Influenza Sinusitis and its Relation to Epidemic Influenza
Free Access from Suburban Emergency Management Project August 4, 2009, Biot #638
(This has been purged from the internet)
July 27, 2009
H.E. Robertson, M.D. of Minneapolis, Minnesota, became a major in the U.S. Army in 1917, serving overseas in the Central Medical Department Laboratory of the American Expeditionary Force in France. In May 1918, he published an article titled “Influenza-sinus disease and its relation to epidemic influenza” in the Journal of the American Medical Association, based on his observations of patients in the hospital of the British Expeditionary Forces in France. May 1918 was during the first wave of pandemic influenza (see graph below). His observations are astute.
Graph showing three pandemic waves: weekly combined influenza and pneumonia mortality, United Kingdom, 1918-1919. Source: http://www.cdc.gov/ncidod/eid/vol12no01/05-0979-G1.htm; accessed July 27, 2009.
Robertson wrote, “A typical attack of influenza usually beings as a rhinitis and spreads from the nasal mucosa throughout the respiratory tract. As the chief symptoms are produced by the involvement of the bronchial tree, attention is naturally directed to the lungs and bronchi as the most important foci for the infection. However, in studying acute cases one is often impressed by the fact that the severity of the disease, best evidenced by the general prostration of the patients, is out of all proportion to the physical signs. Tracheo-bronchitis with abundant muco-purulent sputum, a particularly distressing and often spasmodic cough, and moist rales [wet sounds] uniformly present in both lungs, almost exhaust the positive findings of the respiratory tract. It becomes difficult to understand why a vigorous, previously healthy young adult, should succumb to an infection which in many cases appears to be almost wholly confined to the tracheo-bronchial mucosa. It might even be questioned whether such an individual should die from a primary bronchitis and broncho-pneumonia. In the opinion of many clinicians and pathologists, such a combination is rather rare. (1)
Robertson believed that “in addition to the infection of the respiratory tract per se, “other lesions, almost uniformly neglected by writers on the subject and rarely noted by clinicians or pathologists, may prove to be very seriously important factors both in the clinical picture and in the often fatal outcome of the disease.” (1) What are these lesions?
In October 1917, Robertson says he visited the base hospital zone of the British Expeditionary Forces in France, at which time “Captain Rolland of the Royal Army Medical Corps mentioned his observations in a series of cases of this disease, which had occurred in epidemic proportions and which was highly fatal. The influenza bacillus seemed without doubt to be the causal agent, though pneumococci and streptococci were often also isolated [in the laboratory].” Robertson, however, was most surprised at the “involvement of the sinuses at the base of the skull” during autopsies of patients who had succumbed to influenza.
Robertson noted, “Infection of the accessory sinuses of the nose and skull have [sic] often been noted. As early as 1837, Petrequin stated that frontal sinus involvement produced the headache so often present in [influenza]. Bronchin, in 1884, distinguished the ‘cephalic’ form of influenza by localizations in the nasal fossae, and the frontal and maxillary sinuses. Pfeiffer, however, in his classic description of the etiology and pathology of influenza, does not mention the sinuses. [2]…[Pfeiffer] evidently did not encounter or missed the significance of any sinus complications,” declared Robertson. “In short, sinus disease in epidemics of influenza is either totally disregarded or described as an accidental complication or sequel of the infection of the pulmonary tract.” Robertson believed otherwise.
Location of human sinuses. Source: http://ent.med.nyu.edu/files/ent/u3/nose_anatomy_front.gif; accessed July 27, 2009.
“When, therefore, our first fatal case of influenza tracheo-bronchitis and broncho-pneumonia showed, at postmortem examination, an empyema [collection of pus] of both sphenoid [sinus] cavities, and the pus from these revealed both smears and cultures typical influenza bacilli, the condition was regarded as an interesting but unusual complication. However, as case after case coming to necropsy showed similar or comparable lesions, the circumstances warranted more careful and detailed study,” Robertson noted.
Robertson summarizes fourteen necropsies showing involvement of the sinuses.
In his comment section, he wrote, “It would, of course, be unreasonable to assert that all cases of influenza are accompanied by sinus complications…The number of cases is altogether too small to justify any sweeping conclusions. They do serve most emphatically to emphasize the importance of the sinuses in the respiratory type of influenza.” Why?
First, infection of the sinuses “constantly menaces the pulmonary system, only awaiting suitable conditions of exposure and lowered resistance for hostile invasion, but also furnishes continued sources of toxic absorption, not to mention the direct effect on the well being of the patient from the presence of these local conditions.”
Second, and more important, “is the bearing that these local infections have on prophylaxis and treatment. When their attention had been called to the possible constant presence of sinus disease in patients suffering from influenza bronchitis, the attending physicians adopted local measures of treatment for these conditions, even when their presence could not be diagnosed with any degree of certainty. Local applications to the nasal passage of cocaine and epinephrine solutions often resulted in copious discharges of thick, muco-purulent exudates from the sinuses, with marked relief to the patient, such as amelioration of headache and pain in the eyes, as well as definite betterment of the conditions in the bronchi and trachea.” (1)
Detail of human sinuses. Source: http://www.sinustreatmentcenter.com/scfig3_500.jpg; accessed July 27, 2009.
Robertson summarizes his findings, as follows (two have been omitted):
1. “Epidemics of respiratory influenza (purulent tracheo-bronchitis) have been fairly severe in both the American and the British Expeditionary Forces.
2. In the investigation of cases, both clinically and at postmortem, little attention in the past has been give to the question of accompanying sinus disease.
3. Of eight fatal cases of purulent tracheo-bronchitis due to the influenza bacillus, all but one showed involvement of one or more of the sinuses at the base of the skull by inflammatory processes, probably, in all cases, directly due to the invasion of these sinuses by the influenza bacillus.
4. Appropriate treatment of the sinuses in patients suffering from influenza often served to relieve the symptoms and apparently to hasten convalescence.
5. Investigation of the sinuses during epidemics of influenza is strongly recommended and urged not only on therapeutic but also on prophylactic grounds.” (1)
Robertson’s findings are relevant to today. Effective treatment of influenza sinusitis may prevent spread to the lungs. Treatment, however, is possible only with awareness of the disease entity, i.e., influenza sinusitis.
Notes:
1. H.E. Robertson: “Influenzal sinus disease and its relation to epidemic influenza.” JAMA, May 1918, Volume 70, Number 21, pp. 1533-1535. Available at
2. Pfeiffer’s bacillus, subsequently named Hemophilus influenza, was shown by Martha Wollstein, M.D., in 1919, to be “at least a very common secondary invader in influenza, and that its presence influences the pathological process.” However, patients’ serological reactions that she studied were not “sufficiently stable and clean-cut to signify that Pfeiffer’s bacillus is the specific inciting agent of epidemic influenza.” Source: Martha Wollstein: “Pfeiffer’s bacillus and influenza: A serological study.” The Journal of Experimental Medicine, Volume 30, pp. 555-568, 1919. Abstract available at http://jem.rupress.org/cgi/content/abstract/30/6/555; full text is available at http://jem.rupress.org/cgi/reprint/30/6/555; accessed July 27, 2009.
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