A Synopsis of AFP's "Nephrotic Syndrome in Adults: Diagnosis and Management"

Nephrotic Syndrome in Adults: Diagnosis and Management
CHARLES KODNER, MD, University of Louisville School of Medicine, Louisville, Kentucky
Am Fam Physician. 2009 Nov 15;80(10):1129-1134.
http://www.aafp.org/afp/2009/1115/p1129.pdf

     The common causes of nephrotic syndrome are focal segmental, membranous, minimal change, IgA, and membranoproliferative.  Secondary causes include diabetes, SLE, hepatitis B/C, NSAIDs, amyloidosis, and HIV. The pathology is unknown, but the proteinuria may be the cause of the edema and tubulointerstitial inflammation. Clinical features include edema (lower extremity, periorbital and genital), weight gain, ascites, effusion (heart and lung) and fatigue. Lab values include proteinuria (3-3.5g/day or 3+ on a dipstick), spot protein/creatinine ratio above 3, hypoalbuminemia (<2.5 g/dL),  and possibly an elevated total cholesterol. Complications of nephrotic syndrome include DVT, PE, infection, and acute renal failure.
     Evaluation of these patients involves looking for an underlying cause of the nephrotic syndrome. In addition to the above mentioned lab tests, tests screening for HIV, Hep B or C, amyloidosis, multiple myeloma, syphilis, and SLE should be considered if the history warrants. Biopsy may be necessary to confirm the diagnosis, ut specific recommendations for biopsy are not available.
     Management is dependent on clinician experience as solid recommendations have yet to surface. Sodium and fluid restriction is often done to reduce edema. Diuretics  are often used as well. Whether to use loops or thiazides depends on the rise in creatinine, where loops would be preferred. ACEIs have helped to lower proteinuria. Albumin can help with diuresis, but it has a short half life and high cost. Corticosteroids are a mainstay. They are especially helpful in minimal change disease compared to other diseases. The use of cyclophosphamide should trigger a referral to a nephrologist.

A Brief Synopsis of AFP's "Evaluation of Patients Presenting with Knee Pain: Part II. Differential Diagnosis"

Evaluation of Patients Presenting with Knee Pain: Part II. Differential Diagnosis
WALTER L. CALMBACH, M.D., University of Texas Health Science Center at San Antonio, San Antonio, Texas MARK HUTCHENS, M.D., University of Texas at Austin, Austin, Texas
http://www.aafp.org/afp/2003/0901/p917.pdf
Am Fam Physician. 2003 Sep 1;68(5):917-922.

     The differential diagnosis of knee pain can be broken down by age and location of pain. In children, the three most common conditions are patellar subluxation, tibial apophysitis, and patellar tendinitis. Patellar subluxation is when the patella moves out of it's track, usually laterally. It may be seen in a teenage female who states that her knee "gave way". The dislocation may lead to hemarthrosis and swelling.  Tibial apophysitis is also known as Osgood-Schlatter disease. The pain is typically found at the tibial tuberosity. The pain in intermittent. It is worse when the patient is squatting, walking on stairs, repetitively jumping or during quadricep contraction. Pain is reproduced with passive knee hyperflexion or knee extension against resistance. Patellar tendonitis presents with vague anterior knee pain ad tenderness. Knee extension against resistance will reproduce the pain. SCFE (slipped capital femoral epiphysis) is also seen primarily in children. It is seen in overweight children. They will present with a flexed and externally rotated hip while sitting. Hip pain will be seen with passive internal rotation or extension of the hip. The disease is best seen with CT of the femoral head. Osteochondritis dissecans is degeneration and re-calcification of the articular cartilage and bone. The pain is poorly localized. There is morning stiffness as well. Joint mice ("loose bodies") may be seen in the joint which will exacerbate locking and catching of the joint. 
     Overuse injury is a common cause of adult knee pain. Anterior knee pain may be due to patello-femoral syndrome (chondromalacia patellae). This presents as patellar tenderness with prolonged sitting. Pain may be reproduced with anterior, lateral, or medial pressure to the knee. Medial knee pain may be due to medial plica syndrome. This presents as medial knee tenderness without effusion, which may become inflamed from overuse. Pes anserine bursitis is medial knee pain over the anteromedial aspect of the knee. This will worsen with repetitive use and may be confused with MCL problems. Pain may be reproduced with valgus stress (as well as the MCL, so it is not very helpful). There is effusion at the insertion of the medial hamstrings, but not at the knee joint. 
     Lateral knee pain in the adult may be due to tendinitis of the iliotibial band on the lateral femoral condyle. It is another overuse injury seen in runners and cyclists. The pain is seen at the lateral knee. Noble's test is done by having the supine patient flex and extend his or her knee during pressure over the lateral condyle. Trauma was explained in the previous article so please refer to that one.
     Infection of the knee is a serious condition. Risk factors include corticosteroid use and a weak immune systems. The joint will be red, warm, swollen and tender. Arthrocentesis will show an elevated WBC count (above 50,000/mm3), at least 75% PMNs, elevated protein, and a low glucose concentration.  Possible pathogens include S. aureus, H. influenzae, N. gonorrhoeae, and Streptococcus. There may be an elevated ESR .
     In older adults, the most typical problems are OA, gout/pseudogout, and bakers cyst.  OA in the knee is worse while weight bearing and better with rest. It is asymmetrical. Morning stiffness persists for less than 30 minutes. X rays will show joint space narrowing, sclerosis, and osteophyte formation. Gout of the knee will present with intense inflammation. Synovial fluid will have sodium urate crystal and negative birefringent rods. If it is pseudogout  the crystals will be calcium pyrophosphate and there will be positive birefringent rhomboids. The synovial fluid will be clear or partly cloudy. The WBC will be 2,000-75,000/mm3, high protein, and lower glucose concentration.  
    

     

A Brief Synopsis of AFP's "Evaluation of Patients Presenting with Knee Pain:Part I. History, Physical Examination, Radiographs, and Laboratory Tests"

Evaluation of Patients Presenting with Knee Pain:Part I. History, Physical Examination, Radiographs, and Laboratory Tests
WALTER L. CALMBACH, M.D., University of Texas Health Science Center at San Antonio, San Antonio, Texas MARK HUTCHENS, M.D., University of Texas at Austin, Austin, Texas
Am Fam Physician. 2003 Sep 1;68(5):907-912.
http://www.aafp.org/afp/2003/0901/p907.pdf

     When a patient presents with knee pain, determining the type of pain (onset, location, duration, severity, quality, aggravating and alleviating factors) is the first step. If the knee locks, it could be due to a meniscal tear. Popping can be a ligament problem. If the knee "gives way", the cause could be due to a patellar subluxation or ruptured ligament.
     Specific trauma to the knee can help determine the type of injury. Patients who hurt their knee during a head on automobile collision (such as where the knee hits the dashboard) can damage the PCL. The specific force in this situation is an anterior blow to the proximal tibia. A sports injury (or similar action) that puts force on the lateral knee in a lateral-to-medial vector can damage the MCL. Any kind of pain caused from quick pivoting, tight turns, stopping, or non-contact trauma can damage the ACL.
     The physical exam begins with comparing the bad knee with the good knee.  Special attention should be give to looking for swelling, bruising, redness, and discoloration. Range of motion should be checked as well (normally 135 degrees of flexion). Having the patient contract their quads during knee palpation will help assess for proper patella tracking. Measuring the Q angle (using the lines from the ASIS to the patella and the patella to the tibial tuberosity) can help assess patellar subluxation.
     There are several orthopedic tests that should be added to the physical exam in a patient complaining of knee pain. The patellar apprehension test will detect patella subluxation when the physician puts lateral traction on the kneecap.  The anterior and posterior drawer test checks the ACL and PCL, respectively. With the patient supine and the bad leg flexed 30 degrees at the knee, the lower leg can be pulled anteriorly (to check the ACL) and pushed posteriorly (to check the PCL). In the valgus and varus stress test, the clinician simply abducts or adducts the lower leg to check the MCL or PCL, respectively. The McMurray test assesses the medial and lateral menisci. The patient is supine, with the hip and knee flexed at right angles. The lower limb is either externally or internally rotated while the knee is fully flexed. The clinician can also add some valgus stress while the leg is externally rotated or varus stress with internal rotation. A positive test will be pain at the location of the medial or lateral menisci.
     Whether or not to get x rays can be determined by using the Ottawa Knee Rules. The test requires at least one of the following to recommend xrays;
1. age 55 years or older
2. isolated patellar tenderness
3. fibula head tenderness
4. inability to flex the knee past 90 degrees
5. inability to bear weight on the knee and take four steps immediately and in the ED
if x rays are recommended, the AP, lateral, and merchants views should be taken. Young adults may need additional views to look for osteochondritis. Radiographs are used to find fractures or OA.
     If the joint is warm, tender, fluid filled, or red, lab work (CBC w/diff and ESR) and an arthrocentesis may need if septic arthritis or inflammatory arthropathy is suspected. Hemarthrosis may be seen in a ligament tear or fracture.

I'M DAMN SHARP! A synopsis of AFP's "Diagnosis of Systemic Lupus Erythematosus"

Diagnosis of Systemic Lupus Erythematosus
JAMES M. GILL, M.D., M.P.H., Christiana Care Health Services, Wilmington, Delaware, ANNA M. QUISEL, M.D., Newark, Delaware, PETER V. ROCCA, M.D., Wilmington, Delaware, DENE T. WALTERS, M.D., Christiana Care Health Services, Wilmington, Delaware
Am Fam Physician. 2003 Dec 1;68(11):2179-2187.
http://www.aafp.org/afp/2003/1201/p2179.pdf

     SLE is an inflammatory disease that infects many organ systems, including the skin, musculoskeletal, renal, GI, cardiac, pulmonary, hematologic, RES, and neuropsychiatric system. The disease is more common in women, especially african-american women. There is also a familial predisposition. SLE patients are at high risk of CAD, respiratory and urinary infections. The most common signs in children include fever, arthritis, renal involvement, and alopecia. 
     The diagnosis of SLE requires at least four of the following 11 criteria (the mnemonic IM DAMN SHARP);
Immunoglobulins (Anti-dsDNA, Anti-Sm, Anti-phospholipid), 
Malar Rash, 
Discoid Rash, 
Antinuclear Antibody, 
Mucositis (Oropharyngeal Ulcers), 
Neurological Disorders, 
Serositis (Pleuritis, Pericarditis), 
Hematologic Disorders, 
Arthritis, 
Renal Disease, and
Photosensitivity
     The diagnosis algorithm goes like this. If the patient has manifestations in two or more organ systems, then an ANA test is done. If the titer is less than 1:40, then it is most likely NOT SLE. If an alternative explanation can not be found, then the patient should be referred to a rheumatologist. If the titer is greater than 1:40, then the above 11 criteria should be investigated. Lab studies, including CBC, UA, serum creatinine, ANA, and the immunologic antibodies, should be drawn. 
     Even though the ANA is very sensitive, many patients may have a false negative test early in the course of the disease. ANA can also be false positive due toother connective tissue diseases, including sjogren's syndrome, scleroderma  RA, and juvenile RA. This is why the ANA should be drawn only after the patient presents with at least two clinical manifestations. The other antibodies (Anti-dsDNA, Anti-Sm, Anti-phospholipid) are helpful in patients with a high ANA titer, but who have not met the other clinical criteria.

A Synopsis of AFP's "Update on Subclinical Hyperthyroidism "

Update on Subclinical Hyperthyroidism 
INES DONANGELO, MD, PhD, and GLENN D. BRAUNSTEIN, MD, Cedars-Sinai Medical Center, Los Angeles, California
http://www.aafp.org/afp/2011/0415/p933.pdf
Am Fam Physician. 2011 Apr 15;83(8):933-938.

     Subclinical hyperthyroidism is low TSH with normal free T3 and T4.  The two categories of subclinical hyperthyroidism have either a TSH between 0.1-0.4 mIO/L or a TSH less than 0.1 mIO/L. The cause of subclinical hyperthyroidism is either endogenous (overproduction), due to Graves disease, multinodular goiter, or adenoma, or exogenous (excessive hormone therapy). Other causes of low TSH, besides subclinical hyperthyroidism, include medication (dopamine and glucocorticoids), pituitary TSH deficiency, euthyroid sick syndrome, hypothalamic disorders, and psychiatric illnesses. 
     According to the algorithm in this article, when a patient has suspected subclinical hyperthyroidism, a TSH is ordered. If it is normal, then it's probably not subclinical hyperthyroidism. If it is low, then a free T3/T4 should be ordered. If both are high, the patient has overt hyperthyroidism. If only the free T3 is high, then the patient has T3 toxicosis. If both are normal, then the patient has subclinical hyperthyroidism and more investigation is needed. A radioactive iodine uptake scan should be ordered to determine where the TSH is coming from. If the iodine uptake is increased (or normal) in a diffuse pattern, then the most likely diagnosis is Graves disease. If the uptake is increased in a localized pattern, then the diagnosis is a toxic nodular (or multinodular) goiter. If the uptake is decreased, a thyroglobulin is needed. If the thyroglobulin is decreased, then the diagnosis is exogenous thyroid hormone. If it is elevated, then the patient has subacute thyroiditis.
     Patients with subclinical hyperthyroidism will have elevated HR, more fibrillations, larger left ventricle, and lowered heart rate variability (so no nocturnal dipping). This will lead to an increased risk of cardiovascular events and atrial fibrillation. Treatment consists of methimazole or radioactive iodine. Methimazole help return the cardiovascular issues to normal after the  TSH level is fixed. Iodine does not have the same affect on the cardiovascular complications.
     Subclinical hyperthyroidism can also cause a decrease in cortical bone mineral density. It is more advanced in postmenopausal women. Elevated TSH will increase bone turnover. Treating the hyperthyroidism will stop the bone turnover. 
     Other symptoms of hyperthyroidism include palpitations, nervousness, tremor, heat intolerance, sweating, and lower well-being. There is also a relationship between TSH and cognitive function.
     There is no current recommendation to advise screening of subclinical hyperthyroidism. There is, however, a relationship between low TSH and atrial fibrillation in later life. 

A Synopsis of AFP's "Management of Common Sleep Disorders"

Management of Common Sleep Disorders
KANNAN RAMAR, MD, and ERIC J. OLSON, MD, Mayo Clinic, Rochester, Minnesota
Am Fam Physician. 2013 Aug 15;88(4):231-238.
http://www.aafp.org/afp/2013/0815/p231.pdf

     Most people get about 6.9 hours of sleep a night. The recommended amount is 7-9 hours a night. The four types or sleep disorders are
those who cannot sleep,
those who won't sleep,
those with daytime sleepiness, and
those with increased movements during sleep.
     For those who cannot sleep, the two causes are insomnia and restless leg syndrome. Insomnia is described as difficulty with sleep initiation, duration, quality, and consolidation (amount of uninterrupted sleep). A proper insomnia history include asking questions about onset, frequency, sleep and wake times, sleep environment, evening activities, comorbid psychiatric/ medical conditions, and medications. CBT with hypnotics and sleep hygiene, in combination, have been shown to be synergistic for treatment. Sleep hygiene includes not have pets in the bedroom, no caffeine, no nicotine, no late night exercising, no staring at the bedroom clock, and keeping the bedroom cool. Patients should only lay in bed when they are tired and sleepy.  Antihistamines and melatonin for insomnia have limited effectiveness.  Restless leg syndrome has four parts;
uncomfortable sensation and
intense urge to move legs,
worsening during rest,
worse at night, and
relieved by movement.
If the patient has a low ferritin, then the syndrome can be fixed when the iron deficiency is fixed. Otherwise, the patient can try dopaminergic agonists (ropinirole or pramipexole), opiates, gabapentin, or pregabalin.
     Patients who "will not sleep" have a delayed sleep phase syndrome. These people go to bed late and get up late. They develop daytime sleepiness, insomnia, and functional impairment. The treatment is giving the patient melatonin  before bed and bright light exposure upon awakening. The goal is to gradually give the melatonin and bright lights earlier each week to create a more appropriate schedule.
     Excessive daytime sleepiness is seen in narcolepsy and obstructive sleep apnea (OSA). Narcolepsy has a classic tetrad of;
sleepiness,
cataplexy,
hallucinations upon falling asleep,
hallucinations upon awakening, and
sleep paralysis.
Patients with narcolepsy should be referred to a sleep clinic, which includes polysomnography and a multiple sleep latency test. Medications for narcolepsy include antidepressants (venlafaxine), SSRIs, and stimulants (methylphenidate). OSA is obstruction or the upper airway  during sleep, despite the patient trying to breath. It can cause hypertension, sleepiness, hypoxia, and cognitive impairment. Risk factors include obesity, CHF, diabetes, pulmonary hypertension, stroke, atrial fibrillation, and bariatric surgery. The treatment calls for CPAP or BIPAP.
     Patients who complain of increased movement during sleep usually have REM sleep behavior disorder or periodic limb movement. REM sleep behavior disorder is characterized by elevated muscle tone, causing the patient to act out dreams. It is associated with parkinsonian syndromes. The spouse may notice the patients movements during sleep. Treatment consists of moving dangerous items that the patient may fall on. Melatonin or clonazepam may be helpful. Periodic limb movements are repetitive and stereotypic actions during sleep. Diagnosis is made by polysomnography, finding a movement index greater than 15 per hour (5 per hour in children). Treatment is the same as for RLS.

A Synopsis or AFP's "Prevention and Management of Postpartum Hemorrhage"

Prevention and Management of Postpartum Hemorrhage
JANICE M. ANDERSON, M.D., Forbes Family Medicine Residency Program, Western Pennsylvania Hospital Forbes Regional Campus, Monroeville, Pennsylvania DUNCAN ETCHES, M.D., M.CL.SC., University of British Columbia Faculty of Medicine, Vancouver, British Columbia
Am Fam Physician. 2007 Mar 15;75(6):875-882.
http://www.aafp.org/afp/2007/0315/p875.pdf

     Postpartum hemorrhage is considered when more than 500 ml of blood are lost after delivery. Complications include orthostatic hypotension, anemia, and fatigue. In severe cases, such as when blood loss exceeds 1000 ml, hemorrhagic shock, anterior pituitary ischemia and posterior pituitary necrosis may occur. Risk factors include a prolonged third stage of labor, episiotomy, fetal macrosomia, and multiple deliveries.
     Active management of the third stage of labor is the strategy that is used to minimize the occurrence or postpartum hemorrhage. The parts of active management are;
-administration of oxytocin (or misoprostol) after delivery of the shoulder,
-cord traction, and
-uterine massage after delivery.
Early cord clamping and cutting is no longer part of active management. Delaying clamping has been shown to increase fetal iron stores as well as lowering the risk of anemia. Active management will shorten the third stage of labor. In expectant management, the placenta will separate on its own, but it may take longer, this increasing the risk of third stage complications.
     The four common causes of postpartum hemorrhage are "tone, trauma, tissue, and thrombin". Tone, or uterine atony, is the most common cause of postpartum hemorrhage. Treatment consists of bimanual uterine massage and oxytocin, ergot alkaloids, or prostaglandins. These medications stimulate uterine contraction and vasoconstriction.
     Trauma is referring to laceration, hematomas, uterine inversion and rupture. Episiotomies are discouraged unless absolutely necessary. Lacerations can be sutured.  Hematomas are treated through irrigation and ligation. Uterine inversion is rare but may be related to placental implantation. It looks like blue-gray tissue coming out of the vagina. Treatment consists of grasping the protruding part and pushing it up into the pelvis and abdomen to revert it. If the attempt fails, medications to promote uterine relaxation can be given (magnesium sulfate, terbutaline, nitroglycerin, or anesthesia). Surgery is another option. Once the uterus is properly reverted, medications can be given to increase uterine tone. Rupture of the uterus can occur in women who have a previous history of uterine scarring, previous uterine surgery, multiple cesarean sections, and short intervals between deliveries. Induction and augmentation of labor (prostaglandins, oxytocin, and misoprostol) also increases the risk or rupture. Signs of rupture include tachycardia, late decelerations, abdominal tenderness, circulatory collapse, and increasing abdominal girth.
     Tissue refers to retained tissue or placenta in the uterus. Placental delivery can be spontaneous or accelerated through active management. Oxytocin can also be injected into the umbilical vein. Retained product may need to be removed manually. The placenta can also be invaded into the uterus. "Placenta accreta adheres to the myometrium, placenta increta invades the myometrium, and placenta percreta penetrates the myometrium" (that was stolen straight from the article). Risk factors include older age, high parity, placenta previa, and previous CS. Common treatment includes hysterectomy or methotrexate.
     Thrombin refers to coagulation disorders. Most of these have been discovered before the woman become pregnant. Patients who have pre-eclampsia or placental abruption may develop HELLP or DIC. Excessive bleeding should be evaluate by ordering platelet counts, PT/PTT, fibrinogen and FSPs. These coagulopathies can be treated accordingly.
   

A Synopsis of AFP's "Metabolic Syndrome: Time for Action"

Metabolic Syndrome: Time for Action
DARWIN DEEN, M.D., M.S., Albert Einstein College of Medicine of Yeshiva University, Bronx, New York
Am Fam Physician. 2004 Jun 15;69(12):2875-2882.
http://www.aafp.org/afp/2004/0615/p2875.pdf

     Metabolic syndrome is an independent risk factor for cardiovascular disease and new onset diabetes. The diagnostic criteria for metabolic consists of;
(1) a waist circumference of 40in in men or 35in in women,
(2) a triglyceride level above 150 mg/dL,
(3) a HDL less than 35 mg/dL in men or 39 mg/dL in women,
(4) a blood pressure above 140/90,
(5) an elevated fasting glucose (>110) (impaired glucose tolerance, insulin resistance, or diabetes), and
(6) microalbuminuria.
Lab work that may be related to metabolic syndrome include CRP, platelet aggregation, uric acid, LDL, plasmin activator inhibitor 1, and hyperfibrinogenemia. Other associated conditions include PCOS and NASH. Prevalence of metabolic syndrome is related to increased age and increased body weight.
     Metabolic syndrome is caused by either increased insulin resistance (causing endothelial dysfunction and vascular damage) or by elevated cortisol and alterations in the HPA axis.
     Clinical evaluation includes information about leisure activity and how much time during the day is spent sedentary. Treatment is individualized but focuses on reducing the risk factors. Weight loss will slow the onset of diabetes and cardiovascular disease. Exercise is another important aspect of reducing risk factors in these patients. According to this article, skeletal muscle has the most insulin-sensitive tissue. It also says that the impact of exercise on insulin sensitivity will last up to 5 days (which is why regular exercise is so important). Resistance training and aerobic activity is the best, but any program must be started gradually. Patients need constant encouragement and counseling.
    Diet can make a big impact on reducing risk factors of metabolic syndrome, new onset diabetes, and cardiovascular disease. There are many diets out there, so a referral to a nutritionist or dietitian may provide benefit to the patient. Alcohol used should be used only in moderation.
     Aspirin and statins play a role in benefit. as well, but lifestyle modification play a larger role.

A Brief Synopsis or AFPs "Childhood Eye Examination"

Childhood Eye Examination
AMANDA L. BELL, MD; MARY ELIZABETH RODES, MD, MEd; and LISA COLLIER KELLAR, MD, MSCE  Wright State University Boonshoft School of Medicine, Dayton, Ohio
Am Fam Physician. 2013 Aug 15;88(4):241-248.
http://www.aafp.org/afp/2013/0815/p241.pdf

     Eye examinations should begin at the first well child visit. The purpose is to identify treatable conditions and refer them to the proper specialist. As with all exams, a past medical and family history can reveal important risk factors. The first part of the eye exam is the visual acuity test. It should be done within three years of age. There are charts of pictures instead of letters if the child cannot read. Eyes should be covered individually and tested separately. 20/20 vision may not evolve until the child is six years old, but the vision should at least be equal. The eyes should not be more than two lines apart on the eye chart. The child should not get more than three wrong on the 20/30 line.
     External examination of the eye includes the eyelids, orbits, sclera, conjunctiva, cornea, and iris. The lacrimal sac should be evaluated if there is persistent discharge. Excessive tearing (accompanied with redness and corneal edema) is a sign of childhood glaucoma.
    Pupillary response is another part of the test. Anisocoria is a difference in pupil size greater than 1 mm, which may be a normal finding. Horner syndrome or third nerve palsy may be seen with this test.
     The child should respond to the presence or the physician's face within six weeks, and should be able to follow and track an object within two months. Ocular alignment may deviate as a normal variant for the first four months, but beyond that will require a referral. The corneal light reflex should be equal and symmetrical by six months of age.
     There are three other tests to check for alignment. The cover test is done by covering one eye while watching for the other eye deviate. The cover-uncover test is done by rapidly covering and uncovering the same eye and watching for it to deviate. The alternate cover test is done by alternating which eye you are covering in rapid succession (left right left right...), while watching for deviation. These tests are performed while having the patient focus on a fixed object, one time far and one time near. Strabismus is a cause for referral. Amblyopia is caused from any alteration in vision that affects the image that the brain receives. A child may tilts his or her head to compensate for the abnormality.
     The red light reflex is used to detect ocular alignment, cataracts, refractive, or retinal problems. It is a two part test (which is news to me!) Each eye is checked individually from 12-18" and checked together from 2-3'. The color should be orange/red. Asymmetry of color between the two eyes or presence of a dark or white spot could be leukocoria, retinoblastoma, cataract, or a refractive error A referral is needed.

A Quick Review of AFP's "Preterm Labor"

Preterm Labor
WILLIAM G. SAYRES,JR., MD,Group Health Cooperative, Spokane, Washington
http://www.aafp.org/afp/2010/0215/p477.pdf
Am Fam Physician. 2010 Feb 15;81(4):477-484

     The common causes of preterm labor are spontaneous labor with intact membranes, preterm premature rupture of membranes, and iatrogenic (such as preterm induction). Infant mortality rates increase for those born before 32 weeks gestation.  Some of the risk factors for preterm delivery include a previous preterm birth, infection, tobacco, alcohol, cocaine or heroin use, a history of LEEP, multiple gestations, or periodontal disease. A shortened cervix (less than 3 cm) is a risk factor. Cervical effacement normally starts at 32 weeks gestation.
     Bacterial vaginosis is a risk factor for preterm labor.  Screening and treating with clindamycin will lower the rate of PPROM and low birth weight babies. Diagnosis can be done with a gram stain or by using the Amsel criteria (having at least three of the following;
amine color with KOH,
presence of clue cell,
ph above 4.5, and
a thin vaginal discharge.)
The USPSTF recommends against BV screening due to insufficient evidence. The CDC suggests treatment, with reevaluation one month later.
     Antenatal progesterone has shown benefit in maintaining uterine dormancy. It is recommended for mothers with a previous spontaneous birth before 37 weeks. The three antenatal interventions shown to be effective for women presenting with preterm contractions are;
corticosteroids,
antibiotic prophylaxis against GBS, and
transferring the patient to a NICU.
     The initial assessment of these patients includes gestational age, determining if the membranes are ruptured, determining if the patient is in labor, if there is an infection, and determining the likelihood of a preterm delivery. Assessing the membranes can be done with a fetal fibronectin test (looking for ferning) and a nitrazine test (looking for alkalinity).  The test can be confirmed with a transabdominal amnioinfusion of indigo carmine, or by seeing oligohydramnios on ultrasound.
     All pregnant patients are screened for bacteriuria and pyelonephritis with a urine culture. A rectovaginal culture can be used if the patient was not previously screened. Antibiotic prophylaxis (penicillin, ampicillin, cefazolin, clindamycin, or erythromycin) should be give to those who tested positive. Patients should also be screened for  gonorrhea, chlamydia, BV and trichomoniasis.
     It is important to determine if the patient is actually in labor. Contractions should occur every 6 minutes, the cervix should be dilated to 3 cm or more, and it should be at least 80% effaced. The membranes may have ruptured and there may be bleeding. If labor has begun between 24-34 weeks, corticosteroids (betamethasone or dexamethasone) should be given to help fetal lung maturity. Tocolysis is needed so that the steroids have time to work (48 hours). Examples of tocolytics include indomethacin, Magnesium sulfate, nifedipine, terbutaline, and calcium channel blockers.

A Quick Synopsis of AFP's "Parathyroid Disorders"

Parathyroid DisordersTHOMAS C. MICHELS, MD, MPH, Madigan Army Medical Center, Tacoma, Washington KEVIN M. KELLY, MD, MBA, Carl R. Darnall Army Community Hospital, Fort Hood, TexasAm Fam Physician. 2013 Aug 15;88(4):249-257
http://www.aafp.org/afp/2013/0815/p249.pdf

     PTH is released from the parathyroid glands in response to low serum calcium. The PTH causes the bones to release calcium from the bones into the blood. The kidneys stop losing calcium in the urine and put it back into the system. The kidneys also convert 25-vitamin D into 1,25-vitamin D, which helps calcium absorption in the GI tract. Even though the body has four parathyroid glands, we only need one to maintain normal calcium levels.
     The most common cause of hypercalcemia is primary hyperparathyroidism, due to a single adenoma.  Lesser causes are multiglandular hyperplasia and carcinoma. Most patients are asymptomatic. Risk factors include previous neck radiation, age above 50 years, and being female.  Calcium is elevated and PTH is high or normal. The calcium/ creatinine ratio should be elevated as well. If the ratio is below 0.01, the diagnosis is familial hypocalciuric hypercalcemia. This results from a calcium receptor gene mutation, in which extra calcium in needed for PTH suppression (feedback inhibition). Patients with familial hypocalciuric hypercalcemia present with normal or high PTH, high calcium, and low urinary calcium.
     Surgery is often a curative measure for primary hyperparathyroidism. Parathyroidectomy may be considered if the creatinine clearance is less than 60 ml/min, they are younger than 50, the serum calcium is greater than 1 mg/dL above the upper limit of normal, or the T-score is less than -2.5.  Hyperparathyroid patients who are symptomatic with osteoporosis or osteopenia are candidates for surgery. The surgery will improve bone density and fracture risk. Patients who are unable or unwilling to undergo surgery should take calcimimetics (cinacalcet).
    Secondary hyperparathyroidism will have hypocalcemia, hyperphosphatemia, and low levels of 1,25 vitamin D. Causes include chronic kidney disease (where the vitamin D is synthesized as explained above), low D intake (deficiency), malabsorption, lack of sunlight, and liver disease. Secondary hyperparathyroidism can also be normocalcemic. It would present with low bone density, bone fragility, and osteoporosis. The exact cause is not known. Complications of secondary hyperparathyroidism can be treated somewhat with protein restriction, calcium supplementation, vitamin D supplementation, and calcimimetics. A referral to a nephrologist (NOOOOO!) may be necessary if kidney disease is involved.
     Hypoparathyroidism can happen from damage or removal of one or more parathyroid glands. It can happen from surgery or autoimmune destruction. Pseudohypoparathyroidism is elevated PTH due to tissue resistance. The phosphorus will be elevated as well. If the phosphorus is low, then it is most likely due to  vitamin D deficiency rather than pseudohypoparathyroidism.
     MEN syndromes should also be mentioned in this discussion. MEN is a collection ("Multiple") of "Neoplasia"s in the pancreas, pituitary, parathyroid and adrenal "Endocrine" glands. MEN 2A involves medullary thyroid cancer, pheochromocytoma, and parathyroid tumors. MEN 2B (medullary cancer, pheo, and mucosal tumors) is not mentioned here.

A Brief Synopsis of AFP's "Bleeding and Bruising: A Diagnostic Work-up"

Bleeding and Bruising: A Diagnostic Work-up
Michael Ballas, MD, Wilson Care, Fort Loramie, Ohio Eric h.Kraut, MD, The Ohio State University, Columbus, Ohio
Am Fam Physician. 2008 Apr 15;77(8):1117-1124.
http://www.aafp.org/afp/2008/0415/p1117.pdf

     The differential for bleeding disorders is large. I'm going to begin by breaking down table 1 of this article. There are two types of platelet disorders. Quantitative platelet disorders are commonly due to ITP, TTP, malignancy or viral disease. The common symptoms are bleeding, bruising, petechiae, or purpura. Functional platelet disorders are due to glycoprotein disorders (Bernard-Soulier, Glanzmann) or vWD. Abnormally shaped platelets may be due to Wiskott-Aldrich syndrome or a May-Hegglin anomaly.  Patients with hemophilia will present with joint or soft tissue bleeding. Leukemia will have abnormal blood counts with an abnormal smear.  The other disorders on this chart are more obvious (alcohol, trauma, vitamin deficiency, etc).
     Prothrombin and partial thromboplastin times are helpful in determining where on the clotting cascade the problem is. For review, PT measures the extrinsic pathway (factor VII) and PTT measures the intrinsic pathway (XII, XI, IX and VIII) The common pathway which may prolong both are X, V, II and I.  So if both PT and PTT are normal, the platelets need to be checked (with an old school bleeding time or the new, more popular and less barbaric, Platelet Function Analyzer 100). Prolonged bleeding times can be due to vWD or drugs, such as aspirin. If only the PTT is abnormal, a PTT mixing study can be done. If the PTT corrects, then assays for factor VIII, IX, and XI need to be checked. If the mixing study does not correct, lupus anticoagulant or factor VIII inhibitor may be the cause. Causes also include hemophilia A or B.  A prolonged PT may be due to vitamin K deficiency or Factor VII deficiency. DIC will have prolong PT and PTT with bleeding at multiple sites. 
     A bleeding history can be quantified using a Bleeding Score System. Some patients may have never had a situation for significant bleeding to occur (no surgery, no dental procedures, etc.). Patients with a positive family history of bleeding may be at increased risk of a inherited disorder. 
     Many medications may cause bleeding, including NSAIDs, penicillins, SSRIs, TCAs. cephalosporins, and PTU (I left out the obvious ones). 

A Quick Synopsis of AFP's "Methods for Cervical Ripening and Induction of Labor"

Methods for Cervical Ripening and Induction of Labor
JOSIE L. TENORE, M.D., S.M., Northwestern University Medical School, Chicago, Illinois
Am Fam Physician. 2003 May 15;67(10):2123-2128.
http://www.aafp.org/afp/2003/0515/p2123.pdf

     Induction of labor is the artificial creation of uterine contractions, cervical effacement and dilation.  It is used when the cervix is "unfavorable". Cervical assessment is done using the Bishop score. Up to three points are given to each of the following categories:
Position
Consistency of cervix
Cervical effacement
Dilation %
Station
Patients with preeclampsia or previous vaginal deliveries get extra points. Patients with postdate pregnancy, nulliparity, or PPROM will lose points. A patient with a score less than 6 will usually need cervical ripening. 
     Herbs have had a history of being beneficial for induction. Black haw and black cohosh may have a uterine tonic effect. Blue cohosh is described as being able to stimulate uterine contractions. Red raspberry leaves can increase uterine contractions after labor has begun. The role of herbs have not been studied and the effectiveness is uncertain.
     Sexual intercourse and breast stimulation may help with labor. Nipple stimulation will increase oxytocin. Semen contains prostaglandins. The actual effectiveness lacks support.
     Mechanical modalities include hygroscopic dilators and balloon devices. The idea is that the increase pressure in the uterus will stimulate prostaglandins. Studies showed that both methods are effective for ripening. 
     Stripping the membranes will increase prostaglandin A2 and F2a, which aid in dilation. The method is associated with a lower dose of oxytocin needed, but does not appear to have any other clinical benefit. Risks include infection, rupture, and bleeding. Amniotomy can increase prostaglandin but also has no noticeable benefit in labor. 
     Pharmacologic prostaglandins are effective in cervical ripening. They dilate the cervix and cause uterine contraction. Cervidil and Prepidil are the featured medications in this article. They will increase the rate of a successful delivery. Misoprostol is a PGE1 analog. It is safe and effective when given at the proper dosage. Patients with a previous CS will be at increased risk of uterine rupture if on Misoprostol.  Misoprostol use causes a lower incidence of CS, lower need for oxytocin, and higher incidence of delivery. Mifepristone is an antiprogesterone agent, which inhibits the inhibition of uterine contraction by progesterone. It works well for  vaginal delivery. Relaxin is a hormone which promotes ripening. Studies are insufficient for relaxin at this time. Oxytocin stimulates uterine contraction through a pathway that increases calcium levels. Low dose and high doses are equally effective.
     

A Quick Synopsis of " Thrombocytopenia"

Thrombocytopenia
ROBERT L. GAUER, MD, Womack Army Medical Center Family Medicine Residency, Fort Bragg, North Carolina
MICHAEL M. BRAUN, DO, 1st Special Forces Group, Fort Lewis, Washington
Am Fam Physician. 2012 Mar 15;85(6):612-622.
http://www.aafp.org/afp/2012/0315/p612.pdf

     Thrombocytopenia is a low platelet count (less than 150). Patients with platelet counts above 50 are usually asymptomatic.  Those less than 50 may begin to see bleeding with trauma. Those less than 30 may have spontaneous bleeding, petechiae, and bruising.
    There are three primary causes of thrombocytopenia. Decreased platelet production (1) can be do to bone marrow problems, alcohol, infection, B12/ folate deficiency, or "congenital macrothrombocytopenias" such as Alport's, Wiskott-Aldrich, Bernard-Soulier, or Fanconi. Increased platelet consumption (2) can be due to autoimmune syndromes (SLE, sarcoidosis, antiphospholipid syndrome), DIC, HIT, ITP, infection, HELLP/preeclampsia, TTP, or HUS. Platelet sequestration (3) can be due to alcohol, liver disease, PE, pulmonary hypertension, or gestational thrombocytopenia.
   A peripheral blood smear is very helpful when making a diagnosis. Atypical lymphocytes may be due to a viral infection. Basophilic stippling may be due to thalassemia, alcohol, or lead poisoning. Cryoglobulin may be due to cryoglobulinemia, multiple myeloma, or mycoplasma pneumonia. Giant platelets may be due to ITP or congenital thrombocytopenias. Megakaryocyte fragments may be due to myelofibrosis. Nucleated RBC's may be due to myelofibrosis or hemolysis. Oval macrocytes may be due to B12 or folate deficiencies. Platelet agglutination may be due to pseudothrombocytopenia. Schistocytes may be due to TTP, HUS. DIC, or a defective prosthetic heart. Target cells may be due to chronic liver disease or hemoglobinopathies. I kinda stole this right from Table 4 of this article.
     ITP will oftentimes resolve spontaneously in children. Adults are at a higher risk of bleeding. Secondary ITP is associated with autoimmune disorders, lymphoproliferative disorders, and infections. Almost half of these patients will test positive for ANA and antiphospholipid antibodies (without having the corresponding disease). First line treatment is corticosteroids, immunoglobulin, or rituximab. Second line treatment is thrombopoietin receptor agonists or splenectomy.
     HIT takes about 5-10 days to show a drop in platelet count in patients naive to heparin, but in can drop in hours for those who have had previous heparin exposure.  HIT can be complicated by thrombosis, even after heparin is stopped. Features of HIT include skin necrosis, DVT, PE, stroke, or MI. Testing includes EIA of platelet factor 4/anion complex. By the way, stop the heparin!
     TTP has a clinical pentad. "Klmno" is the mnemonic that I use. It stands for kidneys, low grade fever, microangiopathic hemolytic anemia, neurologic signs, and thrombOcytopenia. It can lead to ischemia and necrosis, and seen mostly in adults. Treatment is plasma exchange.
     HUS is a child version of TTP. It presents with acute renal failure and bloody diarrhea. It is caused by a shiga toxin from E. coli.
     Preeclampsia and HELLP syndrome may have symptoms of thrombocytopenia, headache, vision problems, RUQ pain, hypertension, anemia, elevated liver enzymes, elevated lactate dehydrogenase, and proteinuria, at 20 weeks of gestation. Treatment consists of magnesium.
     Drug induced thrombocytopenia is a common cause of acute platelet drops. It usually takes about 5-7 days for it to occur, with resolution in 1-2 weeks. Medications include, but are not limited to abciximab, carbamazepine, cephalosporins, cimetidine, heparin, HCTZ, interferon, MMR, phenytoin, quinidine, rifampin, TMP/SMX, and vancomycin.
     Some of the infections that can cause thrombocytopenia include hepatitis B and C, HIV, EBV, CMV, parvovirus, VZV, rubella, mumps, malaria, dengue fever, typhoid fever, lyme disease, RMSF, and ehrlichiosis. Liver disease can also be the cause.
     Gestational thrombocytopenia is a benign diagnosis, thought to be caused by hemodilution or accelerated platelet clearance. Mild ITP during pregnancy may mimic gestational thrombocytopenia ,so the platelet count should be watched.
    Thrombocytopenia should be considered when making recommendations about patient activity, especially in contact sports.

A Brief Look Back at AFP's "Dystocia in Nulliparous Women"

Dystocia in Nulliparous Women
SARA G. SHIELDS, MD, MS, University of Massachusetts, Worcester, Massachusetts, STEPHEN D. RATCLIFFE, MD, MSPH, Lancaster General Hospital Family Medicine Residency Program, Lancaster, Pennsylvania, PATRICIA FONTAINE, MD, MS, University of Minnesota, Minneapolis, Minnesota, LARRY LEEMAN, MD, MPH, University of New Mexico, Albuquerque, New Mexico
Am Fam Physician. 2007 Jun 1;75(11):1671-1678.
http://www.aafp.org/afp/2007/0601/p1671.pdf

     Labor that is prolonged or is progressing slowly is known as dystocia. Arrested labor is having contractions for two hours without cervical change. Proper management of dystocia can dramatically affect the rates of c-sections. Labor in recent years has taken a slower rate of progression that previously documented on the Friedman curve. Physicians with strict adherence to the Friedman curve may advise intervention prematurely.
     In dystocia, the four issues that need to be addressed are:
(1) assessment of adequate contractions,
(2) fetal malposition,
(3) cephalopelvic disproportion, and
(4) coexisting clinical issues.
    In the latent phase of stage 1, supportive care (observation, sedation, antihistamines, narcotics and labor augmentation) can be given, but surgical intervention should not be considered this early in the labor. Once the patient is in the active phase of stage one, amniotomy and oxytocin can be considered, which may shorten labor lengths without affecting CS rates. Amniotomy, however, is a risky procedure which may cause variable decelerations (cord compression). The use of intrauterine pressure catheters can measure contractions, but it has no effect on the duration of labor or rate of CS. It may, however, help in deciding when to give oxytocin. If the patient is in arrested labor, waiting an additional two hours has lowered the rate of CS more than 2/3's.
     In the second stage of labor, malposition is a common cause of dystocia. Occipitoposterior position is the most common position. Having the mother go into certain poses (knee-chest, lunging, pelvic rocking, side-lying, among others) may help the child fall into proper position. Manual rotation by the physician is another option. If the second stage of labor is prolonged, it is not an indication for CS.
     Dysfunctional labor can be limited by using methods including:
(1) labor support,
(2) avoiding hospital admission in the latent phase of stage one labor,
(3) avoidance of a elective induction with an unripe cervix,
(4) cautious use of an epidural.
Labor support is best done with a professional, such as a doula. It has shown to lower the incidence of epidurals. Patients unnecessarily admitted, especially in the latent phase, will be exposed to more interventions, such as oxytocin and epidurals. The use of ripening agents (misoprostol, mechanical) has lowered the labor time but has not changed the rate of CS.  The use of epidurals, although oftentimes very appropriate and acceptable (maternal request is one), has led to an increase in operative vaginal delivery. They have no relationship to incidence or CS.

   

A Quick Synopsis of AFP's "Spontaneous Vaginal Delivery"

Spontaneous Vaginal Delivery
Dale a. Patterson,MD, Family Medicine Residency Program at Memorial Hospital of South Bend, South Bend, Indiana Marguerite Winslow, MD, and Coral D. Matus, MD, The Toledo Hospital Family Medicine Residency Program, Toledo, Ohio
Am Fam Physician. 2008 Aug 1;78(3):336-341.
http://www.aafp.org/afp/2008/0801/p336.pdf

     before labor starts, some screening tests may be important. Group B strep (GBS) screening is done on all women at 35-37 weeks. GBS positive women (and those that were not screened) are prophylaxed with penicillin four hours before delivery and every four hours until birth. Ampicillin, cefazolin, erythromycin or vancomycin are alternative medications. Patients with HSV2 during pregnancy can be treated with acyclovir, ganciclovir, or valacyclovir from week 36 until delivery. Patients with active lesions during delivery should have a c-section. All patients should also be screened for HIV. Patients who test positive should get therapy throughout pregnancy as well as a c-section at 38 weeks.
    Labor is divided into three stages. Stage one is from onset of labor to complete dilatation of the cervix. There is a latent and an active stage in stage one. The latent stage becomes active when the cervix dilates to 4 cm. Stage two is from dilatation to delivery. Stage three is delivery to delivery of the placenta. The stages typically last longer than the times previously documented on the Friedman curve.  Patients in the first stage of labor should not be admitted to "L and D" until they reach the active phase. Pain control is the most important intervention in this stage. Narcotics and epidural anesthesia are the two choices, but they can be given in combination. Epidurals increase the incidence of instrument delivery and the lengthen the second stage of labor. Fetal heart rate monitoring is commonly used. Due to its high false positive rates, it has increased the use for c-sections without lowering perinatal mortality or incidence or cerebral palsy. Fetal pulse oximetry and fetal ECG monitoring are other  modalities that have not been well studied (at the time of this article).
     The second stage of labor is where all the pushing occurs. Coached pushing with sustained breath holding leads to a shorter second stage. Delayed pushing prolongs the second stage, but shortens the duration of pushing. The patient can push in any position that she is most comfortable in. Episiotomies increase the risk of perinatal trauma, third degree tears, sexual dysfunction and urinary incontinence. They should not be done. antenatal perineal massage can lower the incidence of perineal trauma. First and second degree perineal tears do not need to be sutured.
     In the third stage of labor, the placenta separated from the uterus. Oxytocin is usually given to help the uterine contract, which decreases blood loss. It also lowers the risk of postpartum hemorrhage.
   

A Brief Synopsis of AFPs "Signs and Symptoms of Childhood Cancer: A Guide for Early Recognition"

Signs and Symptoms of Childhood Cancer: A Guide for Early Recognition
IOANNA FRAGKANDREA, MD, PhD, The Royal Marsden Hospital, Sutton, London, United Kingdom JOHN ALEXANDER NIXON, MD, Epsom and St. Helier NHS University Hospital, Sutton, London, United Kingdom PARASKEVI PANAGOPOULOU, MD, MPH, PhD, Panagiotis and Aglaia Kyriakou Children’s Hospital, Athens, Greece
Am Fam Physician. 2013 Aug 1;88(3):185-192.
http://www.aafp.org/afp/2013/0801/p185.pdf

     childhood cancer is oftentimes a delayed diagnosis because most of the signs and symptoms are nonspecific and are more common in other diseases. Thus, cancer should always be in back of your mind when symptoms don't resolve appropriately. Common symptoms of adult cancer are rare in childhood cancer. Common red flags in childhood cancer include fever, pallor, fatigue, malaise, anorexia, weight loss, lymphadenopathy, hemorragia, headaches, and many more. Prolonged fever of unknown origin can be associated with lymphoma or leukemia. Night sweats, fever, and weight loss (B symptoms) are seen in Hodgkin lymphoma. Lymphadenopathy that does not resolve should be evaluated with further tests, including CBC, differential, ESR, and a chest x ray. Headaches that occur in the morning, at night or that awake the child are suspicious. Accompanied symptoms include vomiting,  irritability, lethargy or developmental delay.
     GI symptoms that may be cancerous include an abdominal mass or new onset constipation.  A mass should be assessed with an ultrasound to rule out neuroblastoma or nephroblastoma. Constipation that does not respond to treatment could be an obstruction or spinal cord lesion. Diarrhea may be associated with leukemia, lymphoma, or VIPoma.
     Bone pain associated with cancer may occur at night or awaken the child. A bone tumor may have associated swelling or deformity. An x ray, CRP, CBC and blood smear will help with the diagnosis. Hematuria may be due to a renal tumor or sarcoma if more common causes are ruled out. Other symptoms include vaginal bleeding, scrotal mass, nonproductive cough, dyspnea, gingival swelling or bleeding.
     Patients with eye symptoms can get a fundoscopic exam to look for abnormalities which include malignancy. Paraneoplastic syndromes are more common in adults, but are seen in wilms tumor and neuroblastoma.
    Medical conditions which may preclude children to malignancy include down syndrome, gardner syndrome, WAGR syndrome, Turner syndrome, von Hippel Landau, SCID, Li-Fraumeni syndrome, xeroderma pigmentosum among many many others.

A Quick Synopsis of AFP's "Diabetic Foot Infections"

Diabetic Foot Infections
FASSIL W. GEMECHU, MD, MetroHealth Medical Center, Cleveland, Ohio, FNU SEEMANT, MD, State University of New York at Buffalo, Buffalo, New York, CATHERINE A. CURLEY, MD, MetroHealth Medical Center, Cleveland, Ohio
Am Fam Physician. 2013 Aug 1;88(3):177-184.
 http://www.aafp.org/afp/2013/0801/p177.pdf

     There is up to a 25% risk of a diabetic developing a foot ulcer in their lifetime. Risk factors include peripheral neuropathy, PAD, and impaired immunity. The most common bacteria in foot ulcers are aerobic gram negative rods, mostly Staphylococcus (including MRSA). Moderate to severe foot ulcers are often polymicrobial, including gram negative bacilli. Necrotic ulcers are more commonly anaerobic.
   A diabetic foot ulcer will have redness, warmth, swelling, pain, tenderness, purulent secretions, and induration. The wound severity can be graded. Grade 1 is for ulcers that are local without any systemic features. Grade 2 is a local infection with erythema less than 2 cm around the wound. Grade 3 has erythema greater than 2 cm around the wound which also affects structures below the skin and subcutaneous area. Grade 4 has signs of SIRS (fever, tachycardia, elevated respiratory rate, or leukocytosis).
     Ulcers that are larger than 2 cm or deeper than 3 mm or over a bony prominence should be investigated for osteomyelitis. Suspicious wounds can be diagnosed by biopsy, x ray, bone scan, or MRI. Probing the ulcer to see if it hits the bone is another option. Although lab values such as ESR, CRP and leukocyte counts may be elevated, absence of these markers does not exclude infection.
     Mild infection can be treated with oral antibiotics  for 1-2 weeks as an outpatient. Reevaluation should occur within 2-4 days.  More severe infections will need empiric broad spectrum antibiotics for 2-3 weeks. Hospitalization should be considered. Blood cultures should be drawn and the patient should be reassessed daily. If the patient does not improve, surgery should be consulted for the possibility of revascularization or amputation.
     Diabetic patients should have their feet routinely inspected at least annually. Patients with sensory loss should have them inspected every 3-6 months. Patients with PAD should have them looked at every 2-3 months. A patient with a history of ulcers should have their feet inspected every 1-2 months.

A Brief Synopsis of AFP's "Thyroid Nodules"

Thyroid Nodules
MARK A. KNOX, MD, Hawaii Island Family Medicine Residency, Hilo, Hawaii
Am Fam Physician. 2013 Aug 1;88(3):193-196.
http://www.aafp.org/afp/2013/0801/p193.pdf

     Thyroid nodules are common findings on physical exam and imaging. They may present as a protrusion in the neck, even causing compressive symptom. Risk factors for cancer in these nodules are a history of neck irradiation, a family history of thyroid cancer (medullary of papillary), and possibly graves disease. The first step in the algorithm requires the physician to do a full history, exam, TSH, and ultrasound. If the TSH is low, a thyroid scan can be done to rule out a hyperfunctioning nodule. If it is hyperfunctioning, radioiodine ablation or surgical excision can be performed. The radioactive iodine does not harm surrounding tissue because of the healthy tissues' low uptake. If the TSH is normal or high, the size of the nodule determines the plan. Nodules 1 cm or smaller can be followed up clinically. Larger nodules can be aspirated by ultrasound guided FNA.
     Aspiration results are classified as malignant, suspicious, benign, or indeterminate/ nondiagnostic. Indeterminate/ nondiagnostic samples can be repeated within a month. If the findings are benign, the patient can be followed with an ultrasound in 6-18 months. If the nodule does not grow, then the follow up interval can be extended to 3-5 years, otherwise a repeat FNA can be done. Malignant or suspicious samples should be referred (the R word!) for surgery. Nodules larger than 4 cm usually require a lobectomy.
     Calcitonin levels can be checked in patients suspected of medullary thyroid cancer, although sufficient evidence for this practice is lacking.   Ethanol injection can be done to recurrent cystic nodules.
     Pregnant women will have higher rates of thyroid nodules, but the rate of cancer is unchanged. Nodules are rarer in children, but the rate of cancer is higher.

A Quick Synopsis or AFP's "Diagnosis of Ear Pain"

Diagnosis of Ear Pain
JOHN W. ELY, MD, MSPH; MARLAN R.HANSEN, MD; and ELIZABETH C.CLARK, MD, MPH
University of Iowa Carver College of Medicine, Iowa City, Iowa
Am Fam Physician. 2008 Mar 1;77(5):621-628.
http://www.aafp.org/afp/2008/0301/p621.pdf

     When a patient presents with ear pain, the ear exam will either be normal or abnormal. The most common causes of ear pain with an abnormal exam are otitis media, otitis externa, a foreign body, or barotrauma. Acute otitis media will have a red, bulging tympanic membrane. Otitis externa (swimmers ear) will have debris over the tympanic membrane as well as swelling and erythema in the ear canal. Barotrauma can occur from an airplane flight or scuba diving. The tympanic membrane or middle ear may be bleeding.
     With a normal exam, the causes are TMJ, dental issues, pharyngitis, tonsillitis, cervical spine arthritis, or idiopathic.TMJ syndrome may have increased pain while talking or chewing food. If the exam is normal, but the cause is not apparent, "worst- case scenario" illness should be investigated. Patients with risk factors for cancer, such a tobacco use, alcohol use, or age greater than 50 years, may need imaging. Patients with risk factors for coronary disease or thoracic aneurysm may need an ECG, chest x-ray, or troponins. Temporal arteritis should also be rules out.
     Malignant otitis externa is severe, deep pain from osteitis of the skull base. It is from Pseudomonas, and is seen in the diabetic and immunocompromised.  Ramsey Hunt syndrome is due to a herpes zoster infection of cranial nerves V, VII, IX, and X. Symptoms include hearing loss, tinnitus, and vertigo. Polychondritis effects the ear cartilage (sparing the earlobe), causing a red or violet auricle. Cholesteatomas are epithelial cysts the destroy the inner ear, ossicles, and facial nerve canal. They should be easily visualized. Tumors causing ear pain are commonly found at the base of the tongue, tonsillar fossa, and hypopharynx. Bells palsy will affect the upper and lower face