A 62-year-old woman presents with epistaxis from the right nostril. Thenosebleed has lasted about 90 minutes, and she has become alarmedby the amount of blood on the tissues and washcloth she has applied to hernose.
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A 62-year-old woman presents with epistaxis from the right nostril. The nosebleed has lasted about 90 minutes, and she has become alarmed by the amount of blood on the tissues and washcloth she has applied to her nose. She denies headache, sinusitis, facial pain, diplopia, and chronic rhinorrhea.
She has had a mild upper respiratory tract infection (URTI), from which she is recovering, but otherwise she was previously in good health. At her annual physical examination 2 weeks earlier, new, mild hypertension (142/90 mm Hg) was diagnosed; lisinopril and low-dose aspirin (ASA) were prescribed. Since she did not have “baby” ASA at home, she has been using standard adult tablets instead.
She has had 3 children by vaginal delivery, extractions of permanent teeth, and a cholecystectomy-all without abnormal bleeding. She has no symptoms of heart failure.
Heart rate is 90 beats per minute and blood pressure, 150/96 mm Hg. Examination of the head, eyes, ears, nose, and throat reveals no sign of any cranial neuropathy. There are bruises on the dorsum of the patient’s right hand and on her left shin, but all other physical findings are normal.
LABORATORY RESULTS ON ADMISSION
Hemoglobin level is 13 g/dL; white blood cell count and platelet count are normal. A chemistry panel and ECG are normal as well. Prothrombin time (PT) and partial thromboplastin time (PTT) are normal; a template bleeding time is 6.5 minutes (normal, 2 to 7 minutes).
Which of the following is most likely responsible for this patient’s epistaxis? A. A previously undiagnosed congenital coagulopathy, such as von Willebrand disease.
B. Aspirin use.
C. Poorly controlled hypertension.
D. Symptomatic onset of hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber syndrome).
E. Presence of a nasopharyngeal neoplasm.
CORRECT ANSWER: B
Epistaxis is one of the most common nontraumatic bleeding events encountered in clinical medicine. As many as 60% of persons experience epistaxis in their lifetime, and about 6% of them present for medical evaluation.1 Peak ages are younger than 10 years and older than 40 years.1
Factors that contribute to epistaxis in otherwise healthy persons. These include nose picking (in children); certain environmental conditions (eg, dry heat in winter); viral URTIs with frequent nose blowing and sneezing; and use of topical nasal sprays/medications.
Systemic conditions that can cause epistaxis. Several more serious systemic conditions have also been suspected to cause epistaxis. Hypertension (choice C) has long been thought to be a major epidemiological factor in epistaxis. However, more current data indicate that any causal association is weak at most.2,3 A prospective study showed that in hypertensive patients, epistaxis incidence was not related to hypertension severity,1 and a population-based study showed no association at all.3 Although earlier studies documented hypertension in many patients with epistaxis, the blood pressure elevations may have been the result of stress and anxiety produced by the episode rather than the cause of it.
Coagulopathies. There is stronger evidence of a causal role for coagulopathy in epistaxis. A recent retrospective study reported that 45% of patients admitted for epistaxis (a subgroup with more severe epistaxis) had systemic disorders with associated coagulopathy.4 These conditions included ingestion of anticoagulants or antiplatelet agents, significant hepatic or renal disease, and previously undiagnosed coagulation disorders.
It is unlikely that this patient has an undiagnosed coagulation disorder, such as von Willebrand disease (choice A). She is 62 and has no previous bleeding history, even in the setting of such hemostatic challenges as childbirth, major surgery, and extraction of permanent teeth. Moreover, her PT and PTT are normal.
However, she has just started ASA therapy. A recent large study evaluating ASA for cardiovascular prophylaxis showed a slight but definite increased risk of epistaxis in patients receiving ASA compared with matched patients not receiving ASA (19.1% vs 16.7%).5 Moreover, this patient has not been using the recommended 81-mg daily dose but a higher dose (325 mg), which has been shown not to enhance cardiovascular prophylaxis but to increase the risk of bleeding.6 Her bleeding time is at the upper limit of normal, and she has several bruises. Thus, her ASA use (choice B)-particularly in the setting of a URTI-is most likely responsible for this episode of epistaxis.
Local pathologies. Several types of local pathology can also present as epistaxis. Hereditary hemorrhagic telangiectasia (choice D) is an autosomal dominant genetic defect of blood vessels that renders the mucosal capillaries fragile and prone to hemorrhage. Mucosal bleeding, especially epistaxis and GI bleeding, is the main manifestation; bleeding episodes typically recur lifelong, resulting in anemia and severe iron deficiency. The capillary telangiectasia can be visualized on endoscopy. Onset is in the second and third decades of life.
Outcome of this case. Physical examination, including nasal endoscopy, revealed no significant local pathology. Topical vasoconstrictors and moisturizing ointments were applied, and the bleeding ceased. Packing was not required. ASA was discontinued for a week, then restarted at a dosage of 81 mg/d. After 4 months, epistaxis has not recurred.
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