Massive Epistaxis from Nasal CPAP T...

Massive Epistaxis from Nasal CPAP Therapy

Nasal CPAP has become a standard form of therapy for patients with obstructive be still apnea syndrome and has eliminated the ne for tracheostomy in many patients. [1-4] It is generally effective and well tolerated and ensues in an improved quality of life, contributing to a compliance rate as high as 85 percent [5-7] The most numerous common adverse effects are nasal congestion and drynes which are particularly hard during episodes of upper respiratory infection. Instillation of saline nose sprays or the use of scope humidifiers have been effective in controlling these symptoms. In-line humidification generally has been regarded as unnecessary for chiefly patients. We report a 75-year-old man with obstructive rest apnea who developed massive epistaxis within couple weeks of starting therapy with nasal CPAP. Following aggressive therapy of his acute bleeding question nasal CPAP was reinstituted with humidification in the CPAP circuit and he has sustained no recurrence.

CASE REPORT

A 75-year-old man complained of a seven-year history of daytime fatigue and exertional dyspnea. The physical examination disclosed morbid obesity, clear lung and a impressible systolic murmur at the apex of his heart. Intermittently he would be noted to have edema of the lower extremities. A chest radiograph revealed clear lung fields and borderline cardiomegaly. Pulmonary function testing showed moderate obstructive airway disease with an [FEVsub1] of 174 L and an [FEVsub1/FVC] of 65 percent Arterial kindred gas levels on room air showed a pH of 738; [PCOsub2] 41; and [POsub2] of 64 The right ventricle was hypokinetic and dilated with a left ventricular ejection fraction of 51 percent by way of MUGA scan. Cardiac catheterization revealed pulmonary hypertension with pulmonary artery urgency of 46/24 mm Hg and a mean constraining force of 32 mm Hg. yet 3+ mitral regurgitation was also noted, he had a normal wedge influence of 12 mm Hg.

A diagnosis of rest apnea was considered due to his pulmonary hypertension and history of daytime fatigue and nocturnal snoring. All night polysomnography revealed an apnea-hypopnea index of 25 episodes for hour and arterial oxygen desaturation to a nadir of 82 percent Initial attempts at therapy with nighttime oxygen alone were bootless and persistent daytime fatigue continued. In addition, the patient unfolded worsening right-sided heart failure with the appearance of coagulopathy (prothrombin time, 16 s) fancy to be due to liver congestion. He was then started in succession nasal CPAP at a influence of 5 [cmH.sub.2.O] (Sleep-Easy II, Respironics) with ready improvement in his level of daytime alertness, although he did complain of nasal stuffiness and drynes Ten days after the initiation of nasal CPAP, he cause to growed epistaxis requiring placement of a right anterior nasal pack. Immediately following removal of this pack, he make knowned profuse bleeding with an estimated line loss of 600 ml in 10 min. A posterior pack was required to command the epistaxis and he was admitted to a community hospital for observation. Laboratory studies at that time were notable for a platelet estimate of 112,000, a prothrombin time of 152 s and a partial thromboplastin time of 356 s Nasal CPAP was discontinued during this time and after three days the posterior packing was remov with no further bleeding. Nasal CPAP was reinstituted sum of two units weeks later with a Cascade Junior in-line humidifier (Puritan-Bennett). He continued to use the nasal CPAP with no further nasal bleeding and continued improved daytime alertness.

DISCUSSION

Serious complications with nasal CPAP are rare. Anderson et al [8] reported a patient with obstructive be dead apnea due to a lax epiglottis who discloseed fluoroscopically confirmed worsening airway obstruction upon nasal CPAP. Bilateral feculent conjunctivitis in one patient also has been reported, possibly resulting from a poorly fitted mask. [9] Sanders et al [7] reported "moderate" epistaxis in individual patient which required only topical antibiotics. Our patient set forths the first reported case of morose life-threatening epistaxis on nasal CPAP.

Despite the ability of the nose to humidify inspired air, the high roll on rates used with nasal CPAP can significantly arid the nasal mucosa. We be moved that this was the case in our patient with resulting ulceration and bleeding. While his coagulopathy undoubtedly contributed to the severity of the bleeding, we do not be wrought up that it was the direct cause.

With increased recognition of the prevalence of rest apnea and with the growing acceptance of nasal CPAP as first-line therapy, we await that epistaxis will become a more frequent complication of this treatment modality. Physicians prescribing nasal CPAP should include a thorough examination of the nose as a part of routine follow-up and erosion of the mucosa warrants early intervention. We raise in-line humidification to be highly successful in our patient and we would consider adding this degree of therapy when there is evidence of breakdown of the nasal mucosa.