This is short summary of metabolism of chylomicrons.
ARBs or ACEI?
ARBs are expensive but evidence suggests they are as good as ACEI and may be beter if you want to prevent strokes. Read more..
Stroke Prevention- Still Confusion?
Recurrence of stroke is disabling event and prevention of such event is important. S MATCH trial showed increased bleeding in patients taking combination of aspirin with Clopidogrel . This study looked at combination of aspirin plus extended release Dipyridamole compared to clopidogel. Study concludes that there is no difference in using either drugs. Aspirin dose used is only 50 mg daily. What do we do with our stroke patient?"For stroke prevention,/ use an antiplatelet drug./ Treat hypertension" Read more.
Read what the editorial has to say..
Migraine with Aura and Stroke in Women
In women, migraine with aura is a risk factor for several ischaemic outcomes including all cause cardiovascular death, stroke, myocardial infarction, angina, coronary revascularisation procedures, and claudication. Read this editorial in BMJ..
Migraine, vascular risk, and cardiovascular events in women: prospective cohort study
Migraine, vascular risk, and cardiovascular events in women: prospective cohort study
5 minute of medicine
This is interesting collection of mterial from BMJ, 5 minute of International medicine. Read now..
(MRSA): “missing the wood for the trees”
August 28, 2008
MRSA is found very where in health care environment including neck ties, steths nad ID badges. While it is helpful to know all the places we may find MRSA, these types of studies really just confirm what should be blindingly obvious — that MRSA readily disseminates within our health care environment. Thus, the hands of health care workers will frequently come into contact with MRSA.
The real issue with the control of MRSA is not the need for more information on environmental contamination, but the need to use the abundant information we already have to curtail the principal way that MRSA spreads in hospitals — via the hands of health care workers, that's us. Read this editorial and there is an interesting comment too...
The real issue with the control of MRSA is not the need for more information on environmental contamination, but the need to use the abundant information we already have to curtail the principal way that MRSA spreads in hospitals — via the hands of health care workers, that's us. Read this editorial and there is an interesting comment too...
Cardiac repolarisation: the long and short of it
August 27, 2008
A summary of all you need to know about Long and short QT syndrome..
ABCD2 Tool for TIA
- ABCD2 tool for assessment of patients with transient ischaemic attack
- A. Age ≥ 60 years = 1 point.
- B. Blood pressure ≥ 140/90 mmHg = 1 point.
- C. Clinical features: unilateral weakness = 2 points, speech impairment alone = 1 point.
- D. Duration > 60 minutes = 2 points, 10–59 minutes = 1 point.
- D. Diabetes = 1 point.
- Total. 0–3 = low risk of stroke, 4–7 = high risk of stroke.
VTE prophylaxis
Current data suggest that VTE prophylaxis is grossly underused in hospitals.
The ENDORSE study (which enrolled over 68 000 medical and surgical patients in 32 countries,) showed that 51.8% of hospital inpatients were at risk of VTE, but only 58.5% of at-risk surgical patients and 39.5% of at-risk medical patients received VTE prophylaxis. Read more article published in Lancet..
The ENDORSE study (which enrolled over 68 000 medical and surgical patients in 32 countries,) showed that 51.8% of hospital inpatients were at risk of VTE, but only 58.5% of at-risk surgical patients and 39.5% of at-risk medical patients received VTE prophylaxis. Read more article published in Lancet..
Addison,s and Stress
Steroid replacement therapy in Addison,s syndrome has gone through various levels. It has been common practice to give higher doses of steroid during medical stress and surgical procedures. Most f the time patient excessive doses and this can lead to various steroid related complications. This review article published in MJA deals with this topic..
CPC 08/08 - Answer
The answer for last CPC case is posted here..
CPC case presentation..
Click on cpcanswer...
THE MOTHER-IN-LAW EFFECT
August 26, 2008
Derek Harwood Nash, one of the pioneers of neuroradiology, wanted to find an easy way to describe the DSA (digital subtraction angiography) behaviour of meningioma. He noticed that the tumour blush in a meningioma comes very early (early wash-in); normally it is very dense and persistent with a delayed wash-out. This reminded him the behaviour of an unwanted guest who comes early and stays late, and the guest that classically do this is actually the mother-in-law. Meningioma has both a dural and a pial blood supply and a sunburst or radial appearance of the feeding arteries. Depending on the location you may have to perform internal carotid, external carotid, ab vertebral injections. In the typical sphenoid wing meninigioma, the middle menigneal artery is enlarged.
Here is link to see mother-in-law effect.
syndicated from NeuroRAZiology..
When can you stop warafarin in unprovoked DVT
Stopping warfarin in unproved DVT is not easy decision. Identifying patients who are low risk has been a difficult task andi find this study published in Canadian Medical Journal very useful.
It concludes that it may be safe for women who have taken oral anticoagulants for 5–7 months after an unprovoked venous thromboembolism to discontinue therapy if they have 0 or 1 of the following signs or symptoms: hyperpigmentation, edema or redness of either leg; a D-dimer level of 250 µg/L or more while taking warfarin; BMI 30 kg/m2 or more; and age 65 years or more.. What about men?it appears that all men are at high risk of recurrence, particularly men with hyperpigmentation, edema or redness in either leg.They found that men had more than twice the risk of recurrence compared with women and that no subgroup of men with a low risk of recurrence could be identified. Read more..
It concludes that it may be safe for women who have taken oral anticoagulants for 5–7 months after an unprovoked venous thromboembolism to discontinue therapy if they have 0 or 1 of the following signs or symptoms: hyperpigmentation, edema or redness of either leg; a D-dimer level of 250 µg/L or more while taking warfarin; BMI 30 kg/m2 or more; and age 65 years or more.. What about men?it appears that all men are at high risk of recurrence, particularly men with hyperpigmentation, edema or redness in either leg.They found that men had more than twice the risk of recurrence compared with women and that no subgroup of men with a low risk of recurrence could be identified. Read more..
Stopping anticoagulant therapy after an unprovoked venous thromboembolism
ACP guidelines
Thyroid Eye Disease
August 25, 2008
Graves Eye disease can be a serious vision threatening condition. There are still unresolved issues in this condition. This is a recent abstract of lecture presentation.
Low LDL and Cancer Risk: Vytorin?
FDA has rejected cancer scare associated with Vyotorin.Meanwhile, the WSJ reports, the House Energy and Commerce Committee sent more letters to Merck and Schering yesterday. The committee wants to see the analysis of the SEAS trial conducted by an outside expert who concluded that the trial’s cancer findings were an anomaly, and the drug doesn’t increase cancer risk. Association of Low LDL with increasing incidence of cancer has been reported.This study says previously reported association of low levels of on-treatment LDL-C and incident cancer, confirmed here, is not driven by statins, and statin therapy, despite producing marked reductions in LDL-C, is not associated with an increased risk of cancer. Further studies are needed to validate these findings, particularly with longer durations of follow-up. Read more..
Lady with purple Hands
August 19, 2008
A 79-year-old woman with recurrent urinary tract infections presented with complaints of “purple” hands.
Bluish-purple discoloration of skin involved her earlobes and hands. The pulse oximeter read 80% to 84% saturation while 100% oxygen was administered at a flow of 15 L/min. Her urine was deep orange, and arterial blood appeared dark brown. Arterial blood oximetry showed a PO2 of 200 mm Hg, with 87.5% oxyhemoglobin and 11.8% methemoglobin. She had normal glucose-6-phosphate dehydrogenase levels, and intravenous methylene blue improved her cyanosis; her methemoglobin levels decreased to 0.3%. Apparently, acquired methemoglobinemia and urine discoloration had been induced by 10 days of phenazopyridine use (200 mg 3 times daily) for urinary tract infection. Urine returned to normal color within 3 days of discontinuing phenazopyridine. This azo dye, often used as a topical urinary tract analgesic, should not be administered for more than 2 days because of potential adverse effects (cytopenias, methemoglobinemia, nephrotoxicity, orange urine discoloration, and transaminitis).1
Methemoglobinemia is caused by excess methemoglobin (normal ≤1% of total hemoglobin) that is formed by oxidation of the iron moiety of hemoglobin from ferrous (normal) to ferric state. Drugs or chemicals, hemoglobin M variants, and congenital diminished activity of erythrocytic NADH-cytochrome-b5 reductase are associated with methemoglobinemia.2 Avoidance or discontinuation of offending drugs and use of methylene blue (once normal glucose-6-phosphate dehydrogenase levels have been confirmed) constitute the main management options.
The role of carbapenems in initial therapy for serious Gram-negative infections
The treatment of patients with serious Gram-negative infections must be both prompt and correct. Numerous studies have demonstrated that mortality risk is significantly increased when the initial antibiotic regimen does not adequately cover the infecting pathogen.
Furthermore, changing to an appropriate regimen once culture results are available does not reduce this risk. Therefore, one must empirically treat serious infections with a regimen that covers likely pathogens. Selecting such a regimen is complicated by the increasing prevalence of resistance to commonly used antibiotics. Moreover, multidrug-resistant pathogens, once limited to hospital-acquired infections, are increasingly being detected in community-acquired infections, especially those involving the urinary and gastrointestinal tracts or in immunocompromised patients. Consequently, the initial antibiotic regimen must have a broad spectrum of activity that includes potential resistant pathogens, as indicated by the local antibiogram. Many multidrug-resistant pathogens remain susceptible to carbapenems despite increasing worldwide antibiotic resistance. This article reviews the role played by carbapenems in the initial treatment of serious Gram-negative infections and the potential effect of emerging resistance on this role. A review in Critical Care examines this role. A future concern is the emergence of more resistance to carbapenems. What will we do when they begin to wear out their welcome? There’s not much else to turn to and the dry antibiotic development pipeline limits future prospects. (And do you think hospitals are safe now!).
Furthermore, changing to an appropriate regimen once culture results are available does not reduce this risk. Therefore, one must empirically treat serious infections with a regimen that covers likely pathogens. Selecting such a regimen is complicated by the increasing prevalence of resistance to commonly used antibiotics. Moreover, multidrug-resistant pathogens, once limited to hospital-acquired infections, are increasingly being detected in community-acquired infections, especially those involving the urinary and gastrointestinal tracts or in immunocompromised patients. Consequently, the initial antibiotic regimen must have a broad spectrum of activity that includes potential resistant pathogens, as indicated by the local antibiogram. Many multidrug-resistant pathogens remain susceptible to carbapenems despite increasing worldwide antibiotic resistance. This article reviews the role played by carbapenems in the initial treatment of serious Gram-negative infections and the potential effect of emerging resistance on this role. A review in Critical Care examines this role. A future concern is the emergence of more resistance to carbapenems. What will we do when they begin to wear out their welcome? There’s not much else to turn to and the dry antibiotic development pipeline limits future prospects. (And do you think hospitals are safe now!).
Obese and Healthy?
Better to Be Fat and Fit Than Skinny and Unfit, New York Times reports. This is in line with my previous post on Metabolically obese with normal weight.
ARB plus ACE: ON TARGET
Okay, moving on to the next common question, “should I add an ARB to the ACE inhibitor?” Read more..
It’s been shown that angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) reduce both proteinuria as well as renal risk (loss of GFR and need for dialysis). What remains unclear, however, is whether a combination of these classes of drugs has an additive effect on renal risk reduction, and whether the effects of ARB and ACE inhibitors are equivalent. Several previous studies have shown that combination therapy reduces proteinuria; however, these trials were limited by their small sample size, short duration of therapy, and did not report on major renal outcomes. The current investigation, the ONTARGET study, published in this week’s Lancet, is a large multi-center, randomized controlled trial that took place over 6 years. Participants were 55 years or older and had established atherosclerotic vascular disease or diabetes with end-organ damage (the baseline mean creatinine was about 83mmol/l). Over 25,000 patients were assigned to ramipril 10 mg daily, telmisartan 80 mg daily, or to a combination of both drugs. The primary outcome was a composite of dialysis, doubling of serum creatinine and death; the secondary outcome was a composite of dialysis and doubling of serum creatinine. The results of this trial may surprise you. Combination therapy reduced proteinuria to a greater degree than either therapy alone. However, both the primary outcome as well as secondary outcome were similar for telmisartan and ramipril but were increased with combination therapy. The study raises interesting questions regarding the relationship between proteinuria and kidney damage and asks if the reduction in proteinuria by itself can be taken as a definitive marker of improved renal function; these questions will no doubt require further investigation. Study limitations include a population that, at baseline, was well-treated with regards to standard cardiovascular therapy and only included a small subgroup with overt diabetic nephropathy. So this population may not represent the majority of patients we treat in our clinic. Overall, this trial suggests that while monotherapy with either an ARB or ACE inhibitor confers similar beneficial effects on major renal outcomes, combination blockade of the renin-angiotensin system may not be the way to go.
It’s been shown that angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) reduce both proteinuria as well as renal risk (loss of GFR and need for dialysis). What remains unclear, however, is whether a combination of these classes of drugs has an additive effect on renal risk reduction, and whether the effects of ARB and ACE inhibitors are equivalent. Several previous studies have shown that combination therapy reduces proteinuria; however, these trials were limited by their small sample size, short duration of therapy, and did not report on major renal outcomes. The current investigation, the ONTARGET study, published in this week’s Lancet, is a large multi-center, randomized controlled trial that took place over 6 years. Participants were 55 years or older and had established atherosclerotic vascular disease or diabetes with end-organ damage (the baseline mean creatinine was about 83mmol/l). Over 25,000 patients were assigned to ramipril 10 mg daily, telmisartan 80 mg daily, or to a combination of both drugs. The primary outcome was a composite of dialysis, doubling of serum creatinine and death; the secondary outcome was a composite of dialysis and doubling of serum creatinine. The results of this trial may surprise you. Combination therapy reduced proteinuria to a greater degree than either therapy alone. However, both the primary outcome as well as secondary outcome were similar for telmisartan and ramipril but were increased with combination therapy. The study raises interesting questions regarding the relationship between proteinuria and kidney damage and asks if the reduction in proteinuria by itself can be taken as a definitive marker of improved renal function; these questions will no doubt require further investigation. Study limitations include a population that, at baseline, was well-treated with regards to standard cardiovascular therapy and only included a small subgroup with overt diabetic nephropathy. So this population may not represent the majority of patients we treat in our clinic. Overall, this trial suggests that while monotherapy with either an ARB or ACE inhibitor confers similar beneficial effects on major renal outcomes, combination blockade of the renin-angiotensin system may not be the way to go.
Quantitative ETA and VAP
Our patients admitted for ventilation get Endotracheal aspirate cultured routinely twice a week. Is this practice cost effective? Does this help in identifying the VAP bug or not? Read this editorial...
Role of quantitative endotracheal aspirate and cultures as a surveillance and diagnostic tool for ventilator associated pneumonia: A pilot study
Role of quantitative endotracheal aspirate and cultures as a surveillance and diagnostic tool for ventilator associated pneumonia: A pilot study
Rheumatic Fever
August 17, 2008
You want to know all about pathogenesis of Acute Rheumatic Fever you can read this article. Syndicated from Clinical correlations.
WHt Ratio in Obesity
Another measure of obesity. It does not matter how we measure but fat is not healthy.Kurth and colleagues report, in the Journal of the American College of Cardiology, that waist-to-height ratio had the strongest association with CVD. Read this article in Journal of ACC.
Sleep Apnea and Stroke in CAD
Sleep disorders are more common in CAD patients and this not frequently recognised. This is associated with increased cardiovascular accidents Patients with CAD should therefore be considered for sleep apnea investigations and subsequent treatment. Read this paper in Circulation..
Thrombolysis in Stroke- another indication
Whe stroke patients show fluctuating neurological signs then it is an indication to five thrombolytics. Says this study published in Archives in neurology.
Central Obesity and Stroke
August 16, 2008
Central Obesity is strongly linked to risk of Stroke. So measurements of central obesity is important in risk assessment of stroke rather than BMI. Read more..
Diabetic Foot Care protocol
A simple protocol can assess the diabetic foot for the presence of predisposing factors for ulcerations and amputation, and can be used to guide treatment, according to recommendations developed by an American Diabetes Association task force.
The protocol consists of a history, general examination, and an assessment of dermatologic, musculoskeletal, neurologic, and vascular factors. Details of the protocol were issued by the American Diabetes Association, with the endorsement of the American Association of Clinical Endocrinologists, in a report in the August issue of Diabetes Care by Dr. Andrew J. M. Boulton and his colleagues in a task force of the ADA's Foot Care Interest Group. Read More....
Smoking and Plavix
Smoking is known to produce hyper reactive platelets but smoking also enhances action of clopidogrel.. Read more. Syndicated from HOTM.
Much has been said repeatedly, that smoking is a no, no, and bad for just about every aspect of our health. And that is true. Smoking obviously does more harm than good. Recently, I read an interesting article on a potential benefit of smoking. In the Aug 12th issue of the J of the American College of Cardiology, Dr Bliden and colleagues from the Sinai Thrombosis Research Center, Baltimore, published their findings in a small study of 259 patients, smokers who were on plavix to see the effects of smoking on platelet function, in these patients. They found that smoking seem to induce some enzymes in the CYP450 system, specifically CYP1A2, to enhance the conversion of clopidogrel to its active metabolite, thereby enhancing the action of clopidogrel. Interesting. In other words, smokers who are also on clopidogrel, have enhance platelet inhibition and so less thrombotic tendency. Apparently, when they reviewed the literature, they found that there was already a hint of this in the larger clopidogrel studies like CREDO, CLARITY, etc. However, I must caution that this is not a prospective randomised study and the numbers are small. Although it may be hypothesis generating and something for us to study further, who smokers should not think that their blood is thinner and so they are less likely to have heart attacks. THAT IS NOT WHAT I MEAN. It is possible that smokers on Plavix, maybe less likely to have a thrombotic event. I think that this theory, merits further study. Be that as it may, we cannot go out there and tell patients with DES to continue smoking and taking plavix, in the hope that they get less DES stent thrombosis. That is an obvious NO,NO. Whatever it is, patients with thrombotic diseases or vascular disease should stop smoking to prevent vascular events, Plavix or not.
The second point that I wish to raise is that Plavix is a pro-drug that needs to be activated via the CYP450 pathway, thereby making it vulnerable to all kinds of potential drug-drug interaction. Omeperazole for example may slow down the activation of Plavix, thereby causing it to be less effective. This is important because, we often use Plavix as an alternative to aspirin, after aspirin gastritis in some patients. Sometimes in this context, we also give them Omeperazole. We must then remember that the Plavix may not act so well.
Much has been said repeatedly, that smoking is a no, no, and bad for just about every aspect of our health. And that is true. Smoking obviously does more harm than good. Recently, I read an interesting article on a potential benefit of smoking. In the Aug 12th issue of the J of the American College of Cardiology, Dr Bliden and colleagues from the Sinai Thrombosis Research Center, Baltimore, published their findings in a small study of 259 patients, smokers who were on plavix to see the effects of smoking on platelet function, in these patients. They found that smoking seem to induce some enzymes in the CYP450 system, specifically CYP1A2, to enhance the conversion of clopidogrel to its active metabolite, thereby enhancing the action of clopidogrel. Interesting. In other words, smokers who are also on clopidogrel, have enhance platelet inhibition and so less thrombotic tendency. Apparently, when they reviewed the literature, they found that there was already a hint of this in the larger clopidogrel studies like CREDO, CLARITY, etc. However, I must caution that this is not a prospective randomised study and the numbers are small. Although it may be hypothesis generating and something for us to study further, who smokers should not think that their blood is thinner and so they are less likely to have heart attacks. THAT IS NOT WHAT I MEAN. It is possible that smokers on Plavix, maybe less likely to have a thrombotic event. I think that this theory, merits further study. Be that as it may, we cannot go out there and tell patients with DES to continue smoking and taking plavix, in the hope that they get less DES stent thrombosis. That is an obvious NO,NO. Whatever it is, patients with thrombotic diseases or vascular disease should stop smoking to prevent vascular events, Plavix or not.
The second point that I wish to raise is that Plavix is a pro-drug that needs to be activated via the CYP450 pathway, thereby making it vulnerable to all kinds of potential drug-drug interaction. Omeperazole for example may slow down the activation of Plavix, thereby causing it to be less effective. This is important because, we often use Plavix as an alternative to aspirin, after aspirin gastritis in some patients. Sometimes in this context, we also give them Omeperazole. We must then remember that the Plavix may not act so well.
On-TIME 2 trial favours Tirofiban in STEMI
Prehospital treatment with tirofiban plus standard anti-platelet therapy improves clinical outcomes in patients with ST-elevation myocardial infarction (STEMI), according to research published in The Lancet if PCI is considered.
Looks like just getting aspirin and Clopidogrel in at the first signs of a heart attack is not enough!Platelets need to be blocked at all costs..
Looks like just getting aspirin and Clopidogrel in at the first signs of a heart attack is not enough!Platelets need to be blocked at all costs..
Beware of Red Bull
Drinking even one can of red bull can produce hyper reactive plateletes and may lead to CV events..Read report from Australia..
Eye view
August 14, 2008
What does this fundus picture show?Look for:
* in young patient, mention you like to examine the eyes for internuclear ophthalmoplegia and cerebellar sign for multiple sclerosis
* Signs of Cushing's syndrome in SLE pts on steroid
* in old patient, look for evidence of vascular diseases such as prominent temporal artery (or old scar indicating temporal artery biopsy) and carotid bruit
(or endarterectomy scar)
Congenital
If congenital, it is usually hereditary with an onset of deterioration in childhood and may be accompanied by nystagmus. Leber's Hereditary Optic Neuropathy, (LHON) or Leber Optic Atrophy is hereditary, but typically has its onset in 20-30 year old males. This is due to a mutation of the mitochondrial genome and hence is passed exclusively through the mothers. Dominant optic atrophy or Kjer's optic neuropathy has autosomal dominant inheritance. It usually presents in early childhood. There are numerous less common genetically related syndromes.[2]
Alternatively, congenital optic atrophy can be caused by a lack of oxygen during pregnancy, labour or in the early days of a child's life. Some drugs taken during pregnancy are also associated with optic atrophy.
Acquired
The acquired type of optic atrophy may be due to blood supply changes in the eye or optic nerve (anterior ischemic optic neuropathy or posterior ischemic optic neuropathy), may be secondary to inflammation or swelling within the optic nerve (optic neuritis), may be a result of pressure against the optic nerve (such as from a tumour), or may be related to metabolic diseases (e.g., diabetes mellitus), trauma, glaucoma, or toxicity (caused by methanol, tobacco, or other poisons). It is also seen in vitamin B12 deficiency and Paget's disease of the bone.
Herbal supplements and surgery
Lots of patients consume herbal medications and some take concoction of many. This article deals with interaction of such remedies during surgery..Read more.
Normal weight Obese syndrome
August 13, 2008
Nearly 20 years ago, it was suggested that individuals exist who are not obese on the basis of height and weight, but who, like people with overt obesity, are hyperinsulinemic, insulin-resistant, and predisposed to type 2 diabetes, hypertriglyceridemia, and premature coronary heart disease. Since then it has become increasingly clear that such metabolically obese, normal-weight (MONW) individuals are very common in the general population and that they probably represent one end of the spectrum of people with the insulin resistance syndrome. Read more..
The opposite may be true as well when obese people are metabolically healthy..Recent publication in Arch. Internal Medicine describes two different phenotypes..
Another study in the same issue of Arch.Internal Medicine concludes that metabolically benign obesity that is not accompanied by insulin resistance and early atherosclerosis exists in humans. Furthermore, ectopic fat in the liver may be more important than visceral fat in the determination of such a beneficial phenotype in obesity.
The opposite may be true as well when obese people are metabolically healthy..Recent publication in Arch. Internal Medicine describes two different phenotypes..
Another study in the same issue of Arch.Internal Medicine concludes that metabolically benign obesity that is not accompanied by insulin resistance and early atherosclerosis exists in humans. Furthermore, ectopic fat in the liver may be more important than visceral fat in the determination of such a beneficial phenotype in obesity.
Rhabdomyolysis
August 12, 2008
Rhabdomyolysis is a serious disorder of muscles and Acute Kidney injury is a consequence of this condition. This editorial deals with this topic nicely.. Read more..
AKI in Rhabdomyolysis
AKI in Rhabdomyolysis
HBA1c is a screening tool for DM
August 11, 2008
HBA1c is an useful tool in the management of DM. It also been a contentious issue whether it can used in screening for DM. This consensus statement is favouring using HBa1c in screening for DM. Read more..
Diagnosing DM...
Simva and Amiadarone: FDA warning
There in increased risk of rhabdomyolysis when simvastatin is combined with amiadarone.More drugs you use more problems we see. Read FDA warning..
Aspirin Resistance: Is this disease driven?
August 8, 2008
Aspirin is one of the most widely prescribed drugs for the prevention of thrombosis in patients with vascular disease. Yet, aspirin is unable to prevent thrombosis in all patients. The term “aspirin resistance” has been used to broadly define the failure of aspirin to prevent a thrombotic event. Whether this is directly related to aspirin itself through biochemical aspirin resistance or treatment failure, or if it is because of aspirin's inability to overcome the thrombogenic aspects of the disease process itself, has not been elucidated. This can have dramatic clinical implications for a variety of vascular disease subsets and is cause for concern, considering the high prevalence of aspirin use for both primary and secondary prevention. Disparities exist in the rates of aspirin resistance among certain patient populations, such as women, patients with diabetes mellitus, and those with heart failure, and across clinical conditions, such as cardiovascular and cerebrovascular disease. Clinical trial data from studies observing resistance have revealed that regardless of study size, dose of aspirin, control for drug interactions and adherence, or assay used to measure platelet function, aspirin resistance is associated with an increased risk for adverse events. Although the evidence is mounting, there has yet to be a consensus on the appropriate clinical response to aspirin resistance.
Taken from abstract in Pharmacotherapy
Sub Therapeutic INR- What is the Risk?
Anticoagulation with warfarin is a two edged sword. Low INR is seen commonly in our clinic and i dont practice bridging heparin therapy. i have been looking for a study that shows that this this practice is safe. This article is published in Pharmacotherapy recently. You can read abstract below.
Study Objective. To quantify the absolute risk of thromboembolism associated with a significant subtherapeutic international normalized ratio (INR) in patients with previously stable anticoagulation while receiving warfarin.
Design. Retrospective, matched cohort analysis.
Setting. Centralized anticoagulation service in an integrated health care delivery system.
Patients. A total of 2597 adult patients receiving warfarin from January 1998–December 2005; 1080 patients were in the low INR cohort and were matched to 1517 patients in the therapeutic INR cohort based on index INR date, indication for warfarin, and age.
Measurements and Main Results. Stable, therapeutic anticoagulation was defined as two INR values, measured at least 2 weeks apart, within or above the therapeutic range. The low INR cohort included patients with a third INR value of 0.5 or more units below their therapeutic range. The therapeutic INR cohort included patients with a third therapeutic INR value and no INR value 0.2 or more units below their target INR range in the ensuing 90 days. The primary outcome was anticoagulation-related thromboembolism during the 90 days after the index INR. Secondary outcomes were times to the first occurrence of anticoagulation-related complications (bleeding, thromboembolism, or death) in the 90 days after the index INR. Four thromboembolic events (0.4%) occurred in the low INR cohort and one event (0.1%) in the therapeutic INR cohort (p=0.214). The differences in the proportions of thromboembolism, bleeding, or death were not significant between the cohorts (p>0.05). No significant differences were noted in the hazard of thromboembolism, bleeding, or death between the cohorts (p>0.05).
Conclusion. Patients with stable INRs while receiving warfarin who experience a significant subtherapeutic INR value have a low risk of thromboembolism in the ensuing 90 days. The risk was similar to that observed in a matched control population in whom therapeutic anticoagulation was maintained. These findings do not support the practice of anticoagulant bridge therapy for patients stabilized on warfarin therapy to reduce their risk for thromboembolism during isolated periods of subtherapeutic anticoagulation.
Worth reading this abstrat too.
Pharmacodynamics of Uniform versus Nonuniform Warfarin Dosages
Study Objective. To quantify the absolute risk of thromboembolism associated with a significant subtherapeutic international normalized ratio (INR) in patients with previously stable anticoagulation while receiving warfarin.
Design. Retrospective, matched cohort analysis.
Setting. Centralized anticoagulation service in an integrated health care delivery system.
Patients. A total of 2597 adult patients receiving warfarin from January 1998–December 2005; 1080 patients were in the low INR cohort and were matched to 1517 patients in the therapeutic INR cohort based on index INR date, indication for warfarin, and age.
Measurements and Main Results. Stable, therapeutic anticoagulation was defined as two INR values, measured at least 2 weeks apart, within or above the therapeutic range. The low INR cohort included patients with a third INR value of 0.5 or more units below their therapeutic range. The therapeutic INR cohort included patients with a third therapeutic INR value and no INR value 0.2 or more units below their target INR range in the ensuing 90 days. The primary outcome was anticoagulation-related thromboembolism during the 90 days after the index INR. Secondary outcomes were times to the first occurrence of anticoagulation-related complications (bleeding, thromboembolism, or death) in the 90 days after the index INR. Four thromboembolic events (0.4%) occurred in the low INR cohort and one event (0.1%) in the therapeutic INR cohort (p=0.214). The differences in the proportions of thromboembolism, bleeding, or death were not significant between the cohorts (p>0.05). No significant differences were noted in the hazard of thromboembolism, bleeding, or death between the cohorts (p>0.05).
Conclusion. Patients with stable INRs while receiving warfarin who experience a significant subtherapeutic INR value have a low risk of thromboembolism in the ensuing 90 days. The risk was similar to that observed in a matched control population in whom therapeutic anticoagulation was maintained. These findings do not support the practice of anticoagulant bridge therapy for patients stabilized on warfarin therapy to reduce their risk for thromboembolism during isolated periods of subtherapeutic anticoagulation.
Worth reading this abstrat too.
Pharmacodynamics of Uniform versus Nonuniform Warfarin Dosages
RCTs and parachutes
In the tight-sphinctered world of academic medicine, it's always delightful to find a journal that still has a sense of humor. The following satirical paper from the British Journal of Medicine made me laugh and laugh.Smith GCS, Pell JP. (2003). Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials. BMJ, 327(7429), 1459-1461. DOI: 10.1136/bmj.327.7429.1459
In a nutshell, this paper rightfully points out that no one has ever done a randomized, controlled trial (RCT) on the efficacy of parachutes. Furthermore,
Advocates of evidence-based medicine have criticised the adoption of interventions evaluated by using only observational data.
To be funny, satire has to contain enough truth about its subject to properly skewer its underlying fallacies. Smith and Pell's excellent paper carries the concept of parachute efficacy through the usual machinery of evidence-based medicine, all the way to the following hilarious reductio ad absurdum conclusion:
We think that everyone might benefit if the most radical protagonists of evidence-based medicine organised and participated in a double-blind, randomised, placebo-controlled, crossover trial of the parachute.
From skimming through the comments stimulated by this paper, it seems that not all of the BMJ readers recognized it as satire, even though the article concludes with the following contributors' statement:
GCSS had the original idea. JPP tried to talk him out of it. JPP did the first literature search but GCSS lost it. GCSS drafted the manuscript but JPP deleted all the best jokes. GCSS is the guarantor, and JPP says it serves him right.
A Bit More on Evidence-Based Medicine
The formal term "evidence-based medicine" (EBM), is a relative newcomer on the medical research scene, and is based on early publications by Cochrane in 1972 and Sackett and Guyatt in the early 1990's. Their idea is a simple one: make clinical decisions based on a synthesis of the best available evidence about a treatment.
Just a few decades later, there are way many EBM advocates who are way too ready to blindly wield EBM like a mighty sword without understanding its limitations. IMHO, one of its biggest limitations is the current EBM definition of "best available evidence". For example, consider the Oxford Centre for Evidence-based Medicine Levels of Evidence (May 2001):
Level Therapy/Prevention, Aetiology/Harm
1a systematic review (with homogeneity*) of RCTs
1b Individual RCT (with narrow Confidence Interval‡)
1c All or none§
2a systematic review (with homogeneity*) of cohort studies
2b Individual cohort study (including low quality RCT; e.g., <80%>Oscillococcinum). However, the solutions usually employed are so dilute there is not a single molecule left of the original agent. Scientific likelihood of any benefit over that of plain water = zip.
Homeopathy counters this with the claim that the diluting water has a "memory" of the original agent, even though it's all gone. However, there is no scientific evidence of such a "memory" effect. Besides, when one considers how much of our planet's water passes through human kidneys, it seems likely that any possible "memory" of Oscillococcinum would be swamped by just the "memory" of used beer.
Bottom line: scientific likelihood of any benefit of homeopathy over that of plain water again = zero/zed/zip.
In this case, the basic science is so overwhelmingly against any benefit that it seems ridiculous to perform an RCT of homeopathic claims. Even if a marginally weak effect were suggested by a clinical trial, the a priori implausibility of homeopathy makes it hard to put much confidence in the result.
Parachutes
The physics of falling bodies, on the other hand, has been understood for a long time, particularly when there is atmospheric drag. The terminal velocity of a falling human in air is about 55 m/s (120 mph). Scientific likelihood of survival = almost 0% (a few fluke cases have been reported of lucky folks surviving parachute failures).
A properly designed parachute can decrease this falling speed to as little as 2.1 m/s, about the speed you'd develop by jumping off a 9 inch stool. Scientific likelihood of survival = virtually 100%.
In this case, the basic science is overwhelmingly in favor of survival. Therefore, I'm willing to take my chances with a parachute during my next plunge from a height -- RCT or no RCT.
Syndicated from samurai radiologist.
Clinician's Long Tails
August 7, 2008
DB has written a series of posts on this concept (here, here, here, here, here and here). There’s little I can add but I wanted to get them into my own links, and going through the exercise below has helped my understanding of the concept.
The long tail refers to the horizontal tail of a power law graph. This is a polynomial function which has garnered great interest because of its applicability to a large number of phenomena in commerce and nature. When applied to differential diagnosis the horizontal axis can be visualized as an array of diseases of increasing rarity the farther away from the origin. The vertical axis represents the probability of the given disease explaining the patient’s presentation. A small number of common diseases are clustered toward the origin (to the left). Toward the right (in the long tail) are uncommon diseases, becoming increasingly rare as the graph approaches the horizontal axis as an asymptote.
Individual diseases in the long tail are uncommon. But, because the tail is long (there are many rare diseases), in the aggregate a significant number of patients is represented. That principle, a challenge for the clinician, is explained here.
DB uses the sore throat as an illustration. Pneumonia is another example. Pneumococcal pneumonia would be near the origin. Blastomycosis, ANCA associated pulmonary capillaritis and bronchoalveolar carcinoma, diseases which can present as “pneumonia”, are in the long tail. For recurrent abdominal pain irritable bowel syndrome would belong on the left, with celiac disease and acute intermittent porphyria occupying positions progressively to the right. And so on.
The challenge of the long tail is knowing when to enter it and, once you do, to generate a wide enough differential diagnosis to encompass the disease the patient has, and finally to select appropriate tests to pinpoint the diagnosis. That’s why the long tail separates clinicians from automatons. Algorithms and guidelines won’t help. Up to Date may not even help! What’s needed is judgment along with a vast fund of knowledge about diseases. Key to knowing when and when not to enter the long tail, as DB explains, is knowledge of natural history. How long, for example, should it take your patient with pneumonia to get better? At what point, as a corollary, should you start searching for another diagnosis?
The description of this cognitive process and the contrast between clinician and automaton makes a compelling case for the revival of the original concept of the internist.
Syndicated from RW.
The long tail refers to the horizontal tail of a power law graph. This is a polynomial function which has garnered great interest because of its applicability to a large number of phenomena in commerce and nature. When applied to differential diagnosis the horizontal axis can be visualized as an array of diseases of increasing rarity the farther away from the origin. The vertical axis represents the probability of the given disease explaining the patient’s presentation. A small number of common diseases are clustered toward the origin (to the left). Toward the right (in the long tail) are uncommon diseases, becoming increasingly rare as the graph approaches the horizontal axis as an asymptote.
Individual diseases in the long tail are uncommon. But, because the tail is long (there are many rare diseases), in the aggregate a significant number of patients is represented. That principle, a challenge for the clinician, is explained here.
DB uses the sore throat as an illustration. Pneumonia is another example. Pneumococcal pneumonia would be near the origin. Blastomycosis, ANCA associated pulmonary capillaritis and bronchoalveolar carcinoma, diseases which can present as “pneumonia”, are in the long tail. For recurrent abdominal pain irritable bowel syndrome would belong on the left, with celiac disease and acute intermittent porphyria occupying positions progressively to the right. And so on.
The challenge of the long tail is knowing when to enter it and, once you do, to generate a wide enough differential diagnosis to encompass the disease the patient has, and finally to select appropriate tests to pinpoint the diagnosis. That’s why the long tail separates clinicians from automatons. Algorithms and guidelines won’t help. Up to Date may not even help! What’s needed is judgment along with a vast fund of knowledge about diseases. Key to knowing when and when not to enter the long tail, as DB explains, is knowledge of natural history. How long, for example, should it take your patient with pneumonia to get better? At what point, as a corollary, should you start searching for another diagnosis?
The description of this cognitive process and the contrast between clinician and automaton makes a compelling case for the revival of the original concept of the internist.
Syndicated from RW.
CPC -08/08
Welcome to the monthly posting NYU Department of Medicine’s Clinical Pathology Conference. Use the link below to review the case, followed by a slide presentation of the radiological findings. Feel free to make your diagnosis by clicking the comment field. We will reveal the answer next week.
Clinical Pathology Conference Case Presentation
Clinical Pathology Conference Images
Click on cpcimages...
Lesson for us: Use proper blood pressure cuffs
Blood pressure that is fluctuating is common in wards and apart from personnel variation, using improper blood pressure cuffs can end up in serious trouble for patients. Read this lesson of the week from BMJ.
Lesson of the week.....
Lesson of the week.....
Treatment for HIV
The availability of new antiretroviral drugs and formulations, including drugs in new classes, and recent data on treatment choices for antiretroviral-naive and -experienced patients warrant an update of the International AIDS Society-USA guidelines for the use of antiretroviral therapy in adult human immunodeficiency virus (HIV) infection.
OBJECTIVES: To summarize new data in the field and to provide current recommendations for the antiretroviral management and laboratory monitoring of HIV infection. This report provides guidelines in key areas of antiretroviral management: when to initiate therapy, choice of initial regimens, patient monitoring, when to change therapy, and how best to approach treatment options, including optimal use of recently approved drugs (maraviroc, raltegravir, and etravirine) in treatment-experienced patients.
CONCLUSIONS: New data and considerations support initiating therapy before CD4 cell count declines to less than 350/microL. In patients with 350 CD4 cells/microL or more, the decision to begin therapy should be individualized based on the presence of comorbidities, risk factors for progression to AIDS and non-AIDS diseases, and patient readiness for treatment. In addition to the prior recommendation that a high plasma viral load (eg, >100,000 copies/mL) and rapidly declining CD4 cell count (>100/microL per year) should prompt treatment initiation, active hepatitis B or C virus coinfection, cardiovascular disease risk, and HIV-associated nephropathy increasingly prompt earlier therapy. The initial regimen must be individualized, particularly in the presence of comorbid conditions, but usually will include efavirenz or a ritonavir-boosted protease inhibitor plus 2 nucleoside reverse transcriptase inhibitors (tenofovir/emtricitabine or abacavir/lamivudine). Treatment failure should be identified and managed promptly, with the goal of therapy, even in heavily pretreated patients, being an HIV-1 RNA level below assay detection limits
Read the original article published in JAMA here
OBJECTIVES: To summarize new data in the field and to provide current recommendations for the antiretroviral management and laboratory monitoring of HIV infection. This report provides guidelines in key areas of antiretroviral management: when to initiate therapy, choice of initial regimens, patient monitoring, when to change therapy, and how best to approach treatment options, including optimal use of recently approved drugs (maraviroc, raltegravir, and etravirine) in treatment-experienced patients.
CONCLUSIONS: New data and considerations support initiating therapy before CD4 cell count declines to less than 350/microL. In patients with 350 CD4 cells/microL or more, the decision to begin therapy should be individualized based on the presence of comorbidities, risk factors for progression to AIDS and non-AIDS diseases, and patient readiness for treatment. In addition to the prior recommendation that a high plasma viral load (eg, >100,000 copies/mL) and rapidly declining CD4 cell count (>100/microL per year) should prompt treatment initiation, active hepatitis B or C virus coinfection, cardiovascular disease risk, and HIV-associated nephropathy increasingly prompt earlier therapy. The initial regimen must be individualized, particularly in the presence of comorbid conditions, but usually will include efavirenz or a ritonavir-boosted protease inhibitor plus 2 nucleoside reverse transcriptase inhibitors (tenofovir/emtricitabine or abacavir/lamivudine). Treatment failure should be identified and managed promptly, with the goal of therapy, even in heavily pretreated patients, being an HIV-1 RNA level below assay detection limits
Read the original article published in JAMA here
Painless mammography?
Breast CT Scanners Promise Painless Alternative To Mammography.
The discomfort of a mammogram can drive some women to avoid the valuable screening, occasionally with dire consequences. Now a new procedure, dedicated breast computed tomography (CT), promises to take the pain out of breast cancer detection.
In the cone beam breast CT scanner, which was first developed at the University of California, Davis, a woman lies face down on a special table with one breast suspended through an opening. A CT scanner rotates around the breast, collecting data that are reconstructed into a three-dimensional image. The total dose of radiation is the same as in a conventional mammogram. Since 2004, the UC Davis researchers, led by John M. Boone, Professor and Vice Chair of Radiology and Professor of Biomedical Engineering, have scanned 160 women with their prototype scanner. In early 2008, the researchers began operating a second prototype device, into which the researchers have incorporated a positron emission tomography (PET) scanner. The PET scanner tracks the metabolic activity of a tumor, if present, so the hybrid CT/PET breast scanner would allow clinicians to, among other uses, precisely localize and monitor the response of a tumor to chemotherapy, determine the extent (or staging) of tumors, and help guide radiologists conducting biopsies.
The clinical trials show that the scanner “is better than mammography for mass detection,” Boone says, while “offering improved comfort to the patient and a better three-dimensional understanding of pathological lesions when they are present.” The scanner, however, is less efficient than regular mammography at detecting the tiny clusters of calcium (or microcalcifications) that can sometimes signal breast cancer. This is because it uses X rays at higher energies than do mammograms, reducing the contrast of the images and the ability to distinguish the calcium clusters. “Thus, we are not making the claim that breast CT is “better” than mammography-yet,” Boone says. The research was described in the talk, “Dedicated Breast CT Imaging of the Breast,” presented July 29, 2008 at the 50th annual meeting of the American Association of Physicists in Medicine.
Reported in Science Daily.
The discomfort of a mammogram can drive some women to avoid the valuable screening, occasionally with dire consequences. Now a new procedure, dedicated breast computed tomography (CT), promises to take the pain out of breast cancer detection.
In the cone beam breast CT scanner, which was first developed at the University of California, Davis, a woman lies face down on a special table with one breast suspended through an opening. A CT scanner rotates around the breast, collecting data that are reconstructed into a three-dimensional image. The total dose of radiation is the same as in a conventional mammogram. Since 2004, the UC Davis researchers, led by John M. Boone, Professor and Vice Chair of Radiology and Professor of Biomedical Engineering, have scanned 160 women with their prototype scanner. In early 2008, the researchers began operating a second prototype device, into which the researchers have incorporated a positron emission tomography (PET) scanner. The PET scanner tracks the metabolic activity of a tumor, if present, so the hybrid CT/PET breast scanner would allow clinicians to, among other uses, precisely localize and monitor the response of a tumor to chemotherapy, determine the extent (or staging) of tumors, and help guide radiologists conducting biopsies.
The clinical trials show that the scanner “is better than mammography for mass detection,” Boone says, while “offering improved comfort to the patient and a better three-dimensional understanding of pathological lesions when they are present.” The scanner, however, is less efficient than regular mammography at detecting the tiny clusters of calcium (or microcalcifications) that can sometimes signal breast cancer. This is because it uses X rays at higher energies than do mammograms, reducing the contrast of the images and the ability to distinguish the calcium clusters. “Thus, we are not making the claim that breast CT is “better” than mammography-yet,” Boone says. The research was described in the talk, “Dedicated Breast CT Imaging of the Breast,” presented July 29, 2008 at the 50th annual meeting of the American Association of Physicists in Medicine.
Reported in Science Daily.
New strain of Malaria in Sarawak
We have to watch out for malaria cases imported from Sarawak with new pattern of fever here too. This new strain seem to multiply faster and produce fever every 24 hours. Read more on this report.
Intervention vs Responsibility
July, 2008 Mayo Clinic Proceedings an article reports the results of a study looking at the value of telemedicine in the management of diabetes. In essence, there were two arms of the study, one with the "usual" management, the other with an endocrinologist available by telemedecine for various problems.
The study found no benefit from having (more or less) instant access to an endocrinologist.
My take on this is that it supports a contention I have about health: It's not about access. It's about patients taking responsibility for their own health. If you are responsible, it becomes your responsibility to learn as much as you can about how to deal with problems, customized to your own situation. So that if you're not doing well, it's your responsibility, not a "failing of the system.Also providing health is not about high tech telemedicine"
The study found no benefit from having (more or less) instant access to an endocrinologist.
My take on this is that it supports a contention I have about health: It's not about access. It's about patients taking responsibility for their own health. If you are responsible, it becomes your responsibility to learn as much as you can about how to deal with problems, customized to your own situation. So that if you're not doing well, it's your responsibility, not a "failing of the system.Also providing health is not about high tech telemedicine"
Diagnosis not to be missed!
August 5, 2008
Infectious disease management involves knowledge of local prevalence and manifestations of diseases. This case history involved a Philippine man who presented with continued diarrhea and eventually died. delay in diagnosis is worrying and how it is important we use using search engines to get information re illnesses.
Read the NEJM problem solving case..
You can go through this power point presentation to leaen more about this infection.
Click on capillariasis...
Chemoprevention of Gastric cancer?
We now know, due to the pioneering work of Warren and Marshall (the duo won the Nobel prize in Medicine in 2005) that Helicobacter pylori is the cause of most stomach ulcers. It has also been linked with stomach cancer. But will eradication of Helicobacter pylori prevent the development of stomach cancer?
Previous trials in this area have shown inconclusive results.
Recently, Japanese workers published work in The Lancet which shows that eradication of H. pylori has an impact on preventing recurrence of gastric cancer.
Read abstract of Lancet article here.
Further reading if you have time..
Previous trials in this area have shown inconclusive results.
Recently, Japanese workers published work in The Lancet which shows that eradication of H. pylori has an impact on preventing recurrence of gastric cancer.
Read abstract of Lancet article here.
Further reading if you have time..
Biotics: what you need to know
Prebiotic is a selectively fermented ingredient that allows specific changes, both in the composition and/or activity in the gut bacteria leading to benefits for the host well being and health. Synbiotic is a combination of prebiotic and probiotic.
Bifidobacteria and lactobacilli have been shown to have potent antipathogenic properties for potentially providing health benefits.
A successful prebiotic has the following properties:
1. Is not destroyed or absorbed in the gut on its journey from mouth to the colon.
2. Undergoes bacterial fermentation in the gut.
3. Selectively promotes the number and/or activity of the indigenous beneficial bacteria like bifidobacteria and lactobacilli
While dietary fiber may act as prebiotic, the most promising however are fructo-oligosaccharides (FOS) because of their selective fermentation towards the more healthy gut bacteria.Galacto- oligosaccharides (GOS) are used in infant formula foods. Both FOS and GOS meet the criteria for prebiotics as outlined above. Inulin type fructans have positive prebiotic effects. Other products with possible prebiotic potential include soybean oligosaccharides from soybean whey. Isomalto- oligosaccharides may be regarded as a quasi-prebiotic since it is partially metabolized in human gut.
Possible health benefits of prebiotics include:
Dose of prebiotic: 5-8 g per day
Products on the market that may be fortified with prebiotics include diary products, health drinks, infant formula, cereal, dried instant as well as canned foods, and pet foods etc.
Do you or someone you know takes probiotics or prebiotics? If yes, in what form do you take and do you think it makes a difference? Please share your thoughts.
Bifidobacteria and lactobacilli have been shown to have potent antipathogenic properties for potentially providing health benefits.
A successful prebiotic has the following properties:
1. Is not destroyed or absorbed in the gut on its journey from mouth to the colon.
2. Undergoes bacterial fermentation in the gut.
3. Selectively promotes the number and/or activity of the indigenous beneficial bacteria like bifidobacteria and lactobacilli
While dietary fiber may act as prebiotic, the most promising however are fructo-oligosaccharides (FOS) because of their selective fermentation towards the more healthy gut bacteria.Galacto- oligosaccharides (GOS) are used in infant formula foods. Both FOS and GOS meet the criteria for prebiotics as outlined above. Inulin type fructans have positive prebiotic effects. Other products with possible prebiotic potential include soybean oligosaccharides from soybean whey. Isomalto- oligosaccharides may be regarded as a quasi-prebiotic since it is partially metabolized in human gut.
Possible health benefits of prebiotics include:
- 1. Improved lactose tolerance
- 2. Improved resistance to pathogens resulting in decrease in gastrointestinal infections and respiratory infections
- 3. Decrease in cholesterol
- 4. Increased bacterial synthesis of vitamins
- 5. Protection against allergies by reducing gut inflammation
- 6. Improved absorption of calcium and magnesium
Dose of prebiotic: 5-8 g per day
Products on the market that may be fortified with prebiotics include diary products, health drinks, infant formula, cereal, dried instant as well as canned foods, and pet foods etc.
Do you or someone you know takes probiotics or prebiotics? If yes, in what form do you take and do you think it makes a difference? Please share your thoughts.
What langauge do we talk to our Patients?
Do you think, as a patient, all the medical terms you need to know is what is a “cholecystectomy”, “CAT scan”, “CVA”, “stenting” and so on. However, as described in an article in the online Bioethics Forum by Carol Levine there is a host of “new language of healthcare" about which patients should be informed and fluent.
She writes:
What do you call a person admitted to a hospital? If you said “patient,” you’re hopelessly out of date. The person lying there awaiting surgery or recovering from a heart attack is a “consumer.” The person examining the consumer is a “provider.” Depending on the situation, she may be a “hospitalist,” “intensivist,” “proceduralist,” “surgicalist,” or other “ist.” If you’re admitted at night, the provider is a “nocturnist.” Ordinary doctors, who don’t have “ists” after their titles, are seldom seen in hospitals these days.
That’s just one example of how health care language is changing. It’s not enough to know clinical terms; you have to know the lingo of health policy and practice to navigate though the health care system.
She writes:
What do you call a person admitted to a hospital? If you said “patient,” you’re hopelessly out of date. The person lying there awaiting surgery or recovering from a heart attack is a “consumer.” The person examining the consumer is a “provider.” Depending on the situation, she may be a “hospitalist,” “intensivist,” “proceduralist,” “surgicalist,” or other “ist.” If you’re admitted at night, the provider is a “nocturnist.” Ordinary doctors, who don’t have “ists” after their titles, are seldom seen in hospitals these days.
That’s just one example of how health care language is changing. It’s not enough to know clinical terms; you have to know the lingo of health policy and practice to navigate though the health care system.
I manged to get this artcle that talks about communication issues in clinical practice. It is entitled "Do patients Understand" what you are trying to say.
Untreated OSA and Mortality
August 4, 2008
Sleep disordered breathing is often missed and if left without diagnosis and treatment will end in increased CV mortality. This is 18 year follow up study that is recently published in Sleep Journal.
Read the abstract of this article...
Read the abstract of this article...
Update on IE prophylaxis- we are moving on!
2007 the AHA issued guidance for IE prophylaxis that greatly simplified the recommendations and proposed substantive changes—changes that would affect hundreds of thousands of patients. Since then, we, and most likely all of you, have been barraged by our surgical and dental colleagues and patients with inquiries—"Are you sure this is the right thing to do? Would you mind putting the recommendation in writing before I proceed?"
Evidence is now moving from "procedure-related bacteremia" toward "cumulative bacteremia" as the more likely cause of most cases of IE. For instance, daily activities such as tooth brushing are estimated to produce bacteremia 6 million times higher than a single tooth extraction. Thus, continued episodic bacteremia due to poor dentition may pose a much greater risk for the development of IE than a single dental procedure.
A final impetus for change was that the guidelines themselves had become more complicated with each revision, with ambiguous recommendations for which specific patient and which particular procedure required the prophylaxis.
Recommendation:-
Evidence is now moving from "procedure-related bacteremia" toward "cumulative bacteremia" as the more likely cause of most cases of IE. For instance, daily activities such as tooth brushing are estimated to produce bacteremia 6 million times higher than a single tooth extraction. Thus, continued episodic bacteremia due to poor dentition may pose a much greater risk for the development of IE than a single dental procedure.
A final impetus for change was that the guidelines themselves had become more complicated with each revision, with ambiguous recommendations for which specific patient and which particular procedure required the prophylaxis.
Recommendation:-
- • Infective endocarditis prophylaxis should be given only to a high-risk subgroup of patients prior to dental procedures that involve manipulation in gingival tissue or periapical region of the teeth or perforation of the oral mucosa.
- • High-risk patients include only those with a: 1) prosthetic cardiac valve; 2) previous infective endocarditis; 3) complex congenital heart disease; and 4) valvulopathy following cardiac transplantation.
- • Infective endocarditis prophylaxis is not recommended prior to gastrointestinal or genitourinary procedures.
Lazy in and lazy out!
Of course, I would expect nothing less. This is America after all, where they encourage laziness in every possible way. I could understand if it was a disability access issue, but I've never seen an escalator that is wheelchair accessible. So that argument doesn't fly. It FAILS
A Journey to Center of Your Mind by VS
August 3, 2008
The Most Electrifying Lecture You'll Ever Hear
I've heard a lot of lectures in my life but never one like this. This is neuroanatomist Dr. Jill Bolte Taylor giving a talk on the functional differences between the right and left hemispheres of the brain. She's passionate about her subject as she actually suffered a massive intracranial hemorrhage that trashed her left brain. Dr. Taylor brilliantly describes the experience and sensations both as a stroke victim and as a scientist.
Not that I want to replicate her experience but man do I wish I could teach like her! Check it out and prepare to be riveted by the most amazing 20 minute talk you've ever heard.
It makes me never want to step up to a podium again.
Not that I want to replicate her experience but man do I wish I could teach like her! Check it out and prepare to be riveted by the most amazing 20 minute talk you've ever heard.
It makes me never want to step up to a podium again.
Morphine conversions
Opioid analgesics are the cornerstone to treatment and control of severe pain. Equivalence of dose potency is not absolute and care must be taken in changing analgesics. In general, it is safer to use a lower regular dose with breakthrough analgesia rather than to convert immediately to the “equivalent” dose.
It is important nevertheless to know the approximately dosage conversions.
Read here Opioid analgesic dose conversions..
It is important nevertheless to know the approximately dosage conversions.
Read here Opioid analgesic dose conversions..
Asthma Treatment
This is a summary of treatment of asthma in adults. This is summarised from National Asthma Council's asthma management handbook.
Summary of treatment of Asthma in adults
PCOS- To give Metformin or not to?
This is a 32 year-old obese female with a history of hypertension, chronic cold urticaria, focal segmental glomerulosclerosis, and polycystic ovarian syndrome who presented for routine follow-up in primary care clinic. The patient was diagnosed with polycystic ovarian syndrome in November 2007. At that time, she presented with irregular menses and dysmenorrhea, at which point pelvic ultrasound revealed polycystic ovaries. The patient was prescribed daily oral contraceptive medication, but was recently advised to discontinue this medication secondary to persistence of irregular menses. Her last menstrual period was 1/3/2008 – 1/10/2008. Her BMI is 30.7 and she had a normal oral glucose tolerance test. The clinical question of whether or not to begin treatment with metformin warranted further discussion:
Polycystic ovarian syndrome (PCOS) affects nearly 5-7 percent of reproductive age women and is characterized by chronic oligo-ovulation or anovulation, androgen excess, insulin resistance, obesity, hirsutism, infertility, and (in some cases) polycystic ovaries (1, 2). These patients are at a markedly increased risk for impaired glucose tolerance, type 2 diabetes, and other metabolic derangements. Metformin, a medication whose major effect is to decrease hepatic glucose production and increase insulin sensitization in peripheral tissues, plays a pivotal role in the treatment armamentarium for PCOS.
The pathophysiology of PCOS is incompletely understood, but is thought to involve multiple interactions among the gonadotropins and androgens, insulin, and the ovaries. Insulin resistance and hyperinsulinemia are central features of PCOS and appear to be responsible for the associations between PCOS and type 2 diabetes, dyslipidemia, hypertension, and other physiological and anatomical cardiovascular maladaptations (3, 4). In brief, there are four concurrent mechanisms of action:
1. Although peripheral tissues such as skeletal muscle and fat are insulin-resistant in this syndrome, insulin actually stimulates the ovarian production of androgens in PCOS.
2. Insulin also stimulates leutenizing hormone production by the anterior pituitary, further driving ovarian stimulation and increasing serum androgen levels.
3. The progressive hyperinsulinemia inhibits hepatic production of sex hormone-binding globulin, a phenomenon that augments circulating free testosterone levels.
4. Finally, insulin inhibits the ovulatory cycle by interfering with gonadotropin secretion, increasing intra-ovarian androgen levels, and directly affecting follicular development.
Inhibiting insulin release with the use of diazoxide or octreotide, improving insulin sensitivity through weight loss, metformin, or thiazolidinediones, and reducing carbohydrate absorption through the use of acarbose have all been shown to lower circulating insulin levels, increase ovulatory frequency or menses, and/or reduce serum testosterone (5). Clearly, the hyperinsulinemia that is so critical to the pathogenesis and natural history of PCOS is a major therapeutic target.
The role of metformin in decreasing the relative risk for progression to type 2 diabetes among patients with impaired glucose tolerance at baseline has been well established (6). Metformin decreases hepatic gluconeogenesis, increases peripheral glucose uptake and utilization, and has an anti-lipolytic effect that decreases fatty acid concentrations (7). In 1996, Nestler and colleagues reported that the administration of metformin to women with PCOS decreased circulating insulin levels and was associated with decreases in ovarian 17,20-lyase activity and the ovarian secretion of androgens (8). However, to date no randomized clinical trials have specifically assessed the effect of metformin on the progression to type 2 diabetes in patients with PCOS. The closest study to accomplish this goal was a 2007 uncontrolled, retrospective analysis of 50 women with PCOS who were treated with metformin for an average of 43 months. The results were very suggestive of a protective effect in this population: none of the participants showed progression to type 2 diabetes, even though 11 of these women (22.0%) had impaired glucose tolerance at baseline (9). Six of the women with impaired glucose tolerance at baseline (55%) had reversion to normal glucose tolerance during the treatment period. Moreover, of the remaining 39 women with normal glucose tolerance at baseline, only 2 (5%) had conversion to impaired glucose tolerance over the 43-month study period, yielding a 1.4% per year annual conversion rate from normal to impaired glucose tolerance. This conversion rate was significantly lower than the 16-19% annual conversion rate reported for women with PCOS who were not taking metformin. In other words, metformin was shown to reduce the annual conversion rate from normal glucose tolerance to impaired glucose tolerance by 11-fold (P = 0.01). Despite being a retrospective analysis of a limited number of patients, this study suggests that long-term treatment with metformin delays or prevents the development of impaired glucose tolerance and type 2 diabetes in the PCOS patient population.
Metformin is increasingly being used to treat the metabolic derangements of PCOS despite the fact that treatment decisions have so far been guided by the results of randomized controlled trials of populations without the polycystic ovarian syndrome. There is limited evidence on the long-term role of metformin for the treatment of insulin insensitivity, few studies on the efficacy of metformin in ameliorating signs of androgen excess (e.g. hirsutism), and conflicting data on how improvement of insulin sensitivity and fertility compares when metformin is used alone or in combination with existing hormonal therapies. Yet despite the current ambiguity on its role, the American Association of Clinical Endocrinologists recommends that metformin be considered as the initial intervention for most women (particularly those who are overweight or obese) with PCOS. On the other hand, other organizations, like the Androgen Excess Society, are more stringent in their recommendations and point out that therapy should not be mandated until well-designed randomized controlled trials have demonstrated efficacy in this population.
As for this patient, a 32 year-old overweight woman with established polycystic ovarian disease and metrorrhagia refractory to oral contraceptive medication, therapy with metformin should be recommended. Whereas oral contraceptive medication aims to correct ovulatory cycling, metformin functions to help rectify the fundamental metabolic imbalance of PCOS. If she decides to pursue pregnancy, metformin can be safely continued in the first trimester and, although recently published studies have found metformin to be inferior to clomiphine for ovulation induction, metformin has proven efficacy in this regard (10). In conjunction with a comprehensive nutrition management program, metformin will likely help the patient lose weight, improve her ovulatory cycling, and diminish her risk for developing type 2 diabetes.
References:
1. The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and longer-term health risk related to polycystic ovary syndrome PCOS. Hum Reprod 2004:19:41-7.
2. Knochenhauer ES, Key TJ et al. Prevalence of the polycystic ovary syndrome in unselected black and white women of the southeastern United States: a prospective study. J Clin Endocrinol Metab 1998; 83:3078.
3. Paradisi G, Steinberg HO, Hempfling A, et al. Polycystic ovary syndrome is associated with endothelial dysfunction. Circulation 2001; 103: 1410-5.
4. Lilloja S, Mott Dm, Spraul M, et al. Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus: prospective studies of Pima Indians. N Engl J Med 1993; 329:1988-92.
5. Nestler, JE. Metformin for the treatment of the polycystic ovary syndrome. N Engl J Med 2008; 358:47-54.
6. Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346:393-403.
7. Bailey CJ, Turner RC. Metformin. N Engl J Med 1996; 334:574.
8. Nestler JE, Jakubowicz DJ. Decreases in ovarian cytochrome P450c17alpha activity and serum free testosterone after reduction in insulin secretion in polycystic ovary syndrome. N Engl J Med 1996; 335:617-23.
9. Sharma St, Wickham EP III, Nestler JE. Changes in glucose tolerance with metformin treatment in polycystic ovary syndrome: a retrospective analysis. Endocr Pract 2007; 13:373-9.
10. Legro RS, Barnhart HX, Shlaff WD, et al. Clomiphene, metformin, or both for infertility in the polycystic ovary syndrome. N Engl J Med 2007; 356:551-556.
Polycystic ovarian syndrome (PCOS) affects nearly 5-7 percent of reproductive age women and is characterized by chronic oligo-ovulation or anovulation, androgen excess, insulin resistance, obesity, hirsutism, infertility, and (in some cases) polycystic ovaries (1, 2). These patients are at a markedly increased risk for impaired glucose tolerance, type 2 diabetes, and other metabolic derangements. Metformin, a medication whose major effect is to decrease hepatic glucose production and increase insulin sensitization in peripheral tissues, plays a pivotal role in the treatment armamentarium for PCOS.
The pathophysiology of PCOS is incompletely understood, but is thought to involve multiple interactions among the gonadotropins and androgens, insulin, and the ovaries. Insulin resistance and hyperinsulinemia are central features of PCOS and appear to be responsible for the associations between PCOS and type 2 diabetes, dyslipidemia, hypertension, and other physiological and anatomical cardiovascular maladaptations (3, 4). In brief, there are four concurrent mechanisms of action:
1. Although peripheral tissues such as skeletal muscle and fat are insulin-resistant in this syndrome, insulin actually stimulates the ovarian production of androgens in PCOS.
2. Insulin also stimulates leutenizing hormone production by the anterior pituitary, further driving ovarian stimulation and increasing serum androgen levels.
3. The progressive hyperinsulinemia inhibits hepatic production of sex hormone-binding globulin, a phenomenon that augments circulating free testosterone levels.
4. Finally, insulin inhibits the ovulatory cycle by interfering with gonadotropin secretion, increasing intra-ovarian androgen levels, and directly affecting follicular development.
Inhibiting insulin release with the use of diazoxide or octreotide, improving insulin sensitivity through weight loss, metformin, or thiazolidinediones, and reducing carbohydrate absorption through the use of acarbose have all been shown to lower circulating insulin levels, increase ovulatory frequency or menses, and/or reduce serum testosterone (5). Clearly, the hyperinsulinemia that is so critical to the pathogenesis and natural history of PCOS is a major therapeutic target.
The role of metformin in decreasing the relative risk for progression to type 2 diabetes among patients with impaired glucose tolerance at baseline has been well established (6). Metformin decreases hepatic gluconeogenesis, increases peripheral glucose uptake and utilization, and has an anti-lipolytic effect that decreases fatty acid concentrations (7). In 1996, Nestler and colleagues reported that the administration of metformin to women with PCOS decreased circulating insulin levels and was associated with decreases in ovarian 17,20-lyase activity and the ovarian secretion of androgens (8). However, to date no randomized clinical trials have specifically assessed the effect of metformin on the progression to type 2 diabetes in patients with PCOS. The closest study to accomplish this goal was a 2007 uncontrolled, retrospective analysis of 50 women with PCOS who were treated with metformin for an average of 43 months. The results were very suggestive of a protective effect in this population: none of the participants showed progression to type 2 diabetes, even though 11 of these women (22.0%) had impaired glucose tolerance at baseline (9). Six of the women with impaired glucose tolerance at baseline (55%) had reversion to normal glucose tolerance during the treatment period. Moreover, of the remaining 39 women with normal glucose tolerance at baseline, only 2 (5%) had conversion to impaired glucose tolerance over the 43-month study period, yielding a 1.4% per year annual conversion rate from normal to impaired glucose tolerance. This conversion rate was significantly lower than the 16-19% annual conversion rate reported for women with PCOS who were not taking metformin. In other words, metformin was shown to reduce the annual conversion rate from normal glucose tolerance to impaired glucose tolerance by 11-fold (P = 0.01). Despite being a retrospective analysis of a limited number of patients, this study suggests that long-term treatment with metformin delays or prevents the development of impaired glucose tolerance and type 2 diabetes in the PCOS patient population.
Metformin is increasingly being used to treat the metabolic derangements of PCOS despite the fact that treatment decisions have so far been guided by the results of randomized controlled trials of populations without the polycystic ovarian syndrome. There is limited evidence on the long-term role of metformin for the treatment of insulin insensitivity, few studies on the efficacy of metformin in ameliorating signs of androgen excess (e.g. hirsutism), and conflicting data on how improvement of insulin sensitivity and fertility compares when metformin is used alone or in combination with existing hormonal therapies. Yet despite the current ambiguity on its role, the American Association of Clinical Endocrinologists recommends that metformin be considered as the initial intervention for most women (particularly those who are overweight or obese) with PCOS. On the other hand, other organizations, like the Androgen Excess Society, are more stringent in their recommendations and point out that therapy should not be mandated until well-designed randomized controlled trials have demonstrated efficacy in this population.
As for this patient, a 32 year-old overweight woman with established polycystic ovarian disease and metrorrhagia refractory to oral contraceptive medication, therapy with metformin should be recommended. Whereas oral contraceptive medication aims to correct ovulatory cycling, metformin functions to help rectify the fundamental metabolic imbalance of PCOS. If she decides to pursue pregnancy, metformin can be safely continued in the first trimester and, although recently published studies have found metformin to be inferior to clomiphine for ovulation induction, metformin has proven efficacy in this regard (10). In conjunction with a comprehensive nutrition management program, metformin will likely help the patient lose weight, improve her ovulatory cycling, and diminish her risk for developing type 2 diabetes.
References:
1. The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and longer-term health risk related to polycystic ovary syndrome PCOS. Hum Reprod 2004:19:41-7.
2. Knochenhauer ES, Key TJ et al. Prevalence of the polycystic ovary syndrome in unselected black and white women of the southeastern United States: a prospective study. J Clin Endocrinol Metab 1998; 83:3078.
3. Paradisi G, Steinberg HO, Hempfling A, et al. Polycystic ovary syndrome is associated with endothelial dysfunction. Circulation 2001; 103: 1410-5.
4. Lilloja S, Mott Dm, Spraul M, et al. Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus: prospective studies of Pima Indians. N Engl J Med 1993; 329:1988-92.
5. Nestler, JE. Metformin for the treatment of the polycystic ovary syndrome. N Engl J Med 2008; 358:47-54.
6. Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346:393-403.
7. Bailey CJ, Turner RC. Metformin. N Engl J Med 1996; 334:574.
8. Nestler JE, Jakubowicz DJ. Decreases in ovarian cytochrome P450c17alpha activity and serum free testosterone after reduction in insulin secretion in polycystic ovary syndrome. N Engl J Med 1996; 335:617-23.
9. Sharma St, Wickham EP III, Nestler JE. Changes in glucose tolerance with metformin treatment in polycystic ovary syndrome: a retrospective analysis. Endocr Pract 2007; 13:373-9.
10. Legro RS, Barnhart HX, Shlaff WD, et al. Clomiphene, metformin, or both for infertility in the polycystic ovary syndrome. N Engl J Med 2007; 356:551-556.
Radiology Case
August 2, 2008
Cough and chest discomfort are presented in a 16-year-old girl diagnosed with pulmonary inflammatory pseudotumor. Which imaging modalities are preferred in diagnosing a lung mass in a young person? Applied Radiology (Source: Medscape Radiology Headlines)
Read more..
Doctor and patient relationship- Is it healthy?
NewYorkTimes Tara Parker-Pope's piece this week hit the nail on the head. The doctor-patient relationship is in trouble...big trouble!
Parker-Pope has a way of accurately encapsulating today's health issues and this issue is no different. Since this is a relationship I know well, I was impressed how accurately she described it - the good, the bad, and the ugly.
I've had many wonderful moments with families but there have been many times I leave a room scratching my head, wondering what I could have done to have helped that family feel more at ease. While I admit there are times I could have phrased something better or been more tactful, there are even more times when all my best efforts don't seem enough. Those are the times that worry me.
My list of why the doctor-patient relationship is in trouble is similar to Parker-Pope's list. In my mind, the major reasons for the decline include, in no particular order:
1. physician dissatisfaction with clinical life
2. physician dissatisfaction with income
3. unreasonable or unfair patient or family expectations
4. "Dr. Google"
5. A decline in the respect given to experts for their education and training
6. A health care system that doesn't allow enough time for good communication
7. People not following advice given without consulting their doctor first then calling to complain they are not better
8. People not understanding that pills and antibiotics are not the cure for most things
9. People not understanding that tests are not the path to most diagnoses
10. People not taking ownership for their own health day to day
One of the doctors interviewed by Parker-Pope described a typical health care encounter almost like a face-off. Great analogy! That is just what it feels like much of the time - but it doesn't have to be that way.
To turn this mess around, we all have to do our part in the system to de-escalate the relationship. Since this is a relationship, everyone has to accept responsibility for what they bring into the room and work on their part of the friction. So, while us docs are working on communication and better listening, patients and families have some work to do, too. They need to cut us some slack and understand we are only human. And, a little respect would go a long way. It is so difficult to try and help someone when they sort of cop an attitude because of something found in a Google search. As I've mentioned in prior posts, reading a medical lithograph and interpreting it are very different. there's a reason we have 4 years of medical school and 3+years of residency training. If people want us to respect their questions and fears, which we all try to do, our expertise has to be respected, too.
As for the medical system, that is broken and needs to be fixed. It is destroying morale and the work environment actually driving doctors from clinical medicine more often than most people want to discuss. We are not being greedy to want to be paid fairly for our time given how many hours a week a logged in caring for people. And, it is not greedy to want to have a family life and some personal time, either. There has to be a way to pay doctors fairly while structuring a work environment that is supportive and recognizes that we all have lives outside of medicine.
The good news is that we are finally having a conversation about this very difficult and important topic. That's the first step to finding a solution and improving the satisfaction on both sides of this face off. If we work at it and succeed, we'll find ourselves still facing off - but on the same side of the puck with both of us against the medical problem. That's the way it used to be, and the way it needs to be again.
Posted by DrGwenn
Parker-Pope has a way of accurately encapsulating today's health issues and this issue is no different. Since this is a relationship I know well, I was impressed how accurately she described it - the good, the bad, and the ugly.
I've had many wonderful moments with families but there have been many times I leave a room scratching my head, wondering what I could have done to have helped that family feel more at ease. While I admit there are times I could have phrased something better or been more tactful, there are even more times when all my best efforts don't seem enough. Those are the times that worry me.
My list of why the doctor-patient relationship is in trouble is similar to Parker-Pope's list. In my mind, the major reasons for the decline include, in no particular order:
1. physician dissatisfaction with clinical life
2. physician dissatisfaction with income
3. unreasonable or unfair patient or family expectations
4. "Dr. Google"
5. A decline in the respect given to experts for their education and training
6. A health care system that doesn't allow enough time for good communication
7. People not following advice given without consulting their doctor first then calling to complain they are not better
8. People not understanding that pills and antibiotics are not the cure for most things
9. People not understanding that tests are not the path to most diagnoses
10. People not taking ownership for their own health day to day
One of the doctors interviewed by Parker-Pope described a typical health care encounter almost like a face-off. Great analogy! That is just what it feels like much of the time - but it doesn't have to be that way.
To turn this mess around, we all have to do our part in the system to de-escalate the relationship. Since this is a relationship, everyone has to accept responsibility for what they bring into the room and work on their part of the friction. So, while us docs are working on communication and better listening, patients and families have some work to do, too. They need to cut us some slack and understand we are only human. And, a little respect would go a long way. It is so difficult to try and help someone when they sort of cop an attitude because of something found in a Google search. As I've mentioned in prior posts, reading a medical lithograph and interpreting it are very different. there's a reason we have 4 years of medical school and 3+years of residency training. If people want us to respect their questions and fears, which we all try to do, our expertise has to be respected, too.
As for the medical system, that is broken and needs to be fixed. It is destroying morale and the work environment actually driving doctors from clinical medicine more often than most people want to discuss. We are not being greedy to want to be paid fairly for our time given how many hours a week a logged in caring for people. And, it is not greedy to want to have a family life and some personal time, either. There has to be a way to pay doctors fairly while structuring a work environment that is supportive and recognizes that we all have lives outside of medicine.
The good news is that we are finally having a conversation about this very difficult and important topic. That's the first step to finding a solution and improving the satisfaction on both sides of this face off. If we work at it and succeed, we'll find ourselves still facing off - but on the same side of the puck with both of us against the medical problem. That's the way it used to be, and the way it needs to be again.
Posted by DrGwenn
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