The most commonly cited "classic article" on the establishment of pilonidal sinus disease (PSD) as a surgical disease was read before the Boston Society for Medical Improvement, November 8, 1880, by R.M. Hodges, MD.1 It was subsequently published in the Boston Medical and Surgical Journal-accessible in the 1880 archives of the New England Journal of Medicine.1 Although this index paper identifies a plausible pathology for PSD, it is written in the professorial English style of the era. The article gives a good description of PSD that endures today.
Hodges1 establishes the PSD pathology by summarizing: "For the development of this rather singular lesion, to which, for the sake of designation, I venture to give the name of pilo-nidal (pilus, a hair, nidus, a nest) sinus." He further concludes the following elements are necessary to support the diagnosis: a congenital coccygeal dimple; abundant pilous development-hence, adult age, and almost of necessity the male sex; and he ends with this conjecture "insufficient attention to cleanliness; consequently, its subjects, as a rule, must be persons of the lower class, and the affection one met with in hospital, or dispensary, rather than private practice."1
Although wound treatment, closure of PSD, and return to functionally are the most important patient goals, as summarized in the continuing education activity on page 469, several interesting gaps in the literature remain. These include epidemiology, causative factors, and the potential for PSD to exist beyond the natal cleft.1
There is a paucity of literature classifying the exact prevalence of PSD, prior to World War (WW) II. During WWII, 77,637 soldiers2,3 were admitted to Army hospitals for PSD from 1942 to 1945.2,3 One author touted that PSD is "apparently much commoner in the military service than in civilian life."3 "This is because (a) pilonidal sinus is a disease primarily of young men, and (b) conditions of military life are conducive to the start of symptoms."3 These military conditions infer lack of hygiene opportunity in the field and driving or riding in jeeps.3
The exact epidemiology of PSD is hard to discern; however, the statistics during WWII remain similar to the statistics of today's papers on the subject.3 Here's a standard prevalence rate of disease calculations: WWII cases of PSD (n = 77,637); population of US Armed Forces members = 16 million; and the prevalence rate of disease is equal to 0.0049. The percentage of cases in this population is 0.49% (4.85/1000).
Surveillance of PSD during the 1991 Gulf War using the standard prevalence rate of disease calculations yielded the following: n = 124.6 (115 males, 9.6 females); population of US Armed Forces members = 584,341. The prevalence rate of disease was equal to 0.000213232 (population percentage = 0.49%; 0.21 cases/1000 persons [0.20 males, 0.016 females]).4
Repetitive external trauma such as "jeep driving or riding" is speculative, given the incidence of PSD in both military and civilian populations remains stable. The fact is that, over time, US military service members continue to drive vehicles made for utility and not comfort. An additional confounding variable is that wartime armed forces are overrepresented in age and sex with the highest risk for PSD.5
Doll et al6 examined the effects that obesity, sweating, and chronically intermittent contamination of the "rima ani" may have on the incidence and recurrence of PSD. In an elegant study, they concluded that sweating due to a higher body mass index did not promote PSD frequency.6 Furthermore, they found that in the natural history of PSD patients experience "embarrassing recurrent infections before the disease is surgically cured; they should not be further insulted by emphasizing 'maintaining excellent personal hygiene' in the discharge letter. Recommending this is insulting, and neither prevents the development of PSD nor its recurrence."
Although the presence of a coccygeal dimple is mentioned as the sine qua non of PSD, numerous case reports indicate other anatomical sites for PSD, including the neck, axillae, interdigital webs of barbers' hands, and in barefoot individuals. The causative factors of PSD remain incompletely understood.
References