A Brief Synopsis of AFP's " USPSTF: Screening for Intimate Partner Violence and Abuse of Elderly and Vulnerable Adults: Recommendation Statement"

A brief review of:
U.S. Preventive Services Task Force: Screening for Intimate Partner Violence and Abuse of Elderly and Vulnerable Adults: Recommendation Statement
http://www.aafp.org/afp/2013/0415/od3.pdf
Am Fam Physician. 2013 Apr 15;87(8):online.

     Intimate partner violence is defined as  any harm (sexual, physical, or mental) done by a spouse or partner. Sexual intimacy is not required for this classification of this type of violence. Between 25-30 percent of people claim to have experienced some form of IPV. The numbers are likely higher due to underreporting. Patients may feel guilt, self-blame, or fear of retaliation which may contribute to the underreporting. Since there are no current standards for screening, this could also be a factor of the underreporting. 
    The USPSTF recommends screening of all women of childbearing age for IPV. Clinicians can use various screening tools including;
Hurt, Insult, Threaten, Scream (HITS),
Ongoing Abuse Screen/ Ongoing Violence Assessment Tool (OAS/ AVAT),
Slapped, Threatened, and Throw (STaT),
Humiliation, Afraid, Rape, Kick (HARK), 
Modified Childhood Trauma Questionnaire-Short Form (CTQ-SF), and
Woman abuse Screen Tool (WAST).

 For example, the four questions asked in the HITS assessment tool are 
"how often does your partner;
1. Physically hurt you?
2. Insult or talk down to you?
3. Threaten you with harm?
4. Scream or curse at you?"
Each question is scored from one to five, depending on frequency (never, rarely, sometimes, fairly often, or repeatedly). A score greater than 10 is positive. [1]  
     Patients who are victims of IPV often develop depression, PTSD, stress, anxiety, substance abuse, suicide, eating disorders, obesity, teen pregnancy, suicide and other conditions. Although studies are limited, there appears to be little harm in screening. Patients who screen positive need to be referred for intervention services. They can be counseled on safety behaviors, community resources, as well as emotional support, education on problem-solving strategies and parenting. Physicians need to be aware of state and local reporting laws.

1.http://www.orchd.com/violence/documents/HITS_eng.pdf
     

A Brief Synopsis of "Updated Guidelines on Outpatient Anticoagulation" from AFP

 A brief synopsis of "Updated Guidelines on Outpatient Anticoagulation"
PATRICIA WIGLE, PharmD, BCPS, and BRADLEY HEIN, PharmD, University of Cincinnati James L. Winkle ,College of Pharmacy, Cincinnati, Ohio, HANNA E. BLOOMFIELD, MD, MPH, University of Minnesota and Minneapolis VA Medical Center, Minneapolis, Minnesota, MATTHEW TUBB, MD, PhD, The Christ Hospital/University of Cincinnati Family Medicine Residency Program, Cincinnati, Ohio, MICHAEL DOHERTY, PharmD, BCACP, University of Cincinnati James L. Winkle College of Pharmacy, Cincinnati, Ohio

http://www.aafp.org/afp/2013/0415/p556.pdf
Am Fam Physician. 2013 Apr 15;87(8):556-566.

This is a very detailed article (see how many authors!)  that i reviewed and I suggest reading it for more information
     For many decades, warfarin was the only option for anticoagulation, besides aspirin.  Recently, newer medications have come on the market.
     Warfarin is an anticoagulant which inhibits vitamin K dependent clotting factors II, VII, IX, and X. Due to the half life of these clotting factors, warfarin can take several days to take effect. In the beginning stages of using this drug, there is a paradoxical increase in clotting risk due to the decrease in protein C and S. Heparin or LMWH is used at the onset of warfarin therapy due to this hypercoagulable state. It is continued until the INR is in therapeutic range for 24 hours. Heparin is eventually stopped and warfarin is used because warfarin is an oral medication and heparin is not.
     Warfarin can be started at 5-10 mg per day and then adjusted, depending on the INR. If it is elevated, but less than 4.5, the dosage can be lowered or held. With levels 4.5 to 10, one or two doses should be held, then resumed at a lower dosage once the INR is therapeutic.  If the INR is greater than 10, the patient may need vitamin K, in addition to holding the medication, to reverse the effects of warfarin. There are many drug and food interactions that can affect the effects of warfarin.  Amiodarone and rifampin, for example, can alter the INR long after the medication has been discontinued. Diet should be maintained while using warfarin  without and drastic changes, such as becoming a vegan.
     Unfractionated heparin works by inactivating factor IIa and Xa by binding to antithrombin. It also prevents the growth of clots. There is a risk of bleeding with this drug as well as an increased risk in HIT.
     The two LMWHs are lovenox and fragmin. It is given subcutaneously. Anti-factor Xa monitoring is not needed. Bleeding and HIT can be an issue, although less likely than unfractionated heparin.
     Fondaparinux is a synthetic analogue of heparin. It had no effect on thrombin formation and only works on factor Xa. It is given subcutaneously as well and does not need to be monitored.
     There are times when anticoagulation needs to be stopped. According to this article, if the patient is to have surgery, warfarin can be stopped 5 days before the procedure and restarted one to two days after. If there is only a low risk of bleeding, perioperative bridging may not be indicated. Otherwise it may be necessary to bridge the patient with LMWH or unfractionated heparin during the perioperative period.
     The biggest issue with warfarin is getting the dosage right, and the constant need for adjusting it. The advent of newer meds is very appealing, due to its ease of prescribing and lack of need for monitoring. Dabigatran is an anticoagulant that is effective in preventing embolism and stroke for patients with nonvalvular atrial fibrillation. Rivaroxaban is effective in prevention of DVT in patients having hip or knee replacement surgery, in treatment of DVT and PE, and prevention of embolism in nonvalvular atrial fibrillation.



   

A Brief Synopsis of AFP's "Evaluation and Diagnosis of Wrist Pain: A Case-Based Approach"

A synopsis of-
Evaluation and Diagnosis of Wrist Pain: A Case-Based Approach
RAMSEY SHEHAB, MD, Henry Ford Health System, Detroit, Michigan 
MARK H. MIRABELLI, MD, University of Rochester Medical Center, Rochester, New York
http://www.aafp.org/afp/2013/0415/p568.pdf
Am Fam Physician. 2013 Apr 15;87(8):568-573.


     Wrist pain can be classified as acute or chronic. Acute pain is typically due to trauma. Chronic pain can be neurologic, systemic, inflammatory, or from an old trauma. History, including the location, timing, and quality of pain can aid in the diagnosis. The diagnoses  that will be discussed here are scaphoid fracture  ulnar neuropathy, and De Quervain tenosynovitis. I will do my best not to use the words "brevis", "minimi", "longus" or "pollicis"
     The lunate and scaphoid are the two carpal bones that articulate with the ulna and radius, respectively. Scaphoid fractures are more common in the young because of the increased surrounding cartilage. The most common presentation is "falling on an outstretched hand". The wrist and anatomical snuff box may be swollen, with tenderness dorsally around the distal radius. Axial pressure on the first metacarpal bone will reproduce pain. With x ray imagining, its is important to order AP, AP in ulnar deviation, lateral, oblique, pronated oblique, and supinated oblique views. They may need to be repeated two weeks later to see if the fracture is healing. A bone scan or MRI may be needed if the x rays are not sufficient. Patients with suspected scaphoid fracture, but negative x rays, should be given a thumb spica cast and repeated in two weeks.
     In the wrist, the ulnar nerve passes through the guyon canal, to the anterior surface of the hand. The nerve splits off and innervates the sensory portion of the medial palm, the muscles of the pinky, and the muscles for thumb flexion and adduction. Compression of the ulnar nerve in the wrist is typically caused by repetitive trauma or a ganglion cyst. The entire length of the nerve should be investigated to rule out issues in the cervical spine, brachial plexus, and ulnar groove . The patient will complain of numbness and/or tingling in the 4th and 5th digits.  Tinel sign and Phalen sign should be part of the exam. X rays should be ordered first. Nerve conduction tests may uncover entrapment in acute injuries. EMG can be used if the issue is chronic. An ultrasound of the nerve may reveal compression. MRI can be a useful if other tests are inconclusive. 
     De quervain tenosynovitis is inflammation of the sheath that encompasses the the tendons of the lateral border or the anatomic snuffbox. Again, the wrist and tissue around the anatomical snuffbox may be swollen. Finkelstein test will be positive. Grind test should be negative (and positive in OA of the thumb MCP joint).  Injection of lidocaine into the joint can rule out arthritis. Appropriate labs may be drawn if an infection is suspected, and further imaging can be considered if needed.
     

A Brief Synopsis of AFP's Rational Use of Opioids for Management of Chronic Nonterminal Pain"

Rational Use of Opioids for Management of Chronic Nonterminal Pain
DANIEL BERLAND, MD, and PHILLIP RODGERS, MD, University of Michigan Medical School, Ann Arbor, Michigan
Am Fam Physician. 2012 Aug 1;86(3):252-258.
http://www.aafp.org/afp/2012/0801/p252.pdf


     Pain management is a large part of why people see their doctors. Most patients assume that all pain needs to be treated with opioids  Opioids are well know to be highly addictive and overused. It is now even more popular than illicit drug use. Overuse of opioids can cause opioid  induced hyperalgesia, where an increase in opioid use causes a paradoxical increase in pain. 
     Acute pain is different from chronic pain. Acute pain can be relieved with opioids while tissue recovery takes place. Chronic pain is from "complex CNS signalling" involved with biopsychosocial factors that will not resolve acute pain therapy. Opioid treatment should not be used in those with chronic central or visceral pain. These factors can be addressed with modalities such as physical therapy, massage, heat, steroid injections, topical lidocaine, or electric stimulations. Diet, exercise, and proper sleep can make a big impact on chronic pain as well. SSRI's are effective for neuropathic pain.  TCA's can be used if the neuropathy is concomitant with headaches, depression, panic disorder or tobacco addiction. Comorbid psychiatric illnesses such as anxiety, depression, or PTSD, should be treated accordingly.  After all these factors are dealt with, then opioids may be considered.
     The patient should have a comprehensive evaluation and their risk of potential abuse determined before beginning them on a trial basis.  The patient should understand that the goal of opioid therapy is to improve function, not decrease pain, per se. A written agreement should be set up instructing the patient not to be treated by multiple physicians or go to multiple pharmacies for the opioids.  Refill policies, "loosing prescriptions , regular drug testing, regular follow ups, and asking for refills early should all be incorporated into this agreement. 
     Morphine is a good first-line therapy because it is long acting, inexpensive, and reliable. Side effects include nausea, pruritus, constipation and drowsiness. Patients with a morphine allergy can be prescribed oxycodone, although it has a higher potential for abuse. Fentanyl patches or buprenorphine are an expensive alternative. Methadone may be an option because of its long action and lower tolerance rates, but it can cause arrhythmias such as prolonged QT syndrome. Multiple opioids should not be used simultaneously and the meds should be consolidated with a narcotic conversion calculator. Total opioid doses over 100 mg of a morphine equivalent is associated with an increased risk of overdose.
     In acute pain, the idea of giving a short acting medication PRN for "breakthrough pain" is common. It has been show that this concept has not improved outcomes and has only increased the risk of misuse and tolerance. Long acting, sustained-release preparations are preferred. 
     Once the therapy has run it course or has been deemed ineffective or unsafe, the medication should be tapered. A slow taper can be done by decreasing the dose by 10% every one to four weeks, and then by 5% for the last 20% of the original dose. Rapid tapering can be done by decreasing the dose by 25% every three to seven days. Therapy should not be continued for fear of withdrawal symptom because they are usually non life-threatening.  WIthdrawal can be tempered with clonidine or tramadol.

A Quick Synopsis of AFP's "Diagnosis and Treatment of Plantar Fasciitis"

A Quick Synopsis of AFP's;
Diagnosis and Treatment of Plantar Fasciitis
JAMES D. GOFF, DO, and ROBERT CRAWFORD, MD, Summa Health System, Akron, Ohio
http://www.aafp.org/afp/2011/0915/p676.pdf
Am Fam Physician. 2011 Sep 15;84(6):676-682

     Plantar fasciitis is an injury, causing sharp pain on the bottom of the heal. It is a sports injury from overuse, running, or prolonged standing. Patients will complain of heel pain after standing up out of bed in the morning, or after prolonged sitting. Walking barefoot may also reproduce the pain. Sharp pain will be observed on the medial aspect of the heel during palpation.  Dorsiflexion of the first toe will also reproduce the pain. Imaging, although unnecessary (unless used to rule out other causes in the differential) will show a heel spur or a thickened plantar fascia. Risk factors include excessive foot pronation, flat feet, obesity, high arch, tight achilles tendon, sedentary lifestyle, and a job the requires prolonged standing or walking. 
     Regardless of treatment, plantar fasciitis should improve within a year. Initial treatment should include rest, activity modification, ice massage  stretching, NSAIDs, acetaminophen  and weight loss. In addition, patients may find relief with heel cups, orthotics, or anterior night splints, all of which can be found over the counter. 
     If the conservative therapy is ineffective, other therapies, such as eccentric stretching, deep myofascial massage, iontophoresis (using electricity to increase absorption of charged topical medicine through the skin), or steroid injections. Extracorporeal shock wave therapy, which is supposed to increase blood flow and healing, has had mixed results. Plantar fasciotomy is a last line therapy which has been effective, but is invasive.  These last two choices are typically reserved for chronic recalcitrant fasciitis, lasting six months or longer.

A "Brief" Synopsis of AFP's "Diagnosis of Urinary Incontinence"

A brief synopsis of; 
Diagnosis of Urinary Incontinence
CHRISTINE KHANDELWAL, DO, and CHRISTINE KISTLER, MD, MASc, University of North Carolina, Chapel Hill, North Carolina
Am Fam Physician. 2013 Apr 15;87(8):543-550.
http://www.aafp.org/afp/2013/0415/p543.pdf

     Urinary incontinence can be a embarrassing situation for patients of all ages. It is not something that comes with age. It is pathologic. The 5 types of urinary incontinence are stress, urge, mixed, overflow, and functional. Stress incontinence is due to sphincter weakness. The patient will lose small amounts of urine during physical activity or with increased intra abdominal pressure. Leakage will coincide with coughing. It is common in obese women and men after prostatectomy.
     Urge incontinence is due to detrusor overactivity due to bladder irritation (from cystitis, prostatitis, atrophic vaginitis, or bladder diverticuli), or loss of neurological bladder control (from dementia, stroke, spinal cord injury, or parkinson disease). Patients will report a sudden and severe desire to urinate and will "not make it to the toilet . Changes in body position or minor sensory stimulation may trigger bladder contraction. They will have a history of variable volume loss, frequency, nocturia, and urgency.
     Mixed incontinence is a mix of stress and urge. Patients report involuntary leakage with exertion, sneezing, coughing or urgency.
     Overflow incontinence is due to impaired detrusor contractility causing overdistention of the bladder. This causes dribbling, hesitancy  and inability to feel when the bladder is full.  This is commonly due to medication side effects or effects from other illnesses (diabetes, MS, BPH, or spinal cord illnesses).
     Functional incontinence will present with variable amounts of leakage caused by cognitive or physical impairment such as dementia, immobility, or mental health disorder
     When diagnosing incontinence, the physician should first rule out reversible (transient) causes  The mnemonic to remember the causes is "DIAPPERS", which stands for
delirium,
infection (UTI),
atrophic vaginitis,
pharmaceuticals ,
psychological disorders such as depression,
excessive urine output,
reduced mobility, and
stool impaction.
     Common pharmaceuticals that may cause this are antihypertensives, pain relievers  antidepressants, antihistamines, and anticholinergics. Once these causes are ruled out, then one of the chronic types of urinary incontinence should be considered. Along with a proper history, a quick questionnaire can be given which ask three questions. It asks if the patient has leaked urine in the last three months and if so, was physical activity, coughing, sneezing, a feeling of urgency, or inability to reach a restroom a contributing factor. It also asks which situations cause the most amount of leakage. A focused physical exam including looking for signs of volume overload, bladder distention, neurological or psychological impairment, will help with the diagnosis. post void residual volume can help determine they type of incontinence  Less than 50 ml is often seen with stress, urge or mixed incontinence. Volumes greater than 200 ml is often seen with overflow incontinence.  Laboratory tests and a "cough stress test (positive in stress incontinence)" may be considered. A voiding diary (of at least three days) documenting frequency of incontinent episodes, leakage, dribbling, fluid intake and nighttime activity is also helpful.
 

A Tachycardic Synopsis of AFP's "Common Types of Supraventricular Tachycardia: Diagnosis and Management "

A brief synopsis of:
Common Types of Supraventricular Tachycardia: Diagnosis and Management 
RANDALLA.COLUCCI, DO, MPH, Ohio University College of Osteopathic Medicine, Athens, Ohio
MITCHELL J. SILVER, DO, McConnell Heart Hospital, Columbus, Ohio
JAY SHUBROOK, DO, Ohio University College of Osteopathic Medicine, Athens, Ohio http://www.aafp.org/afp/2010/1015/p942.html 
Am Fam Physician. 2010 Oct 15;82(8):942-952.


     Besides atrial flutter and fibrillation, there are three common types of SVT. They are AVNRT (AV nodal reentrant tachycardia), AVRT (AV reciprocating tachycardia), and AT (atrial tachycardia). 
     Nodal reentry is the most common type. It is seen in young, healthy women. The reentry occurs inside the AV node itself. The signal takes a slow route down the node (antegrade), and then a fast path back up it (retrograde). A "retrograde P wave" may not be seen on the ECG, but if it is, it will appear as a "pseudo R wave in lead V1".
     AV reciprocating tachycardia occurs shen the impulse passes through the AV node but instead of going to the bundle of his and around the apex of the ventricle, it follows an accessory "short cut"  through part of the heart and back to the AV node. This creates a reentry circuit and a short RP interval, which will vary depending on the specific trail of the shortened path. A delta wave may be seen. The patient may also develop spontaneous atrial fibrillation. 
   AT is caused by a signal being created in a place other than the SA node, commonly "adjacent to the crista terminalis in the right atrium or the crista terminalis in the right atrium". It can also be multifocal. 
     The most common symptoms in SVT are chest discomfort, dyspnea, fatigue, lightheadedness, and palpitations  The palpitations are intermittent. The patient may be told that they have anxiety or panic disorder. Tachycardia may be the only sign in an otherwise normal patient. The history may show symptoms since childhood, onset with coffee, stress, or lack of sleep, or a positive family history. An ECG may show a narrow QRS complex, prolonged QT interval, or delta waves. A wide complex tachycardia may be associated with a bundle branch block. 
     Management can be divided into short and long term, depending on whether the symptoms come and go, or if they are more serious, causing syncope, hemodynamic instability or other dangerous symptoms. Short term management can be performed first by nonpharmacologic treatments such as the valsalva maneuver, vagal maneuvers, or carotid massage (unless the patient may have an atherosclerotic plaque). This will increase vagal tone and decrease heart rate. Pharmacologic treatments include adenosine or verapamil. Adenosine may cause ventricular fibrillation in patients with Wolff-Parkinson-White syndrome.  It is an AV node blocking agent and thus would not work with AT. Verapamil can be used if adenosine does not correct the SVT. It is a negative inotrope,  so it may cause bradycardia and vasodilation. If none of these treatments work, then referral to a cardiologist for treatment with flecainide or propafenone may be necessary. 
     Long term management is considered, depending on frequency, intensity, and quality of life. The options are radiofrequency catherter ablation or intermittent medication. If the patient only experiences episodes a few times a year, they can be given verapamil PRN, known as the "pill-in-a-pocket" method. Ablative therapy has recently been shown to be quite effective with better long term outcomes and cost.