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Year: 2008  Vol. 12   Num. 3  - July/Sept Print:
Original Article
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Vasovagal Attack During Anterior Nasal Packing in Patients with Epistaxis
Ataque Vasovagal durante o Tamponamento Nasal Anterior em Pacientes com Epistaxe
Author(s):
Prakash Adhikari1, Tapas Pramanik2, Paresh Roychowdhary3
Key words:
vasovagal attack, blood pressure, heart rate, anterior nasal packing, epistaxis
Abstract:

Introduction: The incident of fainting during nasal packing to manage epistaxis is not so uncommon. Objective: To observe the effect of anterior nasal packing on blood pressure and heart rate, during the management of epistaxis. Method: Nepalese male patients (n=40; age more than 13 years) attended in Tribhuvan University Teaching Hospital, Kathmandu presenting with active nose bleeding in the Department ENT and Head and Neck Surgery were taken for the study in the time period between July 2005-June 2008. This prospective comparative study was analysed using Z test. Results: The blood pressure and heart rate in patients presented with epistaxis show significantly lower during anterior nasal packing (10414.08/679.35 mmHg, 673.81/min) compared with same patients before packing (13020.3/8314.89 mm Hg, 7334.82/min). Conclusion: Nasal packing during the management of epistaxis shows bradycardia and hypotension and sometimes vasovagal syncope which are mostly due to reflex action through stimulation of vagus nerve and stimulation sympatho-vasodilator fibres of the skeletal muscle.

INTRODUCTION

Epistaxis is one of the most common otorhinolaryngologic emergencies having sudden onset (1-4). Idiopathic epistaxis is defined as any episode of bleeding from nasal cavity without any detectable cause (5). The bleeding may occur from one or many bleeding points particularly Little's area or posteriorly (6). During management of this emergency by introducing nasal packing, it has been noted that some of the patients fainted and exhibited the symptoms of neurogenic shock. Neurogenic shock is a kind of distributive shock in which a sudden burst of autonomic activity produce vasodilatation, pulling of blood in the extremities and fainting. These are called vaso-vagal attacks, and they are short-lived and benign (7). These incidents led us to explore the effect of nasal packing (during the management of epistaxis) on blood pressure and heart rate.


METHOD

Nepalese male patients (n=40; age more than 13 years) attended in Tribhuvan University Teaching Hospital, Kathmandu presenting with active nose bleeding in the Department ENT and Head and Neck Surgery were taken for the study in the time period between July 2005-June 2008. This is a prospective comparative study. Blood pressure of each patient was recorded using aneroid sphygmomanometer as this is a simple and safe method by which blood pressure can be recorded almost accurately. Systolic pressure was determined at the point when the Korotkoff sound became audible and diastolic pressure was measured at the point at which the sound disappeared. Blood pressure was measured during epistaxis and also during anterior nasal packing using the same instrument (aneroid sphygmomanometer-Doctor, made in Japan), in supine position by the first author. Anterior nasal packing was done in all cases using bismuth iodoform paraffin paste. Children, patients with previous history of hypertension, coagulation disorders are excluded from the study. As blood pressure measurement is a part of routine clinical evaluation, and is a non- invasive procedure, local ethical committee approved to do this study easily (ref:328/08) and informed consent were taken from patients. Data were analyzed statistically using Z test.


RESULTS

It is evident from the Table 1 that the patients presented with epistaxis showed significantly lower blood pressure and heart rate at anterior nasal packing compare before anterior nasal packing. The blood pressure and heart rate recorded before anterior nasal packing were 13020.3/8314.89 mm Hg, and 7334.82/min while at the time of anterior nasal packing were 10414.08/679.35 mmHg, 673.81/min respectively.




DISCUSSION

Epistaxis is a common condition and number one emergency as well as frequent with up to 60% of people experiencing one episode in their life time and 6% seeking medical attention (8). The incidence of epistaxis was 60.4/1000 ENT admitted patients per annum in a study done at TU Teaching Hospital (9). Most cases of epistaxis do not have an easily identifiable cause. Both local and systemic processes can play a role in it (10). Epistaxis are managed by cautery (chemical or electric), anterior nasal packing, posterior nasal packing, arterial ligation or by embolization technique. Anterior nasal packing is the most common procedure in epistaxis.

Many patients experienced fainting attack (vaso-vagal attack) at the time of anterior nasal packing. It has been established that strong emotion may cause hypotension. Somehow, the higher brain centers involved with emotions enhance parasympathetic activity to the heart, resulting in markedly decreased arterial pressure and brain blood flow (transient vasovagal syncope). It also stimulates sympathetic vasodilator nerves to the skeletal muscle. The pathway is probably from: Cortex Hypothalamus Midbrain Pons Medulla Lateral horn cells of sympathetic system of spinal cord Sympathetic vasodilator nerves to the vessels of skeletal muscle (7).

Dripping blood from the nose may cause hypotension following strong emotion and not by the blood loss sometimes, since loosing a little amount of blood will not by itself causes serious hypotension in an individual (11). Rather, it resembles emotional fainting, that begins with intense psychic disturbances in the cerebral cortex (12).

Previous clinical reports indicated that packing in the treatment of epistaxis induce nasopulmonary reflex - changes in pulmonary function to cause hypoxia leading to arterial hypoxemia (13, 14). Nevertheless, studies established that pneumatic nasal pack with central airway that allowed a limited airflow did not cause any clinically important alveolar hypoventilation or changes in arterial oxygenation (15, 16). That posterior nasal pack did not alter oxygenation was also reported (16). Report supported that nasopulmonary reflex as previously described in term of primary drop in O2 is clinically irrelevant (17). Although according to the reports no noticeable hypoxemia due to nasal packing takes place, irritation of the nasal /laryngeal mucous membrane due to nasal pack causes reflex apnea by switching off inspiratory centre which causes bradycardia through chemoreceptor sinu-aortic mechanism (18). That might be the cause of bradycardia and hypotension in all patients during nasal packing. In some cases where bradycardia and hypotension were extreme, patients exhibited vaso-vagal attacks. Our study showed that there is significantly lower blood pressure (both systolic and diastolic) and heart rate during anterior nasal packing compared with previous blood pressure and heart rate (before anterior nasal packing).


CONCLUSION

Nasal packing during the management of epistaxis shows bradycardia and hypotension and sometimes vasovagal syncope which are mostly due to reflex action through stimulation of vagus nerve and stimulation sympatho-vasodilator fibres of the skeletal muscle.


BIBLIOGRAPHICAL REFERENCES

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13. Slocum CW, Maisel RH, Cantrell RW. Arterial blood gas determination in patients which anterior packing. Laryngoscope. 1976, 86:869-73.

14. Cavo JW, Kawamoto S, Berlin BP, Zollinger W, Ogura JH. Arterial blood gas changes following nasal packing in dogs. Laryngoscope. 1975, 85:2955-68.

15. Larsen K, Juul A. Arterial blood gases and pneumatic nasal packing in epistaxis. Laryngoscope. 1982, 92:586-8.

16. Jacobs JR, Levine LA, Davis H, Lefrak SS, Druck NS, Ogura JH. Posterior packs and the nasopulmonary reflex Laryngoscope. 1981, 91:279-84.

17. Loftus BC, Blitzer A, Cozine K. Epistaxis, medical history, and the nasopulmonary reflex: what is clinically relevant? Otolaryngol Head Neck Surg. 1994, 110:363-9.

18. Keel CA, Neil E, Joels N. Neural control of heart rate. ln: Samson Wright's applied physiology, 13th ed. Oxford UK; Oxford University Press; 1996, 131.









1. Doctor. MS Resident, Department of ENT and Head and Neck Surgery, TU Teaching Hospital, Kathmandu, Nepal.
2. Doctor. Associate Professor, Department of Clinical Physiology, Nepal Medical College, Jorpati, Kathmandu, Nepal.
3. Professor and Head, Department of Clinical Physiology, Nepal Medical College, Jorpati, Kathmandu, Nepal.

Institution: Department of ENT and Head and Neck Surgery, TU Teaching Hospital.Kathmandu, Nepal.

Address for correspondence:
Dr. Prakash Adhikari, MS Resident
Department of ENT and Head and Neck Surgery
TU Teaching Hospital - Kathmandu - Nepal.

Article received on September 20, 2008.
Article approved on Octuber 15, 2008.

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