Family Practice International

CLINICAL INFORMATION FROM THE INTERNATIONAL FAMILY MEDICINE LITERATURE



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Am Fam Physician. 2000 Mar 1;61(5):1517-1518.

Best's Disease

(Canada—Canadian Family Physician, November 1999, p. 2607.) Best's disease, or vitelliform macular degeneration, is an autosomal dominant disease of the macula. This disorder usually presents in childhood or adolescence as visual distortion or central loss of vision. The characteristic retinal changes may also be found incidentally in affected persons. The retinal dystrophy of Best's disease is described as occurring in four stages: stage 1—retinal pigment epithelial changes, stage 2—vitelliform cysts (or “scrambled egg” appearance), stage 3—pseudohypopyon (leveling out of the vitelliform material) and stage 4—atrophic changes. In advanced stages, the atrophy with attempted revascularization can result in greatly diminished visual acuity.

Presenting Symptoms of MS

(Australia—Australian Family Physician, September 1999, p. 903.) Multiple sclerosis (MS) is a common chronic neurologic disease that can present with almost any neurologic symptom. Approximately 40 percent of patients initially experience limb weakness. The weakness may involve one or more limbs, be symmetrical or asymmetrical, and present suddenly or evolve over time. Accompanying sensory and sphincteric symptoms are also common. A variety of signs may be found on neurologic examination, depending on the site and severity of the lesion or lesions. About one fourth of cases of MS present as optic neuritis, usually with decreasing visual acuity and pain that increases with eye movement. Significantly, 46 percent of patients with optic neuritis develop neurologic symptoms over 13 years of follow-up. Diplopia is also a common presentation of MS, occurring in approximately 12 percent of new patients. Although less common, internuclear ophthalmoplegia is strongly suggestive of MS. Disturbances of sensation, particularly parasthesiae, are reported to be the initial symptoms in 21 percent of patients with MS. One form of sensory disturbance is the “useless hand” syndrome resulting from loss of position sense in one or both hands. Although not pathognomonic for MS, Lhermitte's sign (an electric-like sensation in the back of the legs on flexing the neck) is highly suggestive of the diagnosis.

‘Temper Tantrum’ Elbow

(Great Britain—Journal of the Royal Society of Medicine, September 1999, p. 462.) A child's elbow can be easily injured by forcible traction to the pronated wrist or hand while the elbow is extended. The resulting “pulled elbow” is characterized by slippage of the radial head through the annular ligament, accompanied by a varying degree of stretching or damage to the annular ligament. The common names for the condition are descriptive of the mechanisms of damage (e.g., baby-sitter's elbow, supermarket elbow, temper tantrum elbow, etc.). A history is often given of the child pulling away while being firmly held by the hand, or of the child being swung or lifted by the arms. The child may be unable or unwilling to give a history of trauma. On examination, the arm is held limply with the elbow extended and wrist pronated, and the child resists attempted supination of the arm. Pain is usually reported in the forearm, wrist and elbow, but there is little swelling or deformity. Radiographs show distal shift of the radius and are useful to exclude fracture or bone injury. Because the elbow has to be supinated to take the anteroposterior view, many children report relief of symptoms after the radiograph is taken. In uncomplicated cases, the subluxation can be reduced by forced supination combined with downward pressure on the radial head. A click may be heard or felt as the trapped annular ligament is released. Use of a sling for a few days may assist recovery and protect the elbow from further immediate injury.

Tinea Incognito

(Australia—Australian Family Physician, October 1999, p. 1021.) Tinea incognito is caused by the application of topical steroid preparations to tinea lesions. The lesions may have been present for several weeks; sometimes the condition initially improves with topical steroids but then becomes worse. Patients may have used prescribed topical steroids or obtained medications from friends or family members. Over time, the skin lesions enlarge and may become dusky, raised, scaly or pustular in appearance. Tinea infection may be present at other body sites. Skin scrapings, especially from the edges of tinea incognito lesions, show dermatophytes, often in large numbers. Successful clearing of tinea incognito requires systemic and topical antifungal therapy.

Treatments in Unstable Angina

(Great Britain—The Practitioner, October 1999, p. 706.) Disruption of an atheromatous plaque in a coronary artery provokes a series of responses leading to the formation of a platelet-rich thrombus. While small thrombi may lyse spontaneously or become incorporated into a plaque, larger thrombi tend to cause clinical symptoms, including unstable angina. Despite optimal medical management, approximately 10 percent of patients with unstable angina die or suffer myocardial infarction within six months of onset. Currently, the nonspecific inflammatory marker C-reactive protein may be the only available laboratory indicator of increased risk of cardiac events. More sensitive markers of myocardial damage based on myocardial structural proteins (troponins) are being developed to identify the subgroup of patients with unstable angina who are at greatest risk of cardiac events. Several new treatments are being developed to ameliorate unstable angina and reduce the potential progression to cardiac death or myocardial infarction. Statin drugs, initially developed to lower serum cholesterol levels, are now believed to help prevent unstable angina by stabilizing plaques. Because Chlamydia pneumoniae may be involved in plaque formation or disruption, antibiotic therapy is being assessed. Finally, a number of new antithrombotic drugs are in development to provide more effective treatment than traditional aspirin or heparin therapies.

Establishing the Cause of Vertigo

(Australia—Australian Family Physician, September 1999, p. 883.) A careful history is essential to distinguish true vertigo from symptoms such as dizziness. Vertigo, described as a sensation of spinning, usually results from disturbances of the semicircular canals. When patients complain of disturbances of linear motion, such as sudden falling or tilting, the cause is likely to involve the otolith organs. The length of attacks may provide diagnostic clues. Benign positional vertigo or vestibular peripheral lesions usually cause attacks of vertigo lasting a few seconds. Migraine and vertebrobasilar ischemia may result in vertigo lasting several minutes. Attacks lasting hours occur in Ménière's disease, vestibular neuronitis and labyrinthitis. Neurologic examination of patients with vertigo should include assessment of balance, gait, eye movements and hearing. Specific provocation tests for nystagmus resulting from positional change are particularly useful to diagnose benign positional vertigo. Specialized investigations—computed tomographic brain scanning, audiometry, brain stem auditory evoked potentials and vestibular investigations—should target the most likely cause of vertigo. Potentially serious neurologic disease should be suspected in patients with focal neurologic signs, severe ataxia, nystagmus changing direction, vertical nystagmus and abnormal eye movement.


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