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:
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.
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.
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