A Synopsis of AFP's "Diagnosis and Treatment of Streptococcal Pharyngitis"

Diagnosis and Treatment of Streptococcal Pharyngitis
BETH A. CHOBY, MD, University of Tennessee College of Medicine–Chattanooga, Chattanooga, Tennessee
Am Fam Physician. 2009 Mar 1;79(5):383-390.
http://www.aafp.org/afp/2009/0301/p383.pdf

     The most common bacterial pharyngitis is Group A beta-hemolytic streptococcus (GAS). It peaks in the late winter and early spring.  Differentiating bacterial from viral using history and physical is not effective. GAS infection is suggested if the patient has a sore throat, acute fever, and recent GAS exposure. Cervical lymph nodes, pharyngeal or tonsillar inflammation/exudates are also common.  Cough, coryza, conjunctivitis and diarrhea are more likely due to viral illness.
     The Modified Centor score is used to determine whether antibiotics are appropriate. One point is given for each of the criteria listed below:

Absence of cough +1
Swollen and tender anterior cervical nodes +1
T' >100.4'F +1
Tonsillar exudates/ swelling +1
Age 3-14 yrs old +1
Age 15-44 yrs old +0
Age 45 years and older -1

Patients with a score of one or less do not need antibiotics. Patients with a score of 4 or more should be treated empirically with antibiotics. Those with a score of 2-3 should have a throat culture or RADT. Positive results should trigger treatment with antibiotics. 
     GAS pharyngitis will usually resolve without treatment, but treatment may prevent systemic and community spread. Acute rheumatic fever is a very rare complication. Lemierre syndrome (an internal jugular vein thrombosis) can be caused by untreated  non-GAS pharyngitis, Fusobacterium necrophorum.
     First line treatment includes penicillin, amoxicillin, ampicillin, or clindamycin. Erythromycin can be used in patients with a "TRUE" penicillin allergy. If erythromycin causes GI issues, azithromycin or clarithromycin can be used. The data on tonsillectomy effectiveness is limited.

A Quick Synopsis of AFP's "Management of Foreign Bodies in the Skin"

Management of Foreign Bodies in the Skin
GWEN WAGSTROM HALAAS, MD, MBA, University of Minnesota Medical School, Minneapolis, Minnesota 
Am Fam Physician. 2007 Sep 1;76(5):683-691
http://www.aafp.org/afp/2007/0901/p683.pdf

     All penetrating skin injuries should be evaluated to rule out foreign bodies. Wounds should be evaluated within 24 hours, before the wound closes or inflammation, induration, and scarring sets in. Organic matter, such as wood, thorns or cloth, pose a higher risk of infection than inert matter, such as metal or glass. Pencil lead or graphite may leave a darkened "tattooing" and should be removed. 

   Penetrating wounds should be evaluated for nerve or vessel damage. Imaging is not necessary if the foreign object can be visualized. Depending on the material, a CT, x ray, or ultrasound can be used.  Removing a splinter can be done with tweezers if visualized. If not, the entry wound can be extended with a scalpel,  and opened up with a hemostat. It splinter has entered perpendicularly, or if it is deep in the fat, an elliptical area may need to be cut around the entry wound. pressure around the sides of the wound may help get the foreign body out, or the entire piece of flash may need to be removed. 

     Fishhooks can be removed in multiple ways. Hooks without a barb on the end can be removed by tractioning the hook in the reverse direction of the entry. If there is a barb at the end, as small gauge needle can be inserted alongside the hook to cover or "cap" the barb. downward pressure on the shank of the hook can help disengage the barb from the flesh while it is being removed. 

    Once the foreign body is removed, the wound should be flushed with tap water.  Using high pressure to clean the area may only drive foreign matter deeper into the wound.  Antiseptics such as hydrogen peroxide, chlorhexidine, and povidone iodine are toxic in open wounds. 

     Tetanus vaccine should be given to all wounded patients who have not had a booster in 10 years, those with an uncertain vaccination history, and those with dirty wounds who had not had a booster in five years. Tetanus Ig can be used in those with and uncertain history who have dirty wounds. 

A Quick Synopsis of AFP's "Diagnosis and Management of Gestational Diabetes Mellitus"

Diagnosis and Management of Gestational Diabetes Mellitus
DAVID C. SERLIN, MD, and ROBERTW. LASH, MD, University of Michigan Medical School, Ann Arbor, Michigan
Am Fam Physician. 2009 Jul 1;80(1):57-62.
http://www.aafp.org/afp/2009/0701/p57.pdf

     Gestational diabetes is universally screened for in the USA. Risk factors include glycosuria, obesity, previous infant with macrosomia, first degree relative with diabetes, and history of glucose intolerance. Screening is done using a 50g nonfasting 1hr glucose challenge test at 24-28 weeks gestation. High risk patients can be screened at the first prenatal visit.  Levels should be less than 130-140 mg/dL. If positive, a 100g 3hr oral glucose tolerance test is done. The cutoff values are
95 mg/dL at fasting,
180 mg/dL at one hour,
155 mg/dL at two hours, and
140 mg/dL at three hours.
A patient who hits at least two of these cutoffs is diagnosed with gestational diabetes. Studies show that treatment of gestational diabetes will improve fetal outcomes.
     First line treatment of gestational diabetes includes dietary modification by an experienced nutritionist. If unsuccessful, insulin is considered. The starting dose is 0.7 units/kg/day.  It can be broken up by giving 2/3 in the morning and 1/3 before dinner. The morning dose should be 1/3 short acting and 2/3 NPH. The evening dose is 50/50. For patients unwilling to take insulin, glyburide or metformin are options, although metformin does cross the placenta.
     Screening these patients for anomalies (fetal well-being, estimated fetal weight, and macrosomia) includes twice weekly NST's and amniotic fluid levels in the third trimester.
     During labor, glucose should be monitored only in patients who are taking medication for gestational diabetes (qhr).  Most patients on insulin are euglycemic during labor. Early delivery reduces the risk of macrosomia, but the rates of brachial plexus injuries, hypoglycemia, and clavicle fractures remain unchanged. Postpartum, most mothers do not need continued diabetic therapy.  Half of these women will develop type 2 diabetes within 5-10 years. They should be screened every three years. Lifestyle recommendations (diet, exercise, weight loss) are also advised.

A Brief Synopsis of AFP's "Pulmonary Arterial Hypertension: An Update on Diagnosis and Treatment"

Pulmonary Arterial Hypertension: An Update on Diagnosis and Treatment
RICHARDSTRINGHAM, MD, and NIPAR. SHAH,MD,University of Illinois at Chicago College of Medicine, Chicago, Illinois
Am Fam Physician. 2010 Aug 15;82(4):370-377
http://www.aafp.org/afp/2010/0815/p370.pdf
     Pulmonary arterial hypertension presents as dyspnea on exertion with chest pain, fatigue, and palpitations. It is often asymptomatic. Diagnosis is often delayed, and many times may be an incidental finding.  It has a large differential and may be overlooked. It is diagnosed by an elevated mean pulmonary arterial pressure greater than 25 mmHg at rest (normal is 15 mmHg). Causes can be idiopathic, heritable (BMPR2 gene), drug or toxin induced, or associated with HIV, systemic sclerosis, sickle cell anemia, heart disease, schistosomiasis, or portal hypertension. Physical examination findings include a right parasternal heave, tricuspid regurgitation, a loud second or third heart sound, JVD, ascites, or hepatomegaly. An echocardiogram may show RVH, septal systolic strain/ sprain,  or right axis deviation. A chest x ray may show bilateral hilar enlargement, right ventricular enlargement, or a prominent central pulmonary artery. Routine lab work includes CBC, chemistry, thyroid function, ANA, anti-Scl-70, anti-centromere, and anti-ribonucleoprotein. Right heart catheterization is used to confirm the diagnosis and evaluate the severity.
     Functional classification of PAH is based primarily on symptoms. Class I has no symptoms or limitations of physical activity. Class II has slight limitations of activity with symptoms. Class III has marked limitations with symptoms during less than normal activity. Class III patients are unable to carry out activity without symptoms.
     Standard treatment includes coumadin (INR 1.5-2.5), diuretics, oxygen and digoxin, although randomized trials are lacking. Newer treatment includes prostacyclins (epoprostenol, iloprost, and treprostinil), endothelin receptor antagonists (bosentan and ambrisentan) and phosphodiesterase type 5 inhibitors (sildenafil and tadalafil).  Combinations may be helpful.  Vaccines for pneumococcus and influenza should be given. There is no cure and prognosis is generally poor.

A Synoposis of AFP's "A Primary Care Approach to Substance Misuse"

A Primary Care Approach to Substance Misuse
BRAD SHAPIRO, MD; DIANA COFFA, MD; and ELINORE F. McCANCE-KATZ, MD, PhD University of California, San Francisco, School of Medicine, San Francisco, California
Am Fam Physician. 2013 Jul 15;88(2):113-121
 http://www.aafp.org/afp/2013/0715/p113.pdf

     There is a difference between substance abuse and sustance dependence. Abuse is a pattern due to the substance use, that leads to impairment or distress, which may occur from not fulfilling obligations at work, school or home, substance related legal issues, involvement in dangerous situations, or social/ interpersonal problems. Dependence is seen in patients who display tolerance, withdrawal, a desire to want to stop, giving up previously enjoyed activities, spending a lot of time getting the substance, and using more for longer times.
     Substance abuse should be considered a chronic illness like asthma or diabetes. The management of substance abuse starts with screening, assessing comorbidities, counseling, follow up, and treatment referral, if necessary. Although not recommended by the USPSTF, screening may be justified because of the high prevalence and morbidity of the disease. A screening questionnaire can be employed to help determine if substance abuse is occurring. Counseling the patient can decrease the amount of drug use. This article briefly describes some interviewing techniques which I recommend reading. Most of the principles talk about having the patient come up with the idea or having the patient have "self discovery" rather then "telling them" what to do. The patient will use the consequences of substance use to be the motivation for change.
     The three drugs that can be used to treat opioid dependence are buprenorphine, naltrexone, and methadone. Treatment should have a long term approach with a slow taper. Buprenorphine is a partial mu opioid receptor agonist that can be mixed with naloxone to prevent misuse. Methadone is distributed through special federal programs. Naltrexone is a mu opioid receptor antagonist which can be helpful in patients trying to maintaining abstinence  It has had limited success in non motivated patients. There is not pharmacologic treatmetns for stimulants. Referral to specialized treatment centers can be very helpful and appropriate.  Comorbid mental health conditions may be occurring concomitantly. Patients should be followed up often and regularly.

A Synopsis of AFPs "Cluster Headache"

Cluster Headache
JACQUELINE WEAVER-AGOSTONI, DO, MPH, University of Pittsburgh Medical Center Shadyside Hospital, Pittsburgh, Pennsylvania
Am Fam Physician. 2013 Jul 15;88(2):122-128 
http://www.aafp.org/afp/2013/0715/p122.pdf

     Diagnostic criteria for cluster headaches includes having at least one ipsilateral symptoms in the eye, nose, or face, restlessness, agitation, headaches lasting 15-180 minutes, a headache frequency from one every other day to eight per day, unilateral location, and severe quality. Cluster headaches are typically classified based on duration and frequency of episodes. Chronic cluster headaches have a least one cluster period lasting over 12 months with a remission lasting less than one month. Episodic cluster headaches last less than 12 months but have two or more cluster periods of one week or more. The remission periods in this case should last at least one month.  Triggers include alcohol, vasodilators, histamines, and tobacco. Pathophysiology is not clear.
     Management includes patient education about avoiding triggers and lifestyle modification. First line abortive therapy includes triptans and supplemental oxygen. Medications with weaker evidence include intranasal lidocaine, octreotide, and ergotamine. Prophylaxis consists of verapamil. Oral steroids have not been proven effective but may be used for bridging therapy. Chronic cluster headaches can be treated with verapamil and lithium. Deep brain stimulation may also be considered.
     Pregnant patients should limit the medication treatment as much as possible. gabapentin can be used in addition to the medications described above.

A Quick Review of AFP's "Edema: Diagnosis and Management"

Edema: Diagnosis and Management
KATHRYN P. TRAYES, MD, and JAMES S. STUDDIFORD, MD, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, SARAH PICKLE, MD, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey, AMBER S. TULLY, MD, Cleveland Clinic, Cleveland, Ohio
http://www.aafp.org/afp/2013/0715/p102.pdf 

Am Fam Physician. 2013 Jul 15;88(2):102-110 

     Edema is the accumulation of fluid from the intravascular space to the intercellular space. This is caused by changes in the capillary hydrostatic pressure gradient and the oncotic pressure gradient. The history can help determine the management of the edema. Acute edema can be seen in a DVT, compartment syndrome, a ruptured popliteal cyst, or a new calcium channel blocker script. Chronic edema is seen with systemic conditions such as CHF, kidney, thyroid or liver diseases. Unilateral swelling can be seen in DVT, venous insufficiency, or obstruction. Certain medications such as MAOIs, BBLs, CCBs, NSAIDs, cytokines, and chemotherapeutics can also lead to edema.
     For diagnostic testing, labs such as BNP, creatinine, UA, albumin, D-dimer, and liver enzymes should be drawn.  Examination of the legs for pitting and the feet for Kaposi-Stemmer sign (inability of skin tenting during pinching of the top of the foot) is helpful for the diagnosis of lymphedema. Venous ultrasound is good for DVT. Duplex ultrasound is good for venous insufficiency. Additional imaging, such as an MRI with venography can help find a DVT or May-Turner syndrome (where the left iliac vein is compressing the right iliac artery).  An echo can be used to evaluate pulmonary arterial pressures in patients with obstructive sleep apnea.
     Management of edema usually focuses on treating the underlying condition. Patients with chronic venous insufficiency can use leg elevation and compression stockings. Pneumatic devices can be used if stockings are contraindicated (peripheral arterial disease). Wound care includes emollients and topical steroids. Patients with lymphedema may need manual lymphatic massage, multilayer bandages, compression stockings, or debulking/ bypass procedures if the lymphedema is severe refractory. DVT management consists of anticoagulation and compression stockings. Medication induced edema patients will need to discontinue the offending medication.  Obstructive sleep apnea patients will need positive pressure ventilation.

A Brief Synopsis of AFP's "Early Recognition and Management of Sepsis in Adults: The First Six Hours"

Early Recognition and Management of Sepsis in Adults: The First Six Hours
ROBERT L. GAUER, MD, Womack Army Medical Center, Fort Bragg, North Carolina
Am Fam Physician. 2013 Jul 1;88(1):44-53.
http://www.aafp.org/afp/2013/0701/p44.pdf

     Sepsis kills as many people in hospitals as heart attacks. The progression of sepsis goes from systemic inflammatory response syndrome (SIRS), to sepsis, to severe sepsis, to septic shock. SIRS is defined as at least two of the following; fever (above 38.5c), tachycardia (above 90 bpm), tachypnea (RR above 20) and leukocytosis or leukopenia (above 12 k/mm3 or less than 4 k/mm3). Sepsis is SIRS with the presence of an infection. Severe sepsis is sepsis with at least one sign of organ hypoperfusion/ dysfunction, including mottled skin, increased capillary refill time, decreases urinary output, increased lactate, DIC, platelet count less than 100k/mm3, ARDS/ acute lung injury, or cardiac dysfunction. Septic shock is defined as severe sepsis plus at least one of the following; a systemic mean blood pressure of less than 60 mm Hg, PCWP between 12-20 mm Hg, or the need for vasopressors. Refractory septic shock is defined when the need for dopamine goes above 15 ug/kg per min to maintain a mean bp above 60 mmHg (or norep, epi of >0.25 ug/kg per min).
     The pathophysiology of sepsis includes endothelial damage, vascular permeability, microvascular dysfunction, coagulation pathway activation and impaired tissue oxygenation. Risk factors include extremes of age, chronic illness, malnutrition, immunosuppression, etc. Fever is the most common manifestation.
     Early goal directed therapy must be done within the first 6 hours to benefit patient mortality. Supplemental oxygen, with possible ventilation and intubation, will maintain proper tissue perfusion. The CVP should be maintained between 8-12 mm Hg with colloids or crystalloids. MAP can be maintained at 65-90 mm Hg with vasoactive agents. If oxygen saturation falls below 70%, the patient can be transfused until the hematocrit is at or above 30%. Inotropic agents can help oxygen saturation as well.
     A full set of labs and cultures should be drawn. An echo can be done to detect endocarditis. A CT can check for a pulmonary embolus, pelvic infection, or renal abscess. Antibiotics should be used empirically based on the probable source of infection. Ongoing management includes corticosteroid therapy, glycemic control, low tidal volumes, hemoglobin maintenance, and oxygen saturation.
   

A Quick synopis of AFP's "Nonalcoholic Fatty Liver Disease: Diagnosis and Management"

Nonalcoholic Fatty Liver Disease: Diagnosis and Management
THAD WILKINS, MD, Georgia Regents University, Augusta, Georgia, ALTAF TADKOD, MD, Barrow Regional Medical Center, Winder, Georgia, IRYNA HEPBURN, MD, Good Samaritan Digestive Health Specialists, Lebanon, Pennsylvania, ROBERT R. SCHADE, MD, University of Pittsburgh Medical Center Presbyterian, Pittsburgh, Pennsylvania
Am Fam Physician. 2013 Jul 1;88(1):35-42.
http://www.aafp.org/afp/2013/0701/p35.pdf

     Nonalcoholic fatty liver disease is defined as fatty infiltration of the liver without other causes of steatosis. It has increased in the population with the increase of metabolic syndrome, obesity, and a sedentary lifestyle. There will be hepatocyte ballooning, mallory hyaline, and mixed lymphocyte/neutrophilic inflammatory infiltrates.  Hepatic steatosis is defined as excessive accumulation of fat in the liver (fat in more than 5% of the liver cells). Nonalcoholic steatohepatitis is hepatic steatosis with inflammation and cell injury. 
     The exact mechanism of nonalcoholic fatty liver disease is unknown. Patients are often asymptomatic. Diagnosis is usually an incidental finding. Metabolic syndrome is associated with nonalcoholic fatty liver disease. The criteria for metabolic syndrome includes: 
     An elevated blood pressure (greater than 129 systolic or 85 diastolic) or on meds for hypertension,
     A fasting glucose above 99 mg/dL or on meds for high glucose,
     An HDL less than 50 in women or 40 in men, or on meds for low HDL,
     A triglyceride level above 149 mg/dL or on meds for high triglycerides,
     A waist circumference at or above 35' in women or 40' in men.
     Screening is not necessary, but for patients suspected of nonalcoholic fatty liver disease, a proper history and physical is needed. A full set of labs, including LFT's, ferritin, iron, A1C, lipids, cholesterol, and hepatitis panels should be drawn. Tests can also be done to rule out wilsons, hemochromatosis, a-antitrypsin deficiency, and autoimmune hepatitis. Ultrasound can be done to look for fat in the liver. It cannot, however differentiate steatosis from fibrosis. A CT or MRI may be needed if this is a concern. There are many serological markers for fibrosis which may defer the need for a biopsy. Biopsy is the definitive test in determining hepatic steatosis vs. nonalcoholic fatty liver disease. 
     Treatment is focused on lifestyle management. The main goal is to reduce insulin resistance.  A healthy diet,  weight loss, and exercise is the standard of care for nonalcoholic fatty liver disease. There is mixed information about pharmacology. Prevention includes vaccination for hepatitis A and B, and limiting alcohol use.

A Brief Synopsis or AFP's "Postexposure Prophylaxis for Common Infectious Diseases"

Postexposure Prophylaxis for Common Infectious Diseases

MAZEN S. BADER, MD, MPH, Hamilton Health Sciences, Hamilton, Ontario, Canada, DAVID S. McKINSEY, MD, University of Kansas School of Medicine, Kansas City, Kansas, and Infectious Disease Associates of Kansas City, Kansas City, Missouri

Am Fam Physician. 2013 Jul 1;88(1):25-32.

http://www.aafp.org/afp/2013/0701/p25.pdf

     Every clinicians' biggest fear is to catch some awful disease from a sick patient. It doesn't stop them from running into the ER during an outbreak, but its still in the back of their minds. The most common and effective prophylaxis is childhood vaccinations. They are available for measles, mumps, rubella, varicella, influenza, hepatitis B, pertussis, among others. In the hospital, standard precautions include regular hand washing, gloves, masks, gowns, isolation precautions and others. This article will focus on what to do if you get exposed to something (post exposure prophylaxis, PEP).
     The first thing that should be done if you think you were exposed to something is to figure out if the patient (source) is really infected. This can be done with culture or serology. Also, the patient may not be infectious even if he or she has the illness. Asking the patient when he or she first got sick, treatment, and current symptoms may help.
     Depending on the patient, PEP for hepatitis B will be different. If the person exposed was unvaccinated, then he or she needs immunoglobulin, followed by vaccination. Those vaccinated with a documented inadequate response will need the immunoglobulin, followed by a vaccine booster. Persons with low risk exposure to HIV would take Truvada or Combivir. High risk exposure persons may take Tenofovir with emtricitabine or Zidovudine with lamivudine, plus Kaletra or Atazanavir.
     Unvaccinated patients who become exposed to hepatitis A should be vaccinated within two weeks. If they are unvaccinated and immunocompromised, they should get immunoglobulin.  For varicella, exposed patients can be vaccinated within five days of exposure. Pregnant or otherwise immunocompromised patients will need immunoglobulin. 
     Persons exposed to rabies who are unvaccinated will need immunoglobulin (IM or around the wound if possible). They will also need to be vaccinated on days 0, 3, 7, 14, and 28. Previously vaccinated persons will need a vaccine on days 0 and 3 if they can prove that they have the antibodies, otherwise they get the shot on days 0, 3, 7, 14 and 28 as well.
     Persons exposed to Step A "necrotizing fasciitis" can get penicillin G plus rifampin, clindamycin, or azithromycin. Persons exposed to meningitis will get cipro, azithromycin, ceftriaxone, or rifampin, for up to two weeks. For pertussis, they can take azithromycin, clarithromycin, erythromycin, or TMP/SMX.  Patients exposed to tetanus who were incompletely vaccinated or not vaccinated will need the vaccine. They can have the immunoglobulin if the wound is dirty. Patients exposed to TB should have a skin test, x-ray, and isoniazid with vitamin B6 if needed. Persons exposed to anthrax will need the vaccine regimen plus cipro or doxycycline. Persons exposed to diphtheria should get the vaccination and penicillin.  
    Exposed patients should be counseled on potential risk and adverse effects of the treatment. 
     
   

A Synopsis of AFP's "Acute Knee Effusions: A Systematic Approach to Diagnosis "

Acute Knee Effusions: A Systematic Approach to Diagnosis  
MICHAEL W. JOHNSON, MAJ, MC, USA, Madigan Army Medical Center, Tacoma, Washington  
Am Fam Physician. 2000 Apr 15;61(8):2391-2400     
http://www.aafp.org/afp/2000/0415/p2391.html

     When examining a swollen knee, the history is important. If the cause was from trauma, the diagnosis may be a fracture or tear. A non-injury cause would more likely be infectious, rheumatic, or due to gout.  If trauma is involved, the mechanism or injury is helpful.  Swelling will appear within four hours in a ligamentous injury, as well as for a hemarthrosis. An ACL tear will occur during a non-contact deceleration, a pivoting or cutting movement or during hyperextension. The patient may have heard a "pop". The patient will have a positive Lachman's test, anterior drawer test, and pivot shift test. A PCL tear will occur as a blow right below the knee during knee flexion. There will be a positive posterior drawer and sag test. Collateral ligament injuries will occur with force either left-to-right or right-to-left across the joint. There will be corresponding ligament laxity on the side opposite the blow. Meniscal injury will occur while the knee is twisted or while squatting. They will have positive McMurray's and Apley's test. In a fracture, there will be a history of a direct blow to the knee and an inability to bear weight in the joint.  There may be deformity, crepitus, or ecchymosis. 
     Radiography can be used to assess compartment space narrowing, knee effusions (with a 15-30 degree flexion), and fracture. According to the Ottawa knee rules, an x-ray is required if one or more of the following is present; 
     age of 55 years or older,
     tenderness at the head of the fibula, 
     inability to flex the knee 90 degrees, 
     can't bear weight on knee or take four steps.
An MRI is better for soft tissue damage.  Arthrocentesis can be diagnostic and therapeutic. The fluid should be sent for analysis. Bloody fluid may indicate a fracture or tear. An infection may have low glucose, elevated WBC count, and positive cultures. Gout will have aspirate with negative birefringent rods or needles. Pseudogout will show weakly positive birefringent rectangles or rhomboids. Rheumatoid arthritis will have increased protein, low glucose and a normal WBC count. 
     

A Quick Synopsis of AFP's "Diagnosis and Management of Lyme Disease"

Diagnosis and Management of Lyme Disease
WILLIAM F. WRIGHT, DO, MPH; DAVID J. RIEDEL, MD; ROHIT TALWANI, MD; 
and BRUCE L. GILLIAM, MD, University of Maryland, Baltimore, Maryland
Am Fam Physician. 2012 Jun 1;85(11):1086-1093. 
http://www.aafp.org/afp/2012/0601/p1086.pdf

    Lyme disease is a tick-borne infection of Borrelia burgdorferi from the deer tick Ixodes scapularis. It is commonly found in wooded areas of the northeast US as well as Wisconsin and Minnesota. It occurs more often in the late spring and summer. Once the tick attaches to the skin, it begins to swell with blood. After 36-48 hours,the tick can infect the patient with the spirochete.  
     There are three stages of lyme disease. The early localized stage begins within 2 weeks after exposure. Symptoms include the the "bulls eye" rash of erythema migrans and nonspecific symptoms such as fever, chills, malaise, headache, myalgia, and fatigue. If untreated, it can progress to an early disseminated stage, which includes heart, skin, muscle and neurologic symptoms.  Cardiac involvement can present as chest pain, dyspnea on exertion, fatigue, palpitations, or syncope. AV block may occur as well. Musculoskeletal symptoms include arthralgia, myalgia, and joint swelling. An inflammatory process may present in the synovial fluid over time. Neurologic symptoms are seen in a classic triad of meningitis, cranial neuropathy, and radiculopathy. Involvement may also be seen as neck pain, headaches, facial nerve palsy and ataxia. Late stage lyme disease may present as chronic arthritis or severe neurologic symptoms such as encephalopathy and peripheral neuropathy. 
     Diagnosis can be made with a history of a tick bite and the classic rash, without lab tests. As far as lab tests are concerned, direct methods include testing for specific proteins and nucleic acids, and indirect  methods includes serology and antibody detection. Cultures are no longer performed. When testing is needed, the EIA is performed first with a confirmatory western blot to be done afterwards. It is important to remember that both IgG and IgM will be present in the patient for years and does not an indication of disease course. Treatment it typically doxycycline. Ceftriaxone, amoxicillin, cefuroxime, and azithromycin may be considered in special situations. 
    Prevention consist of avoiding tick infested areas such as forests and high grass areas. A tick check should be done after the activity as well as bathing within two hours of the event. Ticks, if found, should be removed with a tweezer placed as close to the skin as possible without squeezing the abdomen. For ticks that are engorged and that may have been attached for longer than 36 hours, prophylaxis antibiotics can be used (one dose of doxycycline 200 mg). 
      

A Brief Synopsis of AFP's "Sudden Cardiac Death and Implantable Cardioverter-Defibrillators"

Sudden Cardiac Death and Implantable Cardioverter-Defibrillators
MINTU P. TURAKHIA, MD, MAS, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, and Stanford University School of Medicine, Stanford, California
Am Fam Physician. 2010 Dec 1;82(11):1357-1366. 
http://www.aafp.org/afp/2010/1201/p1357.pdf

     Implantable cardioverter-defibrillators (ICDs) are used to prevent sudden cardiac death (SCD) from arrhythmia. Sudden cardiac death (SCD) will either occur from ventricular tachycardia, progressing to ventricular fibrillation or from bradyarrhythmias, electromechanical dissociation, or advanced heart failure. Risk factors for SCD include coronary artery disease, heart failure, arrhythmias, structural disease, or electrical disease.
    An ICD consists of a generator and a lead. The generator includes the battery, capacitor and microprocessor (the big round thing in the chest wall). The lead consists of the pacing tip electrode and one or two shock coils. The lead parts are placed around the right ventricle, or around the left ventricle (specifically the coronary sinus ostium and a coronary sinus vein) in the case of biventricular pacing. The purpose of the ICD is to stop VT or VF with pacing, cardioversion or defibrillation (FYI "synchronized" cardioversion is defined as giving the the heart a synchronized shock (low voltage at the peak of the R wave) to help the heart get back to normal sinus rhythm. Defibrillation, also known as "unsynchronized" cardioversion, is done to get PEA or VF back into a sinus rhythm. It is high voltage at any point along the ECG).
     ICD placement is helpful in primary prevention because the first event of arrhythmia is often fatal. The best predictor of  SCD is LV ejection fraction. Indications for ICD placement include prior VT, VF or syncope, and an ejection fraction below 30-35%. Implantation for secondary prevention includes patients who have survived previous episodes of cardiac arrest from a VT or VF, or those presenting with structural disease.  Candidates for placement should have a life expectancy of at least 7 years for it to be cost beneficial.
     Evaluation of patients who already have an ICD include LV injection fraction, underlying cardiac disease, indication for placement, underlying rhythm, and device manufacturer. Patients who experience an ICD shock should be examined to determine if the shock was appropriate.  Inappropriate causes include SVT's (atrial, junctional or sinus tachycardia as well as PVC's) and device oversensing. Repeated shocks could be due to a recurrent ventricular arrhythmias or a broken lead.
     MRI's are generally contraindicated, although a special magnet can be placed over the ICD to protect it if the imaging is absolutely necessary. Patient undergoing a surgical procedure should not have central venous access on the same side as ICD lead placement.