The Value of Looking

Abstract

Multiple myeloma is a disease of immature and mature plasma cells. These cells, which accumulate in the bone marrow and other tissues, often overproduce monoclonal immunoglobulins. Many of the clinical features of this disease result from the accompanying disordered immune response, which increases susceptibility to infection. Blood levels of normal immunoglobulin often are decreased in patients with multiple myeloma. They may also have quantitative and functional deficits in complement activity. The net result is a sluggish primary immune response, manifested by a slow rise in immunoglobulin M (IgM) titers, and a reduced capacity to synthesize other immunoglobulin classes needed for secondary immune response. There may be impaired synthesis of antibodies that bind to invading bacteria and thereby make them susceptible to ingestion by phagocytes (a process called opsonization). This puts patients with multiple myeloma at high risk of infection by encapsulated bacteria such as Streptococcus pneumoniae or Haemophilus influenzae. In general, the infections seen in patients with multiple myeloma are the same as those seen in patients with sickle cell anemia, aggammaglobulinemia, and other conditions that disorder bacterial opsonization. Our Patient A 65-year-old black man came to the Emergency Department complaining of a single episode of rigor during the preceding night; he was feverish thereafter. Two weeks earlier he had had a cough productive of yellow sputum which persisted for 4-5 days, but had cleared 6 days before the onset of fever. The day after his episode of rigor, he awoke with soreness in his left neck and a mild headache, but no photophobia or diploplia. Aside from known hypertension his history was unremarkable. Physical examination revealed an elderly man who appeared acutely ill. His blood pressure was 160/95; temperature, 38.2 o C; heart rate, 125 beats/min; and respiratory rate, 26 breaths/min. The patient was able to flex and extend his head and neck normally, but unable to turn his head to the left. The left sternocleidomastoid muscle was tense, and palpation of the lateral border of the medial belly of the muscle caused significant pain. The neurological examination was normal, and neither Brudzinski’s nor Kernig’s signs could be elicited. The remainder of the physical examination was unremarkable. The white blood cell count was 21x10 9 / L; hemoglobin, 13.3 g/dL; creatinine, 1.5 mg/dL; and blood urea nitrogen, 24 mg/dL. A chest X-ray was normal, and the electrocardiogram revealed only sinus tachycardia.