Abdominal Pain DYK's (Did You Know)

In medical school I was taught that anorexia was a sign of appendicitis, but apparently that is no longer true.[1]
Patients with peritonitis will sit still and patients with colic will move around a lot. [1]
There was also a cochrane  study that said that you can give patients with acute abdominal pain opioids without fearing that it will interfere with an accurate diagnosis [2]

1 Evaluation of Acute Abdominal Pain in Adults
SARAH L. CARTWRIGHT, MD, and MARK P. KNUDSON, MD, MSPH, Wake Forest University School of Medicine, Winston-Salem, North Carolina

Am Fam Physician. 2008 Apr 1;77(7):971-978.

2 Cochrane Briefs :Opioid Analgesia During Evaluation of Acute Abdominal Pain 
Am Fam Physician. 2007 Oct 1;76(7):971.

OA= Often Asymmetrical; A Synopsis of AFP's "Osteoarthritis: Diagnosis and Treatment" by Keith Sinusas

This is a review of the January 1, 2012 American Family Physician, volume 85 number 1.


OA is a common disorder, but there are other joint disorders that look similar. OA worsens with activity, especially after rest. Morning stiffness usually lasts LESS THAN 30 minutes ( RA is usually longer). Any joint can be involved, but it usually occurs asymmetrically. Heberden and bouchard nodes can be seen. Lab work and imaging isn't that helpful in the diagnosis of OA.
So there is a "stepped care approach" to treatment which is clearly described on table 5 of this article. Basically it's says this: first start with diet and exercise ( water exercises are apparently not at good as land based programs). You can also start the patient off with some acetaminophen or try an NSAID. The next step is to try ibuprofen or naproxen and a different NSAID. If that doesn't work try glucosamine and chondroitin for 3 months. If the patient is still in pain you can move on to opioids. At this point if the patient has severe OA it may be time to consider corticosteroid injections, hyaluronic acid injections and lastly, a joint replacement. Capsaicin cream and SAM-e have also shown some benefit.

Florence Nightingale’s Notes on Nursing Which Apply to the Art of Caring

http://www.consultant360.com/blog/florence-nightingale?utm_source=dlvr.it&utm_medium=twitter

Consultant posted a nice article about Florence Nightingale and how she shaped the foundation of the modern hospital . See the link above for the story. Below is a summary of her basic principles which I took directly from the article.

Florence Nightingale’s Notes on Nursing Which Apply to the Art of Caring

Observe the sick.
Never let a patient be waked out of his sleep.
Avoid unnecessary noise: Whisper outside the room.
View and sunlight are matters of first importance to the sick.
Leading questions are useless or misleading.
Obtain accurate information.*
Be confidential.
Children are much more susceptible than grown people to noxious Influences.†

SYNOPSIS of AFP's Article "Subacute to Chronic Mild traumatic Brain Injury" by Timothy Mott MD, Michael McConnon MD, and Brian Rieger PhD

This is a review of the article in American Family Physician December 1, 2012 pages 1045-1050.


Mild TBI is loosely defined as a transient loss of consciousness, amnesia, change in mental status, focal neurological deficits, and a GCS of 13-15, after a closed head injury. Most patients recover within hours to days, but some symptoms could last 4 weeks or longer. Typical symptoms are headache, nausea, blurred vision, fatigue, irritability, mood, and sleep disturbances. Most of these symptoms should be treated individually, such as antiemetics for nausea, analgesics for headaches, and SSRI's for behavioral problems.
The physical exam should focus on a proper neurological exam, including ALL cranial nerves, reflexes, strength, sensation, and posture. Cognitive and mental exams should also be completed. Imagining is not typically necessary. Patients must be rigorously reassessed and referral or alternative diagnosis must be considered if the condition persists or worsens.
There is not much for treatment in TBI. It is important to manage the specific symptoms and prevent complications. Early education is critical in care as it gives the patient a realistic expectation and reduces anxiety. Patients are urged to rest both physically and cognitively, and to return to normal activities gradually.

SYNOPSIS of AFP's "Weight Loss Maintenance" by SAMUEL N. GRIEF, MD, and ROSITA L.F. MIRANDA, M

Losing weight can be hard, but often the real challenge is keeping it off. Some strategies for maintaining weight loss: http://bit.ly/VQsvk9 


Weight Loss Maintenance SAMUEL N. GRIEF, MD, University of Illinois at Chicago, Chicago, Illinois  ROSITA L.F. MIRANDA, MD, MS, Clay County Hospital, Flora, Illinois
Am Fam Physician. 2010 Sep 15;82(6):630-634.

     So after seeing this tweet from AFP and looking down at my belly I figured this would be a good article to read and review. Lets start with the facts and the stats. We are fat and we all want to be thin. It is killing us.Losing weight is hard and not fun. I can't remember which journal that was from.
     The best way to lose and maintain weight is by diet and exercise. The National Weight Loss Control Registry (NWCR) has found that the three most common factors in success are restricting certain foods, limiting quantity, and counting calories. Decreasing variety of food and not pigging out on weekends and holidays are also common traits of successful weight loss. Other common factors in successful patients are watching less TV, eating breakfast every day, exercising an hour a day, and monitoring their weight with a scale. 
     There is also a concept of "diet disinhibition" which is composed of three things; cognitive restraint, uncontrolled eating, and emotional eating. This refers to binge eating, common to those on overly restricted diets. This doesn't help.
     The two approved medications for weight loss (at the time of this publication) are Orlistat and Sibutramine. These have been shown to be effective in weight loss. Patients need to have a BMI over 30 or a BMI over 27 with medical comorbidities. Some of thee medications have side affects, like oily stool or heart valve problems, which is something to consider when choosing this route.
     Surgery is another option. There are several varieties , from bariatric to full on surgery. Patients have had, not only weight loss, but also remission of comorbid conditions from the procedure. Patients should have a BMI greater than 40 or greater than 35 with comorbid conditions. They also need to attempt a weight loss program, and dieting, for a set amount of time, and be unsuccessful. There is limited RCT's on these procedures and some studies even suggest that pharmacology is as effective as surgery.

SYNOPSYS of American Family Physicians article "Seasonal Affective Disorder, by STUART L. KURLANSIK, PhD, and ANNAMARIE D. IBAY, MD,

This is a review of the article from AFP called Seasonal Affective Disorder, by

STUART L. KURLANSIK, PhD, and ANNAMARIE D. IBAY, MD,

found at Am Fam Physician. 2012 Dec 1;86(11):1037-1041.

     This article on SAD was a good review, and all the research pretty much confirmed what we already know. SAD is basically depression that occurs in the fall and winter months and resolves in the spring and summer. This doesn't mean that every patient who walks into your office with depression around the holidays has SAD. It needs to occur for two seasons in a row.  The amount of depression episodes in the fall/winter must outnumber the number of episodes in the spring summer.  It is more common in women during childbearing years. One interesting factor is that patients have a tendency to have carbohydrate cravings and hyperphagia. This will cause the patients to gain weight. I could see how these patients could be under treated if a young lady comes into your office upset because she gained some extra weight over the holidays. There are some depression tools to help determine if the patient is depressed  Beck Depression Inventory  and Hamilton Rating Scale for Depression)

    Treatment has not changed much recently. The three types of therapy are light therapy, antidepressants, and CBT. Light therapy is done for 30 minutes a day with a specific lux and spectrum.It takes bout 1-2 weeks to kick in. The medications used are typically second generation antidepressants (SSRI's and SNRI's) most commonly Prozac. CBT is not typically done by everyone and more often referred out, do to the expertise needed and time restraints. Combinations of these therapies have been shown to be more effective than any one therapy alone.      

     Prevention has been shown to be effective as well. Patients can begin light therapy or take Wellbutryn prophylactically  n the early autumn. CBT can be done prophylactically as well. Exercise and relaxation techniques can also help.

Cheesecake Factory Medicine

I'm reading an article from the New Yorker By Atul gawande- google Cheesecake Factory medicine and enjoy!

SYNOPSIS of "Hepatitis A", by Samuel Mattheny MD in AFP

This is a review of the article " Hepatitis A, SAMUEL C. MATHENY, MD, MPH, and JOE E. KINGERY, DO, University of Kentucky College of Medicine, Lexington, Kentucky"

Am Fam Physician. 2012 Dec 1;86(11):1027-1034.

     Hepatitis A is an RNA virus, specifically the picornavirus. It is transmitted through the fecal-oral route. It is spread through contaminated water, in day care centers, on raw vegetables, and through "sexual contact that promotes fecal-oral transmission".  The incubation period is about 28 days, at which time onset is abrupt. Signs and symptoms include jaundice, nausea, vomiting, diarrhea, dark urine, fever,  hepato/splenomegaly, headache, and abdominal pain.
     Laboratory tests will show elevated serum transaminase, bilirubin (total and direct) AP, ALT and AST (ALT will be higher). Diagnosis can be made through detection of IgM anti-HAV antibodies. It will become positive within 5-10 days, but will no longer be detectable after 4-6 months. IgG anti-HAV will increase at this time. The virus is shed in the stool during the time after the increase in ALT and before Igm is detectable (pearl or the day!)
     Hepatitis A is self limiting. There is a small chance of relapse, but it wont become chronic. Treatment consists of bed rest, not going to school or work until the fever and jaundice has resolved and avoiding alcohol.
     All children should be immunized between 1 and 2 years old. Immunoglobulin can be used as pre or post-exposure prophylaxis.  High risk populations (illicit drug users, men who have sex with men, health care workers, those with adopted children from endemic areas, with liver disease or clotting factor disorders) should also be vaccinated. Vaccination should be given to travelers going to countries other than Australia, New Zealand, Canada, Europe, or Japan at least 2 weeks prior. If the patient is over 40 years old, immunocompromised, or is leaving before 2 weeks, you can also give immunoglobulin. If the patient does not want the vaccine,  you can give them the Ig, but you would triple the dose to 0.06mL/Kg if they are going to travel for more than two months.
    For post exposure prophylaxis, you can give the patient the vaccine (or Ig) within two weeks of exposure.

Rate vs Rhythm- The Hatfields and Mccoy's of Atrial Fibrillation

So I was listening to the Medscape Family Medicine Podcast on my way to work and there was a three part episode on atrial fibrillation. The guest was talking about treatment and she said that if the patient is symptomatic, then she would consider rhythm control. she also said that she would try an convert almost anyone at least once because rhythm control gives the patient a better quality of life. Rhythm control can be use for younger patients without co morbid conditions. I felt like that was different than what I had had previously learned. It decide to use my new iPhone app "AFP by topic" and read all the articles on treatment for AFIB. Ill discuss anti-coagulation next time.
      Rate control is preferred for patients who are asymptomatic or mildly symptomatic "AFIBers". It improves diastolic filling, coronary  perfusion, and decreases myocardial energy demands. So for rate control, we have beta blockers, calcium channel blockers (diltiazem and verapamil) and digoxin. The calcium channel blockers are contraindicated in patients with structural disease. As a side note, these two calcium channel blockersdo have an effect in the glomerulus, similar to ACEI's and ARB's in patients with CKD. Digoxin is not preferred because it is not effective for rate control during exercise. It can have a synergistic effect when used in conjugation with beta blockers. 
     It is true that rhythm control should be tried at least once because the patient could cardiovert and stay in sinus rhythm for several years without needing medications.  This may also be considered if the patient is young, first time AFIBers. The four main antiarrhythmic drugs are dronadarone, flecanide, propafenone and sotolol. Those patients with structural heart disease my need a different therapy [2].I failed to mention amiodarone. This medication is the strongest antiarrhythmic, but there are many bad side effects (lung damage, liver damage, and pulmonary toxicity), thus it is not considered a first line medication for rhythm control. There have been studies that recommend amiodarone in patients with low injection fraction.
     There have been several studies comparing rate vs. rhythm in atrial fibrillation. The PIAF (2000) study compared therapy with symptoms (palpitations, dyspnea, and dizziness) and showed no difference between the two therapies. It also showed better exercise tolerance and mor frequent need for hospitalization in the rhythm group. The more hospitalizations were do to the more frequent need to recardiovert patients. The PIAF QOL (2003) study showed no difference in quality of life in either group.
The STAF (2003) study compared the to therapies against "primary endpoint" (The primary endpoint was the combination of death, cardiopulmonary resuscitation, cerebrovascular event, and systemic embolism). Again there was no difference.
The RACE (2002) study compared the two therapies against a primary endpoint of a "composite of death from cardiovascular causes, heart failure, thromboembolic complications, bleeding, implantation of a pacemaker, and severe adverse drug effects [3]". Again there was no difference.
The AFFIRM (2002) trial which again showed "no clinical advantage for rhythm control over rate control".  It did however, show that amiodarone was the most effective antiarrhythmic drug. Also, the study reinforced the importance of anticoagulation. 
     SO what does all this mean? Rate control is safer and cheaper. If you put a gun to my head, then I would treat with rate control measures. But it is really a case by case process, especially in those who are highly symptomatic.



1.Am Fam Physician. 2002 Jul 15;66(2):249-257
2.Can J Cardiol. 2011 May-Jun;27(3):388.
3.Pharmacologic Management of Atrial Fibrillation: Where Do We Currently Stand? , by John Camm, MD
Medscape Cardiology, 2005-02-28

SYNOPSIS of "The Hospital Medicine Podcast: Immune thrombocytopenia Purpura" by Dr Gil Porat MD

This podcast was recorded on July 2, 2012 and can be found here: https://itunes.apple.com/us/podcast/hospital-medicine-podcast/id541752791


   This was a very interesting podcast, as are all of Dr. Porat's lectures. So lets start of by saying that platelets are non-nucleated cells that clot to prevent bleeding. Thrombin forms when coagulation proteins bind to the platelet surface. Platelets also secrete factors for platelet repair. They live for about 10 days and 30% of them are sequestered in the spleen.
     Thrombocytopenia is when the platelet count is below 150k. ITP is normally a chronic benign condition. Spontaneous remission is seen in 9% of adults and is even more common in children. The two ways that ITP occurs is through decreasing production of platelets  (by drugs and bone marrow diseases  and decreasing the survival of platelets ( by ITP, TTP sepsis, hypersplenism, etc).
    The type of ITP that Dr. Porat discusses in this podcast is autoimmune induced thrombocytopenia. It is commonly a diagnosis of exclusion after systemic illnesses and medication reactions are ruled out. ITP is commonly an incidental finding on a lab results, but petechiae, purpura, menstrual  mucosal and cutaneous bleeding my be seen.
     Treatment goals are hemostasis and to increase the platelet count to above 30k. If there is no bleeding and the platelet count is already above 30k, then treatment is typically not needed. Otherwise, the first line of therapy is corticosteroids. Improvement should be noted within one to two weeks, although re-occurrence will often be seen after the steroids are discontinued  Splenectomy is considered second line treatment. Patients should have the appropriate vaccinations prior to surgery (pneumovax, H. influenza, and meningococcal . This therapy is associated with a 60% remission rated although physicians should be diligent to watch for inherent side affect of this surgery (i.e, sepsis). Anabolic steroids have also been used for treatment, but may not be appropriate for female patients.
     Rituximab is a monoclonal antibody that decreases the production of B cells. It decreases the antibodies that are destroying the platelets. It has been shown to be effective, but immune suppressants such as this one have several restrictions and warnings as well.
     The newer medications affect thrombopoietin  Thrombopoietin is made in the liver and sent to the bone marrow to tell the megakaryocytes to increase production of platelets. Two thrombopoietin agonists (Romiplostim and Eltrombopag)  have shown to increase platelet counts to greater than 50K in 94% and 87%, respectively. These medications are very expensive, and continual use is needed for them to work. Some of the side effects are elevated LFT's, thromboembolism, and bone marrow fibrosis.
     Lastly , platelet transfusion in emergency situations, although the effect, is temporary. IVIG can be given along side the transfusion to help the effects.

Review of "Diagnosis and Treatment of Acute Low Back Pain" by Dr. Brian Cassazza

this is a review/synopsis of the article "Diagnosis and Treatment of Acute Low Back Pain by BRIAN A. CASAZZA, MD"


Am Fam Physician. 2012 Feb 15;85(4):343-350



     Since my back pain is only slightly better I figured that this would be  an appropriate time to reread and review an article on Low back pain. First off , acute low back pain is pain for 6-12 weeks , between the area of your back from your "lower costal angle to your gluteal fold". I  have never heard that geographic description so I thought I would mention it . So the most common causes are compression fractures, herniated discs,  lumbar strain/ sprain, stenosis, and sponylo's (-losis, lysis, and listhesis). There are also connective tissue diseases, osteomyelitis, aortic aneurysms  and a lot more so you may want to check out this article to see the complete differential. I'm pretty sure I have a lumbar sprain/strain. 
     When you take your history it is important to pay attention to red flags that MAY OCCASIONALLY be associated with a serious pathology. Bowel or bladder incontinence or saddle anesthesia may be a sign of cauda equina syndrome. Vertebral tenderness and weight loss may be a sign of malignancy. Trauma in the elderly could be a fracture.
     Spine pain rarely radiates below the knee. Sacro-iliac pain radiates often to the thigh and below the knee. Nerve root irritation often manifests as leg pain over back pain. L1-L3 radiates to the hip and though whereas L4-S1 radiates below the knee.
Imaging is often not needed (unless in trauma). It may be considered if pain persists beyond 4-6 weeks and you are considering a serious pathology.
For medications, NSAID's or acetaminophen can often relieve low back pain. They all have shown to be squally effective and can be changed at will. Opioiods are commonly prescribed but have shown little evidence of benefit. Epidural spinal injections have recently come under fire do to the fungal meningitis outbreak due to contaminated product. They don't really have any long term benefit although it may provide some temporary pain relief of radiating pain(if you don't mind the meningitis).
     So if you have a patient who wants to get well and isn't just going to pout until you give him/her a percocet script, you can tell him/her this: stay active. Avoid twisting and turning while bending forward. Try to get back to your normal level of activity as soon as possible. Heat packs can help.
     Some things that don't really work err... I mean haven't been shown to be effective are back braces, acupuncture  massage, traction,  or oral steroids. Just think bed rest = Bad rest!

Back pain and a "mental enema" from what I remember of some "Medscape Family Medicine Podcast"

The new issue of AFP is out but my back is too beat up to sit and write :( But I will try out this iPhone app while I am on the pt bed..... I've been listening to the medscape family medicine podcasts but they are real short. They mentioned that in urinalysis, pay attention to albumin (AKA micro-albumin) because it is a good index of cardiovascular health. If a pt has hypertension and glomerular disease, you can consider using verapamil and diltiazam because it causes dilation of the pre and intra glomerular vessels, similar to and ACEI or ARB.
In peripheral vessel disease, classic claudication is only seen in 10% of patients with claudication so be aware of atypical symptoms. ABI is a very good test to do if you are suspicious. You can give them a statin even if their lipid levels aren't that high. There is also some other medication that starts with an "S" and ends with an "L" that you can use. It is also effective to give them an exercise regiment where they walk till they have pain, continue a little more, then take a break and continue when the pain subsides. They should do about 30-45 minutes 4-5 times a day.
Hmm what else... Oh yeah, ticks can also spread a parasite called nabezia(?) which can be seen on a blood smear. In a lipid panel, non-HDL cholesterol is a more important (and cheaper) index than apoE and ... I forgot the other index. Whooping cough is on the rise in Colorado...

Gimme the Keys, Grandpa! - The Older Driver

    Its a well known fact that old people drive like crap. I know you probably think its because they are too busy checking Facebook and texting and tweeting, but you would be wrong. Old people have things like arthritis, dementia, hearing and vision problems. Actually, most older drivers do drive fine and most older drivers are able and responsible enough on their own to stop driving. The purpose of this article is to figure out how to tweeze out all the crabby old bastards who refuse to accept the fact that its time to get a bus pass.
     Fist thing that you want to do is to find out their driving history. Have they gotten into more accidents recently, more tickets, or more "close calls"? What do passengers say about how the older person drivers? Do they feel safe? It also a good idea to review the medications that the driver is on. Changing medications with ones that have fewer unwanted side affects may be beneficial.
    It is also important to consider chronic diseases, especially diabetes. It has been shown that hypoglycemic episodes and improper insulin doses are often seen in automobile injuries[2]. Other diseases, such as epilepsy, heart disease, musculo-skeletal, Parkinson's etc. can contribute to problems driving.
   It is important to check the hearing, vision, cognition (with a Mini Mental Status Exam or Clinical Dementia Rating,CDR), alcoholism (CAGE questions) attention (reciting numbers backwards), and visual spatial skills (clock-drawing test and the Trails B test[3]).   Patients with a Clinical Dementia Rating (CDR) of 1 or more should not drive [3,5]. Referral to an occupational therapist who specializes in driving may be a consideration. A road test to assess the patients competence may also be valuable. Depending on the state, this can be a slippery slope, so it is helpful if the family supports your decision and is willing to help in this transition. Offering to give rides and helping with public transportation can really make a big difference in the quality of an old bastards life. 

1. Marottoli, RA,The Physician's Role in the Assessment of Older Drivers,  Am Fam Physician. 2000 Jan 1;61(1):39-42.

2. Carr, DB. The Older Adult Driver, Am Fam Physician. 2000 Jan 1;61(1):141-146.

3. Carr DB, Duchek, JM, Meuser, TM, Morris Oldr Adult Driver with Cognitive Impairment.Am Fam Physician. 2006 Mar 15;73(6):1029-1034. 

4. Finestone, AJ, Rauch CJ. The older driver: When is it time to take away the keys?,Consultant. 2012. 52;11:753-760.

5. http://alzheimer.wustl.edu/cdrtraining 

Why is My Urine Purple? A Review of the "Hospital Medicine Podcast" 8/30/12, by Dr Gill Porat, MD

This is a review of "The Hospital Medicine Podcast- Uninalysis Pearls for Managing Adult Patients" added on 8/30/2012 which can be found at  https://itunes.apple.com/us/podcast/hospital-medicine-podcast/id541752791 along with many other of his podcasts


    So I listened to this quick podcast on the way to work this morning and it was prety decent. It was a brief discussion on urinalysis. First, Dr. Porat spoke about nitrates. Common urinary bugs convert nitrate into nitrite in the urine, but there are circumstances when this does not happen. There are some bugs, like yeast and E. faecalis, that do not make nitrates. Also, which is particularly interesting, is that if the patient has urinary frequency, and is emptying their bladder often, then the bacteria may not have TIME to make the nitrites. Thus don't assume that a negative nitrate means that the patient doesn't have a UTI.
     Leukocyte esterase is another test that commonly comes back positive on a UA. But where does it come from. Well ,WBC's make it , and it is also released when WBC's get killed, such as when battling an infection. If they all get killed, there will be a positive LE, but you may not see them in the UA... AH HAH! Kind of like in all those action movies where the good guys come to the enemies camp and the bad guys aren't there. The water may even be boiling on the stove and the bacon may still me sizzling... Bear in mind that contamination may give a false positive and lack of pyuria my make it false negative.
    The big "blow my mind" teaser was this idea of purple urine. And no, its not from diluted hematuria. Its from gram negative bacteria. According to Dr. Porat, the GI tract breaks down tryptophan into indole.  The bacteria then converts indole into indigo. This will then "stain the polyvinyl chloride foley bag purple". So the point being is that you have to send the urine for cultures.  While looking for other resources about this reaction, I came across a reference that said that purple urine can also be found in porphyria.
    He also mentions that brown urine can be seen in "diffuse melanosis" and that green urine can be from pseudomonas (or medications). For completeness, red urine is bloody (or myoglobin), milky or cloudy urine is pusy,  orange urine can be from medications or your diet.
 The last important point that Dr. Porat is about urine pH. I'll let you check the podcast if you want to know what he says (TEASER!)





1.MacFaddin, Jean F. "Biochemical Tests for Identification of Medical Bacteria." Williams & Wilkins, 1980, pp 173 - 183

2. http://www.mayoclinic.com/health/urine-color/DS01026

REVIEW-Diagnosis of Deep Venous Thrombosis and Pulmonary Embolism JASON WILBUR, MD, and BRIAN SHIAN, MD

Diagnosis of Deep Venous Thrombosis and Pulmonary Embolism

JASON WILBUR, MD, and BRIAN SHIAN, MD, Carver College of Medicine, University of Iowa, Iowa City, Iowa

This is a quick review of the article found here 

Am Fam Physician. 2012 Nov 15;86(10):913-919.

     Venous thromboembolism  is basically a blood clot that can go to the legs, causing a DVT, or the lungs, causing a PE. DVT's occur twice as often, but if you have one, there is a greater chance that you may actually have both. The etiology is described commonly as "vichow's triad", which is hypercoagulability, alterations in blood flow, and endothelial injury. The WELLS criteria is commonly  used to determine pretest probability. It categorizes patients into low, medium, and high probability. It is used to determine if you want to order a D-dimer. This is a very sensitive test, so you only use it if you think the patient does NOT have a VTE and you want to rule it out. (You may come across an overzealous ER doc who orders this on every patient with a cough, thus you are stuck admitting the patient if the results come back indeterminate). So basically if you have a suspicion, and the WELLS criteria comes back intermediate or high, you are gonna order a compression ultrasound for a DVT. If it comes back negative, THEN you can do the D-dimer. Consider repeating the ultrasound in one week if the d-dimer is positive do confirm the patient is DVT free.
     PE is a little trickier because first you decide if the patient is hemodynamically stable. If they are unstable and critically ill, and they have a high pretest probability (WELLS), you can send them for an echocardiogram of your choice (transthoracic or transesophageal). If they are not critically ill, you have to option to send them for a multidetector CT if it is available, otherwise you cand send for an echo. If the patient cant do a CT, you can consider a V/Q scan. If the CT is positive or if the echo shows right ventricular disfunction, its a PE. If the CT comes back negative, but you know in your heart it a PE, you can continue to evaluate.  You can also consider a pulmonary angiogram if you want more testing, although it will expose the patient to a good amount of radiation. 
   One other thing I wanted to mention is that a patient with a PE may have "S1Q3T3 syndrome" on EKG. Its worth googling if you forgot what it means.
    This article has some nice algorithms and charts, so check it out!

REVIEW- Lactic acidosis podcasts from "ICU rounds-Dr. Jeffrey Guy" Nov 11, 19 2011

     So, I often listen to podcasts and i'd like to incorporate them into my blog. I was listening to a great one by Dr. Jeffrey Guy (at http://www.burndoc.net) about lactic acidosis, which was recorded nov 11,19 2001. Now since I listened while driving, I didnt take notes, so lets see.. (this is more an exercise of my own personal retention rather than a complete synopsis)

     The first thing is that elevated lactic acidosis most commonly is a reflection of decreased oxygen delivery. Lactic acidosis is a biomarker, thus the lactate itself is not the causative agent. Glucose is converted to pyruvate through glycolysis. The pyruvate is then broken down in the kreb cycle, the first enzyme being pyruvate deydrogenase ( I think). BUT if there is no oxygen to support the kreb cycle, then the pyruvate is converted to lactate. It also leads to a build up of lactate. It also produces much less ATP.
     Lactate is removed from the body by the liver and kidneys (and a small part by heart and skeletal muscle) The liver uses the cori cycle to convert the lactate back to glucose (by gluconeogenesis). The kidneys also metabolize the lactate, specifically in the renal cortex[1] -(my first official footnote!). It can also be excreted if there is a whole lot of lactate.
     Dr. Guy also mentions that you should not automatically avoid Ringer's Lactate for fluid replacement. There is not to much lactate in it to make a difference, and the solution is actually at a basic pH (6.6). If you hang Normal saline, although there is no lactate, the large amount of chloride that is in it can cause a hyperchloremic acidosis.
    There are two basic types of lactic acidosis, type A and type B. A is through the decreased oxygen delivery/ increased oxygen demand. Type B is do to other diseases, medications, or inborn metabolic error. There is also a D-lactic acidosis, which is an increase in one of the lactate isomers.
     Basically if you have a patient with lactic acidosis, concentrate more on the cuasative agent rather than getting the lactate level down.
   There was a whole lot more Dr. Guy talked about, so you can check it out on Itunes (ICU rounds) or the website above.
(next time ill listen twice before blogging)


1-http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137458/

REVIEW- "Revised AAP Guideline on UTI in Febrile Infants and Young Children" by KENNETH B. ROBERTS, MD

This is a quick review of the article found here 

http://www.aafp.org/afp/2012/1115/p940.html

Am Fam Physician. 2012 Nov 15;86(10):940-946.

        The  American Academy of Pediatrics has updated its guidelines  for treatment of urinary tract infections in children between two months and 2 years old. A positive culture is now defined as having at least 50,000 colony forming units per milliliter (instead of 100,000) Also, oral medication is as effective as parental treatment.
        The other big changes from the 1999 guidelines is that now both urinalysis and culture should be performed.  Also, performing a voiding cystourethrogram is no longer recommended after the first UTI. It is indicated, however, if the ultrasound shows hydronephrosis, scarring or obstruction. Otherwise it can be considered after recurrent infections.
       According to the algorithm,  if you have any belief that the patient has a UTI, (is between 2 months and 2 years old), and has a fever of at least 38C, you can go ahead and perform a urinalysis by catheterization or you can do a dipstick analysis. A urine collected by a bag is not reliable. If it's positive, you can start treatment, but send cultures first (or you are gonna hear it from everyone). If the culture and UA come back negative you can stop the treatment. You would also adjust the therapy according to the culture sensitivities. Once a UTI is confirmed you can do a renal bladder ultrasound. If it's the patient's second or more UTI, you can perform a voiding cystourethrograph. 
        In general it appears that there is a low threshold for checking urine in a patient with an infection of undetermined origin. Even if the child does not appear to be having a UTI, it should be assessed anyway.
       The patient should be treated with antibiotics for 1 to 2 weeks. 
      As far as prophylaxis for current UTIs there has been shown to be no statistically significant benefit in this age group.

REVIEW- "Universal HIV Screening Recommended by USPSTF"

This is a brief review of the medscape article "Universal HIV Screening Recommended by USPSTF" by Laurie Barclay MD

http://www.medscape.com/viewarticle/774957?src=nldne



     According to the US Preventive Services Task Force, physicians  should screen all patients between the ages of 15 and 65 years for HIV, and  patients of all ages of those who are at increased risk. This is due to better testing procedures and evidence that starting anti retroviral therapy early can lower AIDS-related events or death. The last recommendation for the USPSTF was in 2005. HIV infection occurs approximately 50,000 times each year. One quarter of those infected are aware. HIV is prevalent in approximately 1.2 million people.  1.1 million have been diagnosed with AIDS and over half a  billion people have died from it.

REVIEW-"Diagnosis and management of gonococcal infections" by Mejebi T. Mayor , Michelle A. Roett, and Kelechi A. Uduhiri

Am Fam Physician. 2012 Nov 15;86(10):931-938


This is a quick review of the above article, this is also my first real post!

       Gonorrhia can cause different types of symptoms and can also be asymptomatic. Common symptoms are pelvic pain and discharge. If left untreated it can lead to pelvic inflammatory disease, which can lead to infertility, or it can lead to disseminated disease such as Reiters arthritis. Diagnosis can be achieved by nucleic acid amplification or cervical swab which would show gram negative diplococci. Treatment is typically 250mg ceftriaxone intramuscular as well as azithromycin to cover for chlamydia. We no longer use fluoroquinolones due to its resistance. If a patient does have reactive arthritis we can use long term antibiotics (at least 3 months) , along with other comfort measures. We can give a prescription for the sexual partner (depending on the state you practice in). The patient should be retested in 6 months.
     Gonorrhia should be tested for yearly in sexually active women. The same goes for all high risk men.

Ok my second post ( but still nothing medical)!

So I figured out how to blog on my iPhone! Feeling totally geeky but also feeling like I am taking full potential of what the Internet is. I'm still not sure how this blog is going to evolve but hopefully ill be able to post things that I have learned through patient cases... But for now it will just have to be what I pick up on independent study.

My very first blog ( and my very first original title)

My first order of business is to figure out how to change the name of my blog. Ultimately I would like to use this space to post reviews of medical podcasts, journals, etc., to chronicle what I have done each day to become a better doctor. So today I plan to figure out how this blogging shtuff works!