INTRODUCTION

Idiopathic epistaxis is defined as any episode of bleeding from nasal cavity without any detectable cause(1). Although epistaxis and hypertension are frequent in general population, their clear correlation is still controversial(2). Herkner et al (2000) reported that the patients presenting epistaxis were hypertensive(3). On the contrary, according to some group of scientists the history of epistaxis was not associated with hypertension classified according to the World Health Organization(1,4). Blood pressure of the admitted patients was recorded using aneroid sphygmomanometer following conventional methods(5). Aneroid sphygmomanometer was used as it is a simple and safe machine by which blood pressure can be recorded almost accurately(6,7). This study was done to evaluate whether patients or individuals with epistaxis in emergency department were hypertensive or not.


MATERIALS AND METHODS

There were 49 patients (male: 33, female: 16; age group 20-70 years) having no prior clinical history of hypertension admitted in Department of Ear Nose Throat and Head & Neck Surgery ward of Tribhuvan University Teaching Hospital, Kathmandu, Nepal (from July 2005-June 2006). Patients with history of trauma to nose, local pathology, systemic diseases and bleeding disorders and children were excluded from the study. Their blood pressures were recorded by authors in supine position using aneroid sphygmomanometer (Doctor, made in Japan) when they presented themselves in Emergency Department with active nose-bleeding. Blood pressure was again recorded on the day of discharge, (about a week after the hospital admission) using the same aneroid sphygmomanometer following conventional method5. It was recorded at 9:00 AM and 10:00 AM and average was taken. As blood pressure measurement is a part of routine clinical check up, and is a non-invasive procedure, institutional ethics committee and the subject had no objection on our work. Data were analyzed statistically by using students't' test.


RESULTS

It is evident from the table that both males and females presented with active nose-bleeding showed significantly higher blood pressure compared to their casual blood pressure at the time of discharge from the hospital (p- value < 0.05). For males during epistaxis blood pressure recorded was 142.42±19.20 / 91.51±12.27 mmHg and for females the same was 141.87±20.72 / 91.25±16.68 mmHg (Table-1). After managing epistaxis, the blood pressures of males and females were noted as 119.39±12.23 / 75.15±7.55 mmHg and 118.75±12.04 / 76.2 5±13.10 mmHg respectively (Table 1).

DISCUSSION

Epistaxis is common Otorhinolaryngologic emergency. The bleeding may occur from one or many bleeding points particularly Little's area or posteriorly(8). The blood pressure of both male and female patients during active nose bleeding was noted about 142/91 mmHg. Our results corroborates the previous findings of Herkner et al, that patients with active epistaxis had higher blood pressure at presentation compared with controls2. The results of this study clearly indicated that the patients with active epistaxis had higher blood pressure presentation at emergency department in comparison with their causal blood pressure noted after treatment.

Epistaxis is usually of sudden onset(8). The victim feels bewildered and suffers from anxiety. Anxiety is associated with sympathetic stimulation and secretion of catecholamine which may increase the rate and force of contraction of cardiac muscle causing an increase in cardiac output(9) -- leading to an increase in systolic blood pressure in both male and female counterparts. Sympathetic stimulation leads to vasoconstriction of superficial vascular bed(10). Epinephrine and norepinephrine secreted from the adrenal medulla due to sympathetic stimulation, directly act on blood vessels usually to cause vasoconstriction(9) leading to an increase in peripheral resistance and thereby causing the elevation of diastolic pressure. Existing literature indicates that norepinephrine secretion tends to be selectively increased by emotional stress with which the individual is familiar whereas epinephrine secretion increases in situation in which the individual does not know what to expect(11). The smooth muscles of blood vessels that supply skeletal muscles has both b2 and a receptors; activation of b2 receptors causes vasodilatation and stimulation of a receptors constricts these vessels. Nevertheless, when both types of receptors are activated at higher concentration of epinephrine the response to a-receptors predominates(12). In the present study emotional stress during active epistaxis might cause profuse secretion of epinephrine from adrenal medulla which in turn increased both the systolic and diastolic pressure(12). Despite the fact that during active nose-bleeding patients showed hypertension (BP > 140/90 mmHg); after treatment i.e., at the time of discharge from the hospital, they were found normotensive without any antihypertensive therapy. Although few patients with chronic hypertension may present with non traumatic nose bleeding, results of the present study clearly indicates that epistaxis is not frequently associated with hypertension.


ACKNOWLEDGEMENTS

Authors are thankful to the faculties of Department of Ear Nose Throat and Head & Neck Surgery Tribhuvan University Teaching Hospital for their inspiration, Prof. Paresh Roychowdhary, Head, and Dept. Of Clinical Physiology, and Mr. Arijit Ghosh, Assistant Prof, Dept. Of Clinical Physiology, Nepal Medical College for their active co-operation and help.


REFERENCES

1. Fuchs FD, Moreira LB, Pires CP, Torres FS, Furtado MV, Moraes RS, et al. Absence of association between hypertension and epistaxis: a population - based study. Blood press 2003; 12:145-8.

2. Herkner H, Havel C, Mullner M, Gamper G, Bur A, Temmel AF, et al. Active epistaxis at ED presentation is associated with arterial hypertension. Am J Emerg Med 2002; 20:92-5.

3. Herkner H, Laggner AN, Mullner M, Formanek M, Bur A, Temmel AF, et al. Hypertension in patients presenting with epistaxis. Ann Emerg Med 2000; 35:126-30.

4. Lubianca Neto JF, Fuchs FD, Facco SR, Gus M, Fasolo L, Mafessoni R, et al. Is epistaxis evidence of end-organ damage in patients with hypertension? Laryngoscope 1999; 109:1111-5.

5. Mc Murray J, Northridge D, Bradbury A. The cardio vascular system. In: Muro JF, Campbell IW (editors): Macleod's clinical examination (10th Ed) Edinburgh: Churchill Livingstone, 2000:86.

6. Canzanello VJ, Gensen PL, Schwartz GL. Are aneroid sphygmomanometers accurate in hospitals and clinical settings? Arch Int Med. 2001; 161: 729-31.

7. Gill G, Ala L, Gurgel R, Cuevas L. Accuracy of anaroid sphygmomanometer blood pressure recording compared with digital and mercury measurements in Brazil. Trop Doct 2004; 34:26-27.

8. Pracy R, Siegler J, Stell PM. A short textbook ear nose throat (2nd Ed) Kent: ELBS/Hodder and Stoughton, 1986.

9. Guyton AC, Hall JE. Editors. Text book of Medical Physiology (10th Ed) Pennsylvania:WB Saunders Company, 2000.

10. Landsberg L, Young JB. Physiology and pharmacology of the autonomic nervous system. In Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, editors. Harrison's Principles of Internal Medicine (15th Ed.) New York: Mc Graw - Hill, 2001:438-50.

11. Ganong WF, editor. Review of Medical Physiology (22nd ed) USA: Appleton and Lange, 2005.

12. Westfall TC, Westfall DP. Adrenargic agonists and antagonists. In Brunton LL, Lazo JS, Parker KL, editors. Goodman and Gilman's the pharmacological basis of therapeutics (11th Ed). New York: Mc Graw Hill, 2006:242.









1. Dr. (M.S. Resident in Otorhinolaryngology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal)
2. Dr. (Associate Professor,Department of Clinical Physiology, Nepal Medical College, Jorpati, Kathmandu, Nepal.)
3. Dr. (M.S.Resident in Otorhinolaryngology,Tribhuvan University Teaching Hospital, Kathmandu, Nepal.)

Correspondence to: Dr. Prakash Adhikari, M.B.B.S.,M.S. First year Resident, Department of Ear, Nose, Throat & Head and Neck Surgery, Tribhuvan University Teaching Hospital, Kathmandu Nepal. Tel 00977-1-4414191 Fax 00977-1-4414191 P.O.Box 4972 Email: prakash_ooz@hotmail.com
No financial support was avaliable.

This article was submitted to SGP (System of Publication Management) of R@IO on February 25, 2006 and approved on April 17, 2007 at 09:28:42.