Epistaxis: Etiology, Investigations, and Management
Summary
Epistaxis, or bleeding from the nose, is a disorder that all otorhinolaryngologists will invariably have to deal with, yet it is perceived as a routine problem that is generally delegated to the most junior doctors. In this chapter is information that we hope will rekindle an interest in the condition and encourage readers to consider the range of treatments that are currently available or being developed.
The chapter commences with the epidemiology, etiology, and relationship of epistaxis to other disorders. Details of the vascular anatomy are described. The next section covers the range of evidence-based treatment and outcomes, including alternatives to nasal packs, hemostatic gels and solutions, sphenopalatine ligation, and selective arterial embolization.
The last section presents the current and proposed management protocol for hereditary hemorrhagic telangiectasia (HHT).
Epidemiology
The term epistaxis is derived from the Greek epistazein, meaning “to drip on.”
Incidence
Epistaxis is a common disorder that will affect most of us at some stage in our lives. This can range from minor traces of blood to single, acute, severe bleeds that may be life-threatening. The condition is generally self-limiting, and most people do not go to the hospital. The true incidence is therefore unknown, but epistaxis is estimated to occur in 60% of individuals worldwide at some point in their lifetime.1 Epistaxis has been described as accounting for 33% of ear, nose, and throat (ENT) emergency admissions within the United Kingdom, and the median age of admission was reported as 70 years.2
A recent randomized study on antioxidant use in 2197 mature women ages 50 to 64 years reported significant nosebleeds in 7.6%; these were related to passive smoking.3 Equally, low-dose aspirin in women has been shown to increase the risk of epistaxis to a small degree compared with placebo: 19.1 versus 16.7%, respectively.4 Acetylsalicylic acid has been shown to be associated with a significant increase in the number of operative interventions, a higher recurrence rate, a larger number of treatment episodes, and an increased severity score in patients admitted with epistaxis, but hospital stay and complications were not increased.5 Although physicians are very good at inquiring about pharmacotherapy, they are less proficient at realizing the array of alternative and over-the counter therapies that patients make use of. Garlic, ginkgo, and ginseng are usually fairly benign homeopathic remedies, but they may contribute to a mild systemic coagulopathy, realized only at the time of epistaxis or following endonasal surgery.6
Age
Although epistaxis can occur at any age, there is a bimodal distribution. The condition is common during childhood and invariably occurs from the mucosa overlying the anterior section of the nasal septum. During the adult years, the peak incidence is in the 6th decade, and older people are far more likely to present with a severe acute bleed.
Nosebleeds in very young children (younger than 2 years) are rare and may reflect serious underlying illness or child abuse.7
In the United Kingdom, the recorded annual incidence of primary epistaxis was 27,101 for 2008–2009, of which 2372 were elective admissions ( Fig. 27.1 ).
Chronobiology
Hospital admission rates from epistaxis fluctuate considerably, but in a global 10-year Scottish study they have been described as being more common in the autumn and winter, particularly on weekends.2 A relationship with circadian rhythms has been described with more bleeds occurring in the early morning and evening.8 A study of 1373 patients admitted with acute epistaxis in London considered seasonal variation and ambient temperature but found no relationship between these variables.9 Figure 27.2 shows the seasonal variation in cases of epistaxis.
Etiology
Epistaxis has been categorized as primary (idiopathic) or secondary (due to an identifiable cause). It is estimated that 70% of bleeds are primary. It is also useful to consider etiologic factors as local (to the nose) or systemic (Table 27.1).
Primary Spontaneous Epistaxis
Primary epistaxis refers to spontaneous idiopathic bleeding from the nose. The reason why this happens is not fully understood. However, we can hypothesize that in older people the nasal mucosa and blood vessels become more fragile and more susceptible to spontaneous bleeding.
Spontaneous mucosal bleeding from the anterior nasal septum is common in all age groups, but particularly in children. This area of mucosa is easily accessible to digital trauma, as well as being susceptible to drying and exposure to irritants, but without direct evidence of a definite cause, the bleed is considered idiopathic.
The introduction of endoscopes into clinical practice has led to improved recognition of the bleeding site and more accurate diagnoses. Small vascular anomalies such as hemangiomas are therefore clearly recognizable.
Secondary Epistaxis
Where bleeding is due to a known cause, it is termed secondary. There are many causes of secondary epistaxis, but most are posttrauma or secondary to sino-nasal surgery. Any disorder that disrupts the normal healthy mucosa may induce nosebleeds; conditions include sinonasal tumors, granulomatous disease, septal perforation/ulceration, and environmental/occupational irritant exposure. Nosebleeds are also more likely to occur in nasal allergy, especially if being treated with topical steroid sprays. Postoperative bleeding following skull base surgery also deserves special consideration not only because of the potential for exposure of critical vascular structures, but also for the fact that blind packing may potentiate a neurologic catastrophe.
Other Specific Causes
Deviated Septum
Deviation of the nasal septum can cause mucosal drying and atrophy and is often attributed to being the cause of epistaxis in clinical practice. However, the vast majority of people have some degree of deflection of the nasal septum, and the evidence base to relate septal deviation as a cause of epistaxis is therefore weak. It is more likely that a combination of septal deviation and mucosal drying of the leading convex septal surface causes irritation and subsequent nose picking, which in turn is the more likely cause of epistaxis.
Coagulation Disorders
Probably the most common predisposing factor to epistaxis is the use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), which are often taken as self-medication. This group of drugs affects platelet function. Clopidogrel, prescribed to patients intolerant of aspirin or as an adjunct to aspirin in the management of cardiovascular disease, is also a potent antiplatelet medication. In a UK study examining the risk of epistaxis in 10,241 patients taking antiplatelet medication, the relative risk of epistaxis with aspirin therapy was 9.04 (95% CI [confidence interval] = 5.13–15.96) and 6.40 with clopidogrel (95% CI = 2.3–17.56).10 There was no increased risk of epistaxis with aspirin compared with clopidogrel (RR [relative risk] = 1.4; 95% CI = 0.6–3.4).
Epistaxis is also listed as a side effect of many other medications. Medications known to cause epistaxis are
Topical nasal steroids
Sildenafil (Viagra)
Isotretinoin
Estrogen contraceptive pill
Sumatriptan nasal spray
Anticoagulants, such as warfarin, may also predispose to epistaxis, particularly in situations where the International Normalized Ratio (INR) is poorly controlled or adverse drug interactions have rendered the INR massively elevated.
Unusual causes are the inherited blood coagulopathies (e.g., von Willebrand disease) and systemic blood disorders (e.g., leukemia). Blood group O, more common in whites, is associated with lower expression of von Willebrand factor and as such, has been suggested as a risk factor for epistaxis. Rare systemic diseases with nasal involvement, such as Churg-Strauss vasculitis and amyloidosis, may manifest with epistaxis and should be considered in the differential diagnosis.11,12
Hypertension and Epistaxis
Hypertension is often quoted as being a cause of epistaxis, but a definite relationship has not been proven.13,14 Although it is widely believed that there is an association between hypertension and epistaxis, this remains controversial: both conditions are common, and both are prevalent in older people. Clearly, not everyone with hypertension suffers with epistaxis; otherwise our office practice would truly be overwhelmed. However, when hypertension is detected in association with epistaxis, most would agree that the elevated blood pressure should be investigated and managed appropriately. Hypertension is often considered more likely to prolong the duration of spontaneous epistaxis, but neither this nor an overall association between adult epistaxis and hypertension has been identified.15
Alcohol Consumption and Liver Disease
An association has been described between alcohol consumption and epistaxis, perhaps a consequence of alcohol-induced platelet dysfunction.16 Alcohol was observed to cause a prolongation of the bleeding time, even at low levels of alcohol consumption of between 1 and 10 units per week.
Liver disease should also be considered, as this will affect coagulation not only by reducing the production of most coagulation factors, but also by adversely influencing the clearance of activation products. The vitamin K–dependent factors (prothrombin; factors VII, IX, and X; proteins C and S) may be decreased in acute or chronic hepatocellular diseases. Hepatic failure and cirrhosis may present with the entire spectrum of factor deficiencies when all procoagulant and inhibitory factors are decreased. This is a reflection of impaired protein synthesis.
Hereditary Hemorrhagic Telangiectasia
HHT is a rare but significant cause of severe recurrent epistaxis that will be referred to later in this chapter. The condition is inherited as an autosomal dominant genetic disorder, leading to a weakness of blood vessel walls and vascular malformations. The underlying mechanism is not completely understood. It is characterized by telangiectasias on the skin and mucosal surfaces, which may induce severe and persistent epistaxis and arteriovenous malformations of the internal organs (lungs, gastrointestinal tract, brain, liver, and spine) ( Fig. 27.3 ) (see Video 34, Patient with Severe Refractory HHT, Young′s Procedure ). High-output heart failure may develop as a consequence of shunting of blood between the arterial and venous circulation. Brain hemorrhage or emboli may pose a significant threat to life. The diagnostic criteria are listed in Table 27.2.
Classification of Epistaxis
In addition to referring to primary and secondary epistaxis, nosebleeds have been classified according to the bleeding site. The terms anterior and posterior bleeds were described before the diagnostic use of endoscopes and lack precision. It has been suggested that anterior and posterior should refer to the relationship to the line of the piriform aperture.16 An alternative and more practical classification related to the etiology may be medical and surgical epistaxis (Table 27.3). The logical corollary is that medical epistaxis should be managed in conjunction with, or even solely by, physician colleagues, whereas surgical epistaxis is more amenable to the interventions of otolaryngologists, perhaps utilizing adjunctive interventional radiology.
The incidence of epistaxis from the septum and lateral nasal wall varies between reports. Endoscopic assessment has described 70% of bleeds as arising from the nasal septum.17 However, there is no difference in incidence between the left and right side of the nose.
Vascular Anatomy of the Nose
The nasal mucosa is a dynamic structure with a rich vascular supply. The arterial supply is derived from both the internal and external carotid arteries, with anastomoses between the two systems within the nasal mucosa. The arteries travel within the mucoperiosteum and mucoperichondrium, with the exception of branches that pass along bony canals in the inferior and middle turbinates.
External Carotid System
Arterial blood flows from the external carotid artery to the maxillary artery and then the sphenopalatine artery (SPA) before entering the posterior section of the nose via the sphenopalatine foramen. This carries the greatest supply of arterial blood to the nose. The sphenopalatine foramen itself lies at the posterior end of the middle turbinate.
Anteriorly, blood flows along the facial artery to the superior labial artery before entering the anterior section of the nose.
Considerable anatomical variation of the SPA exists and must be appreciated with regard to SPA ligation or embolization procedures. The artery often subdivides into several branches before entering the nose. Although the number of branches varies according to the reports, ranging from 2 to 10, bifurcation of the maxillary artery before the sphenopalatine foramen is common and occurs in 89% of cases.18 In this same cadaveric study, the maxillary artery demonstrated three common configurations in the pterygopalatine fossa: a single-looped form (18%) and two double-looped forms, E (51%) and M (31%).
A reliable landmark to the SPA is the crista ethmoidalis, sitting just anterior to the artery as it exits the sphenopalatine foramen in almost all cases.19 Furthermore, 73 of 75 cadaveric specimens demonstrated two or more branches of the SPA medial to the crista ethmoidalis.20 Consequently, it is essential to explore the lateral wall of the nose in the region of the sphenopalatine foramen to ensure that each branch of the artery is identified; this may include removal of the crista ethmoidalis to enhance exposure. Because asymmetry of the maxillary and sphenopalatine arteries is unusual, occurring in only 3%,18 it is usually unnecessary to perform contralateral ligation unless, of course, the side of the epistaxis is not clear. Once the SPA exits the sphenopalatine canal, its posterolateral contributions may continue to exhibit significant variability. Lee at al21 noted that in 38% of cases, some portion of the artery may run anterior to the posterior maxillary wall. Furthermore, in 50% of cases, a branch of the inferior turbinate artery extends anterosuperiorly to supply the posterior fontanelle.21 These studies suggest that in a significant proportion of patients, a large tributary of the SPA may be encountered within the posterior maxillary fontanelle. These variations offer an explanation for the etiology of large-volume postsurgical posterior epistaxis following routine limited maxillary antrostomy.
Within the nose, the SPA divides into a lateral and a medial branch. The lateral branch supplies the lateral wall of the nose and the inferior turbinate. The medial branch passes over the anterior sphenoid wall, 1 cm above the posterior choana, to the posterior septum, where it divides into three parts. The superior branch travels anteriorly to anastomose in Kiesselbach plexus.
The posterior nasal artery, often referred to as the septal artery, has been described as passing through its own foramen posterior to the sphenopalatine foramen.
Internal Carotid Artery System
The internal carotid arterial blood travels along the ophthalmic artery through the superior orbital fissure to the orbital apex, then anteriorly to give offthe anterior and posterior ethmoidal arteries ( Fig. 27.4 ). These traverse the medial orbital wall through the frontoethmoid suture to travel in bony canals across the superior ethmoid, entering the anterior cranial fossa through the lateral lamella of the cribriform plate. Within the cranial cavity, both arteries branch, giving rise to terminal branches that supply the dura of the anterior fossa; some branches run inferiorly to supply the superior nasal cavity. The anterior ethmoid artery is the larger and most constant of the two; the posterior ethmoid artery may be absent in up to 30%.
Additionally, the bone over the paraclivial and parasellar carotid may be dehiscent within a well-pneumatized sphenoid sinus. This anatomical relationship provides the opportunity for massive epistaxis derived from this segment of the internal carotid artery secondary to trauma or idiopathic aneurysmal/pseudoaneurysmal dilation.
Venous Drainage System
Generally, the veins follow the course of the arteries within the nasal mucosa. However, there are emissary branches that lead to the cavernous sinus and similar branches from the pterygoid plexus that also pass to the cavernous sinus.
The retrocolumellar vein is a distinctive vessel that is often visible and prominent running parallel to the columella adjacent to the mucocutaneous junction.
Vascular Anastomoses
The mucosa of the anterior nasal septum is supplied by arterial blood from the septal branch of the SPA, the greater palatine artery via the incisive canal, the superior labial artery, and branches from the anterior ethmoidal artery superiorly ( Fig. 27.5 ).
This anterior region of the nasal septum is known as Little area ( Fig. 27.6 ). James Little was a professor of surgery in New York in 1879 when he described the blood supply and management of a bleeding “ulcer” of the anterior nasal septum in four patients. Wilhelm Kiesselbach, a lecturer in otology at the University of Erlangen in Germany, subsequently described three patients with bleeding from distended vessels from the same site.
Cadaveric dissection has shown that there is a consistent triangle of large thin-walled anastomotic arterial vessels in the mucosa over the anterior nasal septum.22
In 1949 another vascular region of the nose was described in the posterior section of the nasal cavity adjacent to the inferior turbinate ( Fig. 27.7 ). This is the Woodruff venous plexus, which comprises large, thin-walled veins with very little muscle or fibrous tissue within a thin mucosa relatively devoid of other structures.23 The area is clearly visible while examining the nose with an endoscope after vasoconstriction.
Clinical Features
The features of epistaxis are best described according to the clinical presentation.
Children usually present in the outpatient clinic with a history of recurrent nosebleeds. These are often described as arising from both sides of the nose. There is no association between hand dominance, believed by some to imply greater ipsilateral nose picking, and pediatric idiopathic epistaxis.24 Bleeding is often perceived as being heavy, but anemia is unusual. There may be features of allergy and rhinosinusitis. Bleeding is usually from the mucosa of the anterior nasal septum. Crusts in the anterior nasal cavity and vestibules are often seen. The child is otherwise healthy.
Adults may also present to the clinic with recurrent spontaneous nosebleeds, but their medical history is often more complex, particularly with advancing years. The bleeding is generally unilateral but can be prolonged in older patients. However, most do not have any other problems from their nose.
Pregnancy is associated with an increased incidence in nosebleeds due to increased nasal blood flow from hormonal changes. Indeed, the prevalence of epistaxis in pregnant versus nonpregnant women has been found to be significantly increased (20.3% compared with 6.2%, respectively).25 Consideration must be given to the well-being of both the mother and the unborn fetus, and epistaxis frequently poses a therapeutic dilemma, mandating close liaison between the otolaryngologist and the tending obstetrician.
Severe acute nosebleeds are very different. The patients usually have either a single episode or a short series of episodes leading up to a major unilateral bleed. It can be difficult to differentiate which is the bleeding side in profuse bleeds. Patients presenting as emergencies with ongoing or recent bleeding will often be agitated and distressed. They may also be hypovolemic, anemic, and have other comorbidities that can be exacerbated by the acute bleeding episode. Most patients recover well from this, but it is always important to remember that it is very easy to underestimate a potentially serious problem.
Evidence-based Treatment and Outcomes
Acute Epistaxis
Patient Stabilization and Initial Control
An acute nosebleed can be an alarming event to a patient and invariably induces a significant degree of anxiety. A moderate bleed may look to be excessive to an untrained eye, and patients will often require reassurance that they have not lost a lot of blood. However, it is important not to be complacent with patients presenting with an acute epistaxis incident, as bleeding can be significant and, rarely, can prove fatal. A clear and logical plan of action should therefore be adopted ( Fig. 27.8 ).
In the United States, the American Heart Association Basic Life Support protocol guides prioritization of consideration in the management of emergency situations. As applied to epistaxis, the first consideration is always protection and management of the airway. Once this is deemed secure, attention may then be turned toward controlling the bleeding while simultaneously establishing vascular access for the provision of volume replacement and hemodynamic support.
Acute nontraumatic epistaxis occurs spontaneously in various situations, and patients will only go to the hospital if the bleeding is persistent and heavy, often resulting in hospital admission for several days ( Fig. 27.9 ). The initial management is therefore to apply first-aid measures to control and minimize the blood loss. However, it has been estimated that only 11% of people could correctly offer suitable first-aid advice in a cohort of 500 respondents who did not have a history of epistaxis.26 Patients on anticoagulants lack knowledge on how to manage a nosebleed, and only 33 out of 60 could name a single useful first-aid measure.27 First-aid measures should include sitting with the body tilted forward and the mouth open. Lying down should be avoided, unless the patient feels faint, thus reducing the risk of aspiration and minimizing the volume of blood ingested, as this is a potent gastric stimulant and may lead to vomiting. Sitting forward decreases the blood flow to the nasopharynx and also permits blood entering the pharynx to be spat out. The patient should be advised to pinch the soft part of the nose, below the nasal bones, and hold for 10 to 15 minutes without releasing, while breathing through the open mouth. This is a long time to apply compression, and fatigue sets in quickly, especially considering there is a high level of anxiety. It is often useful if a relative or neighbor can assist with this maneuver. For epistaxis that persists or is not controlled by this simple measure, a hospital assessment by an ENT physician is mandated.
Assessment and treatment should take place in a suitable room with suction and specialist equipment readily available. An assistant is essential, first, to pass instruments and equipment that are not readily at hand and, second, to assist if the patient faints. Medical and nursing staffshould wear suitable protective clothing and aprons, as the risk of contamination by blood is high.28 Initially, the patient should be sat upright, leaning forward with a bowl beneath the chin. Direct pressure should be applied with finger and thumb across the alar region for several minutes to compress vessels over the anterior nasal septum (Little area), but this will not control posterior nasal bleeding.
The nasal cavities should then be sprayed with a local vasoconstrictor and topical anesthetic solution. After a few minutes the nose should be examined with a headlight and, ideally, with a rigid endoscope. Blood clot should be evacuated and a source for the bleeding identified. If a bleeding point is identified, the application of a small neuropatty (fluid absorption pad) soaked in vasoconstrictor solution directly over the bleeding vessel may stem the flow of blood.
Placing an ice cube in the mouth has also been shown to reduce nasal mucosal blood flow.29
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