CT Study of the Paranasal Sinuses in Allergic Rhinitis
March 15, 1997 3 minutes read
CT Study of the Paranasal Sinuses in Allergic Rhinitis
The relationship of allergic rhinitis to sinusitis is one of great interest, especially since the role of allergic inflammation in the sinus mucosa is indeterminate. Clinically, patients report symptoms consistent with sinus congestion during periods of allergic rhinitis. Single photon emission CT has shown sinus inflammation in allergic rhinitis. This study sought to determine whether sinus inflammation could be detected by limited coronal CT scan during symptomatic allergic rhinitis.
In nine pollen-allergic subjects, CT scans of the nasal passages, osteomeatal complex, and paranasal sinuses were obtained before and during pollen season. All subjects developed signs and symptoms of allergic rhinitis during the pollen season, but none demonstrated clinical symptoms of sinusitis.
Only two of the patients developed interval changes on CT, not consistent with sinus inflammation. Previous studies have shown that subsequent to viral URIs, patients do develop sinus changes demonstrated on CT scan. Additionally, the authors have previously demonstrated that single photon emission CT scan can detect allergic induced sinus inflammation. Hence, the authors conclude that limited coronal CT scan of the sinuses cannot reliably detect allergic inflammation of the sinuses.
Leipzig J, et al. J Allergy Clin Immunol 1996;98:1130-1131.
Clinical Scenario: The tracing in the figure was obtained from a 61-year-old man with shortness of breath and a large globular heart on chest x-ray. How would you interpret this ECG? What is the likely cause (or causes) of the poor R wave progression seen in the precordial leads?
Interpretation: The rhythm is sinus tachycardia at a rate of 125 beats/min. The mean QRS axis is +105°, consistent with right axis deviation (RAD) of moderate degree. Left atrial abnormality (LAA) is suggested by a deep negative component to the P wave in lead V1. There is "poor R wave progression" in the precordial leads.
This tracing highlights the dilemma of trying to formulate the differential diagnosis for poor R wave progression. One or more of three entities must be strongly considered:
1. Left ventricular hypertrophy (LVH)
2. Right ventricular hypertrophy (RVH)
3. Anterior infarction.
Diagnosis of LVH is suggested by prominent voltage (sum of S wave in lead V2 + R wave in lead V6 ³ 35 mm), the presence of LAA, and ST-T wave changes consistent with "strain" (ST segment depression in the inferior leads, T wave inversion in lead V6, and reciprocal repolarization changes in the anterior precordial leads).
Diagnosis of RVH is usually hard to make when there is also LVH because increases in left and right ventricular mass tend to cancel each other out. However, when RAD is found in association with definite criteria for LVH, biventricular hypertrophy most likely is present.
The question of anterior infarction remains. Although anterior infarction cannot be excluded from simple inspection of the figure, one should remember that LVH and RVH can each produce poor R wave progression that simulates anterior infarction. Determination of anterior infarction, therefore, requires independent confirmation (i.e., by history, comparison with previous tracings, serial CK enzyme studies, etc.).
As implied by the history, the patient in this case was found to have congestive cardiomyopathy. Echocardiography revealed biventricular hypertrophy and enlargement. There was no history of infarction.
It is difficult to determine if the shallow, symmetric T wave inversion in lead V6 is the result of ischemia or strainor perhaps both. As a result, we tend to verbalize our impression of this finding as "LVH and strain and/or ischemia."
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