memory, short term memory and long term memories. These scores can be compared as the patient improves or worsens and can be used as a guide.

Always check for a Hepatic Flap (arms extended and hands extended at the wrists with all digits spread open)-- a typical intermittent flexion-extension motion can be seen.

Smell your patient's breath for Liver Breath (fetor hepaticus) and check the eyes for jaundice.

None of the above can delineate acute from chronic decompensated liver disease.

However, the absence of chronic signs e.g. spider naevae, gynaecomastia, palmar erythema, clubbing, Dupytreen's contracture, gross ascites and caput medussa are clues that the disorder may be acute.

Moreover, in acute liver failure, the liver can be enlarged and tender on palpation whereas chronic liver patients tend to have hard and non-tender livers which may be impalpable.

Both conditions have increased bleeding tendencies but acute failure is far more serious as worsening clotting is a sign of worsening acute liver dysfunction. Patients can develop profound metabolic acidaemia and hence, their symptoms may be confused as a respiratory condition through increased respiratory rate from a Kussmaul-type of reactive breathing.

Patients may also present with unconsciousness due to profound hypoglycaemia, something not so common in chronic failure, and this may be due to decreased storage capacity, reduced glycogenolysis and gluconeogenesis in the acutely failing liver. Simply treating with 50% dextrose is not enough as patients may soon become hypoglycaemic again, so an infusion is required.

Of course, liver results showing very high AST and ALT in the thousands is highly significant of an acute process rather than the smaller rise seen in cirrhotic livers.

I hope the above helps you to separate the two conditions, as treatment and prognosis are different especially as acute liver failure patients may require acute liver transplantation.

Elderly Females and UTIs

UTI in elderly patients is a relatively easy diagnosis to make especially with urine analysis and urine culture providing the best clues.

Often, elderly patients present with fever and no urinary symptoms or they may present with just new or worsening confusion.

Obvious causes include long term Foley catheter usage and faecal incontinence causing contamination of the genital tract.

Atrophic female genitalia and with advancing age are other risk factors especially as the female urethra is shorter compared to the male.

Bacteriuria in the elderly is very common and may also be asymptomatic.

When a patient presents with recurrent UTI then further investigation may be warranted.

Patients in hospital or care homes may be infected by medical staff due to poor hygiene or other infectious patients in close proximity.

The infection may be due to a multi-drug resistant bacteria that was not effectively treated previously or the patient has been auto-infected in some way.

Of course, in younger patients, UTI can be precipitated from sexual intercourse. Also remember, elderly patients may also still be sexually active!

Other more unusual things to consider include fistula between bladder and bowel which might be due to malignancy, inflammatory bowel disease, diverticular disease as examples, which leads to direct faecal contamination of the urine.

Questions to ask include: Is your urine dark brown and cloudy? Faeces in the urine. Are there bubbles in your urinary stream on passing urine ? (not just bubbles in the toilet); this is pneumaturia and signifies gas from the bowel escaping into the urine.

The other questions of urinary frequency, nocturia, suprapubic discomfort, dysuria, haematuria, sexual activity and bowel symptoms should also be asked.

With the problem of re-infection, one question to ask the female patient is how they clean themselves following defecation. Females may put themselves at risk of faecal contamination of their genitourinary tract if they clean their anus from posterior to anterior i.e. downwards and forwards between their legs rather than away from the genitourinary tract (inferior to superior direction) i.e. from below upwards and behind them.

As mentioned, the female genital tract is anatomically more at risk of infection as the urethra is shorter than that of the male and it is more exposed to potential contamination.

Recently, on advising a junior doctor of this line of quite intimate questioning for a patient with her second severe UTI, I was met with a look of astoundment from the doctor that this question should be asked at all.

However, when he did ask the question, it was soon determined that the patient was indeed contaminating her genitourinary tract with faeces when finishing defecation and hence, she was auto-infecting herself causing recurrent UTI.

I appreciate that this questioning is delicate and perhaps embarrassing for both doctor and patient, but if established as the cause of the recurrent UTI, then the patient can be advised on how to avoid such problem in the future. Please consider!

Finally and perhaps most importantly, it should be noted that Foley catheters should only be introduced if the patient actually needs a catheter and not for aiding the nurses by reducing their workload. Remember, nursing care also includes patient toileting and if you as doctors are pressurised into inserting a catheter as the nurse is too busy to toilet the patient, then you may be putting your patient at risk of developing a UTI. If the patient does have a catheter, it should be removed as soon as possible and when practicably possible.

Also, hospitals and care homes should have appropriate Infection Control procedures whereby patients with severe infections e.g. pseudomonas, MRSA, are moved to areas where they pose less danger to other patients. That may mean putting patients in single rooms until the infection is cleared.

Infection control staff also advise medical staff on proper hygiene such as hand washing, disinfection and how to manage outbreaks and their importance in the hospital and community setting cannot be taken for granted.

Please let me know your opinions !!!