Viewing By Category : Rotation 6 04-05 / Main
July 12, 2005
Insect bites

Insect bites

This topic might seem trivial but it presents a common complaint. Many times patients cannot tell what has bitten them. The ability to identify the culprit based on the rash's pattern and presentation can be helpful in educating your patients for prevention.

Mites (also see scabies): produce pruritus and/or allergic rxn through salivary proteins deposited during feeding (fall off after feeding). Nonsensitized: 1 to 2 mm pruritic papules; sensitized:  urticaria, vesiculation or granulomatous rxn with fever and LAD. Chigger (havest mites - red bug), attach to the skin in the ankles, waistline, armpits and perianal area after walking through a grassy environment, can cause intense itching. 

Ticks: Attach and feed painlessly. Secretion can produce local rxn, febrile illness and tick paralysis (rare and occur only if bitten by female ticks). Induration, necrosis, and tick granulomas may develop. More on ticks and associated diseases

Begbugs: common sites: face, neck, arms and hands with linear arrangement of two or three lesions in a row ("breakfast, lunch and dinner") (bottom right picture) - pruritic (can be intense), urticaria-like papules. Human is the preferred host - feed once a week and can survive for 6 to 12 mos without feeding.

Fleas: papular pruritic urticaria at exposed bite site (more picture). Both sexes feed on blood. The female flea, after insemination, burrows itself in the skin of the toes and the sole of the foot. The female swells to the size of a pea, produces eggs and dies in the tissue. There is local reaction to the bite and the eggs and dead flea produce reaction. The infested tissue can get infected and gangrenous; auto-amputation is not uncommon. More on fleas

Lice: Three types of sucking lice are important for human health: Pediculus humanus capitis (head louse), P. humanus humanus (body louse) and Pthirus pubis(crab louse). Lice spend all of their life on one very specific host and both male and female feed on blood and leave one host only to transfer to another. Diagnosis is made based on finding nits on eyelashes /hair  or in seams of clothing. Transmission by close physical/sexual contact. Small erythematous papules or blisters. Of note, pediculosis pubis frequently coexists with another STD.

Scabies: "the 7-year itch" - can present in many ways: intraepidermal burrows http://www.dermnet.com/image.cfm?imageID=5745&moduleID=10&moduleGroupID=365&groupindex=0&passedArrayIndex=9 (distribution from most to least common sites: interdigital webs of hands>wrists>shaft of penis>elbows>feet>genitalia>buttock>axillae>elsewhere); scabious nodule , hyperkeratosis/crusting psoriasiform   (more pictures 1 2 3). Sx: pruritus (may not have associated cutaneous findings), LAD in some cases;. More on scabies

Management: Avoid scratching to prevent secondary infection with GAS and or S. aureus causing impetigo or ecthyma (ulceration covered with crusts). Give topical antitpruritics such as Camphor or Menthol to relieve symptoms. Severe cases can be treated with corticosteroids.

Prevention is key. Educate your patients about using insect repellent such as DEET, apply permethrin spray to clothing, spray household with insectides such as malathion, 1 to 4% dust) with special attention to base boards, rugs, floors, upholstered furniture, bed frames, mattresses, and cellar. Also treat flea-infested cats and dogs

July 10, 2005
Atrial Flutter

A 64 year old Puerto Rican woman with no prior cardiac history presented to the Emergency Dept with palpitations, dizziness and shortness of breath. On ECG she was found to be in atrial flutter. She had been under considerable personal stress recently, and was being treated for hypertension with 12.5 mg HCTZ, and 50 mg metoprolol. After pharmacologic cardioversion she was monitored for 12 hours and was in normal sinus rhythm the entire time.

Atrial flutter is a relatively common arrhythmia that can impair the cardiac output, and, if associated with atrial fibrillation, promote atrial thrombus formation that can lead to systemic embolization. It is characterized by rapid, regular atrial depolarizations at a characteristic rate of approximately 300 beats/min.
Symptoms
Most patients with recent onset atrial flutter have symptoms resulting from the rapid heart rate. Typical complaints include palpitations, fatigue, lightheadedness, and/or mild shortness of breath. Less common problems include significant dyspnea, angina, hypotension, presyncope, or infrequently, syncope.
Etiology
Atrial flutter is most often seen in left ventricular dysfunction, rheumatic heart disease (particularly if the mitral valve is involved), unoperated and repaired congenital heart disease, and after cardiac surgery.
Treatment
Four major issues should be addressed in the treatment of atrial flutter:
1. Reversion to normal sinus rhythm (NSR)
Approaches to converting atrial flutter to sinus rhythm are either internal or external DC cardioversion or pharmacologic cardioversion with class IA, class IC, or class III antiarrhythmic agents.
2. Maintenance of NSR
The strategy to maintain NSR includes depressing atrial premature beats, and may require use of class IA and IC drugs, beta blockers, and amioderone, or to prolong the refractory period with Class III drugs.   
3. Control of the ventricular rate in patients
Rate control in chronic atrial flutter, as in atrial fibrillation, usually involves the administration of a calcium channel blocker.
4. Prevention of systemic embolization, particularly in the patient who also has atrial fibrillation
Many patients have periods of atrial flutter associated with episodes or a history of atrial fibrillation. In such individuals, the embolic risk is similar to that in patients with atrial fibrillation and the choice between warfarin and aspirin therapy is based upon perceived embolic risk.

Wellens, HJ. Contemporary management of atrial flutter. Circulation 2002; 106:649
Fuster, V, Ryden, LE, Asinger, RW, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary. A Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology. J Am Coll Cardiol 2001; 38:1231.


postmenopausal bleeding

67 year old female patient came in today stating that she had bleeding from her vagina when she woke up this morning.  She was so sure that blood was not from her urinary tract.  She went through menopause about 20 years ago and she has not had any vaginal bleeding since then.  She had history of regular menstrual cycle and denied using HRT. 

Post menopausal bleeding refers to any vaginal bleeding in a menopausal women other than the expected cyclic bleeding that occurs in women taking HRT.  In this age group, endometrial carcinoma is the most important consideration.  Approximately 10% will have endometrial cancer.  However, most common cause of bleeding in these women is atrophy of the vaginal mucosa or endometrium.  Abnormal bleeding in the genital area is usually attributed to a uterine source, but may rise from problems at multiple anatomic sites including the lower genital tract(vulva, perianal region, vagina, and cervix) and upper genital tract(fallopian tubes, uterus, and ovaries).  In addition, the origin of bleeding may include nongynecologic sites such as urethra, bladder, and bowel.  A large series of 1138 women age 41 to 91 years with postmenopausal bleeding (351 on HRT) reported the following types and frequency of histopathology:  atrophy(59%), polyp(12%), endometrial cancer(10%), endometrial hyperplasia(9.8%), hormonal effect(7%), cervical cancer(<1%), and other(2%).    

Risk factors for endometrial cancer are exposure to high levels of unopposed estrogen, chronic anovulation, early menarche, late menopause, obesity, diabetes, HTN, nulliparity, and a positive family history.  Peak onset is between 50 and 70. 

Common symptoms are postmenopausal bleeding, menorrhagia, metrorrhagia, lower abdominal pain, and cramping.

 Information that is important in the history includes trauma, nature of bleeding, medications, and family history of bleeding disorder.  Pelvic examination determines the bleeding sites and notes any suspicious lesions.  Endometrial biopsy or transvaginal ultrasound can be used as an initial test for endometrial monitoring. Endometrial biopsy allows the doctor to sample small areas of the lining.  Vaginal probe ultrasound is increasingly being used more than endometrial biopsy to evaluate women with postmenopausal bleeding. Vaginal ultrasound measures the thickness of the endometrium. The disadvantage of vaginal ultrasound is that it often does not show polyps and fibroids in the uterus.

 http://www.chclibrary.org/micromed/00061470.html


valerian

I saw a patient last week, an older gentleman, who returned to the office after I had seen him a couple of weeks earlier.  His chief complaint is insomnia, and he looked significantly worse than I had seen him before.  He was more lethargic, some of his words were slurred, and he tripped over himself several times.  He brought in his sleep log and he basically gets about 2-3 hours of sleep a day.  For the past 6 months!  It has gotten progressively worse and he's at the end of his rope.  I did a brief depression screen and had him fill out a questionnaire and there seemed to be no evidence of depression.  He also does not have any stressors in his life.  So, what could we do for him?  He has tried Tylenol PM, Xanex, ambien, and sonata without success.  At this visit, my preceptor suggested valerian, a plant root.

Here is a Handout from the AAFP for patients with insomnia that may be helpful.  In terms of evaluating patients with insomnia, start with a thorough H&P including psychiatric history and family history.  Then, ask the patient to take a sleep log.  Lab tests that can be pursued are polysmnography, multiple sleep latency tests, and neuroimaging.  Multiple sleep latency testing is where the patient is provided with four or five daytime "nap opportunities" consisting of being recumbent in a dark room and requested to fall asleep within 20 minutes during each "opportunity" is helpful in documenting pathologic sleepiness. Most patients with insomnia are not truly hypersomnolent during the day; MSLT testing is indicated only in cases where there is true inappropriate daytime sleepiness.  Non-pharmacologic treatment options include relaxation techniques, stimulus control therapy where the patient is trained to associate the bedroom with sleep, and cognitive behavioral therapy.  Pharmacologic therapies include benzodiazepines and non-benzodiazepines such as zopidem and zaleplon.  

Valerian is a plant root that has been used to treat insomnia.  Study1 is a randomized clinical trial of 42 patients that concluded that valerian is not better than placebo in treating insomnia.  However, the sample size is too small to have adequate power.  Study2 is a randomized clinical trial of 202 patients comparing valerian with oxazepam and it concluded that valerian had similar efficacy to oxazepam with statistically comparable rates of side effects.  Study3 is a review of the literature that concluded that valerian efficacy is inconclusive.  Study4 investigated the combination of valerian and kava in the treatment of insomnia and found that there was no difference in efficacy between the two and that there was a significant increase in efficacy when they are used in combination.  

So I guess the jury's not out yet on the efficacy of valerian.  However, I can tell you that if you saw the patient I saw, you'd care very little about what the studies said and just have him try it.  


Gallstones - straight from the book to the clinic...

This week, I was very excited when I saw a patient who seemed to be describing symptoms straight out of one of my board-review books.  As someone who tends to second-guess herself, I was able to present a patient to my attending knowing exactly what I thought we should do and what the diagnosis would ultimatly be!

The lucky (or not-so-lucky) patient in this case was   overweight and middle-aged, and presented with intermittent right upper quadrant pain over the last 3 months.  The episodes started out about 1X/week, and had steadily been increasing in duration, now occurring every other day, prompting the patient to seek medical attention.  During these episodes, the patient describes the pain as a constant, 8/10, sharp pressure, that occasionally radiates to her back;  the pain starts suddenly, lasts approximately 15-30 minutes, and stops just as suddenly.  It was not relieved by any position, and she had not taken any meds for it.  The pain was also associated with nausea, and diaphoresis.  No vomiting or fever; no constipation or diarrhea.  The patient denied association between meals and the pain, but when closely questioned, each episode began within 1-3 hours of her last meal, which often consisted of fatty foods, including burgers, fries, and steak.  She does not drink alcohol.

The patient had no prior medical or surgical history, but did have a family history of gallbladder disease (Father recently had a cholycystectomy).

Physical Exam at this time was non-significant, with no abdominal tenderness, and a negative Murphy's sign (arrest of inspiration with deep palpation in the RUQ; often positive in acute cholycystitis).  After presenting this patient to my attending, we decided to send the patient for an Ultrasound, which did confirm gallstones and billiary sludge a few days later.

Billiary colic is a result of gallbladder contraction, usually in response to a fatty meal, which forces a gallstone into the cystic duct opening, causing increased pressure in the gallbladder and pain, which resolves when the gallbladder contraction relaxes.  It is often post-prandial, following a high fat meal, and can be associated wtih diaphoresis, nausea, and vomiting.  Physical exam in between episodes is often normal, but may have RUQ abdominal tenderness.  Billiary colic should be differentiated from acute cholcystitis, which is a result of obstruction of the cystic duct and acute inflammation; it is also associated with fever, and an elevated WBC count.

Risk Factors for Gallstones:

  • Women
  • Age > 40
  • Native American, Hispanic, Caucasian
  • Family History
  • Pregnancy
  • Obesity
  • Frequent fasting
  • Rapid weight loss
  • Diabetes Mellitus
  • Sickle Cell Disease
  • Cirrhosis
  • Medications: ex. fibrates, steroids, post-menopausal estrogen, octreotide, ceftriaxone

Possible Complications of Gallstones:

  • Billiary Colic
  • Acute Cholecystitis
  • Emphysematous cholecystitis (acute infection of the gallbladder caused by gas-forming organisms)
  • Mirizzi's syndrome (compression of the common hepatic duct or common bile duct)
  • Hydrops of the gallbladder (gallbladder lumen  becomes distended wtih clear mucoid fluid)
  • Small Bowel obstruction  (gallstone illeus)
  • Bouveret's syndrome (Gastric outlet obstruction)
  • Perforation of gallbladder
  • Acute biliary pancreatitis
  • Choledocholithiasis (stones in common bile duct)
  • Cholangitis (inflammation of common bile duct; billiary colic, jaundice, and fever)

 

Treatment Options for Gallstones:

  • Diet modification (high fiber, high calcium, low saturated fat diet) and expectant management
  • Surgery - Laparoscopic vs. Open Cholcystectomy
  • Non-surgical treatments: Oral bile acid (ursodeoxycholic acid; disolves cholesterol gallstones; patients become asymptomatic over 2-3 months); Percutaneous endoscopic lithotripsy; Extra-corpeal shock wave lithotripsy

 

 

This link is to an article that discusses management of gallstones: http://www.aafp.org/afp/20000315/1673.html

This link is to a patient information website:  http://familydoctor.org/555.xml 

This link is for patient nutrition information:

http://www.johnson-county.com/publichealth/cardiovascular/nutrition.shtml

I should also note that we (aka -my attending), did decide to start the patient on a PPI in the interim (before the ultrasound), in case of Peptic ulcer disease, which was also high on the differential. 


Sialolithiasis
I saw this young female in the office the other day.  She said that she was out with her friends at a Chinese restaurant and she experienced a sudden onset of focal lateral neck swelling with acute pain.  After she had finished eating she went to the ER and by that time the swelling had gone down so they treated her for strep throat with abx.  She experienced these symptoms a few more times and then decided to come in.  

 

On exam it was possible to feel a pea sized stone under the angle of the mandible.  It was determined that she most likely had a submandibular stone.  She was sent for a CT to confirm the dx.  We also gave her a referral to ENT so they could assess whether or not to remove the stone.  Here is a quick overview with some imaging.

 

Treatment is based on the location of the stone.  If the stone is in the anterior portion of the duct and does not pass spontaneously it can be extracted intraorally.  The ductal papilla can be serially dilated with using graded lacrimal probes, the stone is then massaged out.  If the stone is too big, an intraoral procedure under anesthesia is done.  The duct is cannulated and the incision over the stone is created to allow extraction.

 

Stones that are larger and in the hilum or body of the gland may require surgical excision of the gland.  Recently some endoscopic procdeures have been performed which allows one to avoid a transverse cervical incision.  Other options include wire basket extraction under radiologic guidence and different forms of lithotripsy.

Stones that are larger and in the hilum or body of the gland may require surgical excision of the gland.  Recently some endoscopic procdeures have been performed which allows one to avoid a transverse cervical incision.  Other options include wire basket extraction under radiologic guidence and different forms of lithotripsy.Here are some cool pics

 

 

 

 


Peritonsillar cellulitis

 

Last Friday afternoon an older gentleman with Type 2 diabetes mellitus presented to the clinic with a one week history of a sore throat.  The patient described discomfort only on the right side and over the past two days he begun to notice a sense of fullness on that side.  Although his throat has been bothering he has been afebrile throughout this illness and never described any dysphagia.  Aside from the sore throat he hasn't any other symptoms of pharyngitis within the past two weeks.  On exam, his oropharynx was erythematous but no exudate was present.  Additionally the peritonsillar space was erythematous but not exudative or flucuant on palpation.  With this patient's physical findings and a history of a unilateral sore throat for a week I thought he had a small or early peritonsillar abscess but my attending corrected me and said this is more like a peritonsillar cellulitis.  Needlesss to say, I had never heard of such an animal so I wanted find out if there is a connection between cellulitis and abscess. 

Cellulitis is an infection of the skin with some extension into the subcutaneous tissues. While an extremity is the most common location, cellulitis can involve any area of the body.  In addition, cellulitis falls into a continuum of skin infections also including impetigo, folliculitis, carbuncles, and abscesses.  Well there you have it, cellulitis and abscesses are related pathologies where if cellulitis is left untreated, it could progress to an abscess.

In the case of this patient, since he probably had peritonsillar cellulitis, oral Augmentin was the therapy of choice.  Had he presented with a more fulminant infection of the peritonsillar space, incision and drainage of the abscess would be required and probable intravenous antibiotics.

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12126026&query_hl=2


What is paronychia?

I saw a man this past week who came in and said that he bumped his nail yesterday and that it is infected today.  This sounded strange to me, however, I have since learned that this is a classic presentation of paronychia, or an infection of the cuticle.

 Acute paronychia can develop over a few hours.  The nail fold quickly becomes painful, red, and swollen.  There may be yellow pus, fever, or painful glands in the axilla.  This is usually a staph infection, and can often be treated with warm soaks, antibiotic cream and oral antibiotics.  If there is an abscess, it must be drained.  Our patient had an absecess, so we had to open it up and let the pus out. 

 The history for paronychia may be similar to the patient discussed herein, or it may occur in a patient who gives a history of nail biting, finger sucking, trivial finger trauma, finger exposure to chemical irritants, acrylic nails or nail glue, sculpted nails, or frequent hand immersion in water.  It is important to identify patients with diabetes mellitus, immunocompromise, or history of steroids or retroviral use.

 The following features may be found on physical exam:  erythema, edema, tenderness along the lateral nail fold, or fluctuance.

 Infection is usually caused by Staphylococcus aureus or Streptococcus species.  Sometimes you can find a mixed bacterial infection or a mycotic infection.

There are some rare complications to this infection.  The infection may spread to the pulp space of the finger, creating a felon.  The infection may also spread to involve the deep spaces of the hand, there may be ridging, thickening, and discoloration of the nail, or the nail might fall off.  If treated promptly, however, prognosis is usually quite good.

 This link shows some pictures of paronychia: http://www.aocd.org/skin/dermatologic_diseases/paronychia_nail_in.htmlAnd this is a link to an article with more information on this topic: http://www.emedicine.com/emerg/topic357.htm


Plane crash survivors: Risks and presentation of PTSD

This week, a plane crashed on a glacial lake and the survivors of the crash were brought in to the ER.  All but one survived, and the survivors had witnessed his death.   While none of the survivors had serious physical injuries, they had experienced a significant emotional trauma in witnessing the death of one of their fellow travelers.  This experience triggered my thoughts about post-traumatic stress disorder and what could be done to help prevent it in the survivors of this crash.

PTSD is a fairly common mental health disorder that has a lifetime prevalence of about 10% in the US.  It occurs after an individual experiences or witnesses a traumatic event, such as assault, kidnapping, military combat, natural and man-made disasters, severe motor vehicle accidents, diagnosis of a life-threatening illness, rape, incest, and childhood sexual abuse.  Many of these events are common and considering the prevalence of this disorder, it is reasonable to think that most of us will encounter individuals with PTSD at some point in our careers.  In the US, it is most common among refugee, inner city, and war veteran populations.

The key characteristics of PTSD are:  1) exposure to trauma  2) reexperiencing the trauma  3) avoidance of the trauma and 4) increased arousal.

Most people who have experienced a traumatic event will react to some degree when reminded of the event, but those with true PTSD will react with more severe responses such as flashbacks, severe anxiety, and avoidant or combative behavior.  They can also learn to avoid triggers by emotionally shutting down which results in lack of interest in usual activities and developing detachment from others.  They can have difficulty managing their emotions, which can result in emotional outbursts, and often will show other signs of psychiatric illness such as somatization, substance abuse, and self-destructive behavior.

Many of the signs of PTSD overlap with other psychiatric illnesses, and can resemble depression, anxiety and even psychosis.  One key distinguishing feature is the exposure to trauma and reexperiencing of that trauma.  If you're interested in reading more about PTSD in the primary care community, here is an article with a good general overview.

PTSD is also something to be aware of for anyone interested in doing international work, especially in refugee/disaster situations.  Not only for the population that you are serving, but also for the humanitarian aid workers.  Many aid agencies will organize weekly or monthly debriefing sessions for their aid workers with the goal of reducing stress and helping to process traumatic events seen or experienced by the aid workers themselves.  Even if you're not planning to go overseas, exposure to trauma often leads to trauma among emergency workers (paramedics/ firemen) and is something to be well aware of for anyone working with trauma (eg emergency medicine).


Annual Physicals Cause AIDS and Cancer

So just kidding...but I thought it would a fitting end to third year and blogging with this post. Last month a study appeared in the Archives of Internal Medicine that showed that despite NO reccomendation by the AMA that annual physicals examinations of asymptomatic adults result in a decline in mortality or morbidity, most (65%) of primary care physicians believed that it was necessary to have annual physical exams and 90% of them performed such exams. Moreover (but not included in this specific study), most of the public believes that such exams are necessary as well.

Now this is a double barrelled statement, so let me clarify. The annual physical exam was first recommended in the 1920s as an effective way to detect subclinical disease. BY 1947, the AMA officially recommended that all adults over 35 have annual physical exams. By the 1970s, a myriad of studies came out questioning the usefulness of such recommendations and in 1983 the AMA took the first steps to reverse their recommendations concluding that an examination be performed every 5 years before 40 and about 3 years there after.

Now this is an annual physical exam and is not to be confused with a periodic health maintenance which addresses specific age and gender related problems such as mammograms for breast cancer or colonoscopy for colon cancer. The physical exam findings and the especially the laboratory studies- the CBC, BMP, LFT, Kidney Functions, TFT, UA, and EKG- were said to give rise to more FP and negative results that would lead to either unnecessary further testing or at the very least lead to a waste of money.

The second portion of the original statement was that most physicians believed in the utility of the annual physical exam and did them routinely. Again, they cited the fact that it could detect subclinical disease and created a good doctor patient relationship.

Now for my own editorial, my first reaction when reading the study was that it was nonsense. A physical exam is important in detecting hypothyroidism in someone who might have just attributed their fatigue to their life situation, or finding elevated cholesterol, blood sugar, or blood pressure in a healthy individual, and certainly managing these conditions would cause a decrease in mortality and morbidity. But the more I read into it, the more I realized that they were not  NEVER recommending doing the tests or physical exams; rather they felt that doing these tests on everybody, even people with NO risk factors, pertinent history, or pertinent family history was not cost effective. Indeed for some of these tests-like lipids- there are recommendations after 45, but this is based on epidemiological studies.

So it really caused me to reflect on the number of school physicals, camp physicals, and annual physicals that are performed on individuals in my office every day. How my attending doesn't enjoy doing them, because they take up more time than sick visits, and how nobody recommends doing them in the first place.

Well there you go.
http://www.washingtonpost.com/wp-dyn/content/article/2005/06/27/AR2005062701368_pf.html

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15983282&query_hl=2


Dangerous Complication of Warfarin

An obese elderly lady came to the clinic last week with a complaint of breast and buttock pain.  Her history was positive for recent onset a-fib.  She was put on Warfarin therapy 4 days ago.  On PE red, tender plaques were visible on her breasts and buttocks.  According to my doc, this woman exhibited a rare, but dangerous (even fatal) drug reaction: "Warfarin necrosis". 

Adverse effects of warfarin are categorized into hemorrhagic and nonhemorrhagic complications. Although, GI bleeding is the most common hemorrhagic related complication of warfarin, less common nonhemorrhagic complication such as allergic maculopapular eruptions, urticaria , eosinophylic pleuritis , vasculitis , toxic hepatitis, skin necrosis and purple toes syndrome have also been reported.

Warfarin necrosis occurs in 1 in 10,000 patients. It most commonly affects obese women, who develop painful red plaques on the fatty parts of the body - breasts, hips, and buttocks 3 to 5 days after therapy initiation. Hemorrhagic bullae and necrosis follow and may require surgical debridement..  It is thought to be caused by a transient hypercoagulable state due to a reduction in protein C, a natural anticoagulant, prior to a reduction in other vitamin K-dependent coagulation factors.  Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels by inhibiting vitamin K, it can lead to massive thrombosis with necrosis and gangrene of limbs.  Histology shows thrombosis in dermal vessels.

The treatment is therefore vitamin K, heparin, and discontinuation of warfarin. The physician should also attempt to obtain and administer monoclonal antibody-purified protein C concentrate. The key to management is rapid diagnosis of red, painful plaques in fatty areas.

Breast Necrosis picture

Good article here

July 9, 2005
Childhood heart murmurs
I saw a child the other day with a heart murmur and I had trouble determining if it was innocent or pathologic. This is really important to avoid unnecessary anxiety, cost of workup, and/or restrictions.  So I thought I would write a review of childhood murmurs because they are actually quite common.  50% of all children have heart murmurs, and 10% of those are pathologic.

Innocent murmurs
(starting wtih most common)
1) Still's aortic musical/vibratory murmur - early systolic murmur at left lower sternal border
2) Venous hum of late infancy or eary childhood - heard best at upper right sternal border and disappears when child his supine or when light pressure is applied over child's jugular vein
3) Pulmonary flow murmur of late childhood and adolescence
4) Neonatal pulmonary artery branch murmur

Pathologic murmurs
1) VSD - 38%
2) ASD - 18%
3) Pulmonary valve stenosis - 13%

Signs that are reasurring of an innocent murmur:
  • No evidence of failure to thrive
  • no cyanosis, diastolic murmur, holosystolic murmur, parasternal heave, thrill, or murmur that is louder than II/VI)
  • Accentuated by sitting forward and decreases when standing
  • Accentuated by exercise, anxiety, fever, crying
  • No radiation to neck or back
  • Lower (rather than higher) along left sternal edge
When to refer?

For cost reasons, patients with a pathologic cardiaic exam or cardiac symptoms should be referred to a pediatric cardiologist versus doing an echo.  If referred, pediatric cardiologists should be able to diagnose these murmurs with clinical exam only without wasting money on echocardiography.  Sensitivity of clinical exam of all childhood cardiac murmurs if 96% whereas specificity is 95%. 


Guaranteed to be on the test!

I can't begin to tell you how many patients have come in either complaining of a headache or on prophylactic headache medications.  More recently a patient came in and a quick glance at his drug list showed depakote.  Depakote is used for pyschosis, but in this patient it is used for prophylactically for migraines. 

Headaches is one of the most common complaints in the Western world, periodically affecting 90% of adults and almost 25% have recurrent severe headaches.  As with many common symptoms, there is a broad range of conditions, from trivial to life-threatening.  All of us at one point in our lives have experienced a hangover headache that is so painful that it has stopped us from indulging the next weekend.  I just want to breifly outline headaches and their management do it will be easy to identify.

1.  Migraine without aura (common migraine) presents with chronic headaches preceded by nausea and vomiting. Photophobia is usually present. There usually is a family history.  There are various triggers like stress, food, weather changes.  Prophylactic agents for the prevention of migraines are Beta-blockers, amitrypline, paxil, and methysergide.  Sleep during an acute episode is indicated or sumatriptan but not NSAIDS.

2.  Migraine with aura (classic migraine) presents like a common migraine but is usually preceded by a visual irregularity or slight-flashing lights.  Treatment is the same as common migraines.

3.  Cluster headaches: this is diagnosed by its distinctive pattern of grouped attacks of intense, unilateral, periorbital pain with nasal or ocular watering lasting only minutes to 3 hours but recurring over several weeks or months.  Acute attacks may be treated with oxygen or subq sumatriptan.  Prophylaxis is with B-blockers, TCA, and SSRIs.

Tension headache: Presents with occiptal-frontal headache; it is constant.  If the headaches are constant and chronic attempts should be made to identify the casual factors and eliminate those, whether stress, food, etc.  Mild anagesics such as acetominophen, NSAIDs, ASA TCA and SSRIs are used.  But be aware of rebound headaches from overuse of these meds, especially NSAIDs.

For a great website checkout: http://www.nevdgp.org.au/geninf/std_misc/headaches_types.htm

We also know the broad differential on the headahce list that include meningitis, brain tumor, temporal arteritis, and gluacoma and mostly be aware of the patinet who comes in with the "worst headache of my life.  The key to the diagnosis is a good H & P and pattern recognition and recognizing the underdiagnosis of rebound analgesic headache. 


Polycystic ovarian syndrome

I recently saw a young women with a chief complaint of increasing "chin hair" (hirsutism) and an irregular menstrual cycle for the last few years (1 cycle/year).  Upon introduction to the patient and after PE, I could add to the list obesity, significant acne on her back and a high BP.

What's the Dx?

She had Polycystic Ovarian Disease (PCOD) or Syndrome which is also known as Stein-Leventhal syndrome (named after the people who first reported it).  The differential included a virilizing tumor, adrenal or ovarian, Cushing syndrome, Idiopathic or familial hirsutism, Ovarian hyperthecosis, Hilar cell hyperplasia, Premature ovarian failure, Insulin resistance and type II diabetes mellitus, Adrenal hyperplasia (adult onset), hyperandrogenism and androgen-producing tumors, and hyperprolactinemia.

Brief refresher: In the normal cycle, the hypothalamus secretes GnRH > pituitary gland releases LH and FSH. LH > theca cells to increase the production of androgenic precursors.  Concurrently, FSH > granulosa cells > conversion of androgens into estrogens, particularly estradiol > helps follicular development.  During the follicular phase, increasing levels of estradiol > LH surge.  LH surge + estradiol > FSH surge.  FSH leads to follicular maturation and ovulation.

In PCOD, the cycle is disturbed and there are many proposed causes but nothing definitive.  Polycystic ovaries are not the primary cause of amenorrhea or hirsutism in this condition. They are just one sign of an underlying endocrine disorder that ultimately results in anovulation.

Signs/symptoms: The most common presentation is infertility and amenorrhea.  Obesity, occurring in up to 50% of patients (usu. have a high waist to hip ratio). Hyperandrogenism resulting in excess hair growth on the face, chest, abdomen, thumbs or toes, male pattern baldness or thinning hair and in severe cases, deepening of voice and increased muscle mass.  Persistent acne and oily skin (seborrhea).  Acanthosis nigricans: dark patches of skin that are velvety or rough to touch. These occur most commonly on the back of the neck, armpits, area beneath the breasts and exposed areas such as the elbows, knees and knuckles.  Diabetes mellitus, hypertension, hyperlipidemia and CV disease.

Diagnosis: free testosterone (may be elevated), LH (elevated), FSH (nl to low), prolactin, insulin levels (increased) and lipid profile. Also, a pelvic U/S is helpful if other causes are suspected.

Treatment: In the past, management of the condition was directed at treating individual symptoms of PCOS, such as hirsutism, acne or infertility. More recently with the understanding that insulin resistance has a large part to play in the development of PCOS, treatment has shifted towards correcting insulin resistance, which in turn improves many other symptoms of the condition.

-Diet and exercise: weight loss in obese PCOD patients leads to decreased insulin resistance and a fall in testosterone levels.
-Metformin and glitazones decrease insulin resistance and the amount of insulin in the blood. They may also normalize ovulation.
-Spironolactone, a powerful antiandrogen, can reduce acne and also body hair growth over time. It is less effective for alopecia. It cannot be used by women who are trying to conceive as it can cause birth defects.
-OCP, in combination with the antiandrogen, cyproterone acetate, helps control acne and hirsutism. It also improves menstrual irregularities.                                               

Additional note:  If these patients are not treated they are at an increased risk for endometrial and breast CA b/c of high levels of unopposed estrogen.

PCOS support website:  http://www.pcosupport.org/

Images!:

http://www.gabrielleoconnor.co.uk/photos/lhporig.jpg

http://www.patientcareonline.com/patcare/data/articlestandard/patcare/332004/112797/pba023f1.jpg

http://www.advancedfertility.com/pics/pco.jpg

http://www.nlm.nih.gov/medlineplus/ency/article/000369.htm


High At All?

53yo G2P2 obese Caucasian female presented to clinic complaining of intermittant retrosternal chest pain, which has been occurring over the last 2 months. The pain is worse at night and is sometimes worsened by eating. There is no association with activity.  The pt has 25 pack year history of smoking.

Physical exam is unremarkable.

Plain x-ray of the chest reveals a large round midine lucency superior to the diaphragm, which appears to have an air-fluid level. 

Note: The image above is a "mixed" hiatal hernia.

Dx: Hiatal hernia (very informative site**)

The two main types of hiatal hernias are "sliding" and paraesophageal.  Sliding hernias have the gastroesophageal junction located above the diaphragm and may be seen by x-ray in >40% of the population.  Most are asymptomatic, but chest pain and reflux can occur.  With paraesophageal hernias the gastroesophageal junction is located below the diaphragm, but a portion of the stomach (usually the fundus) is located above the diaphragm adjacent to the esophagus.  Unlike sliding hernias which only require symptomatic treatment for GERD, paraesophageal hernias require surgical reduction due to a risk of strangulation.  Signs of an incarcerated para-esophageal include sudden onset pain and vomiting.  Immediate surgical intervention is imperative.  There also exists different combinations of sliding and paraesophageal which are referred to as "mixed" hiatal hernias.

Images:

Lateral plain film

PA plain film

Barium swallow

Barium swallow

Double contrast image of large hiatal hernia

Endoscopic view from stomach looking up

July 8, 2005
Dance Dance Revolution Syndrome!?

So I saw a teenager who complained of some foot sores for several months duration.  He told me he's been playing this Dance Dance Revolution (DDR) video game for many hours a day for many months.  He played it so much, the gamepad broke!  So DDR is a game where you literally dance around with your feet on a game pad and you do these quick, herky-jerky, twisting-turning motions on your feet to the sounds and beats of bumping music.    

He played while wearing his shoes and socks.  After months, he developed pain on both feet and sores that didn't fully heal. 

On physical examination, I saw areas of calloused thickened skin, without exudate, without erythema, no fluctuance.  There was mild tenderness.  There was a central area of umbilication about 0.5 cm in diameter.  There were two of these on both feet, one near the first tarsal and the other around the calcaneous. 

Here are some pics:

Pic 1     

Pic 2    

Pic 3

So I was confident to recommend him to lay off the video gaming for awhile... but apparently, I was surprised to learn that the cause of these plantar warts wasn't the endless hours of dancing, but probably due to HPV 1.

Cutaneous verrucae (or warts) occur commonly in children and young adults.  They are also common among meat handlers, hx of atopic dermatitis, and the immunosuppressed.  Spontaneous remission occurs in 2/3 within 2 years.  Recurrence is common.  Spread is by direct contact, so wash those hands!!!

Diagnosis is based on clinical appearance.  If there is doubt, use a no. 15 blade and scrape of debris. 

Treatment includes: liquid nitrogen, salicylic acid, duct tape, bichloroacetic acid, or cantharidin. 

https://nsas1.amc.edu/get/uri/http://www.utdol.com/application/topic.asp?file=pri_derm/8201&type=A&selectedTitle=1~5

http://health.yahoo.com/ency/healthwise/hw64902

 

 

  

July 7, 2005
The Many Faces of Shingles

In clinic, we saw an individual with a rash that looked suspiciously like shingles but, because it was limited to a tiny area, we couldn't tell if it was dermatomally limited.  The rash and course have since behaved as expected, so shingles remains the diagnosis.

For those who have yet to see a case of shingles, the classic rash involves exquisitely painful, small, fluid-filled blisters on reddened skin, usually preceded by several days (range:  3-14 days) of inexplicable pain, burning, itching, numbness, and/or tingling in the area, with or without constitutional symptoms. 

Shingles is caused by varicella-zoster virus (VZV)--the same virus that causes chicken pox.  Since shingles is a reactivation of the virus, only persons who have previously had chicken pox can develop shingles.  During reactivation, VZV migrates down a nerve fiber to the dermatome innervated.  The rash develops here. 

Treatment-wise, the course of the attack can be reduced by treatment with antivirals (e.g. acyclovir, valcyclovir, or famcyclovir) within 48 hours of symptom onset.  Analgesics are also appropriate.  Pain decreases over 3-5 weeks.  If diagnosis is uncertain, detection of viral particles in the blister fluid or blood can help.

Simple enough, right?

However, some attacks warrant close monitoring.  The following are presentations and sequelae to watch out for:

Secondary infection:  Treated using antibiotic cream or po antibiotics.
Shingles of the upper cheek or temple:  Shingles here may also affect the eye.
Ophthalmic herpes:  Eye affected or soon to be affected.  Referral to an ophthalmologist may be indicated.
Ramsay Hunt syndrome:  Affects facial nerve, causing severe ear pain.  Rash may appear on outer ear, inside ear canal, in mouth, or on scalp or neck.  Can lead to hearing loss, vertigo, and facial paralysis that is usually temporary, but may be permanent.
Hutchinson's sign:  Rash in single spot or cluster on tip of nose.  Suggests that eye will be affected, causing vision loss (temporary or permanent).
Post-herpetic neuralgia:  Long-lasting pain (on the order of months or years) that's difficult to treat.  May be more intense than the initial outbreak pain.  Refer to a pain specialist.  Try alternative therapies. 


Gynecomastia from the use of PPI's

This past week I was amazed to learn about this possible side-effect from PPI's. The patient was being seen in follow-up s/p breast reconstruction. He had been taking this medication for a couple of years and never real notice the breast development until it became quite apparent, non-symmetrical and cosmetically debilitating.

Just as a quick reminder: Gynecomastia is a benign enlargement of the male breast resulting from the proliferation of the glandular component of the breast. This condition results from an altered estrogen-androgen balance, in favor of estrogens, or increased breast sensitivity to a normal circulating estrogen level.

This is relatively common finding that can be either pathologic or physiologic. Certain causes include: primary or secondary hypogonadism, over production (or peropheral conversion) of estrogen from testicular tumors or to ectopic production of human chorionic gonadotropin that has been reported with carcinoma of lung, kidney, GI tract, and extragonadal germ cell tumors. Other causes include chronic liver disease, malnutrition, hyperthyroidism, adrenal tumors, and familial gynecomastia along with drugs as seen in my patient.

The literature linking gynecomastia and prevacid is relatively weak. The are two articles out of Spain showing the link, however, I has unable to view the whole article. I have linked below a good sight the talks about gynecomastia, causes, and how to treat.

I know in my Family Practice office the use of PPI's is overwhelming so keep in mind this cosmetically devastating side-effect, along with the others, and be sure to screen for it so that you can remove the causitive agent in a timely manner.

http://www.ccjm.org/PDFFILES/Bembo604.pdf


Osteoporosis and lack of Vit D

What I have realized in this FP rotation is that these doctors spend a lot of time educating patients in preventive medicine.  If not them in halting the progession of preventable diseases then who will.  Cetainly not the rheumotologist or cardiologist.  By the time the patient gets a referral for these doctors the damage is already done.  The one thing that has frustrated me in talking to these patients is the noncompliance of the patients in taking measures set forth by their doctor.  But that is a another discussion for another day. 

The one diseases that can be prevented which is a significant cause of pain and doctor visits is osteoporosis.  Osteoporosis is a disease that can be prevented and should be. It is an important health issue because the resultant bone fractures cause a great deal of morbidity in chronic pain (leads to narcotic abuse), loss of independence, and loss of function, as well as mortality.  Women clearly in my office do not take enough calcium and Vit D.  The recommended daily calcium for a woman in menopause is 1500 units a day.  More recently data shows that another significnt cause for osteoporosis in women is a lack of Vit D.  We all know form endocrine that calcium cannot be absorbed form the gut if there is no Vit. D.  Vit D comes from our diet and from being exposed to the sun.  IT is recommended that women in menopause take at least 400-800 IU a day. 

Risk factors for the developmentof osteoporosis include a low peak skeletal density reached in young adulthood, increasing age, loss of steroid hormone production (menopause), smoking, nutritional def., and genetically low bone density.  Approximately 14% of white women and 3-5% of white men will develop osteoporosis in thier lifetime.  The prevalence is lower in other ethnic groups.

Another weapon against osteoposis is these bisphosphonates.  These drugs work by inhibiting the resorption of the bone.  So the arsenal against osteoposis is Vit D, Calcium, and bisphosphonates.  The last thing that is needed is patinet compliance. 

In order to catch early osteoporosis and prevent it bone minral density screening sjould be offered to patinets with risk factors for osteoporosis, and to all women older than age 65 years.  The reason that this is so important is that fractures in the elderly can have a devasting effect upon a patients.  Thus a dexa scan in the office setting is the first step.

Treatment:  As described above is multifaceted approach. Adequate calcium intake, Vit D, estrogen replacementm bisphophonates, and finally weight bearing physical activity.  For a great website see http://www.nof.org/ and for a great article see NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy. Jama 2001; 285 (6):785-95

T

July 5, 2005
Pseudosciatica

Like lil james would say... "What?!"

S: Pt presented with the ubiquitous "low back pain". He was vigorously playing with his kids in the swimming pool and bending down to pick them up many times throughout the day using crappy back mechanics.  Lo and behold he awoke with severe dull, achy low back pain, rated now as 8/10.  He has had past back issues but this event was different; he had noticed a left sided radiculopathy with a burning sensation down into his foot. His low back pain had also moved into his buttock and it was difficult to sit for long periods of time or to squat down. He and his wife were on their way to vacationing 4 hours away and he didn't feel that he could make the trip secondary to the intense pain. O: AVSS; 5/5 strength; no sensory loss; straight leg test negative; no TTP along spine or SI joints; in right lateral recumbent position, pain reproduced by 1) flexing knee and hip and applying internal rotation and by 2) palpating along the area of the piriformis with one very tender "hot spot".

A few provocative tests are available:

  • Beatty's maneuver: the patient lies on a table on the side of the nonaffected leg. The affected leg is placed behind the nonaffected leg with the bent knee on the table. Raising the knee several inches off the table causes pain in the buttocks.
  • Freiberg's maneuver: forceful internal rotation of the extended thigh which stretches the piriformis muscle and causes pain.
  • Pace's maneuver: abduction of the affected leg elicits pain in a sitting patient.
  • Mirkin test: the patient should stand, keeping the knees straight, and slowly bend toward the floor. The examiner should press into the buttocks where the sciatic nerve crosses the piriformis muscle, causing pain that starts at the point of contact and that extends down the back of the leg.

What is the relationship of the piriformis to the sciatic nerve, you ask? Well, in 88% of pts studied, the sciatic nerve runs posterior to the piriformis. In the rest, it runs through it or around it. These pts are more prone to having problems with sciatic neuropathy.

Assessment/Plan: Piriformis Syndrome; Therapy includes...

  • Learning and doing stretching exercises for the piriformis muscle (VERY IMPORTANT!) [Examples: 1 2 3 ]
  • Rest
  • Placing ice packs on your buttock for 20-30 minutes every 3-4 hours for the first 2-3 days, or until the pain goes away
  • Taking prescribed anti-inflammatory medications or muscle relaxants
  • Formal Physical Therapy consult if deemed necessary
  • Botulism Toxin Type B or Type A (abstracts showing positive effect on symptom relief)
  • Arthroscopic release (pdf on article explaining technique—very cool!)
Since our pt was going on a vacation and would be sitting in a car for 4-5 hours, we juiced him up with some Percocet. End of story. Thank you.

July 3, 2005
By the way...I've got

I know this may seem cursory but I had a patient come in with the ambiguous "foot pain".  I, not having interest nor a fetish for feet feel disgusted at times and tend to shy away from these problems.  However, they are unavoidable in the FP clinic. A patient may come in with difficult breathing or heartburn and will "oh, by the way, doc" regarding some foot condition.  Yuk.  Anyway, sometimes the problem is relatively easy and can be fixed by some encouraging words and prescriptions.  Here is one such case, here is my story...

Senor Paco had been walking extensively the past five years or so since his retirement and has not had any problems until about 6 months ago when he began to have intermittent pain in the sole of his right foot.  It was an intense, sharp pain that seemed to radiate from the heel towards his toes, most intense in the heel to mid-foot.  It felt burning at times with more pain with walking or other loading exercises.  Over the past few weeks the pain was most intense the first few steps upon getting out of bed and this prompted his visit to the clinic.

Without any further testing, what is the diagnosis?

Plantar fasciitis (American Family Practice Article) , until proven otherwise. The above complaints are the classic symptoms and description.

Conservative Treatment

  • Rest (limit activities)
  • Ice
  • Supportive shoes and/or OTC orthotics or heel cups
  • Lose weight if an issue
  • Stretching (those listed on website and by pulling upper foot/toes toward shin)
  • NSAIDS

Progressive Treatment

Radical Treatment


Oh, it also causes cancer...

So there have been quite a few patients I have seen who smoke and I have attempted to offer smoking cessation options for them.  Many of them have tried some, or all, of the methods and have been unsuccessful.  Others have not tried any and have no interest.  So, as a soon-to-be physician, I was wondering what I have in my arsenal to convince these patients to attempt to stop smoking.  Certainly, most people know of the connection between smoking and lung cancer.  However, despite the publicity blitz of this connection, I still think many patients feel removed from the threat of lung cancer.  In a way, breathing is so intrinsic and subconscious that I think it's hard to imagine the true effects of lung pathology.  So, I thought I would find another connection that would influence smokers to quit and prevent young people from starting.  So, what would be important enough to prevent youngsters from smoking and make current smokers quit...?

In this Study1, 2115 men were studied and it was found that compared with men who never smoked, men who smoked at some time had a greater likelihood of erectile dysfunction and the response was dose-dependent.  Also, Study2 found that smoking is associated with decreased efficacy of slidenafil citrate in patients with erectile dysfunction.  In another Study3, cigarette smoking was associated with a significant decrease in sperm density, total sperm count, total number of motile sperm, and citrate concentration.  In yet another Study4, smoking was found to be a significant risk factor for ectopic pregnancies.  So there seems to be plenty of data out there that shows a connection between smoking and fertility.  While I can not speak for the better half of the species, I can say that most men would probably be willing to consider smoking cessation if they knew it was related to sexual function and reproductive capability.  Yet another tool in the box.  Hope this helps.


temporal arteritis

I saw a patient who is in her mid 30's came to the clinic with a jaw pain and some ear pain on the same side.  The pain is dull quality that is constant throughout the day and worsens with opening and closing the mouth.  The ear pain is also dull in nature and is more of a discomfort than a sharp pain.  She denied any cold symptoms.  She also denied headache, nausea, vomiting, and blurry vision.  After more thorough history and some facial physical exams, she was diagnosed with TMJ syndrome.  The ear pain is referred pain from the nerve that runs behind the ear and innervating the jaw.   However, this post is not about TMJ syndrome but is about temporal arteritis that may present with similar signs and symptoms.  It can be threatening disease if it's not diagnosed properly.

Patient with temporal arteritis is usually an elderly female that have jaw pain and a new headache as classic symptoms.  They can also present with scalp pain, temporal tenderness, and fever.  It is also associated with weight loss, arthralgia, and myalgia.  It is a feared condition because if misdiagnosed, it can lead to a blindness.  My attending physician told me a story of another physician who saw a patient with jaw pain and for some reason, sed rate was not ordered.  A few months later, the patient found herself completely blind in one eye and on the way to the hospital, the other eye also became blind suddenly.  This is a true story! 

The important lesson is when someone comes in with a jaw pain, no matter what his/her age is, you must ordered a sed rate.  If sed rate comes back positive and she has other classic symptoms of TA, you must immediately start them on a high dose prednisone.  In the meantime, temporal artery biopsy is ordered to confirm the diagnosis.  Eye exam must be continuely followed for any improvements or changes.  Interestingly, half of all TA patients also have polymyalgial rheumatica. 

For more information on temporal arteritis, here is a good website:  http://www.aafp.org/afp/20000815/789.html


Duck Itch

A boy presented with a rash on his upper torso and arms after swimming in a chlorinated swimming pool.  He had had the rash before, but only after swimming in ponds and lakes.  On a previous occasion, someone told him he had "duck itch."
 
Duck Itch is also commonly known as Swimmer's Itch.  (For those who like terminology, it's also called Cercarial Dermatitis.)  It's an allergic reaction to schistosome or nematode larvae that are released from infected snails into surrounding water (freshwater and marine) and normally infest the GI tract of waterfowl.  
 
Humans get Duck Itch by exposure to cercarial-infested water.  The cercariae enter the skin and trigger dermatitis in previously-sensitized individuals.  Within 48 hours of exposure, individuals can develop patches of pruritis or tingling, followed by a rash that looks like tiny red pinpoints.  The pruritis returns with increased intensity and the spots enlarge, forming papules or hives.  Pruritis can last 7 days.  The rash spontaneously resolves within several weeks.
  
There's no definitive way to prevent Duck Itch.  Toweling-off immediately after emerging from the water may help, but some species are quick to penetrate the skin, making such efforts futile.  The best way may be to avoid natural bodies of water, but as the patient in the clinic demonstrated, even chlorinated water may not be completely safe!  In general, good rules are to swim in areas away from (1) where ducks like to hang out and (2) the shoreline since cercariae are concentrated at shorelines (theories on this are based on wave patterns and the snail life cycle).

Treatment is primarily symptomatic to stop the itching since the main concerns are scratching and dermal abrasion that can lead to secondary skin infection.  Mild cases may not require treatment.  Severe cases may call for oral steroids (prednisone).
 
For images of Duck Itch, see Photo1, Photo2, and Photo3.
 
Sources (+ for additional information):  Website1Website2,  and Website3.


Prescription Drugs off the Internet

So I had this interesting patient who needed a prescription for Valium and Levitra. He had been using them for a month and the Valium had worked wonders at managing his anxiety and the Levitra had worked wonders...well at you know. But what was amazing about this was that he had purchased both drugs off of the internet and came to the doctors to get a prescription because the internet cost too much. He basically described to me being prescribed Lexapro for anxiety but that he discotinued due to sexual side effects. Or as he put it "I'm 30 (this has been changed to protect the innocent), so when my old lady wants to pound, I have to be ready."

I asked him about the process and he said he was just as surprised as I was about how easy it was to get EVERY type of drug off the web- pain pills, viagara, sleeping pills, benzodizapines. All you had to do was fill out a brief physical history form, write why you wanted the drug, speak to a "physician" on a chat room, and then give them a credit card number.

And so here's the kicker..as far as I could tell, there is no regulation of internet pharmacies.

There are bills that are being debated in Congress but they are still in committee. Take a gander. 

http://ryanscause.org/ryan-haight-bill.html

http://www.10news.com/news/4178402/detail.html

 

 


A Systematic Approach to Behavior Change

In the outpatient setting we see a lot of patients with conditions that are either instigated or exacerbated by lifestyle choices, most often smoking, lack of exercise and poor diet.  In the outpatient setting, there seem to be more opportunities for preventive care and health maintenance, where you have the chance help someone stay healthy rather than react to the disease that they later present with.  During this rotation, I have observed that patients present with varying degrees of readiness for change. 

This lead to a discussion about behavior change with my preceptor about the "transtheoretical model for behavior change," during which I learned about how to assess a persons "readiness for change".  Similar to the different stages of grieving that we have learned about, people also progress through stages of behavior change.  Recognizing where the patient is in that progression enables the healthcare provider to tailor their advice to the patient's level of receptiveness.

Basically, there are 5 stages of behavior change:

Precontemplation is the stage during which the person has not yet considered changing their behavior.  During this stage, the person might ask themselves, "is this a problem?" For example, a smoker who presents to the office for a cough because they think they need a course of antibiotics.  During this stage, people are not ready to change their lifestyle because they have not yet decided that is an important thing to do.  Rather than going through different quitting options with this patient, the physician might be more effective by encouraging the patient to consider that their behavior, eg. smoking, might be detrimental to their health.  Building rapport is important at this stage so that during a follow-up visit the patient might be more receptive to a conversation about the health effects of smoking.

Contemplation is the next stage and is when the person starts to consider lifestyle change.  At this stage, the person has identified a problem (eg that smoking is detrimental to health) and is considering whether there is a need to correct the problem.  During this stage, the physician can encourage the patient to consider whether the pros and cons of change outweigh the pros and cons of their current behavior.

Preparation is the stage during which the person decides there is a need to change their behavior and begins to consider possible plans of action.  During this stage, the patient is ready for a discussion about alternatives for behavior change, such as a comparison of different techniques for quitting smoking.

Action is the stage in which individuals put their plans into action and actually change their behavioral patterns.  During this stage, the patient might ask themselves whether their plan is working.  Making note of goals achieved and providing positive feedback are helpful means to encourage the person to continue with their plan of action.

Maintenance is the stage during which people work to prevent relapse and continue their new behavior.  During this stage the person develops coping strategies to manage "high-risk" situations without relapsing to their unhealthy behaviors.  The physician can encourage the patient to develop coping strategies and help build their confidence to successfully manage these situations.

Because behavior change often seems like a daunting task in the outpatient encounter, I found it helpful to consider the process of behavior change and to try to determine which stage the patient is in so that you can tailor your advice to their level of readiness.  The smoker who was looking for antibiotics was in the precontemplative stage, and a discussion about different quitting strategies would serve only frustrate both the patient and the physician during that encounter.  Another patient who presented for a routine physical admitted to smoking and that he would really like to quit but felt it would be too hard.  Thinking of him in the contemplative stage, he was ready to be encouraged to consider the pros and cons of quitting versus not and to think about which strategies might work best for him.  A third patient, newly diagnosed with diverticular disease, asked what he could do to prevent another flare up, and responded with enthusiasm to a discussion about diet modification - he was ready for action. 

I found a website that describes the "transtheoretical model" in great detail - with an angle for smoking cessation.  Here is an article as well, describing the effectiveness of physician intervention on healthy behavior change

 

 

 


Hand-foot in mouth disease

Hand, foot, and mouth disease (HFMD) is a common illness of infants and children characterized by fever, sores in the mouth, and a rash with blisters. HFMD begins with a mild fever, poor appetite, malaise, and sore throat. One to two days after the fever begins, painful sores develop in the mouth. They begin as small red spots that blister and then often become ulcers. They are usually located on the tongue, gums, and inside of the cheeks. The rash develops over 1 to 2 days with flat or raised red spots. The rash is non-pruritic, and it is usually located on the palms of the hands, soles of the feet, and buttocks. A person with HFMD may have only the rash or the mouth ulcers.

HFMD is caused by enteroviruses. The most common being coxsackievirus A16; sometimes, HFMD is caused by enterovirus 71 or other enteroviruses. The enterovirus group includes polioviruses, coxsackieviruses, echoviruses and other enteroviruses.

HFMD caused by coxsackievirus A16 infection is a mild disease and nearly all patients recover without medical treatment in 7 to 10 days. Complications are uncommon. Rarely, the patient with coxsackievirus A16 infection may also develop viral meningitis. Another cause of HFMD, EV71 may also cause viral meningitis and, rarely, more serious diseases, such as encephalitis, or a poliomyelitis-like paralysis. EV71 encephalitis may be fatal.

HFMD is moderately contagious. Infection is spread from person to person by direct contact with nose and throat discharges, saliva, fluid from blisters, or the stool of infected persons. A person is most contagious during the first week of the illness.

Usually, HFMD can be distinguished from other causes of mouth sores based on the age of the patient, the pattern of symptoms reported by the patient or parent, and the appearance of the rash and sores on examination. A throat swab or stool specimen may be sent to a laboratory to determine which enterovirus caused the illness. Since the testing often takes 2 to 4 weeks to obtain a final answer, the physician usually does not order these tests.

No specific treatment is available for this or other enterovirus infections. Symptomatic treatment is given to provide relief from fever, aches, or pain from the mouth ulcers.

Pictures:

www.info.gov.hk/dh/diseases/CD/HFMDc.htm

http://dermatology.cdlib.org/93/reviews/viral/11.jpg

www.askdrsears.com/html/8/T082902.asp

www.askdrsears.com/html/8/T082902.aspwww.askdrsears.com/html/8/T082902.asp


Alternative/Additional treatment for Exercise-Induced Asthma

Exercised-induced asthma (EIA) is a common complaint with many of the kids we see for their yearly physicals and it's a constant battle to get them on a preventative medication regimen that works so they don't have to rely on albuterol every day they have gym or school activities or sports.  Obviously reducing or eliminating triggers would go along way, but if they have EIA and we want them to exercise and reduce screen time then it's impossible to eliminate exercise as a trigger.  So most kids have their albuterol, which they probably use too much, and salmeterol (or some salmeterol combo) which is associated with a smaller decrease in FEV1 than other treatments but is not useful in acute setting.  Plus a variety of other meds (Ipratropium, Montelukast, Fluticasone or Cromolyn) that can be used for prophylaxis against EIA, but I have seen enough patients that jump from one med to another and try multiple combos and none of them control or prevent EIA or they have undesirable side effects. 

So I looked up info on what is out there for prevention of EIA and was surprised by a few studies that looked at dietary salt and it's relationship with airway inflammation in asthmatics.
The mechanisms unique to exercise that triggers EIA in asthmatic patients have been extensively investigated.  It has been suggested that transient dehydration of the airways activates inflammatory mediators such as histamine, neuropeptides, and the arachidonic acid metabolites, leukotrienes, and prostanoids from airway cells, resulting in bronchial smooth muscle contraction.  Alternatively, it has been suggested that rapid rewarming of the airways following exercise leads to reactive hyperemia resulting in vascular engorgement and perivascular edema, which would further contribute to airway narrowing caused by bronchoconstriction.  Dietary salt influences vascular volume and microvascular pressure, resulting in mucosal edema and possibly narrowing of the airway lumen but researchers are still looking into the exact mechanisms.

Most of the studies I found were about reducing salt not just to a "normal" salt load, but to a low salt diet (<1500mg salt/day).  Based on pre-and post-exercise study of DLCO, spirmetry and sputum cytology a low salt diet was much better than even a normal salt diet.

I know many young patients may balk at a low salt diet, especially with all the obesity we have all been seeing, but this could be a healthy, inexpensive and non-medication method of reducing or preventing exacerbations.


Alcohol Withdrawal and Treatment

As part of my FP site duties, I've been involved in the care of a number of drug and alcohol dependent patients.  Last week I wrote about heroin addiction and withdrawal.  This week I would like to focus on alcohol withdrawal and treatment, particulary the use of librium.

As you well know, alcoholism is extremely common with an estimated 8 million alcohol dependent individuals in the US, 500,000 of which will experience severe withdrawal annually. 

Due to the fact that alcohol is a CNS depressant, its chronic use leads to compensatory overactivity within the central nervous system including the sympathetic autonomic outflow.  Symptoms of withdrawal occur when alcohol is abruptly removed while the compensatory overactivity is still in place.  This leads to altered levels of neurotransmitters within the brain and subsequent withdrawal symptoms.  For example, because GABA is the major inhibitory neurotransmitter in the brain, its receptors are downregulated and its effects decreased in chronic alcohol use.  However, when in alcohol withdrawal, the loss of GABA's influence on the CNS leads to symptoms of hyperarousal.  Other major neurotransmitters at play include elevated levels of norepinephrine secondary to alpha-2 receptor mediated inhibition of presynaptic NE release, and serotonin which plays a major role in both tolerance and cravings.

Withdrawal symptoms vary drastically and can be minor or severe.  Minor symptoms appear within 6 hours of the patient's last drink, resolve within 24-48 hours, and are usually secondary to the before-mentioned hyperactivity of the brain.  They include insomnia, tremulousness, mild anxiety, GI distress, HA's, diaphoresis, and papitations.  More severe symptoms include withdrawal seizures that appear within 48 hours of the last drink and are usually tonic-clonic in nature.  These seizures are found in 3% of alcoholics, and most of those affected usually only have a single isolated episode.  Patients may also experience hallucinosis that develop within 12-24 hours of abstinence and resolve within 24-48 hours.  These hallucinations can often visual but they may also be auditory or tactile.  Delirium tremens may affect up to 5% of withdrawal patients begining 48-96 hours after the last drink.  DTs are characterized by hallucinations, disorientation, tachycardia, hypertension, fever, diaphoresis, and agitation.  DT's should be viewed as serious complications with up to a 5% mortality rate and prompt medical treatment and supportive care is necessary. Withdrawal is a diagnosis of exclusion and various tests such as an LP maybe necessary to rule out other etiologies.  In addition, many patients may have other co-morbidities that must also be addressed in treatment.

The main goal of treating alcohol withdrawal is alleviation  of symptoms and correction of metabolic problems.  Patients are placed in a safe and quiet environment, usually restrained, and IV infusion of normal saline is placed until the patient is euvolemic.  Thiamine is usually administered before any glucose-containing solutions in order to prevent Wernicke's or Korsakoff's syndrome.  Multivitamins should also be given in order to correct any deficiencies. 

Benzodiazepines, particulary long-acting agents such as chloradiazepoxide (Librium) as well as diazepam (valium) are used most frequently in alcohol withdrawal to treat psychomotor agitation and prevent progression of symptoms.  Recent studies have demonstrated that a symptom-triggered therapeutic schedule results in less medication and shorter duration of withdrawal versus a fixed schedule of medication administration.  In cases of refractory DTs, patients may benefit from barbiturates (phenobarbital), especially when combined with BZD's.  Another alternative maybe the use of propofol which also works to overcome the absence of GABA effects on the brain.  Other less studied agents such as centrally acting alpha-2 agonists, beta blockers, carbamazepine, antipsychotic agents, and ethanol have also been utilized with or without benzodiazepines as means of treatment.

Following successful treatment, patients should be carefully screened for dependence and offered long-term follow-up care.

Please refer to the following sites for more info:

www.niaaa.nih.gov

http://findtreatment.samhsa.gov

 


Restless Legs Syndrome

This week we saw a patient that was suffering from poor memory and fatigue due to interrupted sleep and insomnia.  She was diagnosed with Restless Legs Syndrome (RLS) a year ago but had been symptom free for the past 3 months until this week.

RLS can be categorized into primary or secondary RLS.  Primary RLS is idiopathic but there appears to be a genetic basis as 40% of patients with this disorder have a dominant family history of inheritance.  Some nonspecific findings in patients with primary RLS include reduced motor cortex inhibition, spinal flexor reflex hyperactivity, and brainstem relfex abnormalities. While it has been thought that this is a peripheral nervous system disorder, recent studies have demonstrated reduced basal ganglia dopamine receptor binding and 18F-Dopa uptake, which may demonstrate some CNS involvement.  In addition, patients with RLS have demonstrated increased levels of hypocretin in their CSF compared to average individuals.  Secondary RLS can be caused by a number of disorders including uremia due to end-stage renal disease, pregnancy, diabetes, iron deficiency anemia, rheumatic disease, and venous insufficiency.

RLS is common, affecting 5-15% of the population.  It is most prevelant in the elderly but can be found in almost all ages and is equally prevelant in both males and females.  The patient that I saw was in her late twenties. It can be categorized into intermittent, daily, and refractory types.  RLS is characterized by spontaneous and continous leg movements that are associated with unpleasant paresthesias in the legs and sometimes the arms.  These paresthesias occur only when the patient is at rest and are immediately relieved by movement of the affected limbs.  Patients describe these deep rooted sensations as crawling, creeping, pulling, itching, drawing, or stretching.  The skin is usually not sensitive to touch and there is no associated pain. Symptoms progress during the day and are worst at night, usually appearing 15-30 minutes after reclining in bed.  Patients often suffer sleep disturbances due to the involuntary, jerking movements of the legs known as periodic leg movements of sleep.  Patients are usually unaware of these movements and they may briefly awaken the patient from sleep leading to insomnia and daytime fatigue.

Diagnosis of RLS is difficult in light of the vague nature of the disorder.  The international RLS Study Group proposed the four following features as minimal criteria for diagnosis in light of a normal neurologic exam: 1. Desire to move extremities, often associated with paresthesias or dysesthesia.  2. Motor restlessness.  3. Worsening of symptoms at rest with at least partial and temporary relief during activity.  4. Worsening of symptoms in the evening or at night.  Family history may aid in the diagnosis and patients with secondary RLS may have other associated peripheral neuropathy.  Polysomnography may help in making the diagnosis, especially in difficult to treat cases.  It is also important to exclude other causes such as renal failure and iron deficiency with a low ferritin level.  Akethisia secondary to antipsychotic and SSRIs may mimic RLS.  In addition, peripheral neuropathy, lumbosacral radiculopathy, and ordinary leg cramps must be considered in the differential but can usually be excluded if pain is low or absent as in RLS.

Treatment of RLS can be divieded into non-pharm and pharmacotherapy and the course is usually dependent on the type of RLS as well as the response of the patient to treatment.  Non-pharmacologic approaches include mental alerting activities, avoiding medications or substances that may exacerbate RLS (caffeine, nicotine, alcohol), addressing the possibility of iron deficiency, and streching exercises for the posterior leg muscles before bed.  The patient we saw in clinic actually had a low serum ferritin level and was placed on iron supplementation.  Pharmacologic therapy includes benzodiazepines, dopaminergic drugs such as levodopa, and opiods in resistant cases. 

Here's some useful links that I found, hope it helps:

RLS Foundation:  www.rls.org

We Move: www.wemove.org/rls

American Academy of Sleep Medicine

American Academy of Neurology

World Association of Sleep Medicine



 


Post-Polio Syndrome

I saw a patient this week with post-polio syndrome (PPS).  The patient was dismayed that there were no doctors who were real specialists in PPS in this area, and he had visited doctors all over New England to try and get some help.  Unfortunately, there isn't much that is being done for people with this syndrome, as I learned from my encounter with this patient.  This is a syndrome that we don't often see and that we have never formally been taught about, so I thought that I would try to find some information for all of you on this topic.

Post-polio syndrome (PPS) can affect polio survivors anywhere from 10-40 years after the initial paralytic attack of the poliomyelitis virus.  It is characterized by a further weakening of muscles that were previously affected by the initial polio infection.  Symptoms can include fatigue, slowly progressive muscle weakness, muscular atrophy, joint pain, and skeletal deformities (such as scoliosis).  Some patients can even develop spinal muscular atrophy, which appears to be a form of amyotrophic lateral sclerosis (ALS). 

There are about 300,000 polio survivors in the United States who may be at risk for PPS, and doctors believe that PPS affects about 25-50% of these people. 

So, what causes PPS?  The new manifestations of PPS seem to be related to the death of the individual nerve terminals in the motor units that remain after the initial attack of polio.  As these motor units initially healed, these individual nerve terminals might have tried to compensate for the loss of nearby neurons, adding stress to the neuronal cell body.  As a result, the individual may have normal function for a period of time, until excessive sprouting from this cell body may not be able to maintain the metabolic demands of all of their new sprouts, leading to a slow deterioration of the individual nerve terminals.  

Treatment for PPS consists of energy conservation, physical therapy, occupational therapy, speech therapy, sleep apnea treatment and medications.  Medications that are being used to treat PPS include asprin and NSAIDS to help muscle and joint pain, Pyridostigmine, amantadine, selegliline, bromocriptine, and modafinil for PPS fatigue, and lately studies have shown that IGF-1 may improve recovery after exercise.

Here are some links that might be helpful concerning PPS.

http://healthlink.mcw.edu/article/996372413.html

http://www.mayoclinic.com/invoke.cfm?objectid=998F31A7-54A7-4D06-A37E640DF18D9CE7&dsection=8


Inflammatory Bowel Disease

This week, I saw a young patient with a family history of Crohns disease, who presented for follow-up after an episode of 3 days of severe watery, bloody diarrhea and abdominal pain.  She had had no other associated symptoms, and no systemic symptoms; no recent weight loss, no fevers, chills; no change in diet, no sick contacts.  Physical exam at the time we examined her was normal.  Also, stool culture and gram stain was normal.  Last year, she had a similar episode of a few days of watery, bloody diarrhea, but never followed up with a GI consult as recommended.  In between these episodes, she does not have GI symptoms.  We discussed the importance of a GI consult for colonoscopy or sigmoidoscopy, and hopefully she will follow-up as recommended, considering the possibility of IBD.

Since patients with IBD are often first diagnosed by their PMD, it is important to understand the difference between Crohns Disease and Ulcerative Colitis, as well as other possible diagnoses that can cause a similar presentation.

Crohns Disease

  • Symptoms:  abdominal pain, non-bloody diarrhea, mucus from rectum
  • Systemic symptoms:  fever, chills, anorexia, fatigue, weight loss, erythema nodosum, apthous ulcers, arthritis, iritis
  • Disease involves all layers of the bowel wall, and is characterized by discontinuous skip lesions
  • Incidence peaks in the 2nd and 3rd decades, with a smaller peak in patients 55-65.

Ulcerative Colitis

  • Symptoms include: bloody diarrhea, mucus from rectum, tenesemus, constipation, abdominal pain
  • Disease involves the mucosa only, and always involves the rectum.

 

FeaturesCrohn DiseaseUlcerative Colitis
Skip areasCommonNever
Cobblestone mucosaCommonRare
Transmural involvementCommonOccasional
Rectal sparingCommonNever
Perianal involvementCommonNever
FistulasCommonNever
StricturesCommonOccasional
GranulomasCommonOccasional

 

Celiac Sprue

  • Gluten-sensitive enteropathy
  • Symptoms:  bloating, diarrhea, foul-smelling stools

Lactase Deficiency

  • Symptoms:  crampy abdominal pain, floating, foul-smelling stools, diarrhea after digesting dairy products.

This is a link to a great patient information site from the American Gastroenterological association that I found helpful:

http://www.gastro.org/wmspage.cfm?parm1=851 

July 2, 2005
IUDs
Although I have had several Guyanese patients coming in for IUD insertions/removals, only 1% of contraception users in the U.S. use intrauterine devices.  This is extremely low considering that it is very safe, effective, and a popular option for people in other countries.  This underutilization is probably due to various facts, including the lack of basic knowledge that they are even available.  Also a history of negative publicity and misperceptions about risks of ectopic pregnancy, infertility, and infection have scared the American public.

Copper IUD:   The copper is responsible for oxidation in utero with release of copper ions, which block transtubal sperm migration.  This is approved for 10 years although effective for 12, and the pregnancy rate is 1.6% for 7 years.  It is initially expensive but within 5 years, the copper IUD is the most cost-effective method of contraception available.  Heavy menses and dysmenorrhea are the most frequent reasons for copper IUD removal.  Average monthly menses can be increased by up to 55% thoughout the duration of use.

Hormonal IUD
(Mirena): The hormone-releasing IUD is the ideal choice for contraception for women with menorrhagia.  It is approved for use for 5 years although effective for 7.  The probability of pregnancy  after 7 years is 1.1%.  This reduces dysmenorrhea and decreases menstrual blood loss to 40-50% of preinsertion values.  It is as effective s endometrial ablation for menorrhagia and actually can decrease the risk of PID.  Main reason for discontinuation is amenorrhea.

While the mechanism of action is not well known, possible explanations include changes in cervical mucus that inhibit sperm transport, chronic inflammatory changes of the endometrium and fallopian tubes, glandular atrophy of the endometrium, and direct ovicidal effects.

Contraindications are sever uterine distortion, pelvic infection, known or suspected pregnancy, Wilson's disease, and undiagnosed abnormal uterine bleeding.

July 1, 2005
Post Herpetic Neuralgia

An elderly lady came into the office and complained of pain in her scalp and neck for over 2 months.  She said that her neurologist diagnosed her with herpes zoster several weeks earlier and that this pain was a complication.  I asked her where her Zoster rash had been and she stated that she never had a rash, but had burning and tingling in the same region where she now has her chronic pain.   

About 20% of patient with Herpes Zoster go on to develop postherpetic neuralgia (PHN), which is the most feared complication of Zoster. The physiology of this entity remains elusive, but path studies have demonstrated damage to sensory nerves, the sensory dorsal root ganglia and the dorsal horns of the spinal cord in patients with this condition.  

The sign of postherpetic neuralgia is pain that persists for longer than one to three months after the resolution of the typical herpes zoster rash. It is important to remember however, that some patients (as with the patient I saw being a perfect example) may have "zoster sine herpere" or, prodromal symptoms without developing the characteristic rash.  Older age is the most significant risk factor for developing PHN.

Description of postherpetic neuralgia pain:

  • Constant burning
  • Lancinating pain that may be radicular in nature
  • Hyperalgesia + Allodynia (even the slightest pressure from clothing, bed sheets or wind may elicit pain)
Frequency: 1 month after onset of shingles is 9-14.3%; at 3 months, about 5%; at 1 year, 3% continue to have severe pain.  At age 60, approximately 60% of patients with shingles develop PHN, and at age 70, 75% develop PHN

Treatment of herpes zoster has 3 major objectives:
    1. Treatment of the acute viral infection
    2. Treatment of the acute pain asstd with Herpes Zoster
    3. Prevention of postherpetic neuralgia

Antiviral agents (Acyclovir, Valacyclovir, Famciclovir) - decrease the duration of herpes zoster rash and severity of associated pain.  Only beneficial within 72 hours after rash onset (while new lesions are actively being formed).  

Corticosteroids - if used in conjunction with acyclovir will reduce pain asstd with zoster.  Questionable success in preventing postherpetic neuralgia.  Should only be used in pts >50yrs b/c these patients are at increased risk for PHN. 

Treatment of PHN is directed at pain control.  In general, PHN is selflimited, but may take several months to relent.  Thus, certain medications are used to alleviate pain Sx's.

  1. Analgesics - Capsaicin (chili pepper extract!), is the only FDA approved drug for PHN treatment.  Read a study about capsaicin efficacy
  2. TCAs - decrease neuropathic pain. 
  3. Anticonvulsants
Great article about PHN: http://www.aafp.org/afp/20000415/2437.html

Eval of diff Tx modalities for PHN:  http://www.aafp.org/afp/20030401/britishx.pdf

June 30, 2005
"I have a lump near my left eye"

That was the chief complaint of a patient whom I saw the other day. Four days ago, she had a pimple-like bump on the upper eyelid of her left eye. It appeared overnight. The patient did not recall any kind of trauma or irritation that could have occurred to her eye. Over the next few days, that pump on her upper eyelid resolved but she started noticing some swelling/redness at the medial canthus (the region between the eye and nose). The swelling got bigger and became more sensitive to touch. The day before she came in the office (3 days after the onset of bump), she noted a second swelling below the lower eyelid. Other symptoms include excessive tearing of left eye and itching. Denied pain, tenderness with eye movements, increased pressure in her left eye, impairment of vision, purulent discharge or fever. No recent hx or contact with people with conjunctivitis.

On PE, mild edema of upper eyelid of left eye; periorbital erythema; At the left medial canthus, there is a 0.3cm x 0.7cm, erythematous, soft lump with an abcess-like white center that is tender to touch. About 1.5 cm below the lower eyelid of the left eye and 4cm to the left of her nose, there is another swelling that is also tender to touch. Both eyes have PERRLA, EOMI. No sinus pain or tenderness anywhere else around the left eye. No D/C noted. These are the pictures I found that are most closely resembled my patient's condition. Check them out and see what you think this is!!! Pictures 1 2 3 4

An ophthalmologist was consulted and a presumptive dx of dacryocystitis was made. Dacryocystitis is inflammation of the lacrimal system (Lacrima system) It can be acute, chronic or congenital. Interestingly, for some reasons it occurs more frequently on the left eye. Acquired dacryocystitis is primarily a disease of females and is most common in patients older than 40 years, with a peak in patients aged 60-70 years.


Clinical presentation: (book description) sudden onset of pain, erythema, and edema overlying the lacrimal sac region. Tenderness localized in the medial canthal region but may extend to the nose, cheek, teeth, and face; Epiphora (watery eyes), mattering, periorbital edema, decreased visual acuity are common complaints.


Causes: Congenital: incomplete canalization of the nasolacrimal duct, neonatal infection - Staphylococcus aureus, Haemophilus influenzae, beta-hemolytic streptococci, and pneumococci- structure abnormalities of the midface. Acquired: obstruction/stenosis of the lower part of the nasolacrimal system, infection, nasal diseases

Complications: periorbital cellulites, abscess which may lead to blindness, cavernous sinus thrombosis, and death.

Treatments: mild cases: Keflex or Augmentin; if serious cases in which orbital cellulitis/abscess are suspected: hospitalization with IV abx
More info Dacryocystitis, click here
More pictures of dacrycystitis, click here


lichen planis

My attending called me into a room the other day and showed me a middle aged woman with pruritic, flat topped, polygonal, purple lesions with white scale on her wrists and ankles.  She also had white streaks in her mouth.

He looked at me expectantly for a diagnosis, but I had no idea what it was.  Apparently this is the classic presentation of lichen planus.  This is what it looks like: pictures

Lichen planus most frequently affects middle-aged adults.  The etiology is not known, but it is thought to be autoimmune.  It can be associated with certain drugs or with chronic graft vs. host disease. 20-30% of patients with lichen planus have hepatitis C. 

50% of the time it affects the mouth and there can be asymptomatic white streaks or painful ulcers.  They can also have the white streaks or ulcers on the vulva or penis.  Nail or scalp involvement is also possible.

The lesions usually go away in 1-2 years, but they leave behind hyperpigmented macules.  It can be difficult to treat.  Treatment for localized lichen planus is steroid cream.  More systemic disease can be treated with oral corticosteroids or retinoids.

For more info: article


Is that a Carbuncle?
This week a pleasant woman came into the office complaining of a large "bump" in her groin.  She said that it has been there for over a month and that it was extremely painful to touch.  She said that she had been getting this bump in the same spot on and off for the past 20 years.  The patient also gave a history of other, similar lesions in different areas of her body (she had one in each armpit). 

 

So after looking at the area my preceptor and I knew that it was most likely a skin abscess caused by S. aureus, but we did a culture anyway because it was draining.  Surprisingly she had never had it cultured in the past.  I asked my preceptor at the time if it was a Carbuncle or a Furuncle?  I remembered seeing the pictures back in second year, but could not remember the difference.  Well here's what you have been waiting for.....

 

Very simple I know, but one of those things that makes you look smart if you actually know the difference.  People throw the words abscess and boil around all the time and sometimes I wonder if they know what they actually are.  We gave the patient Dicloxacillin 250mg PO Q6h for 14 days because she had no insurance.  You could also use Cephalexin or Cefazolin. Here is how you would treat it.....

 

Carbuncles usually must drain before they will heal. This most often occurs in less than 2 weeks. Carbuncles that persist longer than 2 weeks, recur, are located on the spine or the middle of the face, or that are accompanied by fever or other symptoms require treatment by a health care provider because of the risk of complications from the spread of infection.

 

Antibacterial soaps, topical (applied to a localized area of the skin) antibiotics, and systemic antibiotics may help to control infection. Warm moist compresses encourage carbuncles to drain, which speeds healing. Gently soak the area with a warm, moist cloth several times each day. Never squeeze a boil or attempt to lance it at home because this can spread the infection and make it worse.

 

Deep or large lesions may need to be drained surgically by the health care provider.

 

Meticulous hygiene is vital to prevent the spread of infection. Draining lesions should be cleaned frequently. The hands should be washed thoroughly after touching a boil. Do not re-use or share washcloths or towels. Clothing, washcloths, towels, and sheets or other items that contact infected areas should be washed in very hot (preferably boiling) water. Dressings should be changed frequently and discarded in a manner that contains the drainage, such as by placing them in a bag that can be closed tightly before discarding.

 

 


Gaucher Disease and AVN

During this rotation, I have been amazed with the amount of variablility. I was fortunate to see a patient with Gaucher disease and subsequent AVN. Here is a little refresher on Gaucher's:

Gaucher is an inborn error of metabolism that affects the recycling of cellular glycolipids. Glucocerebroside which ordinarily is degraded to glucose and lipid components, accumulates within the lysosomes of cells. Gaucher's is the most common lysosomal disease. There is about 20,000 cases in the US, 2/3 of which are Ashkenazi Jews.

Clinical manifestations of Gaucher disease results from the accumulation of lipid laden macrophages in the spleen, liver, bone marrow, and bone. However, pathologic lipid accumulation in macrophages accounts for less than two percent of the additional tissue mass in the liver and spleen. the additional increase is attributed to an inflammatory response.

Two pathologic processes occur within bone: deceased mineral density and marrow encroachment. The mechanism for decrease bone mineral density is uncertain. Marrow fibrosis and osteosclerosis result in  localized loss of hematopoiesis. Thrombocytopenia results from decreased platelet production and splenic sequestration.

Approximately 90 percent of patients have type 1 whihc is the nonneuronopathic form. This is most common in the Ashkenazi Jewish population, which has a carrier frequency of 1 in 12. In non jewish, the incidence occurs about 1 in 40,000 live births. Like my patient here who was 47 years old, the age of onset is variable. Some present at 12-24 months, others have no clinical signs until late adulthood.

Clinical features include: splenomegaly, hepatomegaly, bone disease, bleeding, and a small brownish patch of tissue (pingueculae) on the sclera behind the iris.

Fortunately, Gaucher's is one of the few inherited metabolic disorders that can be treated by replacement of the deficient enzyme-glucocerebrosidase. This therapy has shown good results but is time consuming and very expensive according to my patient and is for life. My patient has stopped treatment all together even after suffering from AVN.

The study below looks at Gaucher patients with AVN and the possible associated hypercoaguable state. As well as, a histologically look at Gaucher Disease and quick overview with specific treatment.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11146461&query_hl=3

http://images.google.com/imgres?imgurl=http://pathcuric1.swmed.edu/PathDemo/gen1/gen120.jpg&imgrefurl=http://pathcuric1.swmed.edu/PathDemo/gen1/gen120.htm&h=233&w=350&sz=22&tbnid=1mcf62z-zc4J:&tbnh=77&tbnw=116&hl=en&start=9&prev=/images%3Fq%3Dgaucher%2Bcells%26svnum%3D10%26hl%3Den%26lr%3D

http://www.ntsad.org/pages/gaucher.htm


Steroid Tapering Protocol

I recently had my preceptor pimp me on the exact protocol for steroid tapering.  Of course, I hadn't a clue.  So here is some info that I found.

Indications for Steroid Withdrawal:

  • max benefit reached
  • no benefit appreciated
  • side effects too great (osteoperosis, HTN)

Immediate indications for steroid withdrawal without tapering:

  • steroid induced psychosis
  • Herpes induced corneal ulceration

Pharmacokinetics:

For the PharmDs among us...

  • age and clearance of steroid are inversely related, ie. dose elderly relatively smaller
  • slower clearance rates of steroids in Africans vs. Caucasians 

Basiclally, the protocol for steriod tapering is generalyl stratified into three broad categories of likeliness of Hypothalamic Pituitary Adrenal Axis Suppression (HPA).  Suppression can lead to adrenal insufficiency (bad).   Basically, it depends on: potency, dose, and duration of the steroid.

Likely HPA suppression:

  • 20 mg/day prednisone > 3 wks
  • evening/bedtime dosing
  • Cushingnoid appearance
  • Taper indicated!

Unlikely suppression:

  • any dose < 3 wks
  • daytime dose therapy
  • <5mg/day prednisilone
  • No taper indicated!

Uncertain suppression (gray area):

  • 10-20mg/day prednisone/day >3wks
  • <10 mg day Not at bedtime dose
  • DO: Stress test with glucorticoids OR ACTH stimulation test for further guidance on tapering

Basically, tapering is controversial depending on the study you look at and the disease you look at.  In a study of pts with asthma, COPD, Crohns, Graft vs. Host disease, tapering showed no difference.  However, in another study of children with nephrotic syndrome, a rapid taper led to a significantly higher relapse rate than a slow taper.

Paper on Glucorticoid Withdrawal by Daniel Furst.  Must have secure login first.

https://nsas1.amc.edu/get/uri/http://www.utdol.com/application/topic.asp?file=tx_rheum/5199&type=A&selectedTitle=1~14

June 28, 2005
Otitis Media and a penicillin allergy

Last week, a six year old can to the clinic with his fourth ear infection that year.  Today he had the typical symptoms of otitis media with tympanic membrane erythema, along with a bulging membrane, and a flat tympanogram.  The interesting issue with this case was his allergy to penicillin.  As we should all know by now the first line treatment for acute otitis media is amoxicillin, but what if a child is allergic to beta lactams.  A lot of practitioners like to use azithromycin as a substitute because it is very easy to take and it has solid coverage against streptococcal infections.  The length of treatment with azithromycin is a popular topic of research as is the general efficacy of this treatment.  In the clinic and during my ENT rotation, both physicians stated that treatment with azithromycin was inferior to either amoxicillin or Augmentin.  Both clinicians stated that this anti-microbial had decreased access to the middle ear making it less effective in the area.  After reviewing the recent literature most of which is from the last year, it appears that a three or five day course of azithromycin may be as effective as amoxicillin or Augmentin but there are conflicting results.  In regards to treating a patient who has a known penicillin allergy the literature seems to recommend trimethoprin-sulfa.

            Here are some of the articles that I saw addressing this topic.  I think the take home message is that azithromycin appears to be an effective alternative to beta-lactams for the treatment of acute otitis media, but the literature still recommends TMP-SMX for patients with a penicillin allergy and acute otitis media.

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10886460&query_hl=11

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15933563&query_hl=17

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14506028&query_hl=17

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12888586&query_hl=17

June 26, 2005
I'm tingling and I can't get up

 

This week I saw a patient with a chief complaint of "tingling coming out of my head". He described that over the past week he had begun to notice extremely intense tingling sensations that were traveling down his arms and in his head. The sensations had gotten progressively worse to the point that he was having trouble walking because he was feeling dizzy, and even lying down was not relieving the symptoms.

 

He had been treated for back and neck pain in the past. He had also been switched from paroxetine to bupropion because of sexual side effects approximately 10 days prior to his presenting in the office. His neurological exam was entirely normal, but he was quite insistent that he be given a referral to get at CT scan because he had been researching his symptoms on the internet and was convinced that he had a brain tumor.

 

Because primary care physicians are frequently managing psychiatric complaints of their patients, familiarity with some of the effects of frequently prescribed medications such as the SSRIs becomes essential to practicing effective medicine. The symptoms this gentleman was describing are very similar to those seen in what is being called "serotonin discontinuation syndrome". The drug paroxetine is one of the biggest culprits due to its shorter ½ life in comparison to some of the other SSRIs, although the symptoms have been reported with all of them.

  • In most cases, symptoms begin within 1 to 3 days of drug discontinuation
  • Symptoms cause clinically significant distress or impairment and are not due to a general medical condition or recurrence of a mental disorder
  • Symptoms may include dizziness, light-headedness, vertigo or feeling faint; shock-like sensations or paresthesia; anxiety; diarrhea; fatigue; gait instability; headache; insomnia; irritability; nausea or emesis; tremor; and visual disturbances.

This patient was educated that his symptoms were likely due to his abrupt discontinuation of paroxetine, and it was recommended that he resume taking half is original dose of paroxetine along with the bupropion to see if his symptoms were relieved. He was not satisfied with this plan, and so was given a referral to see a neurologist with the agreement that a CT scan would be ordered if the neurologist thought one was indicated, but in the meantime, he should try restarting the paroxetine. The very next day my preceptor got a fax from him with a profuse number of thank yous and the statement "You were right. But don't get used to it".

The following link is a one page overview of serotonin discontinuation and has some good references to articles discussing diagnostic criteria.

What are the diagnostic criteria, therapy and prophylaxis for discontinuation symptoms due to SSRIs?

 

 


Suck in that gut!

It seems that every other patient I'm seeing, if not every patient, has obesity.  And the relationship between obesity and diabetes and hypertension is clearly evident in these patients as well.  So, I thought I would look up what indicators we as physicians might use to quantify a patient's obesity and relate that to their risk for morbidity.  If we could give the patients a solid number, this may make their obesity more "real" in terms of how it will affect their health.  I have seen so many obese patients with diabetes and hypertension who either don't believe or don't want to believe that their obesity is related to their illness.  They'd much rather take metformin and captopril than exercise or eat a more appropriate diet.

I had always used BMI as an indicator for overweight and obese.  But this study1 shows that waist circumference is actually a more precise indicator of glucose intolerance and diabetes mellitus type 2.  So given that, I found another study2 which shows the cutoffs for waist circumference that can be used to identify increased risk of coronary events.  This study found that in people who are considered to have normal weight (BMI = 18.5 to 24.9), the waist circumference cut off is 90 cm for men and 80 cm for women.  In people who are overweight (BMI = 25 to 29.9), the cut off is 100 cm for men and 90 cm for women.  In people who are obese (BMI = 30 to 34.9), the cut off is 110 cm for men and 105 cm for women.  And in people who are severely obese (BMI > 35), the cut off is 125 cm for men and 115 cm for women.

So there you have it.  Next time a patient looks at you blankly when you suggest weight loss, ask them what their pants size is.  Then convert it to centimeters.  Then tell them that they are at increased risk for coronary events and that if they can decrease their waist size accordingly, they will decrease their risk.  This gives them a definitive number in terms of their present health, and it gives them a number to strive for.  Hope this is helpful.

PS.  I hope the reason why women have a lower cutoff than men in all categories is based strictly on some biological reason that is yet unknown.


off-label uses of neurontin
    This past week I have become well acquinted with the detox facility.  During that time I was educated on the uses of neurontin other than its current recomended uses for epilepsy.  If one goes to his/her palm it clearly states that neurontin is in the class of anti-convulsants and it is to be used for neuropathic pain.  While conducting rounds on the detox floor, my attending was perscribing it almost to everyone who had serious addiction.  She stated that it was wonderful for mood disorders and both situational and clinical depression. It does not treat the addiction but helps "mellow out" the brain. In other word it somehow stabilizes the brain.  This drug had been studied since 1983 and was approved by the FDA for control of epilepsy in 1994.  Parke-Davis has bee successfully conducting long-term clinical trials.
     In 1996, research for other purposes began appearring  and there has been a quiet revolution of patinets and doctors finding that Neurontin is helpful in illnesses other than epilepsy.  Neurontin has a grwoing multitud of medical studies showing it effective for off-label illness such as and not limited to: brain injury, interstitial cystitis, muscle cramps, cocain dependence, TMJ, hemifacial spasms, bipolar disorder, post-operative pain, etc, and it was concluded in one study that gabapentin (neurontin) "represents a novel class of antihyperalgesic agents."  Off-label reseacrh now points to the probabiltiy that neurontin decreases Substance P activity.   As you can see there are tremendous clinical applications for this drug which is a relatively benign drug with little side effects.  It is well tolerated in patinets and it is almost impossible to overdose on it.  It is exclusively excreted unchanged in the kidneys and the molecule mimicks GABA (gama amino butyric acid) and crosses the blood brain barrier
Some evidence based medicine that points to neurontin as effective for spasticity in patients who have upper motor neuron syndrome see below.
Med Clin (Barc). 2005 Jan 29;124(3):81-5
https://nsas1.amc.edu/get/uri/http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15710092&query_hl=1
For research and abstracts on new applications of neurontin see below. Of course as evidence mounts in neurontin effective off-label clinical use more evidence backed by clinical trials will appear in the literature sponsored either by the drug maker or other health care providers which will ultimatley increase its indications  http://home.tampabay.rr.com/lymecfs/neurontin01.htm
Interestingly Pfizer came out with a "me-to-drug" called  Lyrica that is approved for same indications as Neurontin.  I believe the scope of these drugs and their relatively benign side-effect profile is only going to broaden the clinical application.


Compartment Syndrome
So we had a real interesting case in the office last week. The long and short of it was that after a sports injury two days earlier, the patient presented to the clinic with a swollen, painful leg from knee to ankle. Muscles were tender to palpation and the patient could not dorsi or plantar flex his foot. His shin was also pretty cut up. No other symptoms.
So based on his nasty cut,  I thought he had cellulitis, and that's how I presented him to my attending. But then again, what the hell do I know. My attending came into the room and almost immediately told the patient that he needed to get to the ER for surgery.
So basically this patient was clinically diagnosed with compartment syndrome, one of the few orthopedic emergencies.
All of the limbs in the body can be compartmentalized based on muscle groups and the corresponding nervous and blood supply. The muscle are all wrapped tightly in fascia which are not very compliant. So any injury- trauma, intensive muscle use, burns- that results in the extravasation of fluid into these compartments are met with a disproportionate increase in pressure because the fascia will not expand. The increased pressure subsequently compresses the blood supply and the nervous supply resulting in the clinical symptoms of this condition- severe pain at rest, on movement, and paralysis.
Eventually with the arterial and nervous supply cut off to the muscles, necrosis takes place and the increased myoglobin leads to renal failure. Treatment is usually emergency fasciotomy and not only is this life saving but limb saving as well.
A true diagnosis can be made with compartment pressure readings. Normal intracompartmental pressure is usually 25mmHg and even small increases, 30mm Hg and greater requires intervention. Some authors feel that 45mm Hg should be the cut-off for fasciotomy and 30-45mmHg should warrant hospitalization with observation.
And for what it's worth, cellulitis is number one on the differential.

Compartment Syndrome


Falling off Mountains: Wound Management

The clinic/ emergency room/ hospital where I am working sees a good number of people in need of wound care, usually after falling on one of the nearby mountains but sometimes we get injuries from animal bites, broken glass, or car doors.  I've learned a lot about wound assessment and management, as some are repaired primarily, some need irrigation, some need antibiotics, and others need referral to one of the surgical specialties.  So I thought a review of wound care would be interesting.

Assessment.  The initial assessment of a patient with a laceration should include determination of allergies (to anesthetics, antibiotics, and latex) as well as the date of the last tetanus immunization.  Generally, in a clean, minor wound, tetanus booster should be given if the last immunization was > 10 years ago.  For all other wounds (possible infection), tetanus booster should be given if the last was > 5 years ago.

Age of Injury.  Some practitioners close only wounds that are still bleeding or that are gaping.  In my reading, it seems generally accepted that wound closure is beneficial for wounds less than 19 hours except for wounds on the head/neck which benefit from closure up to 24 hours of age.  The reason is that the risk for infection increases the longer a wound has been left open.

Mechanism of Injury.  The mechanism of injury helps determine whether a foreign body might be present as well as the prognosis for healing.  A crush injury (eg the finger slammed in a car door) may require debridement of devitalized tissue to decrease the risk of infection.  Bite wounds incur a greater risk of infection, and are most often left open to heal by secondary intention.  Stab wounds need to be evaluated to determine whether underlying structures have been damaged.

Foreign Body.  Direct wound inspection may not reveal all foreign bodies, particularly shards of glass.  Radiologic evaluation can help reveal foreign bodies that are radiopaque, and is recommended for wounds caused by broken glass and those associated with other foreign bodies if the bottom of the wound cannot be completely visualized.

Wounds that might need Referral to a Specialist.  Injuries that involve underlying structures (neurovascular or tendons) or that penetrate joint spaces need to be operatively repaired and should be referred to a surgical specialist.  Assessment of circulation, sensation (including two point discrimination) will help identify neurovascular injuries.  Tendons should also be assessed for function. 

Type of Closure.  The decision to close a wound by primary closure or to allow healing by secondary intention primarily depends on the risk of infection.  Risk of infection is determined by the age of the injury, mechanism of injury, and degree of contamination.  Any sign of inflammation is an absolute contraindication of primary closure.  Types of injuries that should be allowed to heal by secondary intention include:  deep wounds that cannot be adequately irrigated, contaminated wounds, animal bites, abscess cavities, and late presentation after injury.

This is a long entry already, so but here is a good article about risks for wound infection and the role of antimicrobials.  Next weekend there is a race up the mountain right behind the hospital, which I've heard fills the ER with lots of broken bones and lacerations.  Here is a link about the race if you're curious (plus some pictures of beautiful mountains).


domestic violence
I have not seen any cases involving domestic violence yet, but we also haven't asked about it at all so I was wondering what the evidence and recommendations are for physician screening for domestic violence.  Considering how common and dangerous it is, I would have thought screening would be recommended.   However there does not seem to be much actual evidence in the literature that routine screening improves outcomes for victims.
The United States Preventive Services Task Force (USPSTF) found insufficient evidence to recommend for or against the routine screening of parents or guardians for the physical abuse or neglect of children, of women for intimate partner violence, or of older adults or their caregivers for elder abuse.  Here is a link to their statement and supporting information.
The Canadian Task Force on Preventive Health Care found insufficient evidence to recommend for or against routine universal screening for violence against either pregnant or nonpregnant women, but recommends that clinicians be alert to signs and symptoms of abuse.
The American College of Obstetricians and Gynecologists (ACOG) guidelines on domestic violence recommend that physicians routinely ask women direct, specific questions about abuse.
The Massachusetts Medical Society Committee on Violence recommends asking one question that can be adapted as needed: "At any time, has a partner hit, kicked, or otherwise hurt or threatened you?" This one question has been found to significantly increase the detection rate of partner violence.
So I guess the important thing is to be alert to the possibility of domestic violence, particularly in specific situations.  Patients who should be asked about violence are female trauma victims, female emergency room patients, women with chronic abdominal pain or chronic headaches, pregnant women, women with STD's, and elders with injuries.
It is important to know about the domestic violence organizations, shelters, and hotlines as well as the state laws where you are.  Here is one link to that information.


hyperhomocysteinemia

Hyperhomocysteinemia

I saw an interesting patient this week. This patient was incidentally found to have elevated homocysteine level during a workup for DVT. My preceptor wanted me to research on the topic. To my surprise, there is currently no guideline for management of hyperhomocysteinemia.

Normal range of homocysteine is between 5-15?mol/L. Hyperhomocysteinemia can be classified as
  •  Moderate (15 to 30 µmol/L)
  •  Intermediate (30 to 100 µmol/L)
  •  Severe (>100 µmol/L)

Elevation of homocysteinemia can occur due to:              
   1. Genetic defects in the enzymes involved in homocysteine metabolism  including deficiency in the cystathionine B-synthase (CBS) enzyme, defective methylcobalamin synthesis, or abnormality in methylene tetrahydrofolate reductase (MTHFR) - the latter is  the most common form.  This is a rare autosomal recessive disorder with prevalence around 1/100000. (pathway)
     2. Nutritional deficiencies in folate, vitamin B12 and B6, especially the first two. More common, 5 to 7% of the population, notably in alcoholics and the elderly (may be as high as 30%-40% in this population). Homocysteine level is not as highly elevated as seen in genetic defects.

Although, not appear to be as important as other risk factors such as hypercholesterolemia, smoking, diabetes mellitus, and hypertension, it has been shown that high level of homocysteine (>15?mol/L) is an independent risk factor for atherosclerotic vascular and venous thromboembolic diseases. This is because homocysteine can induce vascular injury by several mechanisms including intimal thickening, elastic lamina disruption, smooth muscle hypertrophy, marked platelet accumulation, and the formation of platelet-enriched occlusive thrombi.Currently there is not enough evidence to recommend screening of hyperhomocysteinemia. According to American Heart Association, it may be reasonable to screen homocysteine levels in high risk people - those with renal failure or those who have personal or family history of premature atherosclerosis.

At present, there are no definitive guidelines on the management of hyperhomocysteinemia. Folic acid (1 mg/day), vitamin B12 (0.4 mg/day) and vitamin B6 (10 mg/day) have been shown to lower homocysteine levels (20-50%), especially the first two. Folic acid can be increased up to 5mg/day as needed to lower the homocysteine concentration below 15 µmol/L. Betaine (trimethylglycine), a methyl donor in homocysteine remethylation, is also used as homocysteine-lowering therapy for people with hyperhomocysteinemia due to inborn errors in the homocysteine metabolism.

According to the Canadian Task Force on Preventive Health care, adults at average risk for cardiovascular disease should take a daily supplement with folic acid (0.4 mg), vitamin B6 (3 mg), and vitamin B12 (9 micrograms

In my research, I also found two studies that show the effect of caffeine in raising homocysteine level. Although the effect is small, it is still a good idea to advise your CAD patients  to cut down amount of coffee intake

https://nsas1.amc.edu/get/uri/http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15748221&query_hl=1

https://nsas1.amc.edu/get/uri/http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15748221&query_hl=1

 (https://nsas1.amc.edu/get/uri/http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15720203&query_hl=3


Simple Physician-to-Patient Education Regarding HOT FLASHES

I have not noticed that many women during their routine annual exams or otherwise complain of hot flashes.  I usually try to ask some questions regarding this especially for post-menopausal women who are not on any estrogens/progesterones.  I have found that these symptoms are often present though, uncovering an opportunity to counsel patients quickly on remedies that might alleviate these symptoms and improve their quality of life for the time being.

As we know, during menopause the body produces less estrogen and progesterone. As a result, the hypothalamus, gets mixed signals: is it hot or cold? This oscillation causes the blood vessels to expand and contract on an irregular and unpredictable basis. Many symptoms that have been relayed to me are: a feeling of heat on the face and neck, perspiration, fulminant sweating, chill following a hot flash, headaches, fatigue, dizziness, loss of sleep, and palpitations. Some have reported an aura that preceeds the hot flash—a feeling of nausea, or a tingling or pressing sensation in the head.

Duration of symptoms can be from 15 to 30 seconds, while others from 3 to 6 minutes or even as long as 30 minutes to an hour. Frequency can be as often as every 90 minutes. Seventy-five to 80% of women going through menopause experience hot flashes. Some are more bothered by them than others.

Triggers for hot flashes include spicy food, hot drinks, alcoholic drinks, white sugar, stress, unexpressed anger, hot weather, hot tubs and saunas, tobacco and marijuana use.

Standard pharmacotherapy however has not proven helpful. SSRIs have not been shown to be effective in reducing hot flashes in post-menopausal women. So what else can be tried?

Strategies to alleviate symptoms include wearing proper clothing and vitamin supplementation. Clothes made of natural fibers like cotton, wool, or silk help disperse heat away from the body. Hot flashes deplete our bodies of the B vitamins, Vitamin C, and Magnesium and Potassium, so it is helpful to increase our consumption of these nutrients as well as Calcium.

For mild hot flashes, Vitamin E with dosages between 400 and 800 IUs daily is helpful in select patients. A study from the Journal of Clinical Oncology showed that 800IU daily helped reduce symptoms in breast cancer survivors (who were uneligible to receive HRT).

Soy and other phytoestrogens, black cohosh, evening primrose oil, vitamin E, the bioflavonoid hesperidin with vitamin C, ferulic acid, acupuncture treatment, and regular aerobic exercise have been shown effective in treating hot flashes in menopausal women, according to Hot Flashes—A Review of the Literature on Alternative and Complementary Treatment Approaches by Hazel A. Philp, ND. This article is very good at reviewing the above therapies and providing evidence for their effectiveness.

In conclusion, most of your post-menopausal women patients experience symptoms consistent with hot flashes.  Many may not mention their discomfort; however, SIMPLE strategies exist that can help improve their quality of life.  Sharing a few of these stategies with patients for only a few seconds can make a positive impact on their health as well as show them that you care for their well-being.


Fibromyalgia
I don't know about you guys, but I have been seeing a lot of patients with Fibromyalgia.  It is difficult to understand this disease because unlike several other organic diseases in medicine it does not have a definitive cause.  In researching this disease I found that there are several interesting neurochemical/autonomic/behavioral/psychological theories to explain this disease which is characterized by diffuse chronic pain/fatigue.  Here is a good site that summarizes a lot of the current research that is going on in the field.  One that is particularly interesting is the study that proposes that Fibromyalgia and IBS may have a similar etiology.  

 

The researchers found that women with IBS demonstrated more activity in an area of the brain called the anterior midcingulate cortex when they experienced the rectal pressure than when muscle pressure was applied to their arms. The midcingulate cortex is a pain-processing area of the brain that commonly is activated in studies of muscular and abdominal pain.

 

In women with both IBS and fibromyalgia, the same brain area was more activated following muscle pressure than following rectal pressure. The researchers say these findings suggest that although the site of body pain is different in IBS and fibromyalgia, the central nervous system mechanisms underlying pain are probably similar.

 

Though the cause of this disease is not well defined there are several treatment options.  Most commonly,  combinations of antidepressants, muscle relaxants and the analgesic Tramadol.  For many patients an NSAID may provide sufficient pain relief.

 

The most important thing is to treat these patients like any other patient with a chronic disease even though a cause is not well defined.  One of the patients I saw having an acute exacerbation of her disease that she believed was caused by recent stressors in her life, mostly family issues.  So to me it seems as if Fibromyalgia can be viewed like COPD in that it is chronic underlying disease that may become acutely worse with a particular insult whether it be infectious, social or psychological.


Diabetic Foot Care

This week, an elderly, diabetic patient with a history of bypass surgery for peripheral vascular disease,  came in with swelling, redness, and pain in her foot for two days.  On exam, the patient had redness and swelling along the dorsum of her foot, as well as her toes.  She also appeared to have a gangrenous ulcer in between her fourth and fifth toe.  Her foot was warm to the touch, and quite painful to even superficial sensation.  There were no pulses palpable in her foot. 

There is a vascular surgeon in the same building as the clinic I am working at, so the patient was luckily able to be seen almost immediately by the vascular surgeon.  After discussion between my attending and the vascular surgeon, it was decided to admit this patient for treatment given this patient's severe diabetic history. 


Diabetic patients are at higher risk for infections, and they are particularly at risk for foot infections, given the compromised vascular supply secondary to diabetes.  Also, many diabetics also suffer from peripheral neuropathy, and therefore can be unaware of trauma to the feet.  Infections can range from cellulitis, to deep skin or soft tissue infections, to acute osteomyelitis, to chronic osteomyelitis. 

This is the link to a study discussing the common bacteria involved in diabetic foot lesions: http://www.ijmm.org/article.asp?issn=255-0857;year=2004;volume=22;issue=3;spage=175;epage=178;aulast=Anandi

This is the link to an image that shows an example of a diabetic foot ulcer: http://dermatlas.med.jhmi.edu/derm/display.cfm?ImageID=-2131110339

This website includes good patient information about diabetic foot care guidelines from the afp that I found very helpful:   http://www.aafp.org/afp/990901ap/990901j.html (sorry, issues with the hyperlink)


Alias: Idiopathic Endolymphatic Hydrops

A patient with long standing Meniere's disease was seen at our clinic last week.  The exact cause of Meniere's is unknown, but current theories hypothesize that increased buildup of endolymph in the inner ear can cause swelling of the labyrinth and thus lead to the acute symptoms listed below.  Other theories include: virus infections of the ear; salt imbalance in the labyrinth fluid; diet; a faulty immune system.

"Meniere's attacks" (transient symptoms): A Meniere's attack can last from 20 minutes to several hours and is usually preceded by an aura.  Post attack  many people experience fatigue and sleepiness.  An attack without vertigo is uncommon.  7/10 people with this disease will be asymtompatic for long periods (weeks-months) of time between attacks.  

  • Dulled hearing in the affected ear(s). The amount of hearing loss varies.
  • Vertigo. 
  • Tinnitus-a ringing, roaring, or buzzing noise.
  • Ear pressure. 
  •  Loud noises may seem unpleasant and distorted.

Symptoms which may become permanent - during attacks hearing loss and tinnitus occur but usually recede/return to normal when the attack is over.  In long standing disease however both of these of these symptoms can become permanent leading to chronic tinnitus and deafness in the affected ear.

Diagnosis: some of the following may be conducted in the evaluation of possible Menier's.  For more detailed info on the tests below see http://www.menieres-disease.ca/diagnosis.htm for good descriptions.

  • Auditory: pure tones and speech discrimination
  • Glycerol: changes in loudness and/or clarity after drinking glycerine (A positive result is specific for active Meniere's disease; a negative result may indicate inactive Meniere's disease, especially when the hearing loss has been present for some time.
  • Electronystagmography: balance function as seen through eye movements.
  • General health evaluation
  • Auditory brain stem response (ABR) and Otoacoustic emission tests
  • Balance testing
  • Antibody measurement
  • Glucose (sugar) metabolism
  • Blood: (evaluating for systemic infection)
  • Magnetic resonance imaging of the inner ear and hearing nerve.

Treatment of vertigo attack:

  • Meclizine (Antivert), Lorazepam (Ativan) Phenergan, Compazine, Zofran, Decadron (dexamethasone)


Prevention of attacks of vertigo:

  • Betahistine is medicine which is thought to increase the blood flow around the inner ear. This may reduce the amount of fluid inside the labyrinth and prevent symptoms from developing.
  • Other medicines such as diuretics or beta-blockers may help in some cases.  Antibiotics (aminoglycosydes) are also being used.
  • Surgery to the ear may be an option if you have bad or frequent attacks of vertigo. Surgery aims to control vertigo which has not been helped by other means. About 1 in 10 people with Meniere's disease have surgery at some stage.
Diet and lifestyle: although there hasn't been any rock-solid scientific data proving the effectiveness of the following, some people obtain symptomatic relief from these:
  • A low salt diet. This may help to reduce the fluid build up in the inner ear.
  • Regular exercise and methods to combat stress.
  • Smoking Cessation. 
  • Food triggers. There seems to be a link between migraine and Meniere's disease in some people. Food triggers are known to cause migraine attacks in some people.

A general overview of the disease: http://www.menieres.org.uk/


Basal Cell Carcinoma

This week I saw two patients with lesions that  were suspicious for basal cell carcinoma.  Both lesions looked exactly the same and were almost in the same exact location (on the forehead).  So I thought I would share some information about BCC, how it presents, and treatment. 

BCC is the most common skin cancer in the U.S. and is most prevelant in fair skinned individuals.  The incidence is estimated to be between 500-1000 per 100,000 and men are 30% more likely to develop BCC than women.  Both environmental and genetic factors contribute to the development of BCC with the main risk factor being prolonged exposure to the sun's UV rays.  In addition, individuals with chronic arsenic exposure, chronic immunosuppression, exposure to radiation therapy, or smokers are more likely to develop BCC.  Acquired mutations in the tumor suppressor gene PTCH has been identified in sporadic cased of BCC which requires two sporadic "hits" and in cases associated with xeroderma pigmentosum which only require one "hit" plus the inheritance of one defective allele. 

The clinical presentation of BCC can be divided into three groups: nodular, superficial, and morpheaform.  Nodular is the most common subtype and presents on the face as a pink or skin colored papule with the lesion having a pearly or translucent appearance that is commonly seen with telangiectatic vessels within the papule (to see picture click: http://www.utdol.com/application/image.asp?file=onco_pix/nodula8.gif ).  Ulceration can be very common.  Superficial BCC is the second most common subtype and most commonly presents on the trunk.  It usualy appears as a scaly papule or plaque that is light red in color, atrophic in the center, and is rimmed with fine translucent micropapules (picture: http://www.utdol.com/application/image.asp?file=onco_pix/superf4.gif ).  Morpheaform (sclerosing) BCC is the least common subtype and presents as a smooth, flesh-colored papule that is often atrophic.  These papules usually have a firm quality to them with poorly defined borders (picture: http://www.utdol.com/application/image.asp?file=onco_pix/sclero2.gif ). 

Diagnosis of BCC can be clinical but confirmation through biopsy (punch or shave) is usually indicated to help indentify the depth of involvement and histologic type.    Prognosis for people with BCC is excellent because lesions usually grow slowly and metastasis is rare.  There can be considerable morbidity however due to local destruction of skin, cartilage, or even bone.  The most common treatment is surgical excision with primary closure which results in greater than a 90% cure rate.  Radiation therapy also has a high cure rate and is indicated in cases where surgical access is difficult or surgery is contraindicated.  In addition, topical therapy through imiquimod cream or 5-fluorouracil have been successful in treating superficial  BCC at noncritical locations such as the trunk or limbs.  Finally, photodynamic therapy (PTD) of presensitized cells is gaining popularity as a modality for the treatment of superficial or nodular BCC. 

I included the following links in case you guys want to know more about skin cancer or BCC.

http://www.skincancer.org/ 

http://www.aad.org/ 

http://www.intelihealth.com/IH/ihtIH/WSIHW000/9339/9528.html

 


Parvovirus

I saw 2 textbook cases of Parvovirus this week - with the "slapped cheeks" and the lacy rash.  I was amazed that it looked exactly how it does in the pictures.  I wanted to learn more about this disease, especially about the epidemiology of the virus to see if these two cases could be connected.

 I found an article in the American Family Physician with a lot of helpful information.  Parvovirus is an extremely common infection.  About 50% of children have detectable parvovirus B19 specific IgG antibodies by age 15 and 50-80% of adults are seropositive.  Infection is most common in late winter and spring and is spread via the respiratory route.  The stages of Parvovirus are as follows:

Stage 1:

            Period of transmissablity

            Mild prodromal illness

            Viremia

            Erythroid progenitor cell

            Development of parvovirus B19 specific IgM antibodies

Stage 2:

            Facial exanthem, or "slapped cheek" appearance

            Clearance of viremia

            Development of parvovirus IgG antibodies

Stage 3:

            Lacy, erythematous maculopapular exanthem on trunk and extremities

            Evanescent course of exanthem over 1-3 weeks

            Arthropathy

I found it especially interesting that infected persons are no longer contagious once the rash is present.  It is also interesting to note that many people (my patients included) never experience (or don't remember) a true prodromal state.  Additionally, the first stage of the disease course occurs after a 4-14 day incubation period, which is the answer to a question that I have been asked several times in the clinic.

The diagnosis of Parvovirus is made clinically.  In terms of treatment, reassurance is the most important component.  The virus is self-limiting and no specific therapy is warranted in most cases.  The things to look out for in terms of complications are arthropathy and erythrocyte aplasia.

Here is the link to the article that I used: http://www.aafp.org/afp/991001ap/1455.html

and here is a picture of the classic "slapped cheeks": http://health.allrefer.com/health/fifth-disease-fifth-disease.html


Bypass Brain
An elderly patient who had had coronary artery bypass had marked cognitive decline.  The decline was first noted soon after the surgery, but the family was uncertain if it might also/instead be Alzheimer's.  The family's physician thought the patient had "Bypass Brain," possibly superimposed on Alzheimer's. 
 
"Bypass brain" is a phenomenon that is commonly noted immediately after CABG, and is present in up to 75% of patients.  Its manifestations range from temporary psychological changes to stroke, and it can present as changes in attention, concentration, memory, or mental agility.  Its presentation is similar to Alzheimer's and chronic dementias and is unexplained by age or other known physiological factors. 
 
Apolipoprotein E-epsilon 4 was implicated in a 1997 study.  (ApoE genes are responsible for neuronal repair after injury.)  The study found that individuals with lower education levels were more likely to have cognitive decline if they had the Apo E-epsilon 4 allele.  Individuals with higher education levels and the allele were less susceptible.  Persons without the allele were also susceptible to cognitive decline, but less so than if they'd had the allele, regardless of educational level. 
 
Bypass brain is a real phenomenon for which the severity appears to be influenced by educational background and genetics.  When patients discuss elective bypass grafts with health care providers, the providers should include in the discussion of risks the bypass brain phenomenon.

June 25, 2005
what is that on your skin???

seborrheic keratosis vs.  actinic keratosis

I saw an elderly in the office with a lot of raised lesions all over his back and some on his face.  The lesions varied in size from 5mm to 10mm and were dark brown in color. I immediately thought of seborrheic keratosis.  However, I found out later that they were actinic keratosis.  My attending physician told me that some actinic keratosis can look just like seborrheic keratosis and the way to distinguish them is just to biopsy them.  I 've always thought of actinic keratosis as having white scaly lesions on top of the erythematous base but it doen't have to be like that all the time.  Some are just pigmented without the base and can look very similar to seborrheic keratosis that has brown, stuck on appearance. 

The major difference between seborrheic and actinic keratosis(aka solar keratosis) is that seborrheic keratosis is a benign epithelial tumor that does not require treatment and actinic keratosis is a premalignant lesion that requires treatment.  Cryotheraphy is typically performed for small lesions and surgical curettage for larger lesions.  Topical 5FU is effective in the area that has multiple lesions.

Here is a website that has some additional info and some pictures.  http://matrix.ucdavis.edu/tumors/tradition/ak-gallery.htmlhttp://www.aad.org/public/Publications/pamphlets/SeborrheicKeratoses.htm


Tylomas and helomas

I know the topic line sounds exotic, but it's about feet and a patient I saw who came in for an "infected callus" as he put it.  I admit I must have been asleep the day we learned about calluses, corns, bunions and the like so I thought I needed a refresher and maybe this interests you...The patient has been bothered by "calluses" for most of his adult life because he wore steel-toed boots for his job and often went without socks.  On exam, the second metatarsal had a ½ cm well defined, circular, thickened, white lesion in the toe cleft.  There was no evidence of infection and full ROM, but it was very painful to touch, was affecting his gait and on the first metatarsal a thickened area of skin was evidence opposite of this lesion.  He was diagnosed with a corn and advised to soak it or seek a Podiatrist to shave it down.  I wanted to know if there were other treatment options and what makes a corn.  Although this may sound stupid but I have never seen a corn before (at least not that kind of corn)...So here's the difference:

Tylomas (calluses) are a diffuse thickening of the outermost layer of the skin, the stratum corneum, in response to repeated friction or pressure.  Calluses are a thickening of the skin without a distinct border, most common over the bony prominences of the feet and hands, may vary in color from white, gray, yellow, brown or red, and may throb or burn. 
Helomas (corns) develop similarly, but differ by containing a cone-shaped core (hyperkeratotic area) with a point that can press on a nerve below and can be very painful.  Corns typically occur at pressure points secondary to ill-fitting shoes, an underlying bony spur or an abnormal gait.  There are 2 types of corns hard corns (heloma durums) which are the most common type and usually located on the plantar aspect of prominent metatarsals or on the dorsal aspect of toe joints and soft corns (heloma molles) which often occur between toe clefts look whitish and occur as a result of bony abnormalities in the toes.  Corns vary in texture from dry to waxy to transparent to a horny mass; has distinct borders; are most common on the feet; may be hard or soft and may be "kissing corns" between 2 toes.

Treatment — Calluses and corns are treated the same.  Self-care:  Patients should be advised to avoid ill-fitting shoes, wear socks to reduce friction, maintain proper foot hygiene and use emollients to keep skin in good condition.  The treatment of choice is application of salicylic acid plasters.  Salicylic acid plaster, 40 percent, is available without a prescription.  Office care: Debulk the callus or corn by paring skin with a no. 15 scalpel blade.  Cut the plaster to the size of the lesion.  Leave in place for 48 to 72 hours; keep dry.  Patients should be advised to remove the white "dead" skin with a metal nail file or pumice stone each night before replacing the patch. Use of the patch should stop once the lesion has resolved.  Follow up if lesions do not resolve within one to two weeks.

**OTC corn removing solutions and plasters containing acid and should NEVER be used by diabetics, those with diminished circulation or diminished sensation because they will not notice destruction of normal skin.

Remedies such as corn paint, cure or plasters will generally only treat the symptom of the corn and not the problem that causes it.

Treatment can also involve special supports (Orthotics) to correct an abnormal gait and stop further deformity.  Medication can relieve the pain and your Podiatrist can recommend surgery if necessary.

Complications that can result from corns include the development of a bursitis - the formation of a painful inflamed fluid-filled sac beneath the corn; development of an ulcer that may even extend down to bone; and infection of soft tissues or bone.

More images and info:

http://www.aafp.org/afp/20020601/2277.html


 


Interstitial Cystitis or UTI???

A 75yo thin Caucasian female presented to clinic one month after tx with Cipro for a possible UTI. Cultures from one month ago were negative and the patient still has symptoms of urgency, frequency, bladder pressure, dysuria, and vaginal pruritis.

The pt has a history of IBS and essential hematuria. 

U/A from today's visit reveals cloudy urine with 3+ hematuria, 3+ leukocytes and a ph of 5. Nitrites were not recorded. 

The nurse practitioner I was shadowing asked the pt if she drank caffiene.  The pt did in fact drink 3-5 cups of black tea a day.  The pt also claimed to have eaten strawberries last week.  A diagnosis of interstitial cystitis was given pending urine culture results.  The pt was given a large list of foods to avoid that ranged from fruits to soy to caffiene.  The pt was upset about all of the foods she must avoid considering that she feels she is already too thin.  However, she seemed willing to comply.

Interstitial cystitis is a clinical syndrome characterized by urinary frequency, urgency, and/or pelvic pain.  The exact cause is unknown, but it may result from abnormal bladder wall permeability, neurologic upregulation, and abnormal mast cell degranulation.  It is most common in Caucasians and before age 50.  There has been a proposed association with caffeine (however, the methods and assumptions made by this study seem weak) and IBS.  There is no current universally accepted diagnostic criteria, however, the potassium sensitivity test is 78% sensitive and 98% specific.  Tx  of IU includes pentosan polysulfate sodium (which helps restore the bladder epithelium), TCA'S or SSRI's, hydroxyzine (which controls allergies), dimethylsulfoxide, and hydrodistension.

I could not find any material showing an association with I.C. and leukocytes in the urine and could not find any studies that showed a clear link between I.C. and diet.    I also could not find any protocol regarding UTI symptoms and negative urine cultures.  Should this elderly pt be put on a different antibiotic (ie. Bactrim) or is it reasonable to wait until her new cultures come back?  Was this "diagnosis" of interstitial cystitis a bit premature and was enough clarification given regarding the affects of dietary restiction.  After witnessing this case and reviewing some of the literature, it is clear that as health care providers we will have to make "judgement calls" in some situations.  If anyone knows of or comes across any info please feel free to contradict anything I've written.

http://www.aafp.org/afp/20011001/1199.html

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1977196&itool=iconabstr&query_hl=11


Mastoiditis - Complication of Otitis Media


Paroditis

Last week, a physician brought me into an examining room to see an interesting case.  In my two weeks at this clinic the other interesting cases I've seen with this physician reaffirmed my painful lack of knowledge in the world dermatology.  Fortunately today's case didn't have any skin lesions.  The patient presented to the clinic after experiencing severe pain along the angle of her mandible the previous evening at dinner.  The pain was transient and she was able to sleep through the night, but the next morning at breakfast she experienced the same pain.  In speaking with her, she had a similar episode after she gave birth to her first child 5 months ago.  Aside from severe pain to palpation along the angle of the mandible the rest of her exam was normal.

With this brief history and exam, I came to the conclusion that this patient had a parotiditis.  Although the story made sense in that the pain was most pronounced after eating, I would expected her tenderness to be more under the mandible instead of a the angle.  Despite this uncertainty, my guess was correct and the treatment in this case was Augmentin along with rehydration.  Dehydration, which in this case may have occurred after delivery of her child or during this hot weather, is predisposing factor to salivary gland inflammation and the parotid is most commonly involved since it has a lower rate of secretion compared to the submandibular gland. 

After having the bugs most responsible for otitis media and community acquired pneumonia pounded into our heads, I wanted to know what the most common causes of parotiditis are.  After reviewing a few articles, it appears that aerobic and anaerobic bacteria both cause parotid infections.  Aerobic infections were most commonly due to S. aureus or H. influenza while anaerobic infections were usually due to gram negative bacilli or peptostreptococcus species.  Because of this broad spectrum of etiologies for parotiditis, Augmentin was a good choice of therapy with its extended coverage of gram negative bacilli along with its beta lactamase inhibitor to overcome possible resistance via plasmid mediated penicillinase.

 

http://jmm.sgmjournals.org/cgi/reprint/51/6/526

June 24, 2005
Peforated nasal septum

Although I already rotated through ENT surgery, I just recently had the opportunity to visualize a perforated septum on more than one occassion. There are many etiologies but I thought I would give you a little background so that if you see one on physical exam you can begin to think of the cause.

The septum is made of cartilage in the front and bone further back. On either side, it is covered with mucous membranes. The cartilage depends upon the blood vessels in the mucous membranes for its nutrition. If the supply is shut off, the cartilage dies leading to perforation.

Common etiologies include: nose rings through the middle of the nose, cocaine, getting the septum cautized because of nosebleeds, rhinoplasty, typhoid, syphilis, SLE, Tb, and harmful vapors such as phosphorus, copper, and cortisone.

Treatment usually requires surgery especially if the integrity of the nose is compromised. Other treatments include saline nasal spray for symptoms relief.

The article attached is a very good overview of cocaine abuse and its physiologic effects. And since it is widely used one should consider this etiology when a perforated septum is found. I also included a couple of pictures.

http://www.annals.org/cgi/content/full/119/3/226

image 1

image 2

June 23, 2005
Early-onset diabetic neuropathy
An elderly patient with a very recent diagnosis (within the last year) of diabetes mellitus (DM) reported new onset of peripheral neuropathy.  The quick onset of diabetic neuropathy was unexpected, so I looked into its prevalence. 
 
According to a 1977 survey, 7% of patients had peripheral neuropathy at DM diagnosis, but it was far more common for patients to have had DM for 25 years before developing neuropathy.  As you know, longer duration of DM is associated with increased risk of neuropathy.  What you may not have known is that the length of the delay of diabetic neuropathy after DM onset also depends on independent factors such as older age, smoking, alcohol, high cholesterol, HTN, and height. 
 
So in an older male who smokes and drinks in excess, don't be surprised to see an earlier onset of neuropathy.  This makes it all the more important to counsel these at-risk patients immediately after diagnosis about diabetic neuropathy and its independent risk factors.
 
Source:  Duby JJ, Campbell RK, Setter SM, White JR, Rasmussen KA.  Diabetic neuropathy:  an intensive review.  Am J Health Syst Pharm.  2004 Jan 15; 61: 160-173.

June 22, 2005
Pityriasis Rosea

A young woman presented to the clinic with a diffuse erythematous papulosquamous rash all over her back, chest, and abdomen.  Her arms, legs, and face were generally spared.  There is no family history.  The rashes appeared as numerous oval shaped patches, that had a very fine white scaly appearance that looked slightly dry.  She also complains of pruritis.

From this brief description, several dermatological differentials should come to mind which includes psoriasis, atopic dermatitis, and hopefully pityriasis rosea.  

Pityriasis Rosea:

  • common in 10-35 yo.
  • mild to moderate pruritis
  • oval erythematous patch, plaques with fine "cigarette paper" white scale
  • "Christmas tree" distribution on trunk
  • pathognomomic herald patch, solitary salmon colored oval patch, 2-6cm in diameter

Atopic Dermatitis:

  • common, chronic, reccurent, pruritic
  • family history!
  • hx of atopy: allergic rhinitis, asthma, dermatitis
  • infantile form (6mo-10yr): face + extensors, red exudative, crusty, oozing
  • adult form: flexural areas (popliteal, antecubital) dry lichenified, pruritic papules 

Psoriasis:

  • pain, tenderness, joint stiffness
  • family history
  • dark red plaques with silvery white scales
  • sharp margins
  • extensors
  • nail pitting, onycholysis

Pityriasis rosea often is misdiagnosed as eczema or psoriasis since there are overlapping symptoms.  Mainly, eczema is pruritic, and psoriasis has a white scaly appearance as well.  If the patient presents only with the herald patch, it can be confused with ringworm.

The main thing that differentiates the three are that in pityriasis, there is no family history, there is no history of atopy, it is a diffuse rash with no flexor/extensor preference, and it has the characteritic Christmas tree distribution and herald patch.

The etiology of pityriasis is idiopathic, but is commonly seen in the fall and spring.  In this patient, it was really cool in that the herald patch was textbook.  It was solitary (on her leg), preceded the diffuse rash by 3 days, oval shaped, salmon colored.  As far as the Christmas tree distribution on back and chest.... well... I suppose it takes a lot of imagination.  It is self-lmited, though treatment  can include topical steroids, UVB light, antihistamines, or natural sunlight.

Here are some pics:  herald patch,  Christmas Tree      

A link to a good review article can be found here on Pubmed, but to get the full version, you will have to do the secure logon.  A general overview of the condition for lay people can be found here

June 21, 2005
Obesity - the need for education on diet/exercise
I know this topic sounds basic to most of us, but that is exactly why I am writing this blog.  As medical students, knowing which is the healthy choice at dinner is almost like brushing our teeth.  (Now whether we actually choose that option is a different story).  That is why I think that we may tend to overlook it more than we should.  We have all heard sometime in the last 3 years that obesity has become an epidemic in this country.

Working in an FP clinic that serves a very low-income population, I think it is significantly more prevalent of a problem and I truly am astounded by the lack of knowledge on basic diet.  Since I've started working in this clinic, I may be able to count on one hand the number of patients that I have seen with a BMI of less than 35.  When I talk about diet to these folks, their first reply is that they eat small portions and lots of vegetables.  Upon probing, one by one, their true eating habits come out.   "I eat lots of salad.... with a cup of blue cheese dressing."  "I love eggs..... I eat tons of egg foo young from the Chinese take out joint next to my house.  And I order a lot so they deliver."  When asked about fruit intake, "Oh I drink a ton of fruit juice."  "And when I go to McDonald's I eat the double cheeseburger instead of the Big Mac."  One asked, "Are fried vegetables bad for you?"  And of course, every one of these patients has DM2, HTN, hyperlipidemia...... and a family history of early MIs.  When talked to about the importance of weight loss, I have gotten numerous responses for unconventional methods like "Can you prescribe me Topamax for that? I know I can lose weight on that." 

The problem is - these patients will not start dieting/exercising unless they are motivated.  And how can you be motivated when you don't understand how effective it can be?  What they need is - education on diet - which is something that we can provide on a basic level!  With a couple patients, I have literally gone through what they eat for each meal and made specific examples of how they can make a healthier choice.  And they have found it very helpful.  It can be difficult because foods that cost less are usually higher in refined grains, added sugars, or fats vs. lean meats, fish, and fresh produce.  But weight loss will significantly decrease their multiple risks for CHD.  I have also seen a couple patients who have been successful on meal replacement plans, like Slim Fast or Meta Fast.  Again, I know it seems basic, but I think it's really important and I think a lot of physicians don't have time -- that's where the med students should come in!

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10203915&query_hl=17

June 20, 2005
Occupational hazards of fishing
I realize that most of you are probably not seeing tons of fishing traumas, but soft-tissue infections (such as cellulitis) with water exposure may be something you come across. I read up on cellulitis with water exposure after seeing a case of cellulitis caused by a gram negative bacteria. It turns out that there are 5 five bacteria that most commonly produce soft tissue infections when there has also been an exposure to water. These 5 bugs are (pneumonic AEEVM): -Aeromonas (gram negative rod) -Edwardsiella tarda (gram positive) -Erysipelothrix rhusiopathiae (gram positive) -Vibrio vulnificus (gram negative curved rod) -Mycobacterium marinum Because treatment is usually started empirically, I think the take home message is to determine whether the skin trauma occured in a water environment or not as this will influence antibiotic choices. Without water exposure, the most common causes of cellulitis are beta-hemolytic strep and staph aureus and empiric treatment is usually a first generation cephalosporin such as cephalexin (Keflex). With water exposure, however, empiric treatment should cover the AEEVM bugs as well as strep and staph. A commonly used empiric treatment in this situation is ceftazidime plus either an aminoglycoside or a quinolone. If it was a seawater exposure, then add a tetracycline to cover for vibrio vulnificus. Also interesting to consider what water exposures include: fresh water, salt water, brackish water, potable water, water in swimming pools, aquariums, and hospital sources of water such as solutions used for respiratory care equipment. Bites from fish, alligators, sharks, and turtles. Puncture wounds from fish hooks or broken seashells are also important in disease transmission. There is also a case report of a localized epidemic of aeromonas cellulitis among a team of mud football players, so watch for that one too. This paper is an old one (1992) but gives a good basic overview of the AEEVM bacteria - and both the intestinal and extra-intestinal manifestations. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1514473&query_hl=4

June 19, 2005
heroin addiction and treatments
For the past year I have been working on a medicinal chemistry project involving the treatment of cocaine and heroin addiction by synthesizing morphine analogs.  Bascially my project was to create a drug to treat another drug that had less side effects.  I know I sound like a geek/nerd but my point is it was not unitl this past week while on my Family Practice rotation that I was actually able to put a face with the disease that I am trying to cure.  I was given an opportunity to attend morning rounds on a detox floor that involved many heroin addicts that were being treated with Suboxone. 
    Suboxone is 2 drugs consisting of buprenorphine and naloxone, and it is used to treat adults addicted to opioid medicines and drugs, such as morphine and heroin.  Suboxone is not the majic bullet that cures addiction, but is part of a complete addiction treatment program that also includes counseling and behavioral therapy.  The reason why this drug contains 2 drugs is clever thinking on makers.  Buprenorphine (this drug looks very similar to the drug I am working on) acts like painkiller medicines such as morphine, street drugs like heoin, and addiction treatment medicines like methadone.  Buprenorphine gives less of a high as these other opiates, and withdrawal or stopping buprenorphine may be easier than stopping these other drugs.  Naloxone, on the other hand, blocks the effects of thes opiates including buprenorphine when injected.  Naloxone is added to suboxone to prevent people from shooting up suboxone (which would give a btter high).  Suboxone is to be taken sublingually, and in this way naloxone has no effect.  If suboxone in injected then it will block the effects of buprenorphine, and the patient will actually feel severe withdrawal symptoms.  Very clever.
    In the past the only viable treatment for heroin addiction was methadone, which is administered in methadone clinics. According to my attending these clinics are usually in the inner-city and resemble "crack houses."  This she said is often a barrier for a lot people to seek treament because they did not want the stigma of being in one of those places.  Now Suboxone maintenace can be perscribed by a FP while the patient makes an office visit.      There is a lot of evidence based medicine to support the clinical effectiveness of Suboxone that is equal to methadone while at the same time removing existing barriers to treatment.  For this evedence based medicine see link below or see J Pain Palliat Care Pharmacother.  2004; 18 (3): 35-45.
    For those interested in learning about the clinical assesment, screening, and treatment plans for heroin addicts the U.S. Department of Health and Human Services published "Clinical Guidelines for the Use of Buprenorphine in the treatment of Opioid Addiction"  These guidelines are the best-practiced evidenced based guidelins on the use of buprenorphine as a new option for the treatment of opioid addiciton.  For this book see http://www.kap.samsa.gov/products/manuals/index.htm.
    https://nsas1.amc.edu/get/uri/http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15364630&query_hl=3


Acute sinusitis

During the last week, I have seen a lot of cases of acute sinusitis referred to as the "common cold" by patients.  Sinusitis is an inflammation of the lining of the paranasal sinus usually caused by bacterial overgrowth in a closed cavity.  The definition of acute sinusitis are that the symptoms last less than three weeks.  The pathophysiology of acute sinusitis is usually preceded by an infection (maybe viral), inflammation or an obstruction of the sinus opening leading to an impaired ciliary clearance of secretions and bacterial overgrowth.  It most commonly affects the ethmoid or maxillary sinuses. 

Presence of 4 or more of the following symptoms is highly predictive of bacterial sinusitis: Unilateral face pain, purulent nasal discharge, ain during mastication, anosmia, headache, fever, nasal congestion, halitosis, toothache, metallic taste and cough.

On PE: Purulent nasal secretions, increased posterior pharyngeal secretions, tenderness overlying sinuses and air-fluid levels on transillumination of the sinuses.

Streptococcus pneumoniae or Haemophilus influenzae causes 70% of cases.  Other Streptococcus species cause 8% of cases.  Staphylococcus aureus, Neisseria species, anaerobes, and other gram-negative rods cause 6% of cases.  Rarely, sinusitis may be caused by fungi, for example Aspergillus or Candida species.

Lab studies are of limited value because the CBC count with differential may be within normal ranges and cultures of nasal secretions are usually contaminated by normal flora.

CT scanning is the preferred imaging method.  A screening sinus CT scan is adequate for diagnosis and less costly than other methods but is only necessary in cases of treatment failure or chronic disease.

First-line therapy generally is amoxicillin, penicillin, trimethoprim-sulfamethoxazole (TMP-SMZ), or erythromycin.  Second-line agents (eg, cefprozil, cefuroxime, cefixime, amoxicillin-clavulanate, clarithromycin) are used for treatment failures or if resistance is suggested.  An adequate trial (ie, 2 courses of antibiotics for up to 21 d) of medical therapy results in relief of symptoms in nearly 85% of cases.  40% of cases resolve without treatment although inadequently treated infection may lead to chronic sinusitis, abscess or meningitis. 

Alternative treatments include: Humidification/vaporizer, warm compresses, adequate hydration, smoking cessation, saline nasal spray (every patient's favorite treatment).

Images:

http://www.aaaai.org/patients/publicedmat/sinusitis/infectedsinus.jpg

http://www.aafp.org/afp/980901ap/slac_f5.jpg

 

http://www.entnet.org/healthinfo/sinus/sinus_questions.cfm


Darier's Disease

We got to diagnose someone with this rare disease I'd never even heard of last week.  A young man presented with an impetigo-type rash on his arm.  He also had papules on his back and his forehead at the scalp area, and cold sores around his mouth.  His mother told me that his father and grandfather also had chronic rashes and she thought they had a disease starting with D.

Based on his symptoms and family history, we ended up diagnosing him with Darier's disease.  Also known as keratosis follicularis, it is an autosomal dominant disease characterized by the loss of adhesion between epidermal cells and by abnormal keratinization. Reccently the abnormal gene has been identified as ATP2A2, found on chromosome 12q23-24.1. This gene codes for the SERCA enzyme or pump (SarcoEndoplasmic Reticulum Calcium-ATPase) that is required to transport calcium within the cell.  The skin lesions are characterised by persistent, greasy, scaly papules which tend to occur over the seborrhoeic areas of the face (scalp margins, forehead, ears, around the nostrils and sides of nose, eyebrows, and beard area), neck, and central chest and back  The nails are also involved, often with longitudinal broad stripes of white and reddish colour.  Widespread infection of the skin with herpes simplex virus or secondary bacterial infections are possible complications.  A skin biopsy will show characteristic histology, known as focal acantholytic dyskeratosis associated with varying degrees of papillomatosis.  Treatment is topical retinoids, or oral retinoids if it is severe.  Here are some pictures for you:

 picture1  picture2 picture3

And a review article on the epidemiology, pathophysiology, and management if you would like to read more:   article


Human Papillomavirus

This is a little comment on direct to consumer (D2C) ads and some info on HPV.  I had a patient ask me what the HPV test was about and could she get that test.  I thought she was referring to a Pap smear, so I explained to her that during a Pap smear they take a sample of cells from the cervix and a lab looks at those cells under a microscope to see if there are any abnormal cells...she interrupted and said she read in a magazine (Oprah no less) about the HPV test.  She read that there's some special HPV test that women need to ask their doctor about because the other test doesn't always get it right.

So I looked up what magazine ad she was talking about and it was called the HPV test, specifically DNAwithPAP™ test for the 13 high risk HPV DNA types.  It was a D2C ad in the magazine that urged all women over the age of 30 and any women under 30 with an inconclusive Pap to ask their doctor to have this test taken during the annual gyn exam.  

On the website it tells women that the Pap test may not find cervical cancer until it's too late, but luckily there's a new test (their test) that detects the abnormal cells and it says that it's ok to tell your doctor what you learned on the website because doctors are still learning about HPV too.  It also claims to have almost 100% detection rate.

What I didn't know until I looked on the CDC website was that they ARE recommending that all women get the HPV test in addition to a Pap over the age of 30 and of course if the are ASC-US.  Maybe I missed this lecture in OB-GYN, but it was news to me and maybe it will help you out.

HPV facts:

-There are over 100 HPV types causing common warts to carcinoma of the cervix, penis and anus to carcinoma of the lung. 
-High risk types are 16 and 18.  Low risk types are 6 and 11.
-The 2 common types you may see in FP include the anogenital warts aka Condylomata acuminate and cervical infections leading to a low-grade squamous intraepithelial lesion (LGSIL) or a high-grade squamous intraepithelial lesion (HGSIL).
-Pap smears should contain samples of cells from the ectocervix, transformation zone and endocervical canal.
-Treatment: Immune modifiers (INF?, imiquimod) mainly for Condylomata and various surgical options for cervical infections (Crypsurgery, LEEP, Laser).


chronic headache

When a person complains of throbbing headache that's been going on for a couple of months, it's tempting to prescribe a potent pain relieving med such as imitrex and assume that it will take care of all the pain and he/she will get better sleep at night.  That's what i thought at least in the beginning...   However, that's not what most physicians do. 

My attending focuses a lot on avoiding triggers when it comes to treating a chronic headache.  He does not immediately pull out his prescription pad and writes a pain med or give free samples of Imitrex.  Instead, he goes over a list of foods that trigger a headache.  Among the most frequent are red wine, caffeine, cheese, chocolate and peanuts.  Sleep deprivation, stress, and dehydration are other causes of chronic headache.  It is important to keep a diary of foods eaten and recognize when the headache occurs.  By doing this, you can eliminate some of the trigger foods that might be causing the daily headache.  

The next thing to do is to make some lifestyle changes.  Some of the suggested changes are maintaining regular sleep patterns by going to sleep and waking up at the same time, exercising regularly, eating regular meals without skipping meals, and reducing stress by avoiding conflicts and resolving disputes calmly. 

Usually, these are things that are offered to the patients during their first visit.  If avoiding triggers and lifestyle changes fail to improve headaches, prophylactic and abortive medications are started.  Popular abortive meds are NSAIDS and triptans(Imitrex).  Prophylactic meds for frequent, severe headaches are B blockers, TCAs, and calcium channel blockers. 

The main point of this topic is that trigger avoidance and lifestyle modifications always come before pharmacologic therapy.  Patients need to become aware of the importance of recognizing triggers that help reduce the frequency of attacks and this will lead to a better sense of well being and improved quality of life. 

This is a website that talks more about management of chronic headache.  http://www.achenet.org/prevention/

  


Impacted cerumen

An elderly patient complained of recurrent impacted cerumen.  He had tried an OTC ceruminolytic, but reported that it had caused pain.  Ceruminolytics can be irritating, so my question is:  Was a ceruminolytic necessary? 

A randomized, double-blinded, placebo-controlled study compared 2 ceruminolytic agents (Cerumemex and Murine) against saline drops, all of which were followed by irrigation with lukewarm water (WaterPik Oral Jet at the lowest-pressure setting), and found no benefit from the ceruminolytics.  On the contrary, the saline was most effective (not significant).  The authors theorized that the saline worked best because it induced swelling of the cerumen epithelial components, leading to loosening and separation of the cerumen particles.  In terms of adverse events, saline placebo had the best profile, with 1 complaint of ear discomfort (1 of 24 patients).  Cerumenex patients (3 of 24) complained of pruritis, contact dermatitis, and vertigo.  Murine patients (2 of 26) complained of pruritis. 

In conclusion, saline drops are an effective, less-irritating alternative to ceruminolytics.
 
Reference:  Roland PS, Eaton DA, Gross RD, Wall GM, Conroy PJ, Garadi R, LaFontaine L, Potts S, Hogg G.  Randomized, placebo-controlled evaluation of Cerumemex and Murine earwax removal products.  Arch Otolaryngol Head Neck Surg.  2004 Oct; 130: 1175-77.


White coat syndrome

I had a very interesting experience last week.  A patient I saw had demanded that the nurse take his blood pressure while sitting in the chair as opposed to sitting on the examining table because he always had higher blood pressures while on the table.  Of course, I was curious about this and I needed practice taking blood pressures so I repeated the blood pressure with the patient sitting in the chair and I got a blood pressure of 130/60.  When I repeated the blood pressure with the patient on the examining table about five minutes later, his blood pressure was 150/70.  It turns out that this patient had a previous bad experience with a physician and ever since then, he would have really high blood pressures when taken on the examining pressures.  I had always heard about the "white coat syndrome," but this patient had a specific psychiatrically traumatic experience that was the root of his physiologic blood pressure elevation.  So I thought I would look up any studies about the white coat syndrome.

The study I found on pubmed basically questions whether there is an association between patients with various psychosocial dysfunction and the white coat phenomenon.  It did not find an association, but it was also very small and the power was inadequate.  In terms of how this subject may be helpful to us future physicians, I think it is important to keep in mind that patients may be nervous when they come to the doctor's office and they may manifest this physiologically.  Practically, if you have a patient who you are unsure is hypertensive based on their office visits, it may be helpful to have them purchase a home kit to take their pressures on a consistent basis.  If they do turn out to be hypertensive, they can still use the kit to monitor their treatment.  Also, I discussed this topic with a grand rounds speaker last week and he stated that he takes blood pressure in the following way.  First, he takes the pressure when the patient first comes into the room.  He keeps the cuff on after taking the pressure, and goes on with his exam.  Then, he takes the pressure again when the patient is laying down for the exam.  Again, he keeps the cuff on after he takes this pressure.  He then completes his exam and talks to the patient.  Finally, he takes the pressure again with the patient standing up before leaving.  So, he takes the pressure with the patient supine, sitting, and standing, and he never takes off the cuff in between readings, thus reducing the  anxiety the patient experiences.

Hope this is helpful.


Carpal Tunnel Syndrome

This week, we diagnosed 2 patients with Carpal Tunnel Syndrome.  While I'm sure many of us were exposed to carpal tunnel syndrome during the surgery rotation, it was interesting to see the initial diagnosis of CTS in a patient.

The symptoms of CTS are fairly straigtforward, caused by compression of the median nerve at the carpal tunnel of the wrist, often due to edema or hypertrophy of the flexor synovium.  The compression of the median nerve causes a numbness in the hand, following the median nerve distribution, which is often worse at night then during the day.  The symptoms are often bilateral, and slowly progressive, leading from "pins and needles" to an aching pain, which is believed to be secondary to ischemia of the median nerve. 

On physical exam, patients often present with a positive Phalen sign (hyperflexion of the wrist leading to parasthesia), and a positive Tinel sign (tapping on the median nerve at the wrist leading to parasthesia), as well as possible thenar atrophy with advanced CTS. 

While definitive treatment is often surgery, initial treatment consists primarily of rest, NSAIDS, and an immobilization splint. 

Helpful Link: http://www.emedicine.com/emerg/topic83.htm


"Chief Complaint

In the first four days of working in my Family Practice clinic, I realized that the chief complaint of a significant number of patients is ancillary to the reason for their visit.  The family practitioner must be able to identify when a patient needs empathy and support in addition to a resolution for their chief complaint.  The following patients are  two examples of many such situations.  In the first case a woman came in for impacted cerumen.  On exam she did have cerumen obscuring her left tympanic membrane but in talking with her the true reason for her visit was some serious medical developments.  Since her last visit three months ago she had a colonoscopy that revealed three polyps, two of which were removed at the time of the procedure.  Unfortunately the third couldn't be removed and she needs to have a partial colectomy.   Needless to say the physician I'm working with immediately realized that this patient needed more than wax removal, and proceeded to encourage her by saying everything will be all right and she has the support of him and her family.  In this fifteen minute appointment, the stress and anxiety that had been building for the past month began to melt away with just a few kind words.

            Another patient presented with back pain since the birth of her second child three months ago.  The pain she describes is spastic in nature located just inferior to her left scapula and at its worst is rated as a 6 out 10.  Although she was obviously in pain her level of discomfort was out of proportion.  Once again the family practitioner noticed this and empathized with her about the time and energy required to care for two children under the age of three.  Once the physician began addressing these issues the patient's level of distress began to dissipate.  In addition to relating to her stresses, he also recommended that she take 40 minutes every day to have for herself.  Being so busy with caretaking, errands, and chores it becomes easy to lose herself, but it is essential that she takes a little time each day to reflect upon the great job she is doing as a young mother.

            Obviously neither of these cases are medically riveting, but they do represent the psychological side of family practice which accounts for over fifty percent of the visits to this clinic.  Unfortunately I had a difficult time finding a article that investigates the frequency of visits that aren't related to the chief complaint but to mental health instead.  The article I did find looked at how patients with unexplained symptoms might be presenting for psychological support and requirements.  It goes on to say that if practitioners can identify such patients it may decrease the need for expensive diagnostic tests and therapy.  Although this study was well designed by taping physician patient interactions and then analyzing any cues by the patients about their need for psychological help, it is severely weakened by its small sample size.  In addition, although they identified the practitioner's inadequacies at recognizing these cues, they didn't provide any recommendations on improving this problem.  I think future studies that investigate the identification and utilization of the psychological cues would be extremely helpful for all primary care physician.

 

http://lysander.ingentaconnect.com/vl=2743536/cl=20/ini=rcgp/nw=1/rpsv/~30000031/v54n500/s5/p171

 


Sinusitis
So everybody in my FP office must hang out with each other because so many patients this week has had some verison of sinusitis. Now not that I'm some know it all, but it seemed that much of the treatment plans had as much to do with sinusitis vs. URI as it had to do with if it was Monday versus Friday.
In Pediatrics, there was the notion that any cold that did not get better within 10 days should probably be treated with emperic antibiotics as sinusitis. In adults, while that also seemed to be the practice, other signs and symptoms when combined can be helpful in differentiating URI v. Acute Sinusitis. These include "double sickening" (biphasic illness), pain with unilateral prominence, purulent rhinorrhea by history, purulent secretions in the nasal cavity on examination, a lack of response to decongestant or antihistamine therapy, facial pain above or below both eyes on leaning forward, and maxillary toothache. "Double Sickness" refers to having a cold and begins to remit but then gets worse in about a week. When someone has two or more of the above symptoms, diagnostic accuracy is 55-75%
Now what I found interesting in researching this blog that even for sinusitis-which is primarily bacterial- antibiotics really show no signifcant decrease in symptoms than placebo. Not only amoxicillin but more broad spectrum antibiotics as well.
However, 90% of patients expected treatment for sinusitis not only in the form of antibiotics but adjunctive treatments such as decongestants.
I think this is a theme we will be seeing a lot in our careers. Patients expectations for treatment and getting a pill might triumph our best evidence. Unfortunately, this might even make practical sense, as patients won't be coming back to the doctor that prescribes no pills for an illness when there are a hundred physicians that will.
Ah placebo....
http://www.aafp.org/afp/981115ap/fagnan.html


Managing Chronic Pain
This past week I saw for the first time how difficult it is to manage a patient who is dependent on hydrocodone for pain relief.  The patient had recently joined the practice and no old records were available.  She adamantly stated that her old doctor had given her the prescription that she was currently taking, and now she needed a refill. 

 

I was working with a younger physician who had not dealt with this type of situation before and was hesitant about writing the script without her old charts.  We spoke with a more experienced physician and he outlined a way to deal with this type of situation.  Up front, he told my preceptor that if he went ahead and gave the script that he may forever be the "easy mark" for future patients.  Among other things, he instructed us to get a detailed drug history from the patient, including all non-narcotic drugs she had taken before the hydrocodone.  He wanted names, doses and length of time on the drug.  He also wanted to know why she changed from the drug and any possible side effects that she may have had. 

 

Getting this detailed history was not easy and the patient was unable to give many specifics.  In the end my preceptor did not give her the hydrocodone.  He was very patient with the woman, but held his ground, stating that he wanted the old records before he would consider prescribing hydrocone.  He gave a script for a non-narcotic pain reliever, offered close follow up and gave her some phone numbers for support groups.

 

 

This article is a nice overview of how to manage patients with chronic pain and drug addiction.

 


Dealing with an angry patient

During my first week at my site, I found myself in the exam room with an upset patient.  As I began to take a history, I realized to my dismay that the patient was becoming quite frustrated with me and with my questions. In fact she even began to mutter to herself, "calm down, calm down" as I was asking about her past medical history and allergies. She told me that if I looked in the chart I would find all the information that I was asking about. As I flipped the blank pages of the chart she continued to tell me that she had provided all the information about her extensive medical history on her last visit.  She began to get very defensive and annoyed as I explained that I did not have any of the information that she had provided on her last visit. (In fact I did not have any record that she had a prior visit). 

I found myself becoming frustrated with this patient who was treating me disrespectfully and who, at first seemed to be acting quite erratically.  I was trying to come up with a plan to diffuse the situation, and frantically began to recall all of the mood and personality disorders that this patient could be characterized as having.  Then I realized that this patient may well have a very good reason to be upset and the difficulty we were having communicating was preventing her from getting the clinical attention she had come to get.   

As students, we get experience in "controlled" difficult patient settings, but this was the first time I had encountered an angry patient by myself.  I wanted to find out if there were some strategies I could have used to handle the situation. (I ended up apologizing; explaining that I did not wish to waste the patients' time, and then I retreated to go and find out if this patient's original chart had been misplaced, which indeed it had). 

Since I'm sure there are frequently occasions in clinics and hospitals where physicians need to deal with angry patients, I looked for some articles about trials of strategies and communication techniques in dealing with angry patients. Anger is a common response to many stressors, and may impede proper care of a patient if not dealt with in the appropriate context. The first article examines physician responses to patients' anger because of a long wait, and the second article goes through several cases providing an example of a physicians' dialogue with an upset patient. 

McCord RS, Floyd MR, Lang F, Young VK. Responding effectively to patient anger directed at the physician. Fam Med. 2002 May;34(5):331-6.

Levinson W. Improving communication with patients. Hosp Pract. 2000;35(4):113-4,117-20,123.


Shoulder Impingement--How to assess and treat

As you might expect, musculoskeletal conditions are a very frequent complaint in the FP clinic.  Just last week, I personally saw five patients with a painful shoulder (general assessment provided by the American Academy of Family Physicians), three of which had symptoms consistent with shoulder impingement.  I know we had one exciting week of orthopaedics but not all of us got to fine tune our examination skills and rather watched others do special provocative tests that were never really explained.  So this is where I can hopefully help a little so when you encounter this patient you can confidently assess them and plan out their proper management.

Impingement is one of the most common causes of pain in the adult shoulder. It results from pressure on the rotator cuff from part of the scapula as the arm is lifted. The rotator cuff is a tendon linking four muscles—the supraspinatus, the infraspinatus, the subscapularis, and the teres minor. These muscles cover the head of the humerus and work together to lift and rotate the shoulder.

The acromion is the front edge of the shoulder blade. It sits over and in front of the humeral head and easily palpated. As the arm is lifted, the acromion rubs or impinges on the surface of the rotator cuff.  This may cause pain and limits movement. The pain may also be due to a bursitis overlying the rotator cuff or a tendonitis of the cuff itself. In some circumstances, a partial tear of the rotator cuff may cause impingement pain.

Symptoms
Beginning symptoms may be mild. Patients frequently do not seek treatment at an early stage.

  • Minor pain that's present both with activity and at rest.
  • Radiating pain from the front of the shoulder to the side of the arm.
  • Sudden pain with lifting and reaching movement.
  • Athletes in overhead sports may have pain when throwing or serving a tennis ball.

Impingement commonly causes local swelling and tenderness in the front of the shoulder. There may be pain and stiffness upon lifting or lowering the arm. As the problem progresses, the patient may have pain at night with loss of strength and motion. In severe cases, loss of motion may progress to a frozen shoulder. In acute bursitis, the shoulder may be exquisitely tender.

Diagnosis
The diagnosis of shoulder impingement is typically done by a thorough H&P. Certain provocative tests are the Neer's and Hawkins' test (pictures, narration, and video of the two tests; scroll down about ½ of the page to find them). These tests involve moving the shoulder passively (through forward flexion, internal and external rotation with the arm abducted 90 degrees, and adducted) with approximately 5 to 10 lb of force directed inferiorally on the acromion, thus narrowing the subacromial space. 

One helpful adjunct is the diagnostic subacromial bursa injection. Local anesthetic and steroids are injected into the bursa and if the symptoms are due to bursitis, this provides significant and quick relief. However, if the symptoms are predominantly caused by tendonitis or a partial rotator cuff tear, this will have little effect and further imaging is needed such as an X-ray and MRI.

X-rays may be helpful especially with a special view called an outlet view, which may show a small bone spur on the front edge of the acromion. An MRI should be rarely obtained but may be necessary if no other cause is found and may demonstrate fluid or inflammation in the bursa and rotator cuff.

Treatment Options
Initial treatment is conservative: rest, physical therapy, and NSAIDs. If no improvement after a 1-2 months, the next line of therapy is a 10 mL injection of local anesthetic (5 mL of 1% lidocaine and 4 mL of 0.5% bupivacaine HCl) and a cortisone preparation (1 mL of triamcinolone hexacetonide). Treatment may take several weeks to months but many patients experience a gradual improvement and return to function. This might be the mainstay of therapy if your patient is not a candidate for surgical repair.

Referral to an orthopedic surgeon is appropriate if shoulder problems persist for 3 to 6 months despite previous therapies or if there is evidence of a medium or large rotator cuff tear, severe shoulder stiffness, or a complicated fracture. The goal of surgery is to remove the impingement and create more space for the rotator cuff. This allows the humeral head to move freely in the subacromial space and to lift the arm without pain. The most common surgical treatment is subacromial decompression or anterior acromioplasty (this is an interactive video showing some of the techniques).

Additional information regarding the Management of Shoulder Impingement Syndrome and Rotator Cuff Tears according to the American Academy of Family Physicians is provided.


Metatarsalgia

Foot pain is a common complaint in FP setting. Metatarsalgia is a term indicating forefoot pain localized under one or more of lesser metatarsals. Causes include abnormal metatarsal length with alteration of weight-bearing forces or toe deformities such as claw or hammer toe which result in displacement of the plantar fat pad and loss of cushioning under the metatarsal heads.

 

The patient I saw has been having foot pain for a few months, describing it as "deep, diffuse pain" in the right foot. Denies any kind of trauma. Walking and standing aggravate it. Resting helps relieve the symptoms. The patient denies swelling, numbness or tingling sensation. On exam, there is tenderness to direct pressure over plantar aspects of the 3rd, 4th and 5th metatarsals. Compression of forefoot elicits a lot of pain. There are no palpable masses but there are calluses under metatarsal heads. The rest of the exam is unremarkable.

 

The treatment for metatarsalgia is very simple, mainly supportive. A metatarsal pad is usually recommended. The pad should be placed proximal to, not directly under, the painful area. If the symptoms continue, you might want to obtain a standing AP and lateral radiograph to rule out metatarsal stress fracture or arthritis.

In cases where pain is intractable despite conservative measures, operative treatment is required. Procedures designed to relieve metatarsal pressure include excision of the plantar condylar prominence, osteotomy to shorten the metatarsal, resection of the metatarsal head, and, in particularly resistant cases, excision of the entire offending metatarsal. The latter procedures may cause increased disability and should be undertaken only after failure of less radical procedures, such as condylectomy.

Anyway, one things I learned from this case - when you do foot exam, pay attention to callus formation including location, thickness and tenderness. Because calluses are formed in response to chronic pressure overload, they can give you hints of how the patient walks, bears weight or any kind of foot deformities

To learn more about metatarsalgia, click here


Lymphadenopathy

The ever enigmatic lymphatic system has been mostly ignored in medical school yet appears to be quite an essential player in many diverse diseases (go figure!).  I had 3 different people in the clinic last week come in with a lymphadenitis +/- lymphangitis in various anatomic locations.

Lymphadenitis involves inflammation of the lymphatic glands. It may occur when the glands are overwhelmed by bacteria, virus, fungi, or other organisms.  Infection then develops within the glands. Lymphadenitis can also occur as a result of other inflammatory conditions or due to circulating cancer cells.

Based on the location of the swollen gland(s), one can usually determine the site of the underlying infection, tumor, or inflammation. http://www.aafp.org/afp/981015ap/ferrer.html. Most commonly, tender lymphadenitis will be the result of a cellulitis or other bacterial infection (usually streptococci or staphylococci).

Lymphangitis involves the lymphatic channels, with inflammation of the channel and resultant pain and localized or systemic symptoms. It commonly results from an acute cellulitis (streptococcal or staphylococcal), or from a skin or soft tissue ascess.

Lymphangitis may suggest that an infection is progressing, and should raise concerns of bacteremia, which can obviously be life threatening. Lymphangitis is often confused with thrombophlebitis, which presents similarly.


LYMPHADENITIS

  • lymph nodes may be swollen, tender, and hard
  • lymph nodes feel smooth or irregular to touch, or soft and "rubbery" if an abscess has formed
  • the skin over a node may be reddened and hot

LYMPHANGITIS

  • red streaks from infected area to the armpit or groin
    • may be faint or obvious
  • throbbing pain along the affected area (common)
  • may involve the lymph nodes
  • fever of 100 to 104 degrees and/or chills
  • individuals may have general malaise, with loss of appetite, HA, and myalgias

A nice algorithm for the assessment of cervical LAD
http://www.rch.org.au/clinicalguide/cpg.cfm?doc_id=5257

2 good articles delineating all of the major lymphatic groups, their associated anatomical areas of drainage and differential Dx's of LAD in each of these particular groups.
http://www.aafp.org/afp/20021201/2103.html
http://www.aafp.org/afp/981015ap/ferrer.html


Empowering Patients

I recently came across a patient who was diagnosed with hypertension.  While HTN is one of the most common things that family physicians manage, this case was interesting  because the patient refused to try any medication and instead was highly motivated to continue lifestyle changes including diet, excercise, and smoking cessation to control the HTN.  This brought up the core issue of having patients take charge of their illness and making them feel empowered by their actions. I thought about the modern state of medicine and how the huge volume of drugs that are perscribed and dispenced daily.  While therapeutics can be a wonderful thing, they have also made it easier for some patients to simply rely on them for combating their ailements with a very passive attitude.  This is especially true for such things as HTN, hyperlipidemia, and even diabetes.  So I deceided to provide you with some information on how a physician can help his/her patients take charge of their health and feel empowered in the process.  The key point here is that old models of simply telling patients what to do have been proven to be ineffective and the there is a new school of thought that encourages active participation through self-management and goal setting.

Patient self-management requires the physician to be an educator with emphasis on patient self-efficacy that promotes confidence in the patient to identify and solve problems with their health on their own.  The key point here is that we have to view the patient as the solution and not the problem and we have to convey this thought to them.   It is a patient centered approach that deviates from the old "do as I say" approach and emphasizes the attitude of patients identifying their illness, habits, responses, weaknesses and motivations and using their knowledge to manage their (chronic) illness.  As healthcare providers, it then becomes our obligation to educate patients not only about the nature of their illness but also about the power that they hold in the day to day management of their health.  We have to support them and challenge them at the same time.  It may seem unatural at first to not tell patients what to do, but this old model is ineffective and we must help patients make lasting changes by challenging them take responsibility for their well-being.  

I included some helpful links that discuss new approaches to empowering patients.  I hope you find them useful.   

Bodenheimer T, Lorig K, Holman H, Grumbach K. Patient self-management of chronic disease in primary care. JAMA 2002; 288:2469-75.
Available online at http://jama.ama-assn.org/cgi/content/full/288/19/2469

Essential elements of self-management interventions. The Robert Wood Johnson Foundation and The Center for the Advancement of Health. December 2001.
Available online at www.rwjf.org/publications/publicationsPdfs/sm_interventions.pdf

Funnell MM. Helping patients take charge of their chronic illnesses. FPM 2000;7(3):47-51.
Available online at www.aafp.org/fpm/20000300/47help.html

Glasgow RE, Funnell MM, Bonomi AE, Davis C, Beckham V, Wagner EH. Self-management aspects of the Improving Chronic Illness Care Breakthrough Series: implementation with diabetes and heart failure teams. Ann Behav Med 2002;24(2):80-7.

Improving Chronic Illness Care self-management support bibliography.
Available online at www.improvingchroniccare.org/resources/bibliography/self-mngmt.html

Lowes R. Patient-centered care for better patient adherence. FPM 1998;5(3):46-57.
Available online at www.aafp.org/fpm/980300fm/patient.html


When to order a Lyme titer
In my first week in the outpatient setting, I have probably seen almost as many lyme titers ordered as I have seen CBC's and other tests requested.  I started to wonder, are all of these tests necessary?  When is it appropriate to order a lyme titer?

Lyme disease is a tick-borne infection casued by the spirochete Borrelia burgdorferi.  It is a multisystem disease that may present as erythema migrans, or may  include joint, neurologic, or cardiac manifestations.  When erythema multiforme is absent, antibodies to B. burgdorferi must be documented in order to make a diagnosis.  About 2.8 million Lyme disease serologic tests (LDSTs) are performed each year in this country, at a cost of $40 per test -- a medical expenditure that exceeds $100 million.

I found an article that examined the appropriateness of the LDSTs ordered.  This study sampled two large Wisconsin reference laboratories for 12 months with a standardized questionnaire.  Tests were categorized as appropriate, inappropriate, or discretionalry, and data was collected via logistic regression analysis.  A test was inappropriate if the patient was asymptomatic, had erythema migrans, or was treated impirically. 

The study found that 20% of tests were appropriate, 27% were inappropriate, adn 53% were discretionary.  An interesting finding in this study was that when a patient (rather than a clinician) requested a test, the test was more likely to be inappropriate.  Additionally, tests were more likely to be patient-requested if they were ordered by an internist or if the patient was >40 years old.  This study hence concluded that many tests are ordered inappropriately and that this is often influenced by patient demand.  Clinicians need to be further educated about testing indications and contraindications.

This article included the following information regarding appropriate and inappropriate uses of the LDST.  Appropriate uses include the following: patient with oligoarticular arthritis, patient with cranial neuritis, patient with lymphocytic meningitis, patient with AV block, and patient with carditis.  Inappropriate uses of the LDST include: patient who is asymptomatic, patient with clinician-diagnosed erythema migrans, patient treated empirically with antibiotics, and serologic test ordered as a test of cure.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15335133&query_hl=8

June 16, 2005
Tinea versicolor and therapy

I know that we have been taught numerous times about dermatologic disordes such as: atopic dermatitis(eczema), psorias, contact dermitits, and tinea. But believe it or not I saw 3 cases of tinea versicolor in the first week of FP.

Versicolor is a superifical infection caused by Malessezia furfur. This is a sprophytic yeast that is part of the normal skin flora.

Clinically this presents as a variety of shades of color. Lesions can be hypopigmented, light brown, or salmon colored macules. A fine scale is often apparent, especially after scraping. Lesions can be small but often coalesce, and are often located on upper trunk and extremities. It is most evident in the summer because the organism produces azeliac acid which inhibits pigment transfer to the keratinocytes, thereby making the infeted skin more demarcated from the uninfected, evenly pigmented skin.

Typical antifungal therapy is teh treatment of choice with cure rates of 70-80 percent. Make sure to mention to the patients that it maybe necesary to treat for weeks to months and normal pigmention may take months to occur. More convenient medications include oral antifungal agents and even selenium containing shampoos used as a lotion.

One of the links below is a good overview of tinea versicolor with a description, treatment, and causes. I have also included a typical image of versicolor. Since most of you will see this in the office hopefully you are now well prepared to shine in the clinic.

www.medicinenet.com/tinea_versicolor/article.htm

www.nlm.nih.gov/medlineplus/ency/images/ency/fullsize/1895.jpg

June 15, 2005
Cornelia de Lange

No, this isn't some kind of French dessert.... So I first came across this syndrome during my pediatrics rotation.  We had an assignment where it described a child whose chief complaint was short stature.  Among the long list in the differential diagnosis was Cornelia de Lange Syndrome or CdLS for short. 

This is the ultra rare "zebra" and has an incidence of 1:10,000 to 1:30,000 live births.  It is interesting in that  the first pediatric patient I saw in my family practice clinic had this syndrome.  I was told that in the area, there are only a handful of children with this syndrome. 

Essentially, it is a diagnosis of exclusion and it is a clinical diagnosis.  Diagnosis is made by history and mainly physical exam.  There are no specific tests used to diagnosis CdLS, though one can refer to a genetic specialist and order some chromosomal analysis to rule out other more common diseases.  It is probably a genetically linked disease since a gene was identified, though the mode of inheritence is unclear since expression is variable.   

Briefly, common characteristics include: low birthweight, slow growth and small stature, and small head size.  There are characteristic facies which can include thin eyebrows which frequently meet at midline, long eyelashes, short upturned nose and thin, downturned lips.  Various cardiac, palate, and musculoskeletal abnormalities are also noted.  Mental retardation is also common. 

Since CdLS is so rare, even UpToDate doesn't have anything on it.  There is a good website that contains general information on CdLS here.  Those pictures of patients are useful to look at.  Below is an article I found on Pubmed. 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15858306&query_hl=1