Correct!
5. All of the above

The chest x-ray shows new bilateral infiltrates, attributed to cardiogenic pulmonary edema.

While all of the above are diagnostic possibilities, the most likely is polyarteritis nodosa associated cardiomyopathy, which occurs in about ten percent of patients with polyarteritis nodosa.

Transthoracic echocardiogram showed normal valvular and right heart systolic function, and an ejection fraction of 26% with no focal wall motion abnormalities.

For the cardiomyopathy and disease progression, he was started on high dose intravenous steroids (methylprednisolone 250mg q 6 hours) and plasma exchange, though the evidence surrounding plasma exchange in HBV-associated polyarteritis nodosa is limited. He rapidly improved, was extubated within two days of initiating therapy and by five days after presentation, his ejection fraction had improved to 55%.

He was ultimately discharged with a plan to continue outpatient high dose IV methylprednisolone and plasma exchange until his HBe antibody turned positive.

References

  1. De Virgilio A, Greco A, Magliulo G, et al. Polyarteritis nodosa: a contemporary overview. Autoimmun Rev. 2016;15(6):564-570. [CrossRef] [PubMed]
  2. Hernandez-Rodriguez J, Alba MA, Prieto-González S, Cid MC. Diagnosis and classification of polyarteritis nodosa. J Autoimmun. 2014;48-49:84-89. [CrossRef] [PubMed]
  3. Matteson EL. Historical perspective of vasculitis: polyarteritis nodosa and microscopic polyangiitis. Curr Rheumatol Rep, 2002; 4(1):67-74. [CrossRef] [PubMed]
  4. Stone JH. Polyarteritis nodosa. JAMA, 2002; 288(13):1632-1639. [CrossRef] [PubMed]
  5. Jennette JC, Falk RJ, Bacon PA, et al. 2012 revised international Chapel Hill consensus conference nomenclature of vasculitides. Arthritis Rheum. 2013; 65(1):1-11. [CrossRef] [PubMed]

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