Ask the Faculty
| VIA E-MAIL |
- View any 2007-2008 program via on demand Webcast
- Follow the Webcast prompts to submit your questions via e-mail
- Check back to the section below to view new FAQs
| | |
FREQUENTLY ASKED QUESTIONS
Choose an area of interest below, to view Frequently Asked Questions
Primary Care Professionals
Diabetes
Osteoporosis
Sleep Disorders
Specialists
Cardiology
Dermatology
Oncology
Psychiatry/Sleep Disorders
Cardiology FAQs
An Evidence-Based Approach to Managing ACS Patients for Optimal Care
Q: Could you comment on the new ACC/AHA guidelines for the treatment of non-ST-segment elevation myocardial infarction (NSTEMI), and how are they different from the previous guidelines?
A: This is a very timely question. The recent update to the 2002 unstable angina (UA)/NSTEMI guidelines was published on August 6th, and it really integrates a lot of the more contemporary data. New trials, new drugs, and new strategies have been incorporated.
One of the important changes is selectively identifying the high-risk patients who should be treated with an early invasive strategy. For those patients with positive biomarkers, heart failure, or other high-risk features, the guidelines re-emphasized the need for an early invasive strategy. They also integrated new data, such as those from ICTUS, which showed that a conservative strategy may be the best approach for low- and moderate-risk patients.
In the realm of pharmacologic therapy, newer agents such as bivalirudin, a direct thrombin inhibitor, and fondaparinux, a factor Xa inhibitor, made it into the guidelines. These agents can be used in conjunction with antiplatelet therapy for patients with UA and NSTEMI. Unfractionated heparin and enoxaparin were given Class I indications for patients undergoing an invasive or conservative strategy. But because of its benefit in reducing bleeding complications, fondaparinux was suggested as the preferred agent in those who were undergoing a conservative strategy.
There were some other differences in the guidelines, such as allowing for the 600 mg loading dose of clopidogrel, which was discussed in the preceding talk. I think that is an option that many physicians favor, especially if there will be a short delay before percutaneous coronary intervention.
All in all, the guidelines are really keeping up with contemporary practice and new data.
Q: A recent presentation by Swann et al. about the OASIS-5 trial pointed out that women with non-ST-elevated myocardial infarction (NSTEMI) have worse outcomes with invasive therapy. How would you change your strategy for treating these patients? Also, would there be female patients that you would send for early intervention, and how would you identify them?
A: Those are very important questions. As a reminder, the OASIS-5 trial was a randomized trial of a little more than 20,000 NSTEMI patients who were randomized to fondaparinux or enoxaparin, followed by angiography or intervention where appropriate.
One hundred eighty-four of those patients were women who received either fondaparinux or enoxaparin, so the first comment should be that this is a very small substudy of the larger trial. Nonetheless, the study found that the early invasive group experienced a higher rate of complications, including mortality.
These data are very worrisome and compelling. They challenge the assumption that data generated from trials that primarily enroll men can be easily generalized to women; I don’t think that that is the case here. These data are compelling enough that we should perform studies with larger numbers of women to define whether this is just a chance occurrence, or whether this really represents a biologic phenomenon.
To answer the second part of the question, I do alter my strategy based on the gender of the patient because generally women are smaller and we have to be more careful about dosing our anticoagulation medications appropriately. I think smaller women have a higher risk of intracranial hemorrhage with thrombolysis during STEMI. Nonetheless, I think the higher rates of complications could be balanced against a strategy of watchful waiting in a high-risk NSTEMI patient because we also pay a penalty of recurrent MI and possibly higher mortality if we choose a conservative strategy over an invasive strategy in these types of female patients.
In other words, the balance is between creating complications by subjecting this group of patients to an early invasive strategy and withholding the benefit of early angiography and intervention. I make the decision based on the health of the patient. The sicker the patient, the more I am interested in bringing her to the catheterization suite and making sure that she doesn’t suffer a recurrent MI.
So I will restratify patients with troponin-positive status, congestive heart failure, or other high-risk markers with an angiogram and revascularize appropriately. Again, if this person is at increased risk of bleeding, I may not pursue an aggressive anticoagulation strategy, and if not pressed to an early invasive strategy, I may treat them conservatively.
To reiterate, these findings are from a very small subpopulation of the OASIS-5 trial and larger trials should be conducted to answer this question.
Q: Do you change your treatment strategy for ST-segment elevation myocardial infarction (STEMI) when dealing with special patient populations?
A: I do, in several different ways. We have to make adjustments for patients with lower body weight, which is often seen in female and elderly patients. We typically reduce the medication dose for such patients. In addition, when treating STEMI patients, we’re learning more and more that you have to take a more conservative approach with the elderly, particularly if you’re using a lytic. For example, if we use enoxaparin in a female over the age of 75, we would not give the bolus. Also, older women often present with greater kidney function impairment, so it would be important to look at their creatinine clearance. The patients who have the greatest risk of dose errors are older females with low body weight. We have to be very careful with the drugs we give, but if given appropriately, drugs do benefit this patient population.
Q: Can you comment on the article recently published by Henry et al. in the August 2007 issue of Circulation about the use of integrated patient-transfer systems and their effect on door-to-balloon times?
A: That was a very important article. It comes from Abbott Northwestern Hospital in Minneapolis, where they’ve done a superb job of initiating treatment within the 90-minute timeline that has been established.
If cardiac catheterization is indicated, it’s very important for the cath lab to get moving as early as possible. More and more facilities are starting to activate the cath lab when the patient is en route to the hospital. If a 12-lead is administered en route and the EMT says, “We think we have an MI,” more and more facilities are taking that as a cue to initiate treatment en route, rather than wait to evaluate the patient in the ER.
Activating the cath lab as early as possible, having ambulances ready to bring patients from one hospital to another, and bringing people straight to the cath lab rather than through the ER are the major ways that we can reduce door-to-balloon times.
Q: Is there any difference in assessing Troponin T vs Troponin I in risk assessment?
A: These two diagnostic tests can both be used in risk scores such as the TIMI Risk Score. There is no difference between the two tests in this regard.
Q: Many expert cardiologists believe that we should establish protocols for the care of cardiac patients, beginning with emergency department care. The program discussed the need to individualize care, even for STEMI patients. How do you see protocols fitting into individualized patient care?
A: We often feel that protocols impede our ability to individualize treatment, but they actually serve as an important reminder of what the minimum standards of care should be. They also help us make important decisions in the heat of the moment. With regard to STEMI patients, protocols can be a very important tool to help determine when we should select primary PCI, what agents need to be used in conjunction with interventional treatment, and when patients may benefit from thrombolytic therapy. The use of protocols should not prevent us from considering specific patient needs; they can be very useful tools for providing better patient care.
Q: What biomarkers are on the horizon for determining patient risk? Will they be more accurate than troponin?
A: The troponin assay is a very sensitive test that can often determine when patients are in the midst of some other disease manifesting as myocardial necrosis. Although I do not think there will be incremental benefits in sensitivity with newer biomarkers like brain natriuretic peptide (BNP), I do think they will allow us to identify, with more specificity, those patients who are at higher risk regardless of their troponin status. Right now, as the program indicates, the 2 mechanisms of risk stratification for NSTEMI patients are troponin status and the presence of ST-segment elevation. The newer biomarkers may help us identify those patients who might benefit from aggressive therapy, regardless of whether they are troponin negative or positive.
Q: A study was recently published about emergency department physicians activating the cath lab before the patient is seen by a cardiologist (Khot et al., Circulation). How will the results of this study affect patient care and outcomes?
A: This paper supports other recent data that looks at streamlining processes to achieve better outcomes with primary PCI. In many institutions, this process is often prolonged because physicians must talk to several providers to activate the cardiac cath lab. Streamlining the process and empowering emergency department physicians to interpret electrocardiograms and activate the cath lab directly is a very important operational change that can reduce door-to-balloon times. The study also highlights the importance of having continuous dialogue between cardiologists and emergency department physicians as part of ongoing quality improvement for patients undergoing PCI.
Q: The program mentioned bleeding as a consequence of antithrombin and antiplatelet agents. Yet patients—especially those who are post-PCI—need these agents. When patients have bleeding, at what point do you consider stopping these agents? Do you stop them all at once? If not, which ones do you stop? If all are stopped, at what point—if at all—do you restart them, and what do you restart?
A: When patients have bleeding, you should consider stopping these agents if you think the bleeding is uncontrolled or if you’re not sure if it is uncontrolled. We often see patients who become hypotensive, manifest hematoma, or have a gastrointestinal bleed. If it can be determined that the bleed is ongoing, can’t be controlled, or that antiplatelet and/or antithrombin agents are compromising our ability to stabilize the patient, then we need to stop these agents.
As the program indicated, the half-life of clopidogrel is such that the duration of effect is going to be 5 days. So we can deduce that the effects of stopping this agent will be apparent a few days down the line. Other agents, like the IIb/IIIa inhibitors, should be stopped when the risk of bleeding exceeds the potential benefit of reducing recurrent MI. So if a patient has any hemodynamic compromise such as tachycardia or hypotension, or is thought to have an uncontrolled bleed, then it is acceptable to withhold these agents.
When deciding how to start adding agents back to patient regimens, it’s best to add them back in order of importance, which is determined by assessing the risk of complications associated with not administering the agent. For example, in post-PCI patients, particularly those who have had a stent placed, stent thrombosis is the primary concern. So the priority would be to add aspirin and clopidogrel back into the regimen first. If it turned out that there wasn’t really a substantial bleed, then you could also add back the IIb/IIIa antagonist.
Q: At what point should a high-risk NSTEMI patient who is acutely ill be transferred from a hospital without a cath lab to one with a cath lab?
A: The simplest answer is that if the physician feels uncomfortable with the patient’s status, then transferring the patient to a hospital with a cath lab would be an option. There are, however, some practical markers that can help physicians make this decision as well. For instance, patients who are experiencing ongoing chest pain, without ST-segment elevation, should be transferred so that an angiogram can be performed (eg, to see if a circumflex occlusion is present and is electrically silent). Also, patients who are experiencing repeated episodes of chest discomfort or ECG change despite aggressive medical therapy including aspirin, clopidogrel, UFH or LMWH, and IIb/IIIa antagonists should be considered for transfer. Other patients to consider for transfer include those who become hypotensive or are tachycardic during episodes of chest pain.
Q: The ACC/AHA guidelines recommend that STEMI patients should receive fibrinolysis in the ambulance on the way to the hospital if the paramedic is trained to administer it. How do you see this affecting the care of patients, given that the recommendations are that patients who present early should go to PCI?
A: In the United States, we don’t administer as much pharmacotherapy in the ambulance as they do in Europe, particularly France, but it’s something we should consider. There are several trials out there that do indicate that pre-hospital drugs, like lytics, improve patient outcomes and have demonstrated a 16% relative risk reduction in mortality. The guidelines indicate that if a patient presents early, lysis is probably a better strategy, particularly if the patient presents within the first 3 hours and if you can get lytics on board very quickly. So yes, primary PCI is a very good strategy, but for those who present early and who can get lytics very quickly, that may be another very good strategy.
Q: Would you change your strategy for treating STEMI or NSTEMI patients based on factors like age, gender, and comorbid conditions?
A: Recently, an article was published in Circulation that indicates that one size does not fit all when it comes to selecting a reperfusion strategy, and that factors such as age, infarct location, and how long the patient has had symptoms will determine appropriate treatment strategies. For example, in a young patient who presents early with an anterior MI, there is only a 40-minute window in which to perform a PCI before you lose the mortality advantage of PCI over a lytic. Therefore, in this patient, lytic therapy may be a very good treatment option. On the other end of the spectrum, in an elderly patient with an inferior MI who presents late, you have more than a 3-hour window before you lose your advantage of PCI over lysis, and therefore, PCI may be a better treatment option.
Q: In light of the results of research conducted by Alexander et al., could you discuss the need for calculation of renal function and subsequent dose adjustment?
A: Alexander, et al. found that we often excessively dose our elderly patients. What we have learned is that if you fail to downwardly adjust the dose of medications like integrilin, enoxaparin, and other similar agents in the elderly, there may be excessive bleeding. Sometimes, creatinine is used to adjust doses for the elderly, but it has been found that creatinine is not a very sensitive method of gauging kidney function. Creatinine clearance, on the other hand, is a much better measure of kidney function, as it accounts for age, gender, weight, and other factors. Therefore, creatinine clearance should serve as our guide for dose adjustment, and, in general, we need to be much more vigilant and aggressive in adjusting doses in patients with creatinine clearance less than 50 mL/minute.
How to ask a question
Dermatology FAQs
Digital Imaging: Improving Dermatology Patient
New FAQs Coming Soon!
How to ask a question
Diabetes FAQs
Managing Insulin Therapy: From Hospital to Home
Q: Can you review the concept of the 1800 rule, as well as insulin-sensitive versus non-sensitive?
A: Dr. Bruce Bode in Atlanta developed this concept. For most patients with type 1 diabetes, he found that the 1500 rule works. In this concept, you divide the usual daily dose of insulin by 1500. For example, if it’s 50 units in a type 1 patient, than the calculation is 50/1500, which is 30. Therefore, it would be expected that 1 unit of insulin would lower the glucose by 30 mg/dL. So if the patient’s blood sugar is 240 mg/dL and your target is 150 mg/dL, that’s a 90 mg/dL difference and you would estimate a 3 U correction. The 1800 rule is used for patients with type 2 diabetes who are more insulin resistant and typically require more insulin to reach the same blood glucose level.
I use 1500 across the board for patients with type 1 or type 2 diabetes. I just set different target glucose levels. Dividing the daily dose into 1500 gives you a very workable estimate that reflects the amount of glucose reduction per unit of insulin, which can then be modified to reflect individual patient factors. Over time, you will see patterns that show the level of glucose reduction per unit of insulin.
Q: Nephrologists recommend not adjusting the insulin infusion or checking blood glucose during dialysis due to danger of causing the blood glucose to plummet afterwards. They believe that no matter what is done to lower the blood glucose during dialysis, the glucose baths they are using will keep the patients’ blood sugar levels around 200 mg/dL. The nursing staff is a little uncomfortable with this. In your opinion, what is the best way to handle insulin infusion for an ICU patient who is also undergoing dialysis?
A: I agree with the nephrologist. There would be little benefit to doing an insulin infusion during the dialysis, but for reasons other than those mentioned. I don’t expect blood glucose levels to plummet after dialysis with IV insulin if the levels have been maintained at an appropriate level. Patients undergoing dialysis are able to maintain a strict glucose level. 200 mg/dL is the most widely used number that they dialyze against using a glucose bath. Even if infusion was continued during dialysis, levels will hover around 200 mg/dL. Because of this, adjusting insulin infusion during the dialysis will not only provide no benefit, but will raise the projection by the nephrologist. So I would discontinue the IV prior to dialysis. When the dialysis is completed, you can restart the IV at the previous level.
Q: When an ICU patient is on his way to the OR, we usually stop the tube feeding and start dextrose (either 10% at 50 mL/hr or 5% at 100 mL/hr and send the patient on to the OR with the insulin drip infusing. Many times, we later find out that the insulin drip and glucose source are turned off when the patient arrives in the OR and the anesthesiologist runs his own fluids. Should the anesthesiologist keep the insulin drip and glucose source infusing during surgery, check blood glucose levels every hour, and manage the patient’s blood glucose with the Stockton chart as we would do in the ICU?
A: Anesthesiologists are a bit more reluctant to accept a constant IV infusion because they would like to prevent hypoglycemia during a procedure. I have found that it can be very helpful to bring the anesthesiologist into the loop and explain that everybody has a basal insulin secretion and that’s why—even with the stress of surgery and IVs—people without diabetes don’t have post surgical hyperglycemia. It is important to make sure that all members of the patient care team are reminded that basal insulin is absolutely required. It is a low dose, buffered by the glucose in the IV. With frequent glucose testing during surgery, there is some assurance that adequate glucose levels are being maintained. Anesthesiologists are happy because patients are not hypoglycemic during surgery and physicians in the post-op care unit aren’t confronted with correcting glucose levels of 0, 200, 250, or 300 mg/dL. I think it’s just a case of education and respecting each others needs. Once other members of the team recognize what a basal insulin IV is going to do for them and for patient health and welfare, things seem to be better for all concerned.
Q: How do you interpret an HbA1c level in a significantly anemic patient who has not yet had a transfusion?
A: HbA1c is a measure of glucose adherence to red blood cells (glycosylation), and therefore is dependent on the lifespan of red blood cells and their volume measured as the hematocrit. In patients who are anemic—those who have hematocrits below 30 for example—there is a lower volume available for glycosylation, and thus the normal range for the HbA1c cannot be used.
In addition, diseases that produce smaller red cells, sickle cell or thalassemia for example, also distort the results. Transfusions, by introducing nonglycosylated red cells, will also lower the measured values.
In such cases, using levels of glycosylated proteins can avoid these pitfalls. The test, ordered as fructosamine, measures the glucose load for a two-week period. It is therefore especially useful in monitoring children with type 1 diabetes, and glucose management during pregnancy. The usual increase in maternal red cell mass that occurs can also make conventional HbA1c measurements difficult to apply, as the 60-90 day "look back" is not useful to the clinician. An ideal fructosamine level is 228 micromol/L or less in all populations, except that the goal is to aim for less than 200 micromol/L during pregnancy.
Q: How was the number 1800 selected for TDD and who developed the formula?
A: Bruce Bode, MD, developed the 1500 rule for use with human regular insulin, and modified it as the 1800 rule for patients using the analog insulins. To use the rule, take the average daily insulin dose and divide it into 1800 to get a value predictive of the amount of glucose lowering that 1 unit of the analog insulin will provide. For example, if the total daily dose is 50 units, using this method, 1 unit of analog insulin will be expected to provide a 36 mg/dl decrease.
This and other methods of intensifying insulin management can be found in: Individualizing Insulin Management by Walter A. Stoller, MD, Postgraduate Medicine, May 2002, Volume 111, Number 5.
Q: For patients on tube feedings, you mention using basal insulin and then also 70/30. Why couldn’t you just use a higher dose of the basal insulin if the patient is on a continuous tube feeding?
A: Using 70/30 several times a day (some physicians will also use NPH four times a day) is intended to mimic steady state insulin after a while, so you won’t have a lot of variation. It is not necessary to use any one strategy, and you are correct in stating that continuous tube feedings match up pretty well to a non-peaking steady basal insulin. So insulin glargine, for example, makes a lot of sense and actually can be used in these patients.
But one concern that most dieticians and providers have with using a longer-acting regimen in these patients is what to do if a tube feeding is interrupted, which can be fairly common. If a patient is on a long-acting regimen and their tube feeding is interrupted for more than an hour or two, you have the option of infusing dextrose that roughly matches the amount that the tube feeding would have provided until the tube feeding can be reestablished. So, although you can use long-acting basal insulin to cover the continuous tube feedings, there will need to be some plan in place to manage the risk of hypoglycemia in the event the tube feeding is interrupted.
Q: How can we develop strategies and implement protocols in our institution that will encourage the house staff to avoid using sliding scale insulin?
A: Sometimes it is automatic to use sliding scale insulin and we need to remind ourselves that we have to pay attention to each patient in order to achieve good glycemic control. One option is to provide physicians with better alternatives by developing insulin order sets that make more sense and are easy to use, so that you don’t have any sliding scale insulin options available unless the physicians write the individual orders themselves. For example, you may want to try a three insulin order program in which the basal insulin order is recorded first, meal-time insulin second, and then correction insulin is recorded last. It can be further simplified by giving each of the dosing options a check box.
Minimizing Diabetic Cardiovascular Complications: The Roles of Rapid- and Long-Acting Insulin in Maintaining Consistent Glycemic Control
Q: Should you shoot for post-meal glucose targets of less than 180 mg/dL?
A: You can definitely make a case for that. If you can get postprandial glucose levels below 180 mg/dL and pre-meal levels on target, that is a good start. However, if HbA1c levels are still above 7, then you may want to be more stringent in further reducing glucose levels.
Q: If you are trying to attain tight glycemic control with insulin, is there a risk of hypoglycemia? If so, is that a potential danger for patients with heart disease?
A: When you tighten glycemic control, especially with insulin, you generally increase the risk of hypoglycemia. Although you want to try to minimize hypoglycemic events, there isn’t really any major cardiovascular risk associated with such events. You shouldn’t let the potential for hypoglycemia deter your attempts to tightly control glucose levels.
Q: How do you decide which insulin to use for basal coverage? With the availability of glargine and detemir, is there still a role for NPH insulin?
A: I’m not sure there’s much of a role for NPH any more. If you have a patient who refuses to take 3 or 4 injections a day, someone who just won’t take that lunch injection, you may still be able to offer NPH in the morning, but the basal-bolus concept essentially precludes using NPH.
As for choosing which insulin to use for basal coverage, glargine works for 24-hours in probably 90% of patients. The other 10% or so require glargine injections twice daily. For those patients, I sometimes try detemir to see if they have the better day-to-day variability that has been touted with that agent. For other patients, twice daily detemir is a reasonable alternative.
How to ask a question
Oncology FAQs
Advances in the Treatment of Metastatic Gastric Cancer
Q: Do you expect to see a decrease in gastric cancer rates in the future due to further recognition, and eradication of H. pylori in Western countries?
A: In industrialized countries, the rate of gastric cancer has decreased, which may be in part because of H. pylori eradication. However, it is more commonly thought to be due to industrialization that has resulted in less reliance on smoked or canned goods and an increased reliance on refrigeration. One aspect about treating for H. pylori is that there seems to be an inverse relationship with the incidence of GE-junction cancers. This seems to suggest that there may be a protective effect of H. pylori on the development of GE-junction cancers. I think we will continue to see a decrease in gastric cancer diagnosis, but as a whole, gastroesophageal disease will remain significant.
Q: As endoscopic ultrasound becomes more widely available, do you anticipate that it will be more broadly used in gastric cancer diagnosis, and, if so, given its limitations, would this modality need to be coupled with another approach?