Letters to the Editor
Measuring Severity of Tinnitus with a Visual Analog Scale
to the editor: We read with interest the article,1 "Diagnostic Approach to Tinnitus," by Drs. Crummer and Hassan in the January 1, 2004, issue of American Family Physician. It carefully and clearly presented the problem of tinnitus and can be a valuable source of information for family physicians and their patients. The authors1 proposed their algorithm for a diagnostic approach to patients with tinnitus. We would like to present our experience in treating patients with this condition.
In the department of Otolaryngology at the Medical University in Gdansk, Poland, as in most centers that manage patients with tinnitus, one of the most important elements of diagnostics is history data.2 Patients classify in a graphic way the pitch and loudness of tinnitus using a visual analog scale (see accompanying figure). Our patients receive questionnaires that assess how troublesome their tinnitus is and its influence on their daily activity and ability to function. We compare results of the visual analog scale and the questionnaires before and after treatment, which helps to objectively assess the therapy results.3
 FIGURE. Visual analog scale of tinnitus. |
Perhaps the algorithm presented in the article1 will result in the addition of some new elements of objective diagnostics of tinnitus, such as positron emission tomography (PET) or single photon emission computed tomography.4-6 One study4 using PET in 10 patients with tinnitus found increased metabolic activity of the predominant auditory cortex. Although the patients complained of bilateral tinnitus, the brain metabolic activity was higher on the left side.4 Another study6 investigated four patients with continuous unilateral tinnitus, which could be altered by clenching their jaws. Using PET, the results showed that when the tinnitus was increased in this way the brain metabolic activity was increased on the opposite side.6 The study6 also found that the hippocampus was activated in these patients but not in the control subjects. Hippocampus activation could offer an explanation for the adverse psychologic effects that patients with tinnitus often experience. The new methods enable physicians to visualize what previously only had been heard and felt.
WALDEMAR NAROZNY, M.D., PH.D.
JERZY KUCZKOWSKI, M.D., PH.D.
BOGUSLAW MIKASZEWSKI, M.D., PH.D.
REFERENCES
1. Crummer RW, Hassan GA. Diagnostic approach to tinnitus. Am Fam Physician 2004; 69:120-6.
2. Tyler RS, Babin RW. Tinnitus. In: Cummings CW, ed. Otolaryngology - Head and Neck Surgery. 2d ed. St. Louis: Mosby, 1993:3031-53.
3. Narozny W, Sicko Z, Kuczkowski J, Stankiewicz C, Przewozny T. Usefulness of hyperbaric oxygen therapy in patients with sensorineural acute and chronic tinnitus. International Congress Series 2003;1240:277-86.
4. Arnold W, Bartenstein P, Oestreicher E, Romer W, Schwaiger M. Focal metabolic activation in the predominant left auditory cortex in patients suffering from tinnitus: a PET study with [18F]deoxyglucose. ORL J Otorhinolaryngol Relat Spec 1996;58:195-9.
5. Johnsrude IS, Giraud AL, Frackowiak RS. Functional imaging of the auditory system: the use of positron emission tomography. Audiol Neurootol 2002;7:251-76.
6. Lockwood AH, Salvi RJ, Coad ML, Towsley ML, Wack DS, Murphy BW. The functional neuroanatomy of tinnitus: evidence for limbic system links and neural plasticity. Neurology 1998;50:114-20.
in reply: Tinnitus is a common symptom that can affect a patient's quality of life. There are many measures to estimate the impact of tinnitus. The visual analogue scale is a reliable method, commonly used in studies to assess the results of therapy, including that of hyperbaric oxygen therapy.1 Positron emission tomography (PET) is a nuclear medicine imaging study, used primarily for oncologic staging, which for a number of years also has been used to investigate tinnitus, along with other objective methods including auditory brainstem responses and auditory evoked magnetic field.2 Our article3 was written from a primary care point of view. Sophisticated imaging such as PET and single photon emission computed tomography were not included in the algorithm in our article3 because their relevance in the diagnosis and treatment of tinnitus in the primary care setting is still undefined.
REFERENCES
1. Narozny W, Sicko Z, Kuczkowski J, Stankiewicz C, Przewozny T. Usefulness of hyperbaric oxygen therapy in patients with sensorineural acute and chronic tinnitus. International Congress Series 2003;1240:277-86.
2. Holgers KM, Barrenas ML, Svedlund J, Zoger S. Clinical evaluation of tinnitus: a review. Audiological Medicine 2003;2:101-6.
3. Crummer RW, Hassan GA. Diagnostic approach to tinnitus. Am Fam Physician 2004;69:120-6.
Management of Traumatic Subungual Hematoma
to the editor: I would like to describe the procedure for traumatic subungual hematoma (see accompanying figure), which I have performed in my office. Management is as follows:
 FIGURE. Chromatic nail hematoma release procedure. |
(1) Clean wound with alcohol.
(2) Lightly twist the point of an 18- or 21-gauge needle back and forth between index finger and thumb after positioning over the hematoma.
(3) After about one minute, you will note a small amount of blood at the tip of the needle.
(4) Clean the dust and blood from the nail with alcohol and proceed while positioning a heparinized hematocrit tube adjacent to the needlepoint.
(5) Blood will be extracted by capillary action into the tube.
(6) Change tubes, pressure, and angle of the needle to extract as much blood as possible.
This procedure is relatively painless for your patients.
Case Report: Late-Onset Eclampsia Presents as Bilateral Cortical Blindness
to the editor: Although preeclampsia is typically diagnosed in the prenatal period, we would like to describe an unusual case of late-onset eclampsia presenting postpartum as sudden bilateral cortical blindness.
The patient was a healthy, 21-year-old black woman, gravida three, para one, with a previous normal pregnancy and no history of hypertension or preeclampsia. She had an unremarkable prenatal course and her blood pressure prenatally ranged from 98/62 mm Hg to 130/80 mm Hg one week before delivery. Urine protein was zero or trace at all visits. She delivered a healthy 2,670 g (5 lb, 8 oz) male infant at term. Blood pressures immediately postpartum were mostly 120s to 130s/60s to 70s mm Hg with occasional pressures of 140 to 150/80 to 90 mm Hg.
Eight days after delivery, the patient awoke with a severe bilateral frontal headache and blurry vision. Over several hours, this progressed to acute bilateral cortical blindness. Initial evaluation showed blood pressure of 169/99 but without proteinuria. Subsequent 24-hour urine collection showed 0.28 grams protein. Computed axial tomography of the brain demonstrated bilateral low attenuation lesions in the cerebral hemispheres; magnetic resonance imaging revealed diffuse altered T2 signals in a posterior distribution. Cerebral angiogram was normal. Twenty hours after the onset of symptoms the patient developed altered mental status and had two tonic-clonic seizures, at which point she was treated with phenytoin (Dilantin) and magnesium.
The patient's headache and vision quickly improved and by 48 hours her vision had returned to 20/20 acuity. Her blood pressure continued to be elevated throughout her hospital stay, at one point reaching 200/110 mm Hg. Three days after admission, she was discharged home on metoprolol.
Preeclampsia in pregnancy is defined as new-onset elevated blood pressure (>140/90 mm Hg) along with proteinuria after 20 weeks of gestation.1,2 Severe cases may progress to eclampsia characterized by seizures. A multicenter review3 of preeclampsia found up to one third of cases developed postpartum with 80 percent of these occurring three to 14 days after delivery. One case report4 describes onset 26 days after delivery.
Although visual changes such as blurry vision or scotoma are common, they may be more typical of late-onset disease.3,5 One study reported visual symptoms in 44 percent of patients with late-onset preeclampsia.3 Acute cortical blindness has been estimated to occur in 1 to 3 percent of patients with eclampsia, although a review of 15 cases noted a prevalence of 15 percent.5 Our patient was similar to patients in that case series including the transient nature of visual loss (four hours to eight days in their review) and mental status changes (three of their 15 patients) but had minimal urine protein and relatively mild hypertension on initial presentation.
Because 90 percent of women presenting with late postpartum preeclampsia have a headache and close to one half have some type of visual disturbance, physicians providing obstetric care should be alert for these symptoms as an unusual presentation of this disease. This case demonstrates that preeclampsia is less common in multiparous patients, but it can be severe when it develops.
REFERENCES
1. ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. No. 33, January 2002. American College of Obstetricians and Gynecologists. Obstet Gynecol 2002;99:159-67.
2. Lipstein H, Lee CC, Crupi RS. A current concept of eclampsia. Am J Emerg Med 2003;21:223-6.
3. Chames MC, Livingston JC, Ivester TS, Barton JR, Sibai BM. Late postpartum eclampsia: a preventable disease? Am J Obstet Gynecol 2002;186:1174-7.
4. Delefosse D, Samain E, Helias A, Regimbeau JM, Deval B, Farah E, et al. Late onset of cortical blindness in a patient with severe preeclampsia related to retained placental fragments. Anesthesiology 2003;98:261-3.
5. Cunningham FG, Fernandez CO, Hernandez C. Blindness associated with preeclampsia and eclampsia. Am J Obstet Gynecol 1995;172:1291-8.
Treatment of Patients with Obstructive Sleep Apnea
to the editor: The article1 on the diagnosis and treatment of obstructive sleep apnea (OSA) provided an excellent overview. However, I would like to add a few additional considerations.
As Dr. Victor suggested,1 family physicians should be able to identify the symptoms of OSA and initiate appropriate treatment. Although the article1 briefly discussed the risk of mortality associated with OSA, it did not mention some of the other serious problems associated with OSA (such as hypertension, coronary artery disease, myocardial infarction, stroke, psychiatric problems, impotence, cognitive dysfunction, memory loss, and death)2,3 that should be considered when discussing the disorder.
Another significant issue concerns the short-term dangers associated with OSA-related symptoms, particularly the risks of engaging in certain activities while impaired by excessive sleepiness. Excessive sleepiness is the primary symptom, and often the most debilitating feature, associated with OSA.3,4 It is reported by approximately 90 percent of patients with OSA and may be incapacitating, resulting in job loss, accidents, self injury, marital and family problems, and poor school or work performance. If the urge to fall asleep during waking hours is uncontrollable and occurs at inappropriate times, it can have the same consequences as inability to sleep at night. Retrospective studies5 show that the rate of traffic accidents among persons with sleep apnea is three to four times the rate among persons without sleep apnea.5 In addition, 50 percent of accidents at work and 25 percent of accidents at home are caused by excessive sleepiness. The individual and societal implications of excessive sleepiness should not be overlooked, and special consideration should be given to managing this symptom as well as the underlying disease disorder.
The author noted that continuous positive airway pressure (CPAP) therapy can reduce problems of excessive sleepiness in patients with OSA. However, despite the use of nasal CPAP, many patients continue to experience residual excessive sleepiness.6 Residual excessive sleepiness may persist in patients with OSA who have insufficient sleep syndrome of a coexisting sleep disorder. In some patients, the underlying sleep-generating mechanisms may be permanently altered as a result of many years of sleep disturbance. These patients may require other therapies such as surgery, additional devices, or medications.
In January 2004, the U.S. Food and Drug Administration approved modafinil (Provigil) as the first and only drug to be used as an adjunct treatment to CPAP to improve wakefulness in patients with residual excessive sleepiness associated with OSA. Clinical studies have shown that patients with OSA who receive treatment with modafinil and CPAP may have significant improvements in daytime wakefulness, sleep-related functional status, overall clinical condition, and quality of life.6 Modafinil is well tolerated and has been used safely for the treatment of excessive sleepiness associated with narcolepsy since 1998. While CPAP remains integral to the nighttime treatment of OSA, the management of the coexisting morbidities and daytime symptoms associated with this disorder must be prioritized as well.
REFERENCES
1. Victor LD. Treatment of obstructive sleep apnea in primary care. Am Fam Physician 2004;69:561-8.
2. Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003;290:1906-14.
3. Guilleminault C, Brooks SN. Excessive daytime sleepiness: a challenge for the practising neurologist. Brain 2001;124:1482-91.
4. Al-Barrak M, Shepertycky MR, Kryger MH. Morbidity and mortality in obstructive sleep apnea syndrome 2: Effect of treatment of neuropsychiatric morbidity and quality of life. Sleep and Biological Rhythms 2003:1:65-74.
5. Suratt PM, Findley LJ. Driving with sleep apnea. N Engl J Med 1999;340:881-3.
6. Schwartz JR, Hirshkowitz M, Erman MK, Schmidt-Nowara W. Modafinil as adjunct therapy for daytime sleepiness in obstructive sleep apnea: a 12-week, open-label study. Chest 2003;124:2192-9.
Send letters to Jay Siwek, M.D., Editor,
American Family Physician, 11400 Tomahawk
Creek Pkwy., Leawood, KS 66211-2672; fax: 913-906-6080;
e-mail:
afplet@aafp.org.
Please include your complete address, telephone number, fax number, and e-mail address. Letters should be submitted on disk, double-spaced, fewer than 500 words, and limited to one table or figure and six references. Please submit a word count.
Letters submitted for publication in AFP must not be submitted to any other publication. Possible conflicts of interest must be disclosed at time of submission. Submission of a letter will be construed as granting the AAFP permission to publish the letter in any of its publications in any form. The editors may edit letters to meet style and space requirements.
| Copyright © 2005 by the American
Academy of Family Physicians. |
