Epistaxis

Nosebleeds are rare in infancy and common in childhood; their incidence decreases after puberty. Diagnosis and treatment depend on the location and cause of the bleeding.

ANATOMY. The most common site of bleeding is the Kiesselbach plexus, an area in the anterior septum where vessels from both the internal carotid (anterior and posterior ethmoid arteries) and external carotid (sphenopalatine and terminal branches of the internal maxillary arteries) converge. The thin mucosa in this area, as well as the anterior location, makes it prone to exposure to dry air and trauma.

ETIOLOGY. Common causes of nosebleeds from the anterior septum include digital trauma, foreign bodies, dry air, and inflammation, including upper respiratory tract infections, sinusitis, and allergic rhinitis. Nasal steroid sprays are commonly used in children, and their chronic use may be associated with bleeding. Young infants with significant gastroesophageal reflux into the nose may occasionally present with epistaxis secondary to mucosal inflammation.

There is frequently a family history of childhood epistaxis. Susceptibility is increased during respiratory infections and in the winter when dry air irritates the nasal mucosa, resulting in formation of fissures and crusting. Severe bleeding may be encountered with congenital vascular abnormalities, such as hereditary hemorrhagic telangiectasia (see Chapter ), varicosities, hemangiomas, and, in children with thrombocytopenia, deficiency of clotting factors, particularly von Willebrand disease, hypertension, renal failure, or venous congestion. Nasal polyps or other intranasal growths may be associated with epistaxis. Recurrent, and frequently severe, nosebleeds may be the initial presenting symptom in juvenile nasal angiofibromas, which occur in adolescent males. The incidence of Kiesselbach plexus bleeding decreases in adolescence

CLINICAL MANIFESTATIONS. Epistaxis usually occurs without warning, with blood flowing slowly but freely from one nostril or occasionally from both. In children with nasal lesions, bleeding may follow physical exercise. When bleeding occurs at night, the blood may be swallowed and become apparent only when the child vomits or passes blood in the stools. Posterior epistaxis can manifest as anterior nasal bleeding or, if copious, the patient may vomit blood as the initial symptom

TREATMENT. Most nosebleeds stop spontaneously in a few min. The nares should be compressed and the child kept as quiet as possible, in an upright position with the head tilted forward to avoid blood trickling back into the throat. Cold compresses applied to the nose can also help. If these measures do not stop the bleeding, local application of a solution of oxymetazoline (Afrin) or Neo- Synephrine (0.25–1%) may be useful. If bleeding persists, an anterior nasal pack may need to be inserted; if bleeding originates in the posterior nasal cavity, combined anterior and posterior packing is necessary.

After bleeding has been controlled, and if a bleeding site is identified, its obliteration by cautery with silver nitrate may prevent further difficulties. Because the septal cartilage derives its nutrition from the overlying mucoperichondrium, only 1 side of the septum should be cauterized at a time to reduce the chance of a septal perforation. During the winter, or in a dry environment, a room humidifier, saline drops, and petrolatum (Vaseline) applied to the septum may help to prevent epistaxis. Three studies examining treatment options (antiseptic cream vs no treatment, petroleum jelly [Vaseline] vs no treatment, and antiseptic cream vs silver nitrate cautery) found no differences between the compared treatments.

In patients with severe or repeated epistaxis, blood transfusions may be necessary. Otolaryngologic evaluation is indicated for these children and for those with bilateral bleeding or with hemorrhage that does not arise from the Kiesselbach plexus. Hematologic evaluation (for coagulopathy and anemia), along with nasal endoscopy and diagnostic imaging, may be needed to make a definitive diagnosis in cases of severe recurrent epistaxis. Replacement of deficient clotting factors may be required for patients who have an underlying hematologic disorder (see Chapter 476 ). Profuse unilateral epistaxis associated with a nasal mass in an adolescent boy near puberty may signal a juvenile nasopharyngeal angiofibroma. This unusual tumor has also been reported in a 2 yr old and in 30–40 yr olds, but the incidence peaks in adolescent and preadolescent boys. CT with contrast medium enhancement and MRI are part of the initial evaluation; arteriography, embolization, and extensive surgery may be needed.

Surgical intervention may also be needed for bleeding from the internal maxillary artery or other vessels that can cause bleeding in the posterior nasal cavity.

PREVENTION. The discouragement of nose picking, and attention to proper humidification of the bedroom during dry winter months helps to prevent many nosebleeds. Prompt attention to nasal infections and allergies is beneficial to nasal hygiene. Prompt cessation of nasal steroid sprays prevents ongoing bleeding

Severe platelet function defects usually present with petechiae and purpura shortly after birth, especially after vaginal delivery. Defects in the platelet GPIb complex (the VWF receptor) or the αIIb-β3 complex (the fibrinogen receptor) cause severe congenital platelet dysfunction.

Glanzmann thrombasthenia is a congenital disorder associated with severe platelet dysfunction that yields prolonged bleeding time and a normal platelet count. Platelets have normal size and morphologic features on the peripheral blood smear, and closure times for PFA-100 or bleeding time are markedly abnormal. Aggregation studies show abnormal or absent aggregation with all agonists used except ristocetin, because ristocetin agglutinates platelets and does not require a metabolically active platelet

This disorder is caused by deficiency of the platelet fibrinogen receptor αIIb-β3, the major integrin complex on the platelet surface that undergoes conformational changes by inside out signaling when platelets are activated. Fibrinogen binds to this complex when the platelet is activated and causes platelets to aggregate. Caused by identifiable mutations in the genes for αIIb or β3, this disorder is inherited in an autosomal recessive manner. For both Bernard- Soulier syndrome and Glanzmann thrombasthenia, the diagnosis is confirmed by flow cytometric analysis of the patient's platelet glycoproteins.

Hereditary deficiency of platelet storage granules occurs in 2 well-characterized but rare syndromes that involve deficiency of intracytoplasmic granules. Dense body deficiency is characterized by absence of the granules that contain ADP, ATP, Ca 2+, and serotonin. This disorder is diagnosed by the finding that ATP is not released on platelet aggregation studies and ideally is characterized by electron microscopic studies.

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