According to Patadia et al., risk factors classically associated with development of Austrian syndrome include immunocompromised status, male sex, chronic alcoholism, dural fistulas, and splenectomy [5]. Although our patient had a preceding viral pneumonia, which likely placed her at a risk for superimposed bacterial pneumonia, none of the abovementioned risk factors were found in our patient. The sequence of infection occurrence starting in the lungs followed by dissemination to extrapulmonary sites likely overwhelmed her immune system. In result, seeding in the sternoclavicular joint space occurred in the setting of bacteremia. According to Shirtliff and Mader, there are three mechanisms of seeding in an SC joint: direct spread of bacteria from an adjacent focus of infection, hematogenous dissemination, and trauma [8], the second of which fits in the case of this patient.
Austrian syndrome complicated by SC joint infection has been reported twice in the literature [7].
An article by Bindroo et al. presented the case of a 60-year-old male, who had known predisposing factors in his medical history, with Austrian syndrome and secondary SC joint infection [9]. However, there were a couple of differences between the two cases: our patient was a female, 68 years of age, and sensitive to penicillin, whereas the patient in the Bindroo et al. article was a male, 60 years old, and resistant to a 6-week course of ceftriaxone [9]. Our case is the first in the literature to present with Austrian syndrome complicated by SC joint septic arthritis in an immunocompetent female with hypertension as her only comorbidity. This case uniquely challenges the common perception that Austrian syndrome occurs in older, alcoholic males. As an immunocompetent female, it is not known whether the syndrome manifested as it classically would have developed in the pre-penicillin era because penicillin was discovered in 1928, and Austrian syndrome was clinically characterized in 1957 [1].
A different study by Sewlall et al. presents a case of an HIV patient afflicted with Austrian syndrome complicated by septic arthritis as a result of “invasive pneumococcal infection” (IPI) [7]. The case was another example of Austrian syndrome that occurred in the presence of underlying risk factors, including male sex and immunocompromised status [7]. Perhaps immunomodulation may not necessarily serve as a defense mechanism against pneumococcal dissemination. However, it may facilitate recovery from Austrian syndrome upon early antibiotic administration, as demonstrated by our patient’s hospital course. The class of antibiotic differed between Sewlall’s patient and our patient because of penicillin resistance [7].
One limitation of the preceding studies, including our case, is the lack of generalizability of results to future cases of Austrian syndrome. The reason is that the timing of antibiotic administration relative to disease onset likely varied from case to case. One case of Austrian syndrome may have progressed more than another case prior to receiving antibiotics. This variability makes it difficult to determine whether disease outcomes are consistently modified as a result of early antibiotic administration. However, earlier administration of antibiotics would logically contribute to a more favorable patient outcome.