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 !!!

Influenza and Asthma!

This week was supposed to be my Winter Holiday, and my family and I had arranged to go travelling in Japan.

However, my whole family developed an Influenzal-like illness thereby putting an end to any travelling !

My son saw a doctor who diagnosed an infective viral exacerbation of asthma and gave him nebulised beta agonist and theophylline powder and my wife was told something like-- 'don't use the inhaler' (albuterol beta-agonist metred dose inhaler from the USA)......without being given any explanation why she should stop.....

This left me confused as it was against all the UK medical training and evidence I had come to know.

I am not a paediatrician, but this did not sound at all right to me, so I have investigated further.

So, on checking UpToDate for childhood asthma, it confirmed that Mild Acute Asthma should firstly be treated with beta-stimulant either via a nebuliser or metered inhaler via a spacer (as was done) and following this, an inhaled steroid should be provided too.

In the UK British Thoracic Society November 2005 guidance for asthma (some 98 pages !!), no where in the acute guidance does Theophylline feature apart from when all else fails in severe acute asthma !!

In fact, moderate to severe asthma suggests substituting inhaled corticosteroid for intravenous steroid, adding ipratropium, and failing that, to give intravenous magnesium or iv beta stimulant (salbutamol / albuterol).

As for adults with acute asthma, theophylline does not show any more improvement in acute asthma than the combined use of beta-stimulant, ipratropium and steroid administration.

I have heard of cases where patients at local clinics have been given iv aminophylline as a primary treatment in acute asthma and then sent to our hospital when they should have been given a beta-stimulant nebuliser and steroids. This kind of therapy is clearly against the current evidence base.

The main place for aminophylline is in chronic respiratory conditions such as childhood chronic asthma, COPD or in patients who are unable to use an inhaler or have poor compliance.

In such cases of chronic asthma, there is evidence that combined with beta-stimulant and steroid, there is better control of asthma symptoms. Here again though, it should not be given in place of beta-agonist or inhaled corticosteroids but rather compliments their beneficial effects. In this setting, aminophylline can allow the reduction of steroid dose and frequency of beta-stimulant use (UpToDate 15.1)

I appreciate that the Japanese Guidelines advocate aminophylline as a second line agent but as far as I am aware, they have not been updated recently.

Aminophylline is a cheap drug and has alot of physiological effects such as bronchodilatation, anti-inflammatory effects and anti-chemotaxic effects against eosinophils, but obtaining therapeutic levels may be problematic and patients already on oral preparations or who drink coffee can develop toxicity which includes: tachycardia, tremor, seizure (<1%),> In such patients, IV preparations should be avoided to prevent such toxicity.

The treatment of acute asthma in the UK and USA is certainly different compared to what I have seen in Japan.

The UK Guidance can be viewed here: http://www.brit-thoracic.org.uk/iqs/sid.08626940972447923509053/
Guidelinessince%201997_asthma_html (PLEASE CUT AND PASTE TO GO TO THE SITE)

The UK guidelines only institute IV aminophylline in the acute setting when nothing else works and patients are in intensive care (adults) or Pediatric ICU (PICU) but certainly not in place of other measures mentioned above.

Please consider before using this drug.

Do you have extensive experience in the use of this drug and agree or disagree with the above blog? If so, please leave a reply as this is an open forum (albeit moderated) and your opinions would be helpful for other junior doctors to learn.

Types of Chest Pain

Whenever I teach a doctor for the first time and the history is about pain, I always ask various questions about the pain to which I get looks of bewilderment because surely pain is just pain, right???????........Wrong.

There are many different types of pain.

Let me take an example about chest pain. I was recently told a short history about a patient with GI bleeding and chest pain.

The doctor had failed to elicit any further history of the pain.

Questions that should have been asked included:

• What type of pain? Severe, crushing, squeezing chest pain (cardiac) [Like an Elephant sitting on your chest] or severe ripping/tearing pain going through to the back (dissection), sharp and/or worse on inspiration or moving (pleuritic), superficial or deep pain (superficial may be from skin / muscle or bone).

• Does the pain radiate any where? To the neck / jaw / arms (cardiac), to the back (dissection), to the abdomen (inferior ischaemia / MI / dissection). Is the pain worse on lying flat and better sitting forwards? (Pericarditic pain).
  

• Did the patient suddenly become acutely breathless with chest pain? (Pulmonary Embolism / Pneumothorax / Dissection / Massive AMI).

• Did the pain come on gradually or suddenly? Gradual pain may be associated with infection / malignancy / unstable angina / chronic and progressive dissection / pleurisy / myositis / shingles. Acute onset pain must always be taken seriously and may signify an MI, PE, Dissection.

• How severe was the pain? Try to use the Pain Scale, with 1 being minimal pain and 10 being the most severe pain imaginable and 5 somewhere in between. Of course, one person's perception of pain is different to that of another person and so the pain score needs to be individualised. This is useful to use as a guide to assess the severity of the complaint.

• Was the pain continuous or intermittent? Ischaemic pain may reach a crescendo of severity before continuing or subsiding. Pleuritic pain is by definition not continuous as it tends to occur during deep inspiration and gets easier on expiration. Did the pain come on or get worse with exertion?

• Did anything make the pain better or worse? Do you have a Nitro Spray? If so, did it make the pain better.

• Did the patient lose consciousness with the pain? PE, Dissection, Aortic stenosis and severe ischaemia, Massive MI.

• Was the patient vomiting with this chest pain and have a grey look and sweaty? Very cardiac sounding but of course can occur with dissection or any cause of shock. The 'grey look' and sweatiness are due to catecholamine output. The vomiting tends to occur with MI but this is not a good discriminator.

Other causes of chest pain include a oesophageal spasm type pain which is sometimes indistinguishable from cardiac chest pain. This pain also improves with nitrate or calcium antagonist but a patient will tend to have a normal ECG during such episodes.

Gastro-esophageal Reflux Disease (GERD) may cause a retrosternal, rising, burning type pain and an acid sensation at the back of the throat. Worst cases can cause vomiting. Patients will also suffer from flatulence.

Spontaneous rupture of the oesophagus can cause worsening chest pain (from mediastinitis) and patients may develop swollen upper chest and neck from surgical emphysema of air beneath the skin. Hence a history of patients eating when the pain started maybe important.

Also, sometimes, chest pain is mistaken as abdominal pain especially in the epigastric area and hence, disorders such as peptic ulceration, cholecystitis, pancreatitis, sub-phrenic abscess etc also need to be considered when thinking of pain in the chest.

Of course, other questions such as previous chest pain history e.g. AMI, angina should be questioned about, including Family History. Smoking history, diabetes, hypercholesterolaemia, history of dissection in the family / PE and DVT should also be asked.

In respect of the above, it is not fully comprehensive and is only a guide on the questioning with regards to emergency history taking of chest pain. It is impossible to cover all aspects of chest pain in this short blog.

However, in this case, the patient had ischaemic sounding chest pain and dizziness with tarry stool and haematemesis. It is likely that the profound haemorrhagic shock caused cardiac ischaemia and dizziness which promptly reversed on restoring the circulation with blood. ECG when patient was pain free was normal. There had not been an ECG when the patient had developed chest pain.

CK and Troponin T were normal. However, Troponin T takes time to rise and for current tests, this should be performed at about 6 hours and NOT on admission as the CK and Troponin are likely to be normal despite the patient sustaining myocardial damage.

If pain sounds atypical for chest pain or other serious pathologies then question about back problems as pain in the chest can occasionally be due to radiation from a spinal source to the anterior chest wall. Also, consider other diagnoses such as Syndrome X (ischaemic sounding chest pain but normal angiography studies, Prinzmentals (Variant) angina, Early Shingles (zoster) before the typical dermatomal rash forms. One should also asking about the patient's current mental health state, as sometimes patients with develop pain with no organic cause. Sometimes, in such cases, patients may be suffering depression and as such, this type of pain is termed psychosomatic or somatisation. However, this is a diagnosis by excluding the more serious causes FIRST.

UpToDate on PDAs

Today I want to talk about my special love (apart from my family of course !! :) ) .....PDAs.

As I have previously mentioned, PDAs are quite popular in Japan, but I consider that they are under utilised here to some degree.

I have discovered that UpToDate can now be used on the Palm based PDA platform such as the LifeDrive and Palm Treo handheld devices running Garnet OS 5.4.

Unfortunately, having tried to run the software on the Sony Clie TH55 (Palm OS 5.2) it does not work ! Hence, if you want to use UpToDate you need a newer type Palm.

Below are some photos of my old LifeDrive with UpToDate running. It is great!!




However, Palm based PDAs are going to become extinct in the future, or at least, that is what is being said in the PDA world, with Microsoft Windows Mobile 5 (Pocket PC) taking over with its multi-tasking capabilities.

However, although UpToDate also support the WM5 PPC PDAs and earlier versions, the software (which I have) does not run on a Japanese language WM5 PDA !!

In fact, after asking for support from UpToDate (which is excellent I might add) they mentioned that UpToDate for Pocket PC does not support 'Chinese Characters'.

So, if you have a Japanese Pocket PC, it would seem that at present, UpToDate will not run either.

My advice would be, if you want to use UpToDate on a PDA, either get a Palm running OS 5.4 or a PDA phone where UpToDate can be accessed via its site on the internet via the PDAs internet browser.

I think that UpToDate is a very good tool for physicians on the ward and now that it is in PDA format, it should become a highly useful tool for the physician who needs a second opinion !

Fever, Cough and Sputum

Here is another great case which has been anonymised to protect patient confidentiality.

Patient was admitted from Outpatients at another hospital with the following:

• Fever
• Cough with sputum
• Chest Pain
• Headache

The fever had come on after a few days of feeling unwell. The patient had recently suffered with influenza and had overcome that illness in February 07. The fever was constant at about 38 degrees. There were no associated rigors. The patient denied sweats except in the last few days leading up to admission.

The cough was a new problem and was productive of yellow / dark coloured sputum. There was no history of haemoptysis. No recent weight loss, or loss of appetite. The patient was a long-term smoker (20/day for 20 years). There was no history of asbestos or TB exposure.

The patient also suffered with left sided chest pain which was worse on coughing and deep breathing. It was described as Sharp and the part could not take a deep breath. The was no description of cardiac chest pain.

The headache only occurred on coughing and was temporal in origin. No eye symptoms and no neck pain or stiffness.

The patient denied earache or throat pain.

The patient denied any leg pain or swelling and there was no complaint of breathlessness.

Previous History included Atypical Angina (angiography was normal) and some asthma.

Drugs included some inhaler therapy for asthma but no angina treatment.

Family history included lung cancer in a near relative.

Social history - patient was married with two children and was in employment in the electronics industry.

The was a pet dog at home but the patient denied allergies to fur.

On further questioning, the was no history of foreign travel or travel to onsen.

On examination the patient looked well. The temp was still 38 degrees, pulse 80 regular, BP 120/70, Sats 94% on room air, RR= 16/min

There was no evidence of lymphadenopathy.

Cardiovascular, Respiratory and Abdominal examination were entirely normal except for pain when pressing on the patient's anterior left upper ribs.

Legs were described as normal.

Blood results were all normal except for a raised CRP of 15. WCC, Neutrophil % were normal.

Differential Diagnosis based on Hx and Physical

• Drugs-- N/A
• Infection--Bacterial post-influenzal pneumonia (staph aureas), pneumococcal pneumonia, H. influenza, Atypical pneumonia e.g. mycoplasma. chlamydia; mycobacterial e.g. TB

--Viral: Influenzal pneumonia, other respiratory viral infections

--Fungal: Cryptococcus

• Endocrine: N/A
• Trauma: N/A

• Inflammatory: Wegener's Granulomatosis, SLE
• Neoplasia: Lung Cancer, Secondary Lung tumours

• Haematological: Leukaemia, Lymphoma, Pulmonary embolism
• Immunological: Goodpasture's syndrome
• Metabolic: N/A

(This is not a complete list-- this was generated during a teaching session)

The patient was examined it was generally normal apart from the superficial chest pain and it was also pointed out that the patient was quite thin.

Chest Roentogen examination was Abnormal. There was a definite discrete circular lesion in the Right Midzone and a possible second circular area in the Left Upper Zone.
The right lesion at its inferior aspect was more radio-dense (white) than the more radiolucent upper area. There was no fluid level present.

The doctors were asked to also examine the bones and one Resident pointed out a 'Moth-Eaten' Left posterior medial rib which was consistent with a pathological aetiology-- perhaps malignancy.

Differential Diagnosis at this Point

Probable Lung Abscess (despite no air fluid level) secondary to Staph aureus after recent influenza; possible anaerobic causation. TB as previously noted, was also considered.
With the presence of a rib lesion, there was a high suspicion of malignancy.
Lastly, Wegener's Granulomatosis also needed to be considered.

CT scan evaluation confirmed abscesses with thick walls and surrounding pneumonia.

No organisms had been grown on culture. The Echocardiogram performed to look for right sided infective endocarditis was Normal although IE could not be ruled out as a cause as the Modified Duke's Criteria show(see previous case of IE). The patient had not been asked if intravenous drugs were used illicitly.

Sputum examination revealed a polymicrobial flora but no specific infecting organism.

TB Ziel-Nielsen stains were negative on two samples.

Samples had also been sent for cytology.

The patient had been started on a second generation cephalosporin without anaerobic cover.

Suggestions

• PCR of sputum for TB, Skin PPD test, Lowenstein-Jehnsen Culture for TB (4-10 weeks wait for growth!)
  
• Add either Clindamycin iv or Metronidazole orally [good bioavailability] (see Sanford Guide 2006 under Lung Abscess)
• Consider bronchoscopy for obtaining brushings, BAL for microbiological analysis (bacteria, mycobacteria and fungi) and cytology and even abscess drainage if necessary
• ANCA test for Wegener's
• Immunoprecipitins for Cryptococcus
• Beta-D-Glucan for identifying presence of invasive fungal infection
• Isotope bone scan to rule in/out metastases in the event that the rib lesion is cancerous
  

The usual cause of lung abscess is from aspiration of anaerobic oral flora. The symptoms consist of fever, cough and dirty sputum. Rigors invariably do not occur in these patients.

Other causes include Staph and occasionally strep species. TB is another cause of lung abscess and should never be forgotten.

Fungal infections include cryptococcus, blastomyces, candida etc...

Atypical type organisms can occur from infections derived from infective endocarditis from the Right Heart in IV drug users.

Non-infective causes include lung malignancy.

Wegener's Granulomatosis results in a necrosis of lung tissue which may simulate lung abscess formation. However, this patient did not have joint symptoms, upper respiratory symtpoms or signs of renal impairment making it an unlikely cause of this disorder.

Dr Aoki

Yesterday, Dr Aoki visited our Institution to be put through his paces on a great case.

The conference went on for 2 and a half hours and I was able to follow most of what was said in Japanese, and even Dr Aoki's jokes !!

It was great to see Dr Aoki's energy for Infectious Diseases and how he broke the case down into its small pieces to come up with a differential diagnosis containing the right answer !!

It reminded me of Dr Tierney's visit last year, although Makoto-san tells better jokes !


The first year doctors have definitely improved in their way of thinking through cases and were easily able to provide answers on how to work up a complex infectious case.

Dr Aoki went through organ systems then specific abnormalities of those systems by using 'VINDICATE' as a medical sieve.

Following the great conference, we went for a meal and ate some great 'Tsubame' locally.

Multiple Pathology-- Pleural Effusions

Today's discussion is about pleural effusions-- it is not a full history today.

A retired male presented with dyspnoea. He was dehydrated and confused and so history was poor.

It was identified that he had a pleural effusion both clinical examination and on chest Xray.

It was noticed that he also had unilateral foot oedema which raised a suspicion of a deep vein thrombosis.

However, his calves were normal temperature, not tender, no distended veins, not red....

The effusion was tapped from the right hemithorax but it became slightly bloody as the liver may have been inadvertedly hit during the procedure.

CT scan was performed which revealed a mass sitting in amongst the pleural fluid.

It was immediately assumed to be a neoplastic lesion, but there were additional ideas !

The analysis of the fluid suggested it was an exudate rather than a transudate making diseases such as heart failure / nephrosis / liver failure unlikely.

On the other hand, with the fluid being bloody and with a possible DVT, it was considered the possibility of PE as a cause for the effusion. Moreover, chronic infections such as Tuberculosis (TB) can cause effusions.

Other causes considered included:

Infection -- as above TB, para-pneumonic effusion, sub-phrenic abscess, unusual parasitic infections
Endocrine -- Hypothyroidism


Inflammatory-- Rheumatoid lung, SLE
Neoplasia: Primary Ca Lung, Secondary tumours, Lymphoma, Lymphangiitis Carcinomatosa

Haematological: Pulmonary Embolism (PE)
Metabolic: Uraemia

The patient underwent ultrasonography revealing a proximal DVT and the spiral CT revealed PE !! However, the pleural fluid was subjected to Ziel Nielsen Stain which was negative BUT the PCR was POSITIVE for TB !!

Hence, in this rather unusual case, it would appear that the cause of respiratory problem was due to multiple pathology.

Infection, for example pneumonia, can increase the risk of PE especially in the first two weeks after an infection although the risk can last for up to a year (Smeeth et al, 2006). This was demonstrated for community acquired pneumonias and not specifically for TB infection.

Moreover, this patient had been lying in bed for several days which again, increased the risk of DVT / PE.

Hence, this patient was treated for TB and PE, both relatively uncommon diagnoses in modern Japan.

Nevertheless, malignancy still needed to be ruled out in this patient, but there were no results confirming this diagnosis.

Things to bear in mind, that despite one cause being found for an underlying disease, if there is a possibility of another cause(s), then they should also be investigated and ruled out alike.

Quiz No 2

Today is a quiz. I have included a short history and physical with some nice pictures for you to interpret. There are no formal blood results for you to rely on.

This patient presented with a sudden onset of cough and dyspnoea.

Patient remained breathless for 4 days before presenting to hospital.

There was no sputum produced and no haemoptysis.

Patient complained of a dull chest ache when coughing. There was no acute / sharp chest pain.

The patient had a previous history of angina pectoris and rheumatoid arthritis.

Daily medications included: Prednisolone, amlodipine, ISDN, ranitidine.

Patient was a non-smoker.

There was no history of DVT /PE.

On examination:

Temperature of 39.1, pulse 120 regular, RR= 25/min, SpO2 95% on 5 L O2, BP 120/80.

Drowsy consciousness but able to answer questions

Dry tongue and decreased skin turgor

Aortic ejection systolic murmur and tachycardia.

Dullness to percussion at left base and coarse breath sounds. No crackles.

Abdomen within normal limits.

Right lower limb very warm more than left. No evidence of calf muscle tenderness / dilated veins / redness / pain. Mild oedema bilaterally but equal in amount.

Blood Gas: Hypoxaemia SpO2 70mmHg (room air), pH 7.46, HCO3 22, pCO2 30

Chest Xray

CT scan

Question 1: Give two possible diagnoses that may coexist.

Question 2: What does the CXR show?

Question 3: What does the CT scan show?

Question 4: What other two important blood tests would you do to separate the two diagnoses?

Question 5: What treatments would you start empirically in this acutely in this patient?

Please send me your answers and they will be moderated and published.

Answers in one week from today !!

Clot versus Bleeding-- The Dilema

This is a great case! I hope you find this interesting. As usual, it has been anonymised.

A male patient of 55 had recently been on a short holiday to Hokaido and had been well during that time.

On coming back to central Japan, he was feeling unwell with a sore throat and was diagnosed with influenza. Unfortunately, he fell over sustained a contusion to the right knee leading to severe bruising and a swollen, painful knee.

He was bed bound for two days and slept most of the time.

On the night of admission, the patient got up from bed and he was seen to slowly slump to the floor with a loss of consciousness for 1 minute. The patient's right arm was seen to move erratically for up to 20 seconds similar to a seizure. There was no tongue biting and no urinary incontinence. The patient awoke after a few minutes and his consciousness was clear.

On arrival to hospital, the patient was noticed to have low oxygen saturations.

Examination revealed mild fever 37.8, pulse 70 min and regular, BP120/80 (lying), RR 24/min. SpO2 was 80%, Patient was over weight.

Red throat.

CVS- JVP- not raised. Sounds 1 + 2 normal. No mumurs.

RESP- mild right sided crackles that mostly cleared on coughing.

ABDO: Within normal limits.

NEURO: NAD

Right Lower Limb: Swollen, severely bruised. Right patella was painful and easy to move. There was a mild patella tap consistent with a probable intra-articular bleed.

The left leg was normal.

ABG: revealed normal pH but severe Hypoxaemia (PaO2: 52mmHg).

CXR: Nothing focal. No pneumonia or other obvious lung pathology.

ECG: NAD

Bloods: Slight neutrophilia and raised CRP.

Knee Xray: No obvious fracture seen.

CT head: NAD

In view of the collapse, and profound hypoxaemia with the history of leg injury and immobilisation plus an overweight body habitus, Pulmonary Embolism was suspected.

A Spiral CT was performed which showed thrombus in the right and left pulmonary vessels. A perfusion scinitigraphic scan was performed which showed multiple small perfusion defects consistent with small PEs seen on the spiral CT.

Doppler scans of the lower limbs showed no evidence of thrombus.

Echocardiogram revealed a relatively normal pulmonary artery pressure of 26mmHg but the Right Ventricle was slightly distended with 1st degree Tricuspid Regurgitation. Ejection fraction was 68%.

Hence, the physicians had made the great diagnosis of PE.

The patient was eventually commenced on heparin treatment by his physicians.

The patient's limb remained unchanged and the heparin was successful.

An excellent comment I received from a senior doctor suggested that in such cases heparin should always be commenced even if the patient's limb becomes compromised whilst treating PE to save the patient's life.

That is a tough decision to take for any doctor and is the balance between treating the patient but also trying to do no harm to your patient.

Do you agree with this approach?

What would you do in such a situation?

Without your comments other doctors or students are unable to learn so please give your opinion on this blog.

Seizures

Todays comment is in respect of seizures.

There are many, many causes of seizures and when a patient presents in a post-ictal state with there being little or no history available, it becomes the physicians responsibility to hunt for the cause.

For example, we recently had a case of a 65yr old diabetic female who presented with a new history of seizures. As always, this case has been anonymised.

She had been previously well.

She was diabetic, with an old MI and had been a smoker in the past.

She was taking anti-hypertensive agents, atorvastatin and aspirin.

She had three seizures and was treated with a phenytoin infusion which halted the seizure activity.

Blood pressure on admission was 199/95

The patient had apparently not bit her tongue nor had any incontinence.

When examined by a senior doctor, the patient the following day, GCS was 15/15.

Pupils equal and reactive to light. The patient was complaining of a severe bitemporal headache and neck pain. It was painful flexing the neck forwards.

The patient had clearly bitten her tongue and she had dry faeces on her legs suggestive of faecal incontinence.

Cranial nerve examination was normal apart from chronic diplopia that predated this event.

Tone was normal throughout the lower limbs.

Pronator drift was absent.

Power and reflexes were normal throughout.

Babinskis were negative.

Kernig's Test produced BACK PAIN but the patient had had a lumbar puncture the night before.

All bloods were negative and CRP was 0.01

CXR was normal.

CT and MRI had been considered non-diagnostic, but when I reviewed the scan I noticed a very small intracerebral haemorrhage that was very easily missed. There was no SAH visible.

However from the above, it was clear that this patient being a diabetic with hypertension and on aspirin succumbed to an intracerebral haemorrhage resulting in recurrent acute generalised seizures.

In view of the positive meningeal signs it was of concern to me that there may have been subarachnoid extension of bleeding.

On the other hand, the neck pain and headache may have been due to his severe seizure activity and the lower back ache may have been related to the previous traumatic lumbar procedure.

The patient had her aspirin stopped and under went a CT angiogram which revealed no SAH and the patient was referred for a neurosurgical opinion.

However, the only way to truly rule out an SAH is to perform a repeat lumbar puncture to look for xanthochromia.

The above case is an excellent example of a common cause of seizures.

Always consider the back ground previous medical history and always look at the drugs as these may cause or complicate seizures.

In her case, being diabetic on insulin could have resulted in an hypoglycaemic seizure; being an ex-smoker could have caused lung cancer, cerebral metastases and secondary seizures. Being hypertensive and taking aspirin can result in intracerebral bleeding and secondary seizures as in this case. Taking anti-hypertensive agents such as thiazide or loop diuretic agents can result in hyponatraemia and seizures.

The history is of prime importance if it can be elicited from friends or family.

Please let me know your comments.