Chronic Rhinitis
REX MOULTON-MRRETT. MD, VICTOR PASSY, MD. DOROTHY HORLICK, MPH. CT MT. and
GEORGE RAUEL, MD, Irvine and Long Beach, California
METHODS AND MATERIAL
Fifteen patients from the Otolaryngology-Head and Neck Clinic at the University of California- Irvine Medical Center and Veterans Medical Center Long Beach were included in the study between February 1992 and September 1993. Criteria for inclusion in this study were a history of at least 3 months of nasal obstruction that continued after at least a 4-week course of intranasal steroids, the finding of an enlarged membranous head of the inferior turbinate, cytology negative for infection (<5 white blood cells/HPF for 10 HPFs examined), and no significant nasal septal deviation, perforation, or polyps. All histories, examinations, and procedures were performed by a single investigator. Patients were questioned for past or a family history of allergy, current medications, duration, and precipitating events related to their symptoms. The diagnosis of VMCR was made if less than 25% nasal eosinophilia was found. ACR was distinguished from NAECR by the history of positive skin testing or a personal and family history strongly suggestive of atopy.
Nasal obstruction was subjectively graded as follows: 0, absent; 1, unilateral when recumbent; 2, bilateral recumbent; 3, unilateral upright; and 4, bilateral upright. Diminished nasal airflow was subjectively graded as follows: 0, normal; 1, mild; 2, moderate; 3, near total; and 4, total absence of airflow. Inferior turbinate size was graded from 1, if mildly enlarged, to 4, if the nasal cavity was completely occluded. After patient consent was obtained, topical neosynephrine with 4% lidocaine was applied to the nasal cavity. The head of the inferior turbinate was injected with 0.5 ml of 1% lidocaine with 1:100,000 epinephrine. A sterile Teflon-coated 6-mm IC tip (Redfield Corp., Montvale, N.J.) (Fig. 2) was placed along the anterosuperior edge of the head of the inferior turbinate on a setting of 1.0 to 2 seconds for a total of 6 to 10 exposures (Fig. 3). The number of exposures and duration of each exposure were noted for each turbinate. The procedure was repeated one to two times within 6 weeks if the patient continued to complain of nasal obstruction and if the head of the turbinate remained engorged. All patients continued to receive intranasal steroid medication and were encouraged to apply saline solution for at least 3 weeks after ICIT.
Symptomatic improvement, clinical examination findings, and complications of surgery were recorded during each clinic visit (at 1, 3, 6, and 18 months), and a telephone dialogue was maintained. Response to therapy was graded as follows: - 1, worse; 0, unchanged; 1, mildly better; 2, moderately better; 3, much better; and 4, resolved.
Posterior rhinometry was performed on an additional seven patients (not included in this study) before, 3 weeks after, and 6 weeks after ICIT according to the method of Warren?3 Photodocumentation was achieved with an Olympus P-3 nasophatyngoscope, camera, monitor, and high-resolution VHS recording device (Hitachi Denshi America, Ltd., Woodbury, N.Y.).
Cadaveric inferior turbinate was used to determine the relationship between exposure time and depth of injury. Discrete eschars were created for exposure times of 0.5 to 3 seconds, followed by routine fixation, decalcification, longitudinal sectioning, staining with hematoxylin and eosin, and light microscopic evaluation for the presence of cellular destruction.
