Kevin is surprised that there is so much acute care ..

Christian (Red) impressed with the am't of stuff Family Physicians needs ta know. 

Mike (short hair) impressed with how much time one can take off.  Here's an interesting article on family physicians and time off.

Guy in hat (Dale) .. was compelled by the ancillary team efforts that can occur in family medicine .. lotsa opportunities.

Bill was impressed with how nice family physicians are.  Yeh .. we are all cool too.  So warm and fuzzy.

Marina was struck with how it just makes sens that the FAMBILY sees the same physician.

Samantha worked with Dr Bob and she was impressed that he has to play so many roles ... such as ..

• Counselor
• Beahvioral Health Counselor
• Nutritionist
• Maternal Care Provier
• Medication Advisor
• Natural Medicine Consultant
• Evidence - Based Lunatic
• Health Educator .. use the 'fake RX to make them happy

...

At first it was scary but then when it was nut so scary it was easier.. It was supposed to be EBM ... but it's also useful for more causual "fyi" tricks of the tade with each other ..

blah blah blah

Case History:

A 42 yo male comes with complaints of a dull ache in his left suprapubic region. He states that the ache is worst when he extends his torso. He says that his father had an inguinal hernia that he "let go too long" and had complications. He is very concerned that like his father, he has an inguinal hernia. On physical examination, there is an asymmetric bulge over the left suprapubic region. The hernia exam was positive on the left, and not the right. It was not determined whether this was a direct or indirect inguinal hernia. The patient was referred to surgery.

Differential Diagnosis:

Inguinal hernia is neither the only type of abdominal hernia nor the only source of abdominal pain. This case is a straightforward example of an inguinal hernia. For a review of other types of hernias and other causes of abdominal pain see http://www.aafp.org/afp/20010801/431.pdf . Inguinal hernia requires surgical repair, but a family physician must be ready to answer patient’s questions about surgical repair for this common type of injury.

What does the literature say?:

The two common types of surgical repair for inguinal hernia are laproscopic inguinal hernia repair (LIHR) and conventional open inguinal hernia repair (OIHR). A recently study ( http://www3.interscience.wiley.com/cgi-bin/fulltext/106562715/PDFSTART ) compared outcomes of LIHR versus OHIR. This meta-analysis of 29 clinical trials analyzed many end-points including complication rate, hernia recurrence rate, duration of operation, duration of hospital stay, return to normal activity and return to work. LIHR performed better in four of the six end-points: the rate of post-operative complications (odds ratio 0.62 with 95% CI), days to return to normal activity (mean 4.73 days sooner), days to return to work (mean 6.96 days sooner), and time to discharge from hospital (mean 3.43 fewer days). However, LIHR had a higher risk of short-term hernia recurrence (odds ratio 1.51 with 95% CI) and an increase in the time of operation (mean 15.20 mins longer).

Why is this information important and what did I learn?:

This information is important because it will help a primary care physician answer patient questions about a surgical procedure for which you are referring them. Patients will have questions and apprehension about a surgery, as the patient in this case did. With the data provided in this article, a primary care physician would be able to explain surgical options, as well as the risks and benefits. This information impacts patient care because after the surgical repair, you will still be the patient’s primary care physician and must be educated about the potential complications that may result from the procedure performed on your patient.

A stylishly dressed overweight 25 year old woman was complaining of sharp pain in both wrists, especially (but not exclusively) when she moved her wrists. The diagnosis of carpal tunnel syndrome was a little dubious, as the pain she described did not quite fit the profile of median nerve compression and carpal tunnel inflammation. My preceptor decided to do a little more investigating before he started the treatment.

My question: What are the options for treatment of carpal tunnel syndrome in this woman?

A systematic review examined the treatment options for carpal tunnel syndrome. About 50% of patients will get better on their own with no intervention. Local corticosteroid injections and to a lesser extent oral corticosteroids also had high success rates. Wrist splinting was a good option, but non-compliance was high. However, compliance was increased if the wrist splint was only to be worn at night (many patients only experience symptoms at night, and so this may have been an even better treatment modality). Surgery had mixed results - those patients who elected to have the surgery within 3 years of the onset of symptoms fared better than those who waited and had the surgery later. Nerve and tendon gliding exercises, yoga, and chiropractic treatment were found to have little benefit but also little harm. NSAID use, however, was contraindicated because it had little efficacy and resulted in unpleasant gastrointestinal side effects.

For this patient, probably the best and least invasive treatment would be to use the wrist splint at night and to relieve symptoms. Most likely the carpal tunnel syndrome (if that was what it was) would cure itself. If the patient continued to have symptoms, corticosteroid shots – or most likely the oral pills as this patient was afraid of needles – would be the next step. If the corticosteroids failed to relieve the wrist pain, then surgery should be seriously considered.

Case:  While seeing patients with obesity, DM type II, and hypertension, it is always prudent to give them evidence-based advice about dietary modifications that would lead to decreased likelihood of long-term complications and mortality.  I have been talking to my patients about the immense benefits of following the Mediterranean diet and I finally searched the literature to find some evidence to back up my beliefs.  I honestly think that it would be more effective if showed this data to our patients (and explained it in simple language) instead of just telling them to stay away from fats and sweets or “put some windex on it.” =] Salut!!

 

Question:  Does a Mediterranean diet reduce mortality?

 Summary:  It's hard to go wrong with pasta, olive oil, and red wine, and it may even make you live longer! There have been numerous ecologic studies suggesting that a Mediterranean diet high in vegetables, legumes, fruits, nuts, cereals, olive oil, fish, and alcohol; moderate in cheese and yogurt; and low in saturated lipids, meat, and poultry is associated with greater longevity. This is the largest prospective study to date of this hypothesis. The researchers identified 25,917 community-dwelling Greeks, and excluded 3874 with coronary heart disease, diabetes mellitus, or cancer at enrollment. They did a detailed assessment of diet and lifestyle, and rated the participants adherence to the Mediterranean diet on a scale from 0 (not at all) to 9 (perfect adherence -- lots of veggies, seafood, wine, and pasta!) The median follow-up was 3.7 years. This was not a randomized trial, so the outcomes were adjusted for age, sex, smoking status, body mass index, and energy expenditure. The mean body mass index was 28.1 for men and 28.8 for women, making them a slightly pudgy group; 60% were women and more than half of all participants had never smoked. Other than the ratio of monounsaturated lipids to saturated lipids, individual dietary factors were not associated with mortality. However, every 2-point increase in the Mediterranean diet score was associated with a 25% reduction in the risk of death from any cause, a 33% reduction in the risk of death from coronary heart disease, and a 24% reduction in the risk of death from cancer. The benefit was greater in women, in persons older than 55 years, in never-smokers, in heavier folks, and in sedentary persons.

 

Significance:  This excellent study lends further strength to the association between a Mediterranean diet (rich in vegetables, legumes, fruits, nuts, cereals, olive oil, fish, and alcohol and low in meat) and a reduction in all-cause morta
 

I like pediatrics. A mom brought in her newborn baby boy with concern about her baby's cord. The cord remnant was still attached to the umbilicus, but only by the paired arteries and the vein. The little remnant was grey, boggy, and smelled a little off. The kid's mom had been cleaning the cord with soap and water, as instructed by the OB nurses at the community hospital where she delivered. This is called "dry cord care" for some reason.  Alternately, cords are cleaned using isopropyl (rubbing) alcohol.

Which one is better? Alcohol or soap and water? Turns out that alcohol is the answer. Babies whose cord stumps were cleaned with soap and water were significantly more likely to be colonized by lots of different pathogens and foul odor or exudate was also more common. Omphalitis can be a dangerous infection, prevent it by recommending swabbing with alcohol.

Having seen quite a few jaundiced babies the past month, I've been trying to get an idea for which of them need to have their bilirubin checked. Breastfeeding is common in the patient population here, so physiologic jaundice is pretty common. None of the reisdents or preceptors could really give me a good evidence-based bedside test to triage jaundice babies, so I asked my old pediatrician. He found me an ancient article that addresses this issue in a very old-timey doctor kind of way. Dermal icterus progresses from head to toe in a predictable way:

Where              Range of Total Bilirubin

Head                 4.3-7.8    

Chest                5.4-12.2

Pelvis                8.1-16.5

Extremeties     11.1-18.3

Hands and Feet    >15

Here's a look at phototherapy and how to treat jaundice - treatment depends on how old the kid is and there gestational age.. BTW - there's an element of breastmilk that inhibits the glucoronidation of indirect bilirubin, making breast-fed babies prone to jaundice ("physiologic jaundice"). Good luck on the exam.

Thanks for your attention and good luck on the shelf!

Case History:  A 45 year old female patient presented to the office for a followup of her hypertension for which she is taking motorprolol.   She claims that she has had significant weight gain over the last six months and attrributes it to her feeling "down" and not wanting to do anything.  She seems to have a somewhat apathetic attitude towards taking care of herself.   It is important to agknowledge at this point that a true psychological problem might exist, and also that the link between depression and weight gain has been previously established.  What does this tell us about the need to screen for depression? 

A very interesting article from the journal Family Practice seeks to provide us insight into the relationship between various independent variables and weight gain.  In this sample of women aged 35–47 years, psychological factors were the major predictors of gaining 10 lb during a 4-year follow-up period. Few of the other measures, including baseline hormone values, were correlated with subsequent weight gain. These findings suggest that screening for depression and anxiety may be important clinical assessments to identify women at increased risk of substantial weight gain.

Two patients this past week helped make me look good. The first was a 37 year old female with anhistory of bipolar D/O. She is married, with two children. She moved to the area last year, and first presented to our practice for a PCP visit last March, when she was depressed and borderline suicidal. She had a history of bipolar D/O, but no note to that extent was made in the chart at the time. She had been on SSRI's in the past, but did not like the sexual side-effects of the SSRI's. The MD who saw her in March, apparently blind to the Bipolar Hx, started the patient on a combination of Zoloft and Wellbutrin. (BTW, anacdotal reports are that the addition of low dose Welbutrin to a low-dose SSRI tackles depression well, and mitigates the anorgasmia typical with the SSRI's alone!) Within a month the patient was fired from her job, was sleeping less than four hours a day, and was self-medicating with alcohol at the rate of 4-5 beers/day. She made it for six months like this, driving her family and friends nuts. One evening last week she found herself sanding the hardwood floors in her kitchen at three in the morning because they looked dirty and she was overcome with an urge to refinish them. It was at this point that she realized something was wrong and she called to make an appointment. Being in the room with her was exhausting, she spoke twice as fast as me, was animated, laughing and smiling, and never sitting still. We switched her to a mood stabilizer (Depakote) and kept her on the Wellbutrin with an appointment to F/U in two weeks and a referral to the psychiatric NP in our practice.

Patient two was a thirty two year old depressed female. She is out of work with a (legitimate) back injury, living with her boyfriend (also depressed). She has been depressed about her work and injury status, and feeling the "I had never pictured being here at 32 years old, WTF is happening with my life?" anxieties. She came in after two episodes of suicidal ideation. The first she got through on her own. The second caused her to call the county crisis hotline number. She is currently on Zoloft at 75mg/daily. On further questioning, she had had S/I in the past, when her father was ill with cancer three years ago. She had her Zoloft bumped up to 150mg daily at the time. After her father past away and her llife stabilized, still taking the 150mg Zoloft daily, she left her husband, met and left a boyfirend, quit her job, moved to Minnesota for a guy she met online, dumped him, started binge drinking, had sex with ten men in a one month period, and spent all of her life savings. Thinking at the time that perhaps the Zoloft was not needed, she self d/c'd it. Three weeks later she moved back to NY and met her current boyfriend. They have been together for two years. Her depression cropped up again after her work injury five months ago and started on the Zoloft again at 75mg.

So, do we increase the Zoloft to 150mg again? Heck no! By asking about her manic history, it becomes apparent that this patient typifies the Type II Bipolar disorder, that is a bipolar disorder with predominant depression. If we give her just antidepressants, we will lift up the depressed moments, but the normal days will become manic ones. The appropriate first line management for this patient is a combination of a mood sabilizer and an anti-depressant, typically wither an SSRI or Welbutrin.

Conveniently, I had gone home a the end of the day and had read "Bipolar depression: pharmacotherapy and related therapeutic strategies" after patient number one, and was able to totally impress my preceptor when patient two came in. I humbly recommend that you do the same.

After discussing bipolar d/o with the patient, you could see a light-bulb go on over her head as she exclaimed, "Yes! Thats me!" She left with a prescription for Seroquel to add to her 75mg Zoloft, no refills, and a f/u appointment with the same psychiatric NP the first patient went to. By not giving her any refills, we guaranteed we would see her in the near future and get her into the right care. We also discussed her S/I, made sure she had a plan in place if they recurred, and signed a no-harm contract with her.

Without investigating for the history of Mania, it is easy to misdiagnose a depressed bipolar patient as suffereing from a purly depressive mood disorder. The subsequent misguided pharmacotherapy had disasterous consequenses for patient 2 in the past. Make sure you look for it. Depression is the presenting symptom for bipolar patients in over 70% of cases.

Background:  Pica is an eating disorder characterized by the compulsive intake of non-nutritive substances such as dirt, clay, soap, and ice.  If dirt is your cuisine of choice, we call it geophagia.  Those who prefer to eat ice would be said to have pagophagia.  Indeed, the description of this peculiar phenomonenon goes back to Greco-Roman civilization, and patients of all ages even today are walking in with these strange compulsions.

Question:  What do a pregnant woman who eats dirt, a child who eats clay, and a middle-aged woman who eats ice have in common?

Answer:  Iron deficiency anemia.

Discussion:  Pica is a frequently underestimated problem, especially during pregancy.  One article indicates a prevalence of pica during pregnancy as ranging between 8 and 65%, and more specifically 23 to 44% in Latin America.  It is hypothesized that the unusual cravings are due to iron deficiency anemia.  An observational case control study done on children with pica in India found that the plasma iron and zinc levels were 20% and 45% lower, respectively, than in matched control children without pica.  Furthermore, a case report described a 42-year-old woman with severe iron deficiency anemia possibly related to chronic gynecological bleeding who was also found to eat about 80 ice cubes per day over the last 5 years.  After iron supplements corrected her anemia, the pagophagia completely disappeared in less than 15 days and did not recur for the entire year during which she was followed.

Conclusion:  Iron deficieny anemia may be the cause of unusual cravings for dirt, ice, cornstarch, etc.  This compulsion may be cured simply by adding iron to the diet.  Be sure to especially ask your pregnant patients about unusual cravings.  If patients come in describing these peculiar cravings, check their hemoglobin and hematocrit and try iron supplements.

Author's note:  Admittedly, the evidence to support iron deficiency anemia as the cause of pica is limited.  But when you consider that the cure would be a simple iron pill, and that a simple iron pill would not bring in the big bucks for any pharmaceutical company, and that most studies are being funded by drug companies, it's not terribly surprising.  So this is what the literature has to offer.

History:

A 27 y/o AA female pt. is seen in our Wall Street Clinic for a BP check and on exam I noticed a diffuse, symmetric, hypopigmented macular rash with confluent semi-circular borders on the pt.'s back.  The pt. remarked that her rash happens when she eats "acidy foods like tomatoes and ketchup." It turns out that she is always eating these acidy foods, but does not always have the rash.

Discussion

As you can see in these photos (especially the top one), her rash (and upon further questioning her history) was pathognomonic for Tinea Versicolor infection.

In caucasians and light skinned individuals, Tinea manifests itself as a hyperpgmented macular rash with confluent borders. Upon significant sun exposure, only the surrounding skin tans resulting in a hypopigmented macular area. African americans and darker skinned individuals present with Tinea infection with HYPOpigmented rashes. See here for specific description of signs and symptoms.

There are NO known diet restrictions that would prevent recurrence of Tinea (so grab those 20 ketchup packets).

Keep in mind that derm differentials are extensive so leave room for error -

DDx-

Pityriasis alba

Vitiligo

Seborrheic dermatitis

Nummular eczema

Treatment

Succesful treatment may be sought via Itraconazole 1 day/month or Ketoconazole shampoo (Nizoral)

 

In summary, tomatoes don't matter.

Each day a patient (or more like 20 patients) walks into the clinic with cholesterol problems.  Diet and exercise are of course the 1st-line treatments, but in the patient population of downtown Schenectady, I haven't seen this work yet.  So, we put these people on different drugs depending on their specific lipid problems.  You know, a fibrate like Tricor if we want to get their triglycerides down, niacin if we really want to work on their HDLs (and if they can tolerate the stuff), and of course a statin for LDLs.  Zocor, Lipitor, Pravachol, etc...these guys are the wonder drugs of cholesterol, right?  Well, kind of, until you put a patient like Patrick on a full dose statin and either its not working as well as it should or he starts getting myalgias. 

So, what is our recourse?  Well, the newest member of our arsenal is Zetia (ezetimibe).  My question is whether or not the patients we are putting on this newbie are getting any benefit.  So I tracked down this study that looked at almost 800 patients who had primary hypercholesterolemia and added 10 mg of Zetia or placebo to their previous statin regimen.  Sure enough over 70% of them were able to reach their LDL-C goals compared to less than 20% on the statins alone.  Since Zetia works by blocking cholesterol absorption you are probably thinking that these patients were on the can 6 times a day.  According to this study, however, no differences in adverse effects were reported.  Cool.  To bad the study only lasted for a few months.    

Anyway, if your patient isn't so thrilled about his muscle pains on full-dose statins, throw some Zetia into the mix...at least for now.        

Football players and infectious mononucleosis go together like oil on teflon. But a few weeks ago these two characters met in a duel. In one corner stood the formidable opponent – a 17yr old football hero, his brain is saying to get back into the game, his spleen is saying, "hold on there a minute, buddy." In the other corner – Mr.Mononucleosis, a lean mean spleen-rupturing machine. And the doctors in a small-town clinic in Berne got to play referee.

Two weeks ago our friend the football hero came down with a case of mono. He recovered quickly and presented to our clinic for a recheck. Examination revealed no lymphadenopathy, no splenic enlargement and a patient who was feeling great with no signs of fatigue. To his dismay, however, he was told that he was to stay away from contact sports but would be allowed to stand on the sidelines and engage in activities that did not involve any direct tackling/trauma. He agreed and all was said and done… until 3 days later. The night before his symptoms set he decided to go for a light jog to get back into shape for the upcoming sports season. The next morning he appeared in our office with severe 12/10 pain, guarding around his left quadrant, and an inability to lie flat on his back due to the extreme pain. We rushed him to Albany Med’s ER where a CT scan revealed splenic enlargement with no signs of rupture and normal labs. Diagnosis - ?. Treatment – fentanyl and an overnight admission to D7 for observation. Thankfully his spleen had not ruptured and was most likely causing pain by pressing against the abdominal wall. But how could a light jog have caused such symptoms? And what level of activity should we recommend for future patients recovering from a bout of mono?

Athletes do seem to recover quicker than non-athletes according to two studies comparing West-Point cadets to Yale undergraduates. (no offense to all you buff Yale grads) However, this may be a reflection of an enhanced desire or perceived need for the athletes to resume more strenuous activities than true recovery from the illness. Athletes, in general, should wait atleast 3-4 weeks from the onset of their illness to return to weightlifting or strenuous activity. Furthermore, if the athlete is going to engage in a high-risk, collision, or contact sport at such a time, radiologic evaluation of the spleen may be necessary. Simple absence of splenic enlargement on abdominal palpation may not be enough.

Such guidelines beg the question of whether light jogging would fit under the category of "strenuous activity." Currently our patient is recovering and has not had any more complications. He was discharged the following day and sent home with pain medications. Lucky for him he did not experience a splenic rupture—a situation presenting with a grave prognosis due to the highly vascular nature of the spleen. As for football season, unfortunately our patient will be cheering in the stands rather than playing on the field this year.

Case History:  A 31 year old woman presented with the feeling that the room was spinning, and her symptoms were made worse by movements of her head, i.e., when shifting positions in bed.  Patient denied vomiting.  To make a diagnosis, the doctor will often perform a test called the Dix-Hallpike maneuver. In this procedure, the doctor holds your head in a certain position and asks you to lie quickly backward over a table. As you do this, the doctor will look for abnormal eye movements and ask if you experience vertigo.

The most effective treatment is a procedure called "Epley's maneuver", which can reposition the stones inside your inner ear.  Occasionally, medications such as antihistamines, anticholinergics, and sedative-hypnotics may be prescribed to reduce the symptoms of vertigo, although these are often minimally effective.

The article cited here talks about a modified Epley's maneuver for the self treatment of benign paroxysmal positional vertigo.  Patients with suspected benign positional vertigo can be instructed to perform the Epley's maneuver, as outlined in the article, with expectations that the vertigo will improve with time. 

 

Case History:

A 16 yo female comes with complaint of left lower back pain for the past 4 days. The pain is worst when she urinates. She was diagnosed with Crohn’s Disease 2 years ago and is being treated by a gastroenterologist. She is not currently having an exacerbation of Crohn’s, and reports that she has never felt this pain before. She is not sexually active and at the time of the visit was having her menstrual period. On physical examination, the patient had LLQ tenderness, with no rebound or guarding. The left lower back pain was not reproducible on palpation.

Differential Diagnosis:

The differential diagnosis of LLQ tenderness in this patient is complicated due to her Crohn’s disease. It is possible that the back pain and LLQ tenderness is an atypical Crohn’s exacerbation for her. Patients with Crohn’s disease are also at risk for ureteral stones and fistulas. The fact that the pain is worse with urination suggests the presence of a stone. It is also possible that her back pain is due to menstrual cramping. In a typical female, the differential diagnosis of LLQ tenderness includes ectopic pregnancy, PID, and ovarian cyst. Since the patient is a virgin, ectopic pregnancy and PID is unlikely. The diagnosis of a cyst is supported by the onset of pain during menstruation. The patient was sent for an abdominal ultrasound that revealed a 3cm by 3cm cyst on her left ovary.

What does the literature say?:

This case is complicated and I honestly did not think of ovarian cyst at the time as a possible diagnosis. The literature confirmed that ovarian cysts are common lesions that are frequently overlooked and misdiagnosed. A retrospective analysis of 134 females under age 19 showed that ovarian cysts account for 60.4% of ovarian lesions in the pediatric population. The second most frequent lesion was neoplasm at 32.8% of the lesions.(http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15301042)

Another study demonstrated that ovarian cysts can be confused with other conditions in adolescents, especially appendicitis. In this study (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15094575) 297 adolescent females that had either appendicitis or ovarian cysts were studied retrospectively. Of these females, 38% were given a preliminary diagnosis of appendicitis in the ER, 3 of whom were eventually discovered to have an ovarian cyst at surgery.

Why is this information important and what did I learn?:

This information is important because it might save a patient unnecessary and possibly invasive diagnostic procedures. When patients present with abdominal pain gastrointestinal causes are frequently thought of first. However, what the above studies suggest is that in adolescent females, one must also consider ovarian lesions. In this case a mis- or non-diagnosis would be costly, since complications of ovarian lesions range from infertility to death.

Last week, a 19 y/o male came into the office with cough and sputum production.  He said that he had to go to the Urgent Care clinic because his 'cold' symptoms had gotton so bad.  The urgent care clinic had diagnosed this patient to be having an acute episode of bronchitis.  Good.  What did they give him? Azithromycin.  Not good.

We all know that patients like to get something from the doctor when they come into the office, but sometimes antibiotics are completely the wrong thing to do.  It ends up that the most common causes of bronchitis are viral in origin.  Convincing the patient that these signs and symptoms will go away without antibiotics may be difficult, but it is the right thing to do.  Obviously, bacterial causes for bronchitis and pneumonia should be rules out with a CXR, but if a patient comes in with 'run of the mill' bronchitis, routine antimicrobial use is actually not recommended (Ann Intern Med 134:521, 2001).  

So what do you do -- say 'you got bronchitis. sucks for you.'  Well you gotta so something, and you should do something.  If you know its influenza, raminadine is a good idea, but it is often only helpful within the first 48 hours of disease.  If the patient wants to feel better, help him reduce his symptoms -- cough.  Dextromethorphan, or Robitussin DM will do wonders.  If the patient is really having trouble breathing, a short acting beta 2 agonist (albuterol) may not be a bad idea. 

The point is to inform the patient that antibiotics are not a cure all.  Rather, when used in the wrong circumstances, they can be hazardous by creating resistance.  Patients must realize that viral etiologies are common causes for many common infections.  Symptomatic treatment can many times be achieved from over the counter meds, or home remedies.  If patients have this knowledge, it will greatly help us in reducing the rise of multidrug resistant bacteria.   

I saw a patient on Friday whose legs were killing her. Just from the history she gave it seemed pretty clear that she was suffering from sciatica, so I did my exam and got ready to bring in my preceptor. Before I left the room, though, I listened to her heart, lungs and carotids. I was surprised to hear a bruit that wasn't noted in her chart.

I mentioned it to the doctor and, after she told the woman that her leg pain was indeed caused by sciatica, she listened for and confirmed the bruit. The next thing the patient knows, she has a referral in her hand for a carotid ultrasound and the doctor is talking about the risk of stroke. This wasn't what she'd bargained for when she came in with sore legs, and she was visibly shaken.

So, I wondered just how good a predictor of dangerous carotid artery disease auscultation really is. It turns out that in asymptomatic patients like this one, it isn't the best. A study done at the Mayo Clinic determined that bruits like the one I heard have predictive values of 74% for atherosclerosis in the external carotid, and only 16% for intracranial atherosclerosis.

This article from the Annals of Internal Medicine (full text with some nice links to related articles) concludes that a bruit by itself is an inadequate predictor of high grade disease, but is associated with increased long-term incidence of stroke, myocardial infarction and death. So we should continue to wield our Littmanns, but should look carefully for risk factors and symptoms associated with carotid artery disease. And we should be careful about how much we frighten folks when sending them out for confirmatory studies based on what we hear.

 

The common cold is ubiquitous in the family health care setting, yet its treatment is evasive. Antibiotics? Less than 0.1% of URIs have a bacterial etiology. Vitamin C? Zinc? Lots of fluids? Gargle with salt water? Chicken soup for dinner?

R.P. was a 14 year old young woman (one of many such patients) who came in with her mother complaining of a sore throat, headache, sneezing, and myalgia. And after a quick examination she was sent on her way with no prescription, just some commonly heard advice: rest, fluids, vitamins...

Chicken soup has been used as a remedy for the common cold (and probably many other ailments) for centuries. But does it really work? There are no double-blind, randomized controlled studies to prove its efficacy, and yet... This article briefly summarized what is known about the effects of chicken soup on the common cold (as well as describing the perfect recipe for the soup): the hot vapors loosen bronchial secretions, increase nasal mucous velocity, improve ciliary function, and inhibit neutrophil chemotaxis. This interesting property of chicken soup on neutrophil chemotaxis has been shown in vitro by Rennard et al.

What about the other therapies? Some doctors are strong proponents of one therapy, and others claim that it makes no difference. Unfortunately, studies have also fallen on both sides of the fence - some clearly show the therapy makes a difference, others show no difference at all. One small study of 50 volunteers examined the effect of zinc acetate lozenges taken every 2-3 hours while awake on the duration of symptoms (sore throat, nasal discharge, congestion, sneezing, cough, muscle ache, fever, headache) of the common cold. Their study conclusively showed that the zinc acetate halved the duration of the symptoms from 8.1 to 4.5 days.

So in conclusion, there is no final verdict. Although personally I strongly believe in these questionably proven treatments, I would be curious to see how strong is the placebo effect in treating the common cold.

Something must've been in the Clifton Park water, because this past week three random guys came to the office complaining of the exact same symptoms.  They'd just be hanging out when, all of a sudden, their hearts would feel like they were jumping out of their chests.  They would get very sweaty and out of breath, even though they weren't even doing anything physical.  These were all somewhat young guys who were not at the age for a heart attack and had no other risk factors.

They had what is known as premature ventricular contractions, which are extra beats made by the ventricles.  If often makes the heart feel like it's skipping a beat or that it is beating out of one's chest.  It doesn't usually last very long and comes and goes.  Sometimes it shows up on an ECG of an asymptomatic person.  Ninety-nine percent of the time, PVC's are completely benign.  However, Family Practice physicians have to screen patients that complain of PVC's because of the extremely rare risk of sudden cardiac death.  The prevalence of sudden cardiac death is approximately 1 in 250,000.  Certain risk factors, such as CAD or a family history of sudden cardiac death, increase the chance of having the condition. 

So, how do we screen for this rare condition?  One article describes the various electrocardiographic arrhythmia tests to assess risk in people with PVC's.  ECG's are a cheap and quick screening test for people with PVC's.  If symptoms persist or the ECG comes back abnormal, then the physician may want to send the patient for a stress test or have them wear a heart monitor to record their cardiac activity for a longer duration.

So, what did we tell them to do?  1) Cough really hard.  2)  Grab a magazine and pretend that you have to poo.  3)  Pop a couple of beta-blockers to help calm down your sympathetic system

Background:  Two very concerned parents come in with their 8-month-old baby, complaining that the baby has been tugging on her right ear and crying more than usual (for a baby).  They want to do everything they can to make their baby better and they demand antibiotics for an ear infection. 

Appropriate use of antibiotics is a big issue these days with concerns of side effects and of course resistance, so SHOW ME THE EVIDENCE!

Objective:  To assess the quality of evidence to support antibiotic therapy in acute otitis media in children under two, a population considered a risk group for poor outcome.

Design:  A systematic review was conducted searching library databases for articles from 1966 to 1997 to identify placebo-controlled trials of antibiotic therapy for acute otitis media in children under two. 

Results:  Of the possible 115 papers reviewed, only 6 met the inclusion criteria.  And of these, 2 had a quality rating under 40% and only one had a quality rating over 70%.  After all that searching, no statistically significant difference was found between children treated with antibiotics vs. placebo for acute otitis media.

Conclusion:  As mentioned previously, SHOW ME THE EVIDENCE!  The high prescription rate of antibiotics among children under two with acute otitis media is not supported by evidence from published trials.

Take Home Message:  Keep the lines of communication open with the parents about the risks, benefits, and alternatives in the treatment of acute otitis media.  Writing a Rx for antibiotics is meant to make the child feel better, not just the parents.

We are all aware of the amazing benefit of Papanicolaou smears for women who are sexually active.  It is an incredible screening tool for cervical dysplasia and has markedly improved the detection and treatment of cervical cancer.  Without a doubt, women who are sexually active (particularly if they have more than one partner) should be examined annually with a PAP smear. 

A question arises however when we consider women who have had hysterectomies for benign gynecologic disease.  Should these women continue to get regular PAP smears?  In such cases, the test would not be used to screen for cervical cancer, but rather to detect vaginal intraepithelial neoplasia or vaginal squamous cell carcinoma.  The smear would be taken from the vaginal cuff, just below where the cervical os would normally be.

I found an article that discusses the extremely low risk for vaginal neoplasia in women with prior hysterectomies.  In a study with 9610 smears from women who had undergone hysterectomies, 104 smears (from 79 women) showed abnormal findings.  After those smears were categorized, 52 were categorized as atypical squamous cells of undetermined significance, 44 were low-grade squamous intraepithelial lesions, 6 were high-grade squamous intraepithelial lesions, and 2 were squamous-cell carcinomas.  In five of the women, biopsies showed vaginal intraepithelial neoplasia type I or II, while there were no biopsy-proven cases of vaginal cancer.  The article concludes that the prevalence of abnormal findings on PAP smears after hysterectomy is "extremely low". 

So what does that mean for us?  Many clinicians still choose to do annual PAP smears on women without uteruses.  How do we then decide what to do?  This past week, my preceptor and I performed an annual GYN exam on a 48-year-old woman who had undergone a hysterectomy 15 years prior.  She did not have an oophorectomy so her ovaries were still intact.  She was perimenopausal and experiencing crampy pain on one side of her abdomen.  Because we were going to do a bimanual exam to examine this woman's ovaries, my preceptor decided to go ahead and get a PAP smear from the vaginal cuff area.  She stated that in her practice, if a woman with a prior hysterectomy still has ovaries, she does a PAP smear along with the bimanual exam.  In her patients who have had total hysterectomies and oophorectomies and who do not need bimanual exams, she does not do a PAP smear.  After all, as seen above in the article, the risk for vaginal cancer is very low. 

Now to me, this seemed like a nice practice guideline.....if you are going to do a bimanual exam on a woman, go ahead and get a smear of the vaginal cuff since it is such an excellent screen for vaginal neoplasia.  However, if there is no bimanual exam, don't put the patient through the discomfort of an annual GYN exam with PAP smear to screen for such a rare disease.

Note:  This is all in reference to patients who do not have any added risk factors for vaginal cancer such as HPV infection, prior cervical cancer, smoking, and having a mother who took DES while pregnant (b/w 1940 and 1971).  Such women with risk factors should continue to be screened for vaginal neoplasia, even after a hysterectomy.

We're enjoying your posts -- and we're learning a lot.  I hope that you all are learning from your patients, preceptors .. and your colleagues through this assigment, of course).

I posted a few times early in the rotation (1,2,3) and outlined for you how I think that this exercise should be undertaken.  I'll repeat myself a bit here .. as it seems that several of you need a reminder. (hint, hint).

This assignment is to DOCUMENT the learning that you are doing in your practices .. and to EDUCATE your colleagues.  Since you are all having different experiences and reading different atricles, this exercise should be a way for you to share important information with each other.

What's important information?  We're hoping that you learn the concept of POEMs.  Here's another good review.  This is old hat for you by now - right?

What's a POEM?

1. They address a question that we face in clinical practice. 
2. They measure outcomes that we and our patients care about: symptoms, morbidity, quality of life, and mortality.
3. They have the potential to change the way we practice
   

So the POEM part is relevant to how you select your article.  The next part that's important is how you present your work. 

Your readers would much rather see a link to the interesting article (or the abstract) instead of a reference.   References are so '90's ... c'mon folks, this is 2004 ... I'm even thinking that we should make links to the full text, pubmed or hubmed resource required, and full references forbidden.  Perhaps this would get the point across!

You needn't write a long essay -- nor do you need to format the entry so formally as most of you are doing.  Recall that I told you that the primary audience is the other students.  Do you really talk to each other this way?   I doubt it.  So lighten up.  This is supposed to be fun AND educational .. not so formal as many of you are writing.  I think you're making it a more difficult assignment than it needs to be!   

Oh, One more Thing.  If you are pasting the entry from MS-Word or another editor .. or from the Internet, please do a little select-all once you get the text here and change the font to Arial and xx-small.  It will make things much easier to read. 

A 55 year old woman with stage 2 hypertension came in for a regular check up. Her hypertension was well controlled with medications, but during the visit she mentioned that she likes to work in her garden and that she had already been bitten by two ticks during the summer - one last week and one two months ago. She was concerned about Lyme disease and asked if there was some kind of test that could be done to see if she was infected. The doctor was reluctant to order the test, as the patient was asymptomatic. (The serum test for Lyme consists of an ELISA test for IgG and IgM against Borrelia burgdorferi, followed by a Western blot to confirm.)

Question: How useful is this test in this patient? Under what circumstances should a patient be tested for Lyme disease?

According to this article (1), the false positive rate is very high, especially in low-risk patients. In fact, the diagnosis of Lyme disease should be a clinical one and the serum test should be done only to confirm what is suspected clinically. This article cited another one (2), a review of literature, which recommended testing for Lyme only if the pretest probability of having the disease (do these words sound familiar?) is between 0.20 and 0.80, because if the pretest probability is low (ie. the patient has few clinical signs of Lyme disease), and the serologic test is positive, it is most likely a false result. So the doctor was right in explaining to the patient that testing her for exposure to Lyme disease in the absence of symptoms was ineffective.

References:

1. A Review of Lyme Disease

Brown SL, Hansen SL, Langone JJ. Role of serology in the diagnosis of Lyme disease. JAMA. 1999 Jul 7;282(1):62-6.

2. Laboratory Evaluation in the Diagnosis of Lyme Disease

Tugwell P, Dennis DT, Weinstein A, et al. Laboratory evaluation in the diagnosis of Lyme disease. Ann Intern Med. 1997;127:1109-1123.

3. More About Lyme Disease

 

Case History

A 26 year old male with a history of asthma and allergic rhinitis presents to his family practice physician.  Patient occasionally has exacerbations when attempting to perform any sustained physical activity.  The patient has been on the long-acting beta₂ agonist salmeterol qD.  Patient has tolerated the medication well and has had no adverse side effects.  No other significant past medical history.  Immunizations up to date.  NKDA.  Family history significant for diabetes mellitus (maternal father).  Occasional alcohol use.  Denies tobacco use.  Review of Systems negative.

This meta analysis is very important for proper initial management of exacerbations in adults with asthma.  It is well known that the optimal treatment for a patient at the family practice level will depend on both the information available regarding efficacy of treatments and information from patient feedback.  It is reasonable, therefore, that patients with asthma are treated via different mechanisms, but a starting point for treatment should consider the above information:  Inhaled corticosteroids in combination with beta2 agonists provide the greatest reduction in exacerbations in adults with asthma.  Patient feedback regarding tolerance, side effects, and efficacy will ultimately fine tune the treatment.

Case History

A 48 year old male presents with a chief complaint of a painful, swollen right first metatarsal.  The patient has a past medical history significant for hypertension and gout.  The hypertension is treated with a beta blocker.  He is presently on indomethacin (indocin) 25 mg QID.  He is presenting with an exacerbation of his gout.  Family history significant for gout (father).  Social history significant for frequent alcohol use (beer) and a diet high in animal meats and protein.  Review of systems negative except for painful right first metatarsal.  Patient had been previously advised of the necessity for changes in diet and lifestyle.  Blood test shows elevated serum urate levels.  Patient was started on a course of allopurinol

The information presented in the article is very important in understanding the treatment protocol for patients with gout.  The acute exacerbation of the gout can be often adequately treated with analgesic drugs like indomethacin, however, in cases of chronic hyperuricemia due to overproduction, the xanthine oxidase inhibitor allopurinol may also be used.  This is important for treating the acute exacerbation of gout as well as controlling future recurrences. 

 

What was Learned?  It is important to recognize from this case that a number of diseases are treated with combination therapy in order to exploit differences in the mechanisms of action of various drugs.  In this case, statin drugs with niacin were used to aggressively treat the patient’s LDL-C and HDL-C, respectively.

Patient Impact:  In the management of dyslipidemias it is important to optimize the patient’s lipid profile with respect to LDL-C, HDL-C, and TG in order to achieve maximal CAD risk reduction. 

The diet debate has been going on for years now:  Atkins, South Beach, Zone Diet versus the traditional low-fat, low-calorie diets.  At least two out of every three patients that walk through the office I'm at get the nutrition lecture.  But my preceptor doesn't give them the standard low-fat, low-calorie deal; rather, they are urged to get into the "Zone."  The Zone diet is basically a modified Atkins that focuses on an ideal protein/carbohydrate ratio.  The plan emphasizes low-carb, high-protein choices (lean meats, nuts) in addition to fruits, vegetables, and dairy products.  It shuns the high-carb (and low-protein) breads, rices, pastas, and potatoes.  My question is, of course, do the data prove it works?

Well, I couldn't find anything that looked at the Zone diet specifically but a few recent studies have compared low-carb diets to traditional low-fat diets.  Here's one of those studies:  So last year the New England Journal published a study that took 63 obese participants (with no other co-morbidities per se--i.e., they were not diabetics but they probably had some insulin resistance going on) and randomly split them into two diets.  The first group was to eat low-carb, high protein, high-fat foods while the others stuck with high-carb, low-fat, and low-calorie menu options. 

So, what did they find you ask?  Well, the low-carbers lost more weight at the 6-month mark, but by one year the differences were no longer statistically significant.  In addition, the study found that the low-carb peeps also had greater decreases in their triglycerides and greater increases in their HDL (more than could be explained by weight loss alone).  In fact, the traditional dieters dropped their HDLs--a known protector against cardiovascular disease. 

Atkins for everyone?  Well, not so fast.  Following sixty-three participants for 1-year hardly has the statistical power (or something like that) to invert the food pyramid, but at least for the time being I don't have to feel bad about telling our obese patients to reach for the peanut butter and celery instead of the wheat bread.    

My preceptor and I were working up a patient with problem hypercholesterolemia whichn had proven refractory to two different statins. The patient was also treating his "heart" condition with diet and exercise and with a number of suppliments he had been taking. The suppliments in question included, among other things, 1600u of Vitmin E a day, 1000mg vitamin C, flax seed oil, fish oil, selenium, etc. There were a total of about 26 a day. I wondered if he just put milk on his pills in the morning for breakfast. My preceptor commented that the patient probably had the most expensive urine of anyone in his practice, and said that he recalled a study in NEJM a few years ago which found that Vitamin E and statins had an antagonistic effect, but couldn't remember the specific. Being a good little clerk, I ran off to the computer to find the study in question.

I had heard that Vitamin E was "good for your heart." I, in fact, with a family history of males dropping dead of CAD in thier fourties, have been taking 800u of it daily with my Lipitor, presuming it to be doing me some good. It says right on the bottle from GNC: "good for heart, blood vessels. etc."

Unfortunately, such were not the findings of a study published in NEJM in 2001, "Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease." Statins are now firly well documented to provide cardio-protective effects. They also have a great LDL lowering effect, but not much of a boost in patient's HDL levels. Niacin, on the other hand, shows a great boost in HDL levels, but not much of an effect on LDL. Several epidemiologic studies (Framingham et. al.) have documented a presumed protective effect of antioxidants on cardiac health. The autors randomly and in blinded fashion assigned people with known previous CAD and similar lipid profiles to receive either Vitamin E, Vitamin C, beta-carotene, and selenium; simvastatin and niacin; or both. Patients has angiogram before randominzation and again after three years. The authors were looking for a change in proximal coronary artery stenosis. Secondary patient oriented clinical end-points of death, AMI, CVA, and need for angioplasty were also followed. The authors found the least degree of stenosis and disease end-points in those who received both simvastatin and niacin, but not antioxidants. Those who received antioxidants alone had the worst outcomes, and those who received both were in between. Take home lesson? If you've allready got CAD, the statin/niacin combo may be of greater benefit without supplimentary antioxidants.

This study was limited in that there was no placebo group. No effort was made to establish whether antioxidants were better than nothing in patients who were not taking statins. All patients had pre-existing CAD as documented by symptoms, history, and angiography. No effort was made to tease out the individual effects of the antioxidants, Is it beta carotene interfering with a statin while Vit E, C and selenium are doing good? Or are all of them attenuating the statin effects? For that matter, is the interaction between the antioxidants and niacin, or the antioxidants and simvastatin? Or only the combination of all  three? The only real direction I have for the application of antioxidants is in the preexisting CAD patient taking BOTH simvastatin and niacin. Still, it doesn't look good for Vitamin E.

I went lookgin for studies clearly linking antioxidants to CAD, independant of statin use.

Vitamin E: A large meta-analysis of Vitamin E studies looking at CAD has concluded that Vitamin E has essentially no useful role in the treatment of CAD, independant of statin use.

Coenzyme Q10: A single but well-constructed clinical trial has found that Coenzyme Q10 significantly reduced the number of cardiac events, including AMI and cardiac death, from 45% to 24.6% among patients recruited immediately after thier first MI, given a one-year follow-up. Most, but not all, patients were also receiving treatment fro lipidemia.

Fish Oil: Another RCT looked at the use of fish oil, Vitamin E, or both in the prevention of repeat cardiac events among recent AMI patients over the course of a 3.5 year follow-up. As you might expect by now, Vitamin E showed no benefit, but no liability either. Fish oil (n-3 polyunsaturated fatty acids, n-PUFA), showed a reduction in adverse endpoints (12.3% vs. 14.6%). The findings were statistically significant for n-PUFA, but with a large NNT of 44. The study included a placebo group, and all patients received thier otherwise prescribed medications, including those for lipidemia where appropriate.

Conclusions: Vitamin E is not very usefull in treating CAD, and although none of these studies look at it, one has to question is it has a role in preventing CAD either. It potentially antagonizes the cardio-protective effects of a combination statin-niacin regimen, although the individual effects of niacin or statin use have not been teased out. I am going to be starting Coenzyme Q10 this week. Eat fish.

Case History:

A 42 yo alcoholic male comes with a 4-month history of pain in his left shoulder. He has been experiencing shoulder pain since falling in the street and hitting his shoulder on a curb, and the pain is not getting better despite taking 600mg of Motrin per day. His history is significant for "throwing out his shoulder" while playing baseball when he was 23. On physical examination, the patient has no tenderness over the AC joint; the area is not inflamed, swollen or red; the patient has full range of motion; no paraesthesia, weakness or numbness is present. However, the bony prominence of his left shoulder is slightly higher than the right and having the patient elevate his left arm and touch his right shoulder aggravated his discomfort. No other movement seemed to cause his pain. The patient was referred to orthopedics for further evaluation.

Differential Diagnosis:

The differential diagnosis of shoulder pain involves injury or disease of several structures, including the rotator cuff, glenohumeral joint, sternoclavicular joint, biceps tendon and the acromioclavicular joint. A careful history and physical examination is key to diagnosis. Fortunately, there are movements that can be done in the office that will help determine the point of injury. These provacative tests are detailed in http://www.aafp.org/afp/20000515/3079.html.  The particular test that elicited pain in this patient is the cross-arm test and is used to test the AC joint. A recent study evaluated the clinical effectiveness of these maneuvers for diagnosis of AC joint injury (http://journal.ajsm.org/cgi/content/full/32/3/655). The cross-arm test has the greatest sensitivity (77%) of those tested, with a specificity of 79%. The most specific test was the active compression test. The results of this study suggest that a combination of tests, and not a single test, should be used to diagnose AC joint injury.

Common injuries of the AC joint are sprain, dislocation and degenerative joint disease. In this patient, the history of direct trauma to the shoulder and the asymmetric elevation of his left acromion process (known as a "stepped" deformity) suggest AC joint separation. Degenerative change in the AC joint is very common, especially in people over 40, and must also be considered. The first line of therapy for AC joint injury is conservative management with an NSAID, ice and rest. It is not clear whether this patient did or could follow conservative management. If 2 months of conservative management fail to improve the patient’s condition, imaging should be ordered. A radiographic view of the AC joint would be sufficient to determine if degenerative changes or a separation is present. An MRI would only be needed if rotator cuff involvement is suspected. http://www.aafp.org/afp/20000515/3079.html part. A radiograph will allow the physician to determine the extent of injury and course of treatment. In the case of AC joint separation, minor cases might only need further conservative therapy, and more severe cases might require surgery.

What did I learn?

I learned that analysis of the shoulder and shoulder pain can be performed in a simple, yet logical manner. For me, orthopedics is intimidating and complex, but the above-cited articles really took the mystery out of the shoulder for me.

Why is this information important and how does it impact patient care?

This information is important because a familiarity with the anatomy and analysis of the shoulder may save the patient a potentially expensive and time-consuming visit to a specialist. And if a referral to a specialist is required, you will be more confident in your referral with this knowledge.

A 55  year old policeman  came to our office for an annual visit.  He had a history of high cholesterol but other than that, no major health problems.  When I asked him about his blood pressure, he said that he had been told he was a “little” hypertensive and had been advised to lose weight but was on no medications.   When I examined him, his blood pressure in his left arm was 146/90 and in his right arm was 148/92.  Also significant on exam was that his PMI was laterally displaced but he did not have any additional heart sounds.

MY QUESTION:
When do you initiate treatment for high blood pressure? Was this patient considered hypertensive?

WHAT I FOUND:
According to the latest report by the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure, (National Institute of Health, May 2003) systolic blood pressure of greater than 140 mmHg is considered to be an important cardiovascular risk factor, even more so than diastolic blood pressure. People with systolic blood pressures between 120-139 or diastolic blood pressures between 80-89 are considered “prehypertensive” and should adopt healthy lifestyle changes such as exercise and weight control.   According to the guidelines, the goal blood pressure to achieve is less than  140/90 or, if your patient is diabetic or has chronic kidney disease, less than 130/80.  Blood pressure measurements should be recorded on three separate visits before labeling someone with high blood pressure.

CONCLUSION: Looking back in his chart, we noted that our patient had had previously elevated readings so we started him on a thiazide diuretic at a low dose and told him to return for follow-up.  If he had been diabetic, we would have considered started an ace-inhibitor as a first line drug instead because of its other beneficial effects.   As I had felt an enlarged heart on physical exam, I also requested an EKG and 2D echo for further evaluation which showed left ventricular hypertrophy.  This was a sign that this patient had had longstanding uncontrolled hypertension causing this end organ damage, making it even more important that he control his blood pressure right away.

Among this week's office visitors was a 67 year old woman who is a natural vasculopath. Despite never smoking and generally living right, she has had two stents, three bypasses and a re-stenosed graft in the past five years.

Her chief complaint this week was hip pain, which she assumed was due to arthritis. Upon examining her, the doctor agreed. The patient asked about a drug she has seen advertised, "Celebrate or something?" My preceptor said, "It's Celebrex; and yes it might help." But then the woman asked if Celebrex might also harm her heart.

She was referring to a media report of a meta-analysis published in JAMA that suggested a link between the use of COX-2 inhibitors and MI/thromboembolic events. However, this study, published 6 months later in The American Journal of Cardiology found no such relationship - even when controlling for the concurrent use of aspirin. Interestingly, both studies analyzed data from the same source!

So the jury is still out. But until a definitive study is undertaken, patients will continue to see confusing media reports and marketing claims. The best response to their questions, at least for now, may be what my preceptor told this patient: It's unlikely that a COX-2 inhibitor will cause a heart attack or stroke, but since you tolerate ibuprofen well, you might be more comfortable continuing to take that.

Clinical Question:

Do benefits of HRT for post-menopausal symptoms and disease risk outweigh the risks, when compared with frequently used alternative treatments such as Black Cohosh?

Answer:

According to a 2002 study published in JAMA combined hormone replacement therapy is not beneficial enough to be recommended for routine disease prevention in post-menopausal. This study showed that the adverse effects (specifically for an average age of 64 years[pt distrib- 50-79 yrs.]) such as those shown in the earlier HERS study - inc. CHD, inc. invasive breast cancer, inc. stroke, and inc. thromboembolic disease).  Increased risk for early breast cancer is specifically what led to an early end of the trial.

On the other hand,  younger women without any risk factors for CHD or breast CA may see substantial reduction of vasomotor symptoms as well as prevention of osteoporosis with treatment of up to 5 years.

Black cohosh (Cimicifuga racemosa) is known for its ability to treat menopausal symptoms (as well as labor induction, PMS, dysmenorrhea, etc...) such as vasomotor flushing (hot flashes) in studies lasting up to 6 months. Some research has shown that it is as effective as estrogen replacement for some symptoms.

There are concerns of hepatotoxicity with Black cohosh, especially in combination with other hepatotoxic drugs - MONITOR LFT's!!!!!

Conclusion:

Young woman (<50) and no CHD/ breast CA risk factors - HRT or Black Cohosh is fine as long as LFTs are monitored and HRT is not used for longer that 5 yrs.

Older woman (>50) with variety of risk factors- use discretion with HRT as it substantially increases risk for CHD, STROKE, BREAST CA, THROMBOEMBOLIC DZ if used for prolonged time. Black cohosh may be used with LFT monitoring.

Without a doubt, the worst part of local anesthesia is the injection itself. If there were a way to make the injection less painful, that would be great.

There have been studies that have looked at the temperature of the injectate. It doesn't really help to warm up the injection - patients feel the same degree of pain upon injection whether its room temperature or body temperature.

The best way to reduce the sting of a local anesthetic is to buffer the solution. A recent study emplyed a group of 85 people who took one for the team and had bilateral vasectomy performed - one cajone was numbed with buffered xylocaine, the other with unbuffered xylocaine.

Buffered xylocaine is prepared by making a 10:1 of anesthetic to sodium bicarbonate (e.g. 20ml Lidocaine 1% to 20ml sodium bicarbonate solution).

This may not be necessary for every injection, but for kids, wimps and sensitive areas it should make life easier for us and them.

Case:  This past week as I was taking a full history from a hypertensive patient, I asked him whether or not he was taking any supplements or OTC medications.   "My wife is forcing me to take a vitamin E supplement every day because she says its good for my heart," he said.   Although I had heard similar statements from our beloved Dr. Hof (remember the nice lady), I was still skeptical about the efficacy of vitamin E in prevention of heart disease.   I did find an article on the subject matter and I plan to use the information from this article to educate my patients accordingly.

Question:  Are antioxidants effective in preventing heart disease?

Summary:  In this study, the authors searched MEDLINE to identify randomized trials of vitamin E and beta-carotene in primary and secondary prevention of heart disease.  To minimize the effect of publication bias, they excluded trials with fewer than 1000 subjects. They also only included studies from developed countries to reduce the potential effects of nutrient-poor diets.  They identified 12 studies; 8 used beta-carotene and 7 used vitamin E. Of the 12 studies, 7 were for primary prevention and 5 for secondary prevention. More than 130,000 patients participated in the studies of beta-carotene where all-cause mortality was 7.4% in the actively treated patients and 7% in the control group (P = .003; number needed to kill [NNK] = 250). There was a similarly small but significant increase in cardiovascular mortality among patients receiving carotene (3.4% vs 3.1%; NNK = 334; P = .003). Carotene had absolutely no effect on stroke events (2.3% for treated and controls). The data were homogeneous across studies for these end points. More than 81,000 patients participated in studies of vitamin E. All-cause mortality was the same in treated and control patients. The event rate was also the same for cardiovascular mortality in treated and control patients and for stroke rate. Finally, to see if the best possible face could be placed on this, they combined all end points and found that the end point of any bad thing was identical in patients receiving vitamin E or placebo. These data were also homogeneous across studies.

Significance:  Beta-carotene and vitamin E offer no protection against all-cause mortality, cardiovascular mortality, or stroke in either high risk or low risk patients.

Docusate sodium (AKA Colace) does more than soften stool...it effectively gets rid of cerumen (AKA ear funk).

Background: We all make it, some more than others.  We all clean it, some more than others.  Ear wax, otherwise known as cerumen in medicalese, can often impede visualization of the tympanic membrane.  In fact, an adult male patient came into the office just the other day with so much cerumen impaction that it was drastically affecting his hearing.  He was advised by the EBM-friendly physician to go to his local drug store and purchase Colace OTC, which is sold as a stool softener.  Poke a hole in the geltab with a clean needle, and squirt the contents into each ear to soften the cerumen.  He has yet to return for follow-up, but check out this study.

Objective: The perfect cerumenolytic agent has yet to be discovered.  Until then, which is better: docusate sodium (Colace) or triethanolamine oleate (Cerumenex)?

Design: Randomized double-blinded controlled trial conducted in the ER of SUNY Stonybrook on 50 patients, with a mean age of 40.  Patients with cerumen impaction received intra-aural instillation of 1mL of either docusate sodium or triethanolamine polypeptide.  If not completely cleared in 15 minutes, the external ear canal was irrigated with 50-100mL of normal saline.

Results: The ability to completely visualize the tympanic membrane was signficantly greater after treatment with docusate sodium vs. triethanolamine polypeptide (81% vs. 35%; 95% CI, 22 to 71).

Conclusion: Stool softener (Colace) has a whole new market in cerumen impaction.  Indeed, it is even more effective than triethanolamine oleate, which is sold as a cerumenolytic.

A seven year old boy is brought into the clinic for a possible wrist fracture. In the course of obtaining his medical history, I found out that he is being treated for an asymptomatic giardia infection. He has specifically had no history of diarrhea or foul smelling stool. This diagnosis was made by a naturopath who examined the boy's stool. How the naturopath examined the stool and came to the diagnosis is unknown. Because the boy's parents strictly adhere to a regimen of natural remidies, he is not being treated with an antibiotic such as metronidazole. Instead, he is being treated with wheat germ, according to his parents.

Although this boy's giardia infection cannot be verified, I was mystified by the idea of treating giardia with wheat germ. Just for kicks, I did a literature search on giardia and wheat germ to see if there were any studies available.

A small Canadian study found that cyst passage decreased by 50% in asymptomatic subjects taking metronidazole supplemented with wheat germ compared to those taking metronidazole alone. There was no clinically significant difference in symptomatic patients who took metronidazole and wheat germ or metronidazole alone. However, symptoms seem to have resolved more rapidly in the subjects taking wheat germ in addition to metronidazole.

There are some studies in the medical literature that have looked into how wheat germ may work in treating giardia infections. One study found that wheat germ agglutinin inhibits the excystation that is crucial to the initiation of infection by giardia. Another study has found that N-acetyl-D-glucosamine residues (GlcNAc) are major structural components of both giardia trophozites and in vivo cysts. Wheat germ agglutinin binding was markedly reduced after the trophozites and cysts were treated with N-acetyl-beta-D-glucosaminidase, supporting the notion that wheat germ agglutinin reacts with GlcNAc. In an additional study, cell cycle analysis revealed that parasites grown in the presence of WGA were arrested in the G2/M phase.

There appear to be no published large, double-blinded studies that have looked into the treatment of giardia infections with wheat germ. The research looking into this concept, however, has yielded very intriguing results in my opinion. As we deal with the problem of antibiotic-resistance and reducing the use of antibiotics, could wheat germ (or some derivative)be an effective and accepted method of treatment for giardia in the future?

Case:  Last week, a 75 year old widowed Eastern European immigrant presented to the clinic for a follow-up of her mild dementia stemming from what was recently diagnosed as early Alzheimer's.  On review of systems she stated that for the past few weeks she had been feeling a little nausea, kind of dizzy at times, had lost some appetite, and noted some swelling and joint pain in her wrists.  The chart said that she had  recently been placed on Aricept (donepezil) but of course when I asked her if she was still taking it she told me she had stopped a couple days ago because she "didn't really know what it was for and it wasn't helping her anyway."  When my preceptor heard this, he of course put her back on it and kindly explained to her how important it was for her to take this medication.

Question:  So I started wondering, while symptoms she was experiencing in the weeks prior were potential minor side effects from this medication, did she really need to be taking it anyway?  We can't do much for Alzheimer's so what was the point of her taking and paying for yet one more medication and living with its minor yet burdensome side effect profile.  Were we really helping her or were we just making ourselves feel better by offering her a pill for illness that will eventually take away her memories and other cognitive abilities.     

Analysis:  Well, I found an article from this year to counter my skepticism.  The analysis looked at 16 clinical trials ranging from 12, 24, or 52 weeks and included over 4000 participants.  The results showed statistically significant improvements in global clincial state (determined by an independent clinician) and activities of daily living and behavior.  The study noted that at the higher doses, some patients experienced minor side effects but very few actually left the trial.  They acknowledged, however, that no significant changes were reported in patient-rated quality of life scales and that there were obvious limitations to assessing nonspecific and vague criteria like global clinical state.  

Regardless, while we are still far from curing or reversing Alzheimer's, it seems that the evidence suggests that patients with dementia should be on Aricept for 52 weeks or more to at least slow the progression of this devastating disease.                

       

HPI: A 24 yo single mother comes with a 4-month complaint of "disturbing thoughts." She reports that she has been having nightmares about her and her daughter "not being there." When asked if she thought she would hurt herself or her daughter, she replied that she has been having nightmares about being harmed with guns, but she has no guns in her house. Upon further questioning, she revealed that she has thoughts of overdosing on Neurontin that had been prescribed for pain following a finger amputation 4 months ago. She also has trouble sleeping, has had a 30# weight gain in the last 4 months and has difficulty concentrating in school. She also has had episodes of shortness of breath and chest tightness that mostly occur at night. She reported that she had similar, but less severe, feelings 7 years ago, shortly after the death of her newborn son. Her father has schizophrenia and she is afraid the same is happening to her. When offered a plan for managing her symptoms with medication on an outpatient basis, she revealed that she felt it would be better if she were hospitalized. She was then sent to the Crisis Intervention Center at CDPC for evaluation.

Diagnosis: This patient is experiencing a major depressive episode. The diagnosis of depression in both men and women is based on similar criteria (see DSM-IV). The symptoms of depression are sub-divided into psychological (depressed mood, reduced interest in activities, feelings of guilt, suicidal thoughts, etc.) and physical symptoms (insomnia, change in weight, difficulty concentrating, decreased energy, etc.). However, there are differences in the presentation of depression between men and women that the clinician should be aware of. First, depression is about twice as common in males than in females. Second, females present earlier with depressive episodes that last longer. Also, the association of depression with panic attacks, as with this patient, is greater with females. Finally, females experiencing depression attempt suicide more frequently, but are less successful. In addition to differences in presentation, females respond to antidepressant therapy differently. Since, the absorption of antidepressants and plasma concentration of antidepressants in females is greater than males, doses might need to be adjusted lower. Also, the clinician must be careful in the choice of treatment for women who are possibly pregnant because certain drugs have been deemed safer than others (http://www.aafp.org/afp/990700ap/225.html).

Why is this important and what did I learn: This information is important because like many other medical conditions, the clinician must be aware of the gender-dependent presentation of depression. Armed with this knowledge, a proper plan for treatment may be established. This information impacts patient care because it is with this information that a clinician may make a decision about treatment. Given that the antidepressant dose for females is possibly lower than in males will prevent potential harm for the patient. Also, the clinician must be sensitive to the possible increased length and severity of the illness in female patients.

For information to distribute to female patients with depression see http://familydoctor.org/443.xml.

Case History: If you would like to skip a long history, scroll down to the next bold heading, otherwise, for a relevant patient interaction - - >(This case is a follow-up on the 34 y/o male deck-hand with glucosuria from last week's POEM.) 

    This was a difficult case where the patient was very upset with me for jeopardizing his job b/c we (my supervising physician and I) wanted to follow the glucosuria with a random blood glucose to determine our pt.'s DM status.

Upon taking a random blood glucose and catching a lot of slack from the patient because he, "would lose his job if we didn't sign his physical form!", the results came back several days later with a random blood glucose well over 300. (Over 200 is indicative of DM). 

When we informed our patient, he suddenly (and much to my surprise) recalled being diagnosed with DM several months earlier and maybe did not eat a cake, soda, and several bags of candy the night before his exam. His response was that he was trying, 'Herbal therapies, doc, and could you just sign my forms for my job!'

Regardless of intriguing and sad moral lesson that I learned....the question for this week's POEM became -

Query- Are any herbal therapies potentially useful in treatment of Diabetes Mellitus?

Of the interesting array of alternative therapies for Diabetes to be found here (including alcohol and caffeine), the references to Cassia Cinammon (Cinammon Oil) sparked my interest.

It turns out that, "Polyphenolic polymers such as hydroxychalcone found in cassia cinnamon seem to potentiate insulin action. These compounds seem to increase phosphorylation of the insulin receptor, which increases insulin sensitivity. Increased insulin sensitivity may improve blood glucose control and lipid levels. Cinnamon extracts also seem to activate glycogen synthetase and increase glucose update."

Summary -  Food, Derivatives (2), Supplements, and Dental Hygiene products with Cassia Cinammon extract may be beneficial in, "alleviation or possible prevention and control of glucose intolerance and diabetes," (1) for patients who are resistant to conventional therapy modalities.

_____________________________________________________________

1. Anderson RA, Broadhurst CL, Polansky MM, et al. Isolation and Characterization of Polyphenol Type-A Polymers from Cinnamon with Insulin-like Biological Activity. J Agric Food Chem 2004;52:65-70.

2. Jarvill-Taylor KJ, Anderson RA, Graves DJ. A hydroxychalcone derived from cinnamon functions as a mimetic for insulin in 3T3-L1 adipocytes. J Am Coll Nutr 2001;20:327-36.

And if killing 2 birds with one stone isn?t enough, early treatment with angiotension receptor blockers was projected to improve life expectancy and reduce costs in hypertensive patients with type 2 diabetes and microalbuminuria ? Cheaper is better.

Atypical Chest Pain

CASE HISTORY: Mrs. C, a 55 year old diabetic lady, presented to our clinic for a routine visit and prescription renewals. On review of systems, she told me that when she climbs a flight of stairs, she develops a "stomach-ache" which has become worse recently along with some shortness of breath. She attributed this to her gastric reflux and was about to go home when  I decided to ask some more questions. Though she was an obese lady, she said she was able to do her activities of daily living without much difficulty until the past week. Also significant was that her father had died of a heart attack at a young age and along with diabetes, she also had high cholesterol. An EKG we did in our office revealed ST-T changes in the inferior leads that were new from a prior visit.

MY QUESTION: What are the usual symptoms of cardiac chest pain? Would it be reasonable to pursue a cardiac work-up in this patient?

WHAT I FOUND:

According to an article in the New England Journal of Medicine (The Evaluation of Chest Pain in Women by Douglas et al), women having ischemia or acute coronary syndrome often present with atypical symptoms. Most of the clinical data and trials conducted previously describing symptoms that people present with were done on men so women may not complain of  classic "crushing, substernal chest pain radiating down the left arm".   Therefore, women presenting with chest pain suggestive of coronary heart disease should undergo a full assessment of risk, including laboratory testing of cholesterol subfractions and triglycerides. An estimate of the likelihood of coronary heart disease should be made on the basis of cardiac risk factors. The patient should be educated about the importance of coronary heart disease as it is the number one cause of death in women.

CONCLUSION: In this case, with EKG changes and a lady with multiple cardiac risk factors including diabetes, high cholesterol, age, postmenopausal status,  positive family history and obesity, we decided to refer her to a cardiologist immediately.  Another important fact I learned was that diabetics often have an atypical presentation of chest pain so it is very important to obtain a careful history.

A 17 year old mother came to our office this week with her five day old baby. In her first-visit paperwork, she noted that she had smoked throughout the pregnancy, but "only 3-4 cigarettes a day." The baby, as you might suspect, was a peanut, but appeared otherwise healthy and alert.

The "you should really quit smoking" ship had clearly already sailed in this case, and the stressors in this girl's life (new baby, dicey home life, financial instability) made it unlikely that a lecture would change things. So the question for me was what could I suggest that would minimize harm to the baby without alienating the mother? Our objective, after all, is to build rapport with this girl so that she will feel comfortable bringing her baby in for ongoing care.

It turns out that "smoking hygiene" has a significant effect on the risk of hospitalization for newborns. Smoke in the same room as your baby, and her risk of being hospitalized goes up by 56%. Smoke while feeding her, and the risk jumps by 298%.

So in this case, suggesting that she step into the next room when she has to light up seems a reasonable first step down the tricky path of extinguishing the smoking habit without overwhelming this new mom and driving her away.

Case:  Having worked in a family health center for the past two weeks, I am simply amazed by the number of diabetic patients we encounter on a daily basis.  Almost all of these patients are obese individuals with Body Mass Indices of more than 30.  We continuously encourage these patients to be mindful of their diets and take up sensible exercise programs.  It is well known that uncontrolled elevated blood glucose could potentially lead to a myriad of complications such as diabetic neuropathy, nephropathy and microvascular retinopathy leading to blindness.  Although diet and exercise are important components of lowering blood glucose levels in diabetics, pharmacological means are needed in some instances in such patients.  There are many types of glucose-lowering drugs on the market designed for Type II diabetic patients (and it seems like every month there is a new drug available on the market) but not all these drugs offer protection against long-term morbidity and mortality associated with Type II DM.

    Managing hypertension is a frequent challenge for any primary care physician.  With the variety of treatments available and the diversity of the patient population, it is often difficult to establish a concrete system for prescribing the right medications.  This week, I had an interesting encounter with a 67-year-old caucasian woman with moderate hypertension.  When she was first diagnosed 2 years ago, the physician prescribed an ACE inhibitor (Monopril) since that is the recommended first-line treatment for hypertension.  Unfortunately, with that drug she experienced  mild angioedema around her lips.  Angioedema is one side effect that is known to occur with ACE inhibitors, and in some instances it can be quite severe and life threatening.   

    When this patient became bothered by her angioedema, she requested a change in her medication.  Since angiotensin receptor blockers are often better tolerated than ACE inhibitors, the physician decided to prescribe Benicar (olmesartan).  While the ARB was effective in treating the hypertension with no angioedema,  the drug did cause the patient to experience incredible fatigue.  She found this to be unbearable and thus asked again to try a different drug.  At that time, she was switched back to a different ACE inhibitor to see if the adverse effects could be minimized.  The physician prescribed Mavik (trandolapril) which is also known to be effective and well-tolerated.  Finally the Mavik allowed the patient to manage her hypertension without facing intolerable adverse effects.  When I met her at her follow-up appointment, she discussed how much happier she is now with Mavik.  She feels good and has had minimal side effects since beginning the drug 2 months ago.

    Now while this case may seem to be a simple one of juggling drugs to fit a specific patient, it taught me a valuable lesson in the treatment of hypertension.  When a patient experiences an adverse effect with one drug of a certain class, it is often instinctive to try the patient on a new class of drugs....particularly in this case where there is ample material supporting ARB's over ACE inhibitors.  In this article in Hypertension Research, an ARB (valsartan) proved to be most effective in reducing pulse pressure when compared to an ACE inhibitor (temocapril) and a long-acting Ca channel blocker (nifedipine).  Furthermore, the ARB showed potential for decreasing arterial stiffness in addition to its antihypertensive effects.  Seems like a good deal, right?  However, as clinicians, we must remember that patients do not always fit perfectly into a published study.  In this case, the patient did better with a different ACE inhibitor than she did with an ARB.  So in the end, we must listen to the patient's complaints and try not to get frustrated when medications don't seem to be panning out, especially if we've tried several classes of drugs.  What patients need most is our patience and perseverence in finding the best drugs for them as individuals so that they can manage their illnesses with the least amount of adverse effects possible.

Case History:
An 8 yo female presents with a one-week history of worsening sore throat, difficulty swallowing, and headache.  The patient’s general appearance was lethargic and uncomfortable.  The patient reports no history of coryza.  Physical examination findings were as follows: the patient was afebrile; swollen cervical lymph nodes; swollen and erythematous tonsils; highly erythematous oropharynx with a whitish exudate.  The patient also had very bad breath.  Without further physical examination or laboratory testing, the patient was prescribed PenVK (150mg bid) for 5 days.

Differential Diagnosis:
In this patient the differential diagnosis of strep throat includes streptococcal pharyngitis, infectious mononucleousis and viral pharyngitis.  The patient’s age, presenting symptoms and presence of exudate support the diagnosis of streptococcal pharyngitis.  Streptococcal pharyngitis most commonly effects patients of ages five through nine.  In contrast, infectious mononucleoisis most commonly effects patients age 15-24.  Further, patients with infectious mononucleosis will present with enlarged posterior lymph nodes and a history of exposure to infected patients.  Viral pharyngitis is the most common cause of sore throat and is associated with symptoms of coryza.  (Sloane et al. Essentials of Family Medicine, Fourth Edition)

Diagnosis:
In this case, it is likely that the patient had streptococcal pharyngitis, based on physician’s subjective assessment, and the patient was treated appropriately.  However, a physician’s subjective assessment of streptococcal pharyngitis has been demonstrated to be not as accurate as either a clinical prediction guide or rapid antigen test (http://gateway.ut.ovid.com/gw1/ovidweb.cgi).  Interestingly, a clinical predication guide (see http://www.aafp.org/afp/20010415/1557.html) was shown to be as accurate as the rapid antigen test strep (http://gateway.ut.ovid.com/gw1/ovidweb.cgi), calling into question the necessity of the rapid antigen test.

Why you should care:
This is a simple, yet very important teaching case for several reasons.  First, sore throat is a very common complaint in the primary care setting.  The National Ambulatory Medical Care Survey of 2002 (http://www.cdc.gov/nchs/data/ad/ad346.pdf) lists sore throat as the sixth most common presenting complaint of patients seen in the office, representing 2.1% of all office visits.  Second, the differential diagnosis of sore throat consists of illnesses with serious complications if not properly treated.  For example, untreated streptococcal pharyngitis may result in suppurative complications, including endocarditis and otitis media.  It is fear of these complications that motivate antibiotic therapy.  However, antibiotic therapy is thought to only provide a modest benefit in preventing these complications (click on URTI link at http://www.nntonline.net/).  This means that the patient may only have needed symptomatic treatment or a most a “fold and carry prescription”, to be filled only if symptoms worsen.  Finally, improper treatment of sore throat may harm the patient.  For example, administering amoxicillin, which is an option for treatment of streptococcal pharyngitis, improperly to a patient who has infectious mononucleosis may result in a rash.

What I learned and why it helps the patient:
In this case, I learned the differential diagnosis of sore throat.  Further, I learned that following a simple clinical predication rule could save the time and expense of a laboratory test.  Finally, I learned that antibiotic therapy is not always necessary in cases of streptococcal pharyngitis.  This information impacts patient care by reducing patient costs, in terms of having to pay for unnecessary laboratory test and prescriptions.  Also, reducing unnecessary antibiotic therapy will prevent development of resistant strains of bacteria.

If your practice is anything like the one I'm in, is seems as though every other patient you meet has high cholesterol. Some of my patients welcome the idea of going on a statin, but others want nothing to do with starting a medication they may be on for the rest of thier life. Many want to try diet and exercise first. Just how much of a difference can be made with diet and exercise? Is the diabetic with confirmed CAD and an LDL of 180 reallly going to be able to meet his goal of 70? Even 100? I went to find out...

While there are a bunch of scientifically great articles out there, the best common sense practical article I could find was from the American Academy of Family Practice (www.aafp.org).

In an article on dietary therapy for preventing and treating coronary artery disease, Steven Masley gives me the answers I've been looking for and then some.

The best results for dietary change in LDL's were published by Dr. Dean Ornish, founder of the Ornish diet plan. In a reasonably unbiased study, he found that strictly following his program resulted in an average of 37.4% reduction in thier LDL. Most of our patients are not going to follow the program to the T, however.

The reasonable value suggested by Dr. Masley is a 30% reduction in LDL values with diet and exercise alone. What does that mean for our patients?

If your patient has no risk factors other than hypercholesterolemia, and his LDL is 170, shure, let him try diet and exercise for a few months and bring him back for a check-up. He has a reasonable chance of lowering his LDL below his 130 target. If he's a diabetic with CAD, on the other hand, its not likely to work. He would need almost a 60% reduction in his LDL to reach his ATPIII goal of 70, double what he can be expected to accomplish with diet and exercise. Start him on the statin now, and offfer to taper it down as his numbers improve. 

 

Case History:  A 34-year-old mother, Ms. S, came to seek advice as to whether her 2 year-old daughter should receive the varicella vaccine. Her daughter is a healthy child with no history of major medical problems. The pregnancy and delivery were without complications. Her daughter has responded well to all previous childhood vaccines thus far. The mother heard about the benefits of the vaccine on the news and she is interested to learn more and see if it would benefit her daughter. Ms. S is a single parent and is concerned that if her daughter does get chicken pox she won’t be able to take time off of work. How effective is the vaccine in preventing chicken pox?

Significance:  Before the introduction of the varicella vaccine, almost 4 million cases of chickenpox occurred each year in the United States, resulting in 11,000 hospitalizations and 100 deaths. Varicella is now the leading cause of vaccine-preventable death in children. The major concern with the vaccine has been its long-term efficacy. Although it is not yet certain how long immunity is sustained, it is estimated that detectable antibodies are present for up to 20 years. Chickenpox is major nuisance for the child and the family. Children miss school and parents miss work. In addition to itching and fever, some children develop accompanying complications such as pneumonia and infections.

Reference:  Seward JF, Zhang JX, et al. Contagiousness of varicella in vaccinated cases: a household contact study. JAMA. 2004 Aug 11;292(6):704-8.

Summary: The purpose of this experiment was to determine whether the varicella vaccine was effective in preventing chicken pox. The study involved the community of Los Angeles, CA and involved approximately 320,000 people. History of varicella cases were collected from various organizations, households and schools. Information about varicella history, vaccination status and demographics were collected and analyzed. The study found that among contacts aged 1 to 14 years exposed to varicella, the attack rate was 71.5% if they were unvaccinated and 15.1% if they were vaccinated. Vaccine effectiveness for prevention of all disease was 78.9% (95% CI, 69.7%-85.3%); moderate disease, 92% (50-500 lesions) and 100% (clinician visit); and severe disease, 100%.

Conclusion: The varicella vaccine is highly effective in preventing moderate and severe disease and approximately 80% effective in preventing all disease. In a healthy child it is recommended to administer the varicella vaccine in order to prevent the likelihood of getting chicken pox.

The CV exam of a well child checkup - normal, normal, normal, normal... then, what? What if you hear a systolic ejection murmur at the left sternal border of a 8 year old boy in perfect health? Is it a small VSD nobody has picked up yet? Maybe its the dreaded and lethal IHSS (hypertrophic cardiomyopathy), or maybe its a Still's murmur - A.K.A. an innocent murmur that's totally benign and the child will grow out of. We talked about this breifly in the lecture on sports physicals during the orientation week, but I understood less than I listened to. I found an article that really explains all this well.

The way to differentiate between a Still's murmur and hypertrophic cardiomyopathy is to decrease venous return to the heart. There are different ways to do this:

1. Have the child Valsalva - up to you how you get the kid to do this.

2. The squat and stand - squatting is not the crucial phase, its the standing up that causes a breif moment of hypotension before the vessels in the legs can constrict and adjust the BP. For that moment, venous return is less. Brief tangent: children with Tetralogy of Fallot will instinctively squat to increase venous return when they start to feel hypotensive.

If the murmur gets WORSE (louder) when the child stands up, then that's BAD. In IHSS the aortic outflow tract is narrowed by that hypertrophic cardiac tissue, when venous return is decreased, the already narrowed passage has less blood in it and is narrower and more turbulent (louder). If the murmur gets BETTER when the child stands that's GOOD - that favors a diagnosis of a Still's murmur (which has a vibratory or musical nature according to probably the same people who think that some wines have a "spruce" or "licorice" flavor).

That said, if the kid has chest pain, family history of Marfan's, Down syndrome, increased precordial activity, decreased femoral pulses, abnormal S2, clicks, any loud or harsh murmur then its recommended that you refer them to a cardiologist.

Want practice? Click here.

? Is infantile colic a medically treatable condition?

I don't know about you guys but I have not had a lot of exposure to the care of an infant. Last week I encountered colic. It is defined as iconsolable crying for more than three hours per day, for more than three dyas per week and for longer than three weeks in a healthy and well-fed infant. Colic is common in the first six months of life (up to 25% of infants). It is more common in males and is a self- limited condition. The cause of the colic is unknown ( if it is not an organic cuase contributing to the 5% of colic pain). It was almost a revelation when I learned that there is no medically proven efficacious treatment for infantile colic in the U.S. 

I saw A., a two-month-old boy who presented with inconsolable crying for four days. The parents were so disstressed they took him to the ER two days prior to the visit to the office. He was ruled out for the organic cause of distress, diagnosed with colic and given Mylicon with no success. The parents( and me too) wanted to initiate medical treatment of the condition because they thought the incessant crying being a symptom of a  serious disease and were afraid. However, my preceptor and the article called Infantile Colic in the August 15th, 2004 issue of American Family Physician (p.735-739) , http://www.aafp.org/afp/20040815/735.html taught me that medications, diet, and behavioral changes were not successful in alleviating colic in babies. The article was a review of several RTC's (randomized controlled trials). Commonly, the doctors prescribe Mylicon ( an OTC drug for decreasing bloating) or anti-cholinergics for reduction of the muscle spasm). Those medications play a more important role in calming the parents insisting on medications, but there is no proven advantage of them over the placebo. The breast-feeding versus the formula, and carrying or rocking a colicky babiy did not prove effective. In fact, doctors recommend no changes in the baby's diet during colocky episodes. Some doctors recommend herbal teas, such as chamomile, peppermint, fennel, etc to sooth the baby.

Results & Conclusion: So far, reassurance of the parents in the self-limited character of the condition and acknowledgement of the difficulties that the parents face is the mainstay of colic management. An important part of care is to advise the parents to seek help from their family members in order to get rest and adequate sleep. Physical fatigue and emotional disstress that the parents share with their colicky child during a prolonged periods of colic can impact adversely on the parents' health.  

Importance: This case was an important learning experience for me because I was strongly believing in the idea of pain management and patient's comfort as a physician's first priority in all instances. Not seriously treating this infant's pain seemed scary to me and the parents. However, in the instant when medications are mostly helpless in this discomforting for the baby and the parents condition, we need to step aside from this common belief and develop the ability to build trust and reassurance of the parents as the standard of care.

 

 

Cranberry juice to prevent that unpleasant burning during urination: A randomized controlled trial from the friendly folks of Finland

Background: 30% of females have at least one UTI, which translates into 7 million doctor visits per year.

Objective: This study attempted to determine whether recurrences of urinary tract infections can be prevented with cranberry-lingonberry juice or with Lactobacillus GG drink.

Design: In an open randomized controlled trial, 150 women with urinary tract infections caused by Escherichia coli were randomly divided into three groups: 50ml of cranberry-lingonberry juice concentrate daily for six months, 100ml of lactobacillus drink (who thought this was a good idea?!) five days a week for one year, or no intervention.  The women were followed for one year with the main outcome being the first recurrence of symptomatic urinary tract infection confirmed by culture.

Results: After six months, 16% of the women drinking cranberry juice, 39% of the women in the lactobacillus group (lucky ladies), and 36% of the women without intervention had at least one symptomatic urinary tract infection confirmed by culture (P=0.023, NNT=5, 95%CI 3-34...see Dr. Mayer for a translation).  Benefit was still seen at 12 months.

Conclusion: A glass of cranberry juice can significantly reduce recurrence of urinary tract infection in women vs. doing nothing.  And on a side note, don't drink lactobacillus.

 

     This past week I met a 32-year-old white female who complained of increased sexual dysfunction since starting Zoloft (sertraline) 12 weeks ago.  She came into the office to discuss a change in medications since she and her husband were very unhappy with the side effects she was experiencing.  Although the medication had improved the symptoms of her depression and anxiety, she could no longer tolerate the adverse effects of the drug, which primarily involved decreased sexual desire and difficulty reaching orgasm. 

     An article in the Journal of Clinical Psychopharmacology discusses the adverse effects of SSRI's, particularly the onset of sexual dysfunction in patients taking the drug.  The study shows that in a subgroup of females reporting no sexual dysfunction at baseline, 11.8% report decreased sexual desire and 14.3% report orgasmic dysfunction at week 24 of taking fluoxetine.  In a similar subgroup of men, 16.7% reported decreased sexual desire and 18.9% reported orgasmic dysfunction. 

     Since this 32-year-old patient is one of three females that we saw last week with similar complaints, we decided that perhaps Zoloft (or other SSRI's) is not the best choice for ongoing depression and anxiety.  We decided to instead put the patient on Effexor (Vanlafaxine) for her symptoms.  This drug does not seem to have the same adverse effects on sexual function, and its effectiveness for treating depression may even be better than the SSRI's.  A study in the International Journal of Neuropsychopharmacology discusses venlafaxine when compared to fluoxetine for outpatients with depression and concomitant anxiety.  It emphasizes the greater efficacy of venlafaxine in treating the symptoms of depression/anxiety and the fewer adverse effects (such as sexual dysfunction) with that drug.  Fewer patients in the venlafaxine subgroup reported at least one adverse event when compared to the fluoxetine group. 

     In summary, I think we should be careful in prescribing Zoloft immediately to someone with ongoing depression and anxiety.  While it does work well for many patients, an atypical antidepressent like Effexor might actually be the better choice in the end.

Looks like I'm scoring these things a bit more conservatively that you all are .. so I thought I'd let you in on how I'm grading (hint hint)

Recall that this exercise is for you to find and describe an article that relates POEM to your colleagues.

Patient Oriented Evidence (that) Matters.

So .. I give

• 3  stethoscopes  for good, interesting writing and efficient use of hyperlinking.  This includes accurate analysis of the article (you interpret it correctly) and describe it well.   The useful article will provide us with RELEVANT and VALID information with little work.
• 1 stethoscope for Patient Oriented information.  This means I can explain it to grandma -- and that she will think it's important.  Example: an article that describes lower risk of death for treatment of hypertension with beta-blockers.  Death is a patient oriented outcome.  Example of something that is NOT patient oriented:  a study that demonstrates lower LDL with statin use.  Get it?  Grandma doesn't know or care about her LDL.  LDL is the intermediate outcome.  She cares about death, or MI or stroke.   A medication that lowers LDL by 600% but caused liver facilure and kills 80% of those who take it would look GREAT if we look at the LDL .. but would look pretty bad if we look at how many patients are alive at the end of the trial.
• 1 stethoscope for a study that presents Evidence that Matters.  Is the study relevant?  You don't have to say "this study is relevant because ... "  (so please don't) ... The reader should be able to interpret relevance easily.  In general .. this means that the topic is relevant to the practice of family medicine, and to the question you have posed

As you see - I'm heavily weighting the quality of writing and presentation.  If you don't write something well - the readers won't read it and your efforts will be wasted.  Patient Oriented Evidence is also important - as it's a core component of what we're trying to teach you: a method of discriminating between information that is important and relevant to your patients .. vs information that may be interesting .. but may not be relevant or important.

Finally - please feel freee to click on the "comments" for any post.  I've made a few comments here and there .. and you all should feel free to comment on each others' work. 

--------------------------------

Oh yeah -- remember that you can't reveal any information about a patient that might be identifiable.  I'd say that initals are even unnecessary.   Invented names are OK .. as are invented initials, genders, etc.. ;-)

A 49-year young obese female is brought into a rural clinic by her sister complaining of left leg pain.  She denies any recent trauma.  She states that her right leg is fine.  She is largely confined to her bed due to alcoholic encephalopathy and previous traumas related to excessive alcohol consumption.  On physical exam, her left leg is found to be grossly swollen, red, and warm relative to her right leg.

Her signs and symptoms are highly suggestive of deep vein thrombosis.  Furthermore, the potential for catastrophic consequences in DVT make a rapid diagnosis and initiation of proper treatment essential.  Imaging studies, particularly ultrasound and venograms, are ideal in verifying this diagnosis.  In less-than-ideal settings where imaging is not available, such as in a rural clinic, what does a doctor do?

When symptoms and the presence of risk factors strongly suggest DVT, treatment with low molecular weight heparin, such as enoxaparin, can be started while the patient is being transported to a facility where imaging studies can be obtained.  HOWEVER, unnecessary treatment can be significantly minimized in patients who truly do not have DVT's by testing their D-dimer levels.  A study published in the New England Journal of Medicine in 2003 found that a normal D-dimer level can safely rule out DVT without ultrasound imaging (negative predictive value of 99.1%).  Furthermore, D-dimer tests are so cheap, fast, and widely available that even the out-in-the-boonies rural clinic that I'm at now can perform them. 

Although most of us will probably practice in areas where ultrasound and venograms are readily available, we should strongly consider the use of D-dimer levels when ruling out DVT.

Case:  A 21-year old morbidly obese female (she was >300 lbs) presented to the clinic with a 2 week history of heavy menstrual bleeding.  Her menses have never been regular and, while her flow has been heavy for years, the past two cylcles brought her in to the clinic for treatment.  This is her third trip and she is at her wits end.  She has been unable to leave the house because her flow is so heavy and she complained that it is becoming too expensive to buy sanitary napkins at the rate she requires them.  At her first presentation she was prescribed DepoProvera, which  was successful in inducing cessation of bleeding, but make her next cycle even heavier.  The second time, bleeding stopped but resumed 2 weeks later, bringing her to the office at the end of her fourth week post treatment, which is now.  The patient wondered if she could try 'The Patch' for regulation.  This predicament prompted me to ask why this woman was so refractory to the standard therapy and what could be done for her.

Background:  By definition, menometrorrhagia is irregular intervals of heavy menstrual flow, or menses of prolonged duration.  In most women, dysfunctional uterine bleeding (DUB) is due to hormonal imbalance, as opposed to other causes of DUB such as pregnancy, systemic illness or structural lesion (fibroids, neoplasm).  In obese women, estrogen is stored in peripheral adipose tissue.  This increased estrogen suppresses hypothalamic release of FSH, leading to anovulatory cycles and consequent unopposed action of estrogen on the uterus.  The standard treatment for DUB is cyclic medroxyprogesterone acetate (MPA):  10-20mg/day for 10-14 days monthly for 3-5 months.  One study however, showed that obese women experience DUB for twice as long as women who are not overweight and tend to be resistant to MPA.  So, what could be done next? 

Plan:  The patch was not an option since, according to the package insert, efficacy could not be reported for women >198 lbs.  While it has been shown that weight reduction leads to restoration of normal menses in 50% of obese patients (NEJM 1953; 249:835), this was not an immediate option.  Other treatments include prostaglandin-inhibitors (NSAIDS), GNRH-agonists, hysteroscopic endometrial ablation, laser electrodiathermy and hysterectomy, but there have not been any randomized clinical trials done to date that point to the best option for obese patients.  I was able to find one study that is currently ongoing that IS exploring the efficacy of intensive medical therapy vs. hysterectomy, in the framework of a randomized clinical trial, in women who have failed the MPA protocol.  The medical therapies include:  1.  combo low dose OCPs (21 days active, 7 days placebo) +/- prostaglandin synthase inhibitors  2.  continuous OCPs  3.  alternative progestogens (oral or IM forms) or 4.  a Levonorgestrel-releasing Intrauterine system.  However, obesity provides an extra challenge since, like the patch, most standard OCPs are not proven in women >200 lbs. 

Hopefully, this study will provide an answer.  A Finnish study has concluded that the intrauterine system, although efficacious in obesity, has a side-effect of increased pelvic pain.  For my patient, at least right now, endometrial ablation may be the way to go.

 

Moderate wine drinkers have lower hypertension-related mortality: a prospective cohort study in French men.

My patients are not french men .. can we generalize?

Background: For a given blood pressure, the risk of death from coronary artery disease is much higher in northern Europe and the United States than in Mediterranean countries.

Objective: In this prospective cohort study, we tested the hypothesis that regular wine drinking reduces the hypertension-related risk of death.

Design: We used data from 36 583 healthy middle-aged men who had normal results on an electrocardiogram and were not taking drugs for cardiovascular disease risk factors. The subjects underwent a comprehensive health appraisal at the Center for Preventive Medicine between 1 January 1978 and 31 December 1985. Mortality from all causes and from specific causes during a 13-21-y follow-up was recorded.

Results: In a Cox model adjusted for 6 confounding variables, moderate wine drinkers (those who consumed <60 g alcohol/d and no beer) with systolic blood pressure (SBP) of 158, 139, or 116 mm Hg had significantly lower risks of death from all causes by 23%, 27%, and 37%, respectively, than did abstainers. Even for the highest quartile of blood pressure, moderate wine drinkers were protected from all-cause mortality. No significant reduction in all-cause mortality in relation to SBP was observed in other drinkers (those who consumed > 60 g alcohol/d or who consumed beer and wine).

Conclusion: A moderate intake of wine is associated with a lower risk of mortality from all causes in persons with hypertension

Case History:  A 48-year-old man comes in with his wife because he has had lower back pain since March. He has experienced pain like this many times before, but age has a way of slowly making aches and pains much more difficult to bear.  Since he works in construction and his back is his income, so to speak, he has been out of work for the past month due to the pain.  He doesn't like visitng the doctor, but the pain is becoming an issue for him and his employment.  He had been taking ibuprofen for the pain, but was wondering if he had any other options.  What was all the fuss about Vioxx and Celebrex commercials that he had seen on TV?

Since no guidelines for treating chronic lower back pain currently exist, most patients are treated with NSAIDs, which has never been clearly shown to be effective.  An article in Spine looked at the efficacy and tolerability of rofecoxib in treating chronic lower back pain.  They performed two replicate placebo-controlled, parallel-group, 4-week, double-blind studies in which the patients were randomized to either a placebo, 25 mg of rofecoxib, or 50 mg of rofecoxib.  They found that rofecoxib significantly reduced the back pain and was well tolerated.

Significance:  Chronic low back pain is such a common and debilitating problem among adults today.  Many people have a hard time taking NSAIDs for long periods of time due to their gastric toxicity.  Cox-2 inhibitors have been shown to be just as effective as an anti-inflammatory and analgesic agent, yet they do not have the same harsh effects on the stomach.

Reference:  Katz, Nathaniel MD, et.al.  Efficacy and Safety of Rofecoxib in Patients with Chronic Low Back Pain:  Results from Two 4-week, Randomized, Placebo-Controlled, Parallel-Group, Double-Blind Trials.  Spine.  Volume 28(9): pp 851-858.  1 May 2003.

CASE HISTORY:

Working in a clinic on Wall St. in the heart of the financial district of NYC provides for some interesting variety in patient population. Amidst the white-collar alcoholics and stock-traders suffering from anxiety induced hypertension, a well-appearing 32 year old male 'Deck-Hand' w/ 10 pack year history presented to our office for a check-up for his new job. Our deck-hand's new ship was set to raise anchor this coming Tuesday, and as he put it, he, "needs this job, and they will sail with or without me!" Unfortunately, for the deck-hand, his urine sugar came up as a 4+. His explanation, "I ate cake, soda and candy for dinner last night." Our next step was to take a random blood sugar and inform him that we would NOT be able to clear him for duty, until the results came back negative or his Diabetes was 'under control."

CLINICAL QUESTION:

Is urine glucose a legitimate preliminary screening tool for Diabetes in an outpatient setting?

References:

Two separate articles have confounding results,

the first discusses urine glucose as a screening tool - "Prevalence of abnormal glucose tolerance in Khon Kaen Province and validity of urine stick and fasting blood sugar as screening tools."

the second discusses urine glucose as a monitoring tool - (Journal of Family Practice. 34(4):495-7, 1992 Apr.) "Urine glucose testing: reliable backup for whole blood glucose monitoring."

PATIENT RELEVANCE:

 According to the first article the validity of the urine stick as a screening tool in communities was insufficient, with a sensitivity of less than 20 per cent. Therefore, "It is concluded that the urine stick is not a useful screening tool and the method of using blood sugar concentrations for screening have to be improved before it can be applied within communities." - keep in mind this is specific to the population from the Khon Kaen Province;

According to the second article, "Urine glucose testing may provide a reliable backup for suspect whole blood glucose values and may prevent catastrophic events requiring expensive hospitalization." - in this case the relevance applies to monitoring (not screening) and in situations where whole blood glucose levels are 'suspect.'

I suppose there are some patients that will always remain in our memories, no matter how much time has elapsed since that one encounter. I had the opportunity of meeting my first such patient this past week. She came in with an interesting history:

An 86 year old woman presenting with complaints of chest pain radiating down her arms, diaphoresis, and nausea that occurred 2 hrs ago. After being briskly whisked off to get an EKG, our unfortunate expectations were confirmed: inferior wall MI. She had experienced a heart attack, and now here she was sitting in our office, plain as day, trying to figure out what to do next. Our advice? We took no sides, but rather informed her of her condition and the possible options. She could go to a hospital where she would possibly undergo invasive procedures, or go home with some B-blockers and aspirin. She chose the latter and decided to let fate do the talking. But it got me thinking: what's the prognosis for such an elderly woman who decided to go with conservative pharmacological therapy  vs percutaneous coronary intervention(PCI)?

According to this article, primary PCI in the elderly with AMI is significantly more effective than conservative therapy. Mortality rate was almost two times lower in patients who underwent primary PCI. However, the mean ages of patients participating in this study were 78.8 (PCI) and 80.4 (conservative rx). Results of invasive therapy of AMI in the elderly were also compared with those obtained in younger patients. All reports unanimously documented higher mortality and complication rates in the elderly, thus questioning whether invasive therapy in patients aged >75 years is justified. For an 86 year old woman with a long history of medical problems and sensitivities to various drugs, the benefits vs risks of PCI must be weighed.

Though I am still not completely sure of which course of action was best, this experience really cemented in my mind how every case has to be considered on an individual basis and how the ultimate decision must lie in the informed patient's hands. As the woman left the office, she said something remarkable that stood in contrast to all the serious events unfolding in the background.  "Okay Doctor-In-Training," she said, "I have one last important question for you. Do I get a lollipop and sticker before I leave?"

Case:  This past week I had the opportunity to encounter 2 patients with Diabetes Mellitus Type II.  Both of these patients had elevated fasting blood glucose levels (500 mg/dl and 149 mg/dl).  I noticed that when encountering diabetic patients, the first thing physicians discuss with the patient is the importance of lowering blood sugar and not giving as much significance to the patients' hypertension and/or hyperlipidemia.  Both of my patients were non-compliant and hypertensive individuals and their lipid profiles were not known at the time of visit.  As I was sitting today at Barnes and Nobles, sipping my cup of Colombian joe adulterated with skim milk and fake powdery chemical called Equal, I formed the following question in one of my intact and smooth brain gyri unaffected by USMLE Step I. 

Question:  What would be more important on the long-term cardiovascular morbidity and mortality risk in diabetic patients?  Would lowering the serum lipids, blood pressure, or blood glucose afford patients equal protection against cardiovascular disease?  This question is a momentous one since 50-75% of deaths in diabetic patients is caused by cardiovascular diseases.  To this end, I searched high and low and found the following article from our friends in JAMA.  Enjoy cool cats!

Article:  Huang ES, Meigs JB, Singer DE.  The Effect of Interventions to Prevent Cardiovascular Disease in Patients with Type II DM.  JAMA 2001; 111: 633-42

Summary:  This Meta-analysis study looked at various randomized, controlled, double-blinded studies comparing the effects of medicating cardiovascular risk factors in diabetic patients such as increased serum glucose, hypertension, or hyperlipidemia.  This study found that significant and large protection against CV events (MIs and CADs) were obtained when blood lipids (RR=0.75; 95% CI: 0.61-0.93) and blood pressure (RR=0.73; 95% CI: 0.57-0.94) were lowered in Type II DM patients.  Although lowering blood glucose is also important in preventing microvascular disease in such patients, it is not as important or significant in lowering CV morbidity and mortality (RR= 0.87; 95% CI: 0.74-1.01).  In plain Persian language, lowering blood pressure and lipids decreased the CVrisk in diabetic patients by 25% and 27% respectively, while lowering of blood glucose lowered the CV risk by a not so significant 13%.

Significance:  This meta-analysis clearly shows us that physicians not only should treat high blood glucose in Type II diabetic patients, but more importantly  they must also aggressively treat such patients for any potential hypertension and/or dislipidemias.  In doing so, a large number of unnecessary CV events will be prevented and precious medical resources will not be wasted.

 

Case History: An eighteen year old female came to the office with complaints of a runny nose, cough, headaches, nausea and lack of energy for the last seven days. She had come to the office one week prior when her symptoms had begun and was prescribed a course of antibiotics (amoxicillin) because previous bouts of sinusitis and bronchitis had progressed to pneumonia.

 

While the majority of upper respiratory infections are the result of viral infection, antibiotics are often prescribed to rule out a bacterial cause and to prevent the possibility of a secondary bacterial infection. With the threat of antibiotic resistance creating “super-bugs” and the lack of benefit to patients with a solely viral cause of infection, I was curious to find out more about what factors play a role in the decision to prescribe antibiotics for acute URI’s.

 

The Scoop: In this observational study involving 15 primary care practices in Michigan, patient and physician surveys were distributed during visits for acute URI’s. The study found that the physical findings most associated with antibiotic prescriptions included sinus tenderness, rales, ronchi, post-nasal drainage, and discolored nasal discharge. Also, patients older than 18, sick for more than 14 days, and seen in urgent care clinics were more likely to receive antibiotics. Patients expected antibiotics if they perceived that the drug had helped treat similar symptoms in the past. Signs that decreased antibiotic usage included the presence of clear nasal discharge on examination.

 

Usefullness: This information will be useful in designing interventions to decrease inappropriate antibiotic prescribing for upper respiratory infections.

Case History: An 18 month old boy was brought in by his mother for a well-child visit.  The boy appeared healthy and was all smiles.  The physical exam was unremarkeable, and there was nothing signifying disease in the history given by the mother, except that the boy had been found to have high blood lead levels at a previous visit (at another hospital).  At the time the family (mother, father, 5 children) had been living in an older apartment, but they had moved out since. 

Reference: Text  (This study was conducted in Ohio, but it cites similar studies in the Northeast region.)

Lead poisoning in children can have devestating effects (abdominal pain, lethargy, mental retardation, ataxia, convulsions, coma), but many children exhibit no symptoms despite high lead levels.  It is important to screen children in whom exposure to lead is suspected.  New York state law does not mandate that all children be screened, but it does require the screening of children with risk factors for lead exposure.  What might these risk factors be?  Living in a home that was built before 1960 and low socioeconomic status are the predominant factors (study).  If a child (6 mos-5yrs) comes for a visit and you suspect these risk factors, a blood lead level should be obtained as it could save a lot of pain and disability for that child as well as for the family (and society as a whole). 

Well, after only a week at this central NY family practice I've learned a lot of things. Here are two:

1. Most patients have a friend or relative who is a font of knowledge about nutraceuticals.
2. The only physiological effects that most nutraceuticals seem to have is their ability to make physicians roll their eyes.

So I was a little bit surprised when an elderly patient asked my preceptor about glucosamine/chondroitin sulfate for her osteoarthritis and the doctor said, "I think you should try it." Instead of the usual "save your money," or "well, it probably can't hurt you," Dr. Grace cited studies like this one (full text for JAMA subscribers here) and told the patient that the supplement might actually help her knees.

The study linked above is a metanalysis that finds evidence of probable efficacy for glucosamine/chondroitin sulfate preparations even after making quality adjustments for study design flaws, involvement of manufacturers and publication bias.

It's nice to be able to offer patients some hope for a new way to ease their osteoarthritis pain. Bear in mind, though, that supplements like chondroitin sulfate aren't covered by insurance, and they're not cheap.

Thanks to Joyce and Michael for being brave and posting first (and second).

Based on these posts - I'd like to amke some suggestions as we move forward.  I want you  all to think carefully anout your audience.  The primary readers are your colleagues .. not faculty.

So ..

a) when you give us a URL .. try to make the link to a publicly available resource like the medline entry rather than a link to something deep inside of AMC's resources.  If - based on the abstract in medline - we want to follow it and find full-text .. we can go there ourselves.

b) If you are linking us to the reference or the abstract in medline - you don't need to type out (or cut/paste) the whole reference.  We can follow the link .. right?  So the reference is just extra words to make the poor reader wade through.   Hyperlinks are the modern version of footnotes.  Mrs Finklebaum (4th grade English teacher) taught you to use footnotes so the reader can make it through your paragraph without reading the whole reference.  Do that here too.

c) You don't need to explain why this is patient oriented or why it impacts patient care.  That should be self-evident.  Tell us why you think it's important or useful.  Remember - these posts should be QUICK to read, but provide your readers with good, USEFUL information .. and a bit of editorial flair to keep the readers interest extra points for humor) and show us that you are a human. 

Take a look at this editorial in Bandolier - one of my favorite resources for evidence-based medicine .. and this very well done review of  "Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials."

A 55 year old unmarried woman with Parkinson's disease, treated by deep brain stimulation and sinemet, came to the office complaining of rib pain when she bends forward at the waist. Upon further questioning it becomes clear that this only occurs once per week, is not very painful, and resolves almost immediately. Later in the encounter, the patient explains that her sister passed away recently and that they were very close. Her quite elderly, pain-in-the-ass mother then moved in with her and she had taken on the burden of her mother's multiple health care problems as well as her own. She then admits to being pretty depressed, feeling lifeless (doesn't get happy, sad, angry), chronic fatigue, and has had a loss of libido (who saw that one coming?). She was on Wellbutrin and did well until her sister's death, and then was switched to Paxel soon after because she was maxed out on Wellbutrin and still feeling down.

This article (Okun MS, Watts RL. Depression associated with Parkinson's disease. Neurology; Vol. 58-4. Feb 26, 2002) discusses the clinical features and treatment of depression in parkinsonism. Interestingly, the symptoms of depression can, and often do, preceed the motor symptoms of Parkinson's disease. It isn't clear however, if the depression is exogenous (from the idea of having a chronic disease) or endogenous (a feature of the cells in mood-controlling areas dying or loosing ennervation from diseased cells), or both. Also, depression is a known side-effect of Sinemet - the combination levodopa/carbidopa drug that elevates DA levels in the brain. 

SO, what to do? Depression is so common in parkinsonian patients (40%) that its treatment should be standard of care. How to treat it? Stopping their Sinemet isn't really an option, so...

1. Counseling - this one-two punch has been shown to have better outcomes than just throwing drug at the problem and not processing issues with the patient.

2. Antidepressants - TCA's are one way to go, but have some anticholinergic effects that may limit use in parkinsonian patients so the SSRI's are probably a better option. The patient above was on Paxil - and even though it was probably at least partially responsible for her loss of libido - we increased her dose from 20mg qD to 37.4 mg qD to help stabilize her mood and try to revitalize her. Also, some of the SSRI's can be activating - which is great if the patient is having trouble with declining motor activity, not so good if it makes them jittery. And there's one less horny old lady out on the streets... which is nice.

Hi folks.

1. Elizabeth relayed some of your questions to me.  Hmm .. let's see .. You do need to post every week.  It's not so hard. You'll see.  Please try to make "real" URLs so that others can directly link to the articles you mention.  This will make your posts much more USEFUL (hint hint).
2. PDA download does work remotely .. I've tried it several times.  YOu've got to log in through the http://nsas.amc.edu ... site
3. Here's an example post from someone else .. which I found this morning on http://www.medlogs.com - a medical weblog aggregator.
4. I've posted my own little sample post below.  Remember that this little project should be a good way for you to be documenting waht you're learning.  It's an online learning community we're building here -- a way for you to share "high yield" clinical tidbits with your peers and mentors.  So have fun with it and you'll see that it can be easy.

 

-------------------------

Example post:

This recent article in JAMA looked at whether 200 IU for vitamin E would prevent upper or lower respiratory infections in nursing home residents:

The researchers concluded: "Supplementation with 200 IU per day of vitamin E did not have a statistically significant effect on lower respiratory tract infections in elderly nursing home residents. However, we observed a protective effect of vitamin E supplementation on upper respiratory tract infections, particularly the common cold, that merits further investigation."

(my italcis)

This is interesting and potentially compelling.  There is some evidence that Vitamin E enhances immunity in elderly adults (and some evidence that this may not be widely generalizable) - yet previous studies - while reporting a trend in diminsed infections - had not reported significiant outcomes.   The present study is the first to demonstrate a significant effect of Vitamin E supplementation.

The obvious question is whether we would advise our elderly patients to take Vitamin E on a daily basis. 

Hmm .. Well, it's certainly inexpensive ... and the reported side effects are negligible .. so I suppose it is not likely to hurt -- and MAY help - so this could be an appropriate adjunct for some patients.

Test entry for Wed. morning

www.pubmed.gov

Hello class!