A 62-year-old man with history of chronic lymphocytic leukemia (CLL), hypothyroidism, transient ischemic attack, and treated pulmonary tuberculosis presented to the emergency department with a complaint of low back pain for one month. The pain had worsened on the morning of presentation, and was described as a constant dull ache, 9/10 in severity, on the left paraspinal muscle region without radiation.
The pain had been improving, but started to worsen again over the past week, intensifying that morning when he sneezed and twisted toward the left. He also admitted to a two-week history of painless hematuria without other urinary symptoms, and feeling weak and tired with a poor appetite for several days. He had completed treatments for CLL a year earlier. He denied recent travel or sick contacts.
His tuberculosis infection had occurred 20 years earlier, and was treated with two drugs for one year. A cervical lymph node biopsy was his only surgery. The patient denied any allergies, and was only taking aspirin and levothyroxine. His last chemotherapy treatment was also a year earlier. The patient was a smoker who had cut down from two packs to half a pack a day. He denied illicit drug use, but did admit to social alcohol consumption. He had no family history of hypertension, diabetes, or premature coronary disease. He was retired and used to work as a toll booth attendant in the Bronx.
On physical exam, he was noted to be tachycardic with a heart rate of 119 bpm. He was normotensive at 120/68 mm Hg, afebrile at 98.3°F, respiring at 20 with an O2 saturation of 95% on room air. At first glance, the patient appeared cachectic and thinly built but in no apparent distress. His pupils were equal and reactive, conjunctiva pink and sclera anicteric. His otic exam showed no signs of infection.
He had poor dental hygiene and a normal pharynx. His neck was supple, nontender, without cervical lymphadenopathy, JVD, or carotid bruits. His heart revealed a normal S1/S2 without murmurs, rubs, or gallops. Breath sounds were clear and equal bilaterally with normal chest excursion. His abdomen revealed normal bowel sounds, it was nondistended but diffusely tender without rebound or guarding.
Interestingly, his back was tender diffusely over the lumbar area, which was worse on the left side. There was no ecchymosis or other lesions. There was mild dextroscoliosis present. The patient did not have costrovertebral tenderness and the left paravertebral muscles were boggy. His extremities revealed normal range of motion. They were nontender to palpation, with normal distal pulses and without edema. His skin was warm, dry, with good turgor, and no apparent lesions or exudates. Neurologically, he was awake, alert, and oriented. His cranial nerves were intact, and no gross deficits were identified.
Laboratory tests were ordered, including a CBC and chemistry panel as well as lumbar spine x-rays. (Fig. 1.) The CBC included a WBC of 11.0 × 103/mm3, hemoglobin of 10.2 g/dL, hematocrit of 29.2%, and platelet count of 394 × 103/mm3. The chemistry panel revealed that the patient was hyponatremic with a sodium level of 124 mEq/L. The remainder of the chemistry panel was normal, and included a potassium of 4.4 mEq/L, chloride of 87 mEq/L, bicarbonate of 0.8 mEq/L, BUN of 9 mg/dL, creatinine of 0.8 mg/dL and glucose of 123 mg/dL. Because the patient had hyponatremia, he was given a 500 ml bolus of normal saline and placed on maintenance fluids with normal saline at 100ml/hr. His pain was moderately controlled with two tablets of oxycodone/acetaminophen 5/325.
The patient had an admission chest x-ray performed which interestingly showed an 8 cm mass. (Fig. 2.) Consultations were requested, and he was admitted to the hospital. A chest CT scan (Fig. 3) was performed, which corroborated with the chest x-ray finding of an 8 cm mass. Further imaging performed including a renal ultrasound, which revealed a large heterogeneous mass posterior to the left kidney. Subsequently, a CT scan of the abdomen/pelvis was performed (Figures 4 and 5), revealing a large complex cystic paraspinal mass within the left psoas muscle with an accompanying epidural collection and bony erosion (Fig. 5) along the anterior L4 vertebra.
Brain CT revealed a focal low density within the left lentiform nucleus extending into the left corona radiata without mass effect or hemorrhage. The patient was started on sulfamethoxazole/trimethoprim (Bactrim), penicillin G, and metronidazole (Flagyl), but developed neutropenia thought to be secondary to the sulfamethoxazole/trimethoprim. The regimen was changed to amikacin (Amikin) and imipenem-cilastin (Primaxin) and continued on penicillin G until final identification of the organism. Blood and respiratory cultures grew out Nocardia farcinica. Despite aggressive treatment, the patient expired following two months of hospitalization.
Diagnosis and Treatment
Systemic and pulmonary nocardiosis is an uncommon gram-positive bacterial infection caused by aerobic actinomycetes. The classification is based on the location and extent of the disease and includes pulmonary, CNS, cutaneous, and disseminated disease. Risk factors include chronic lung diseases, alcoholism, malignancy, HIV, solid organ or hematopoietic stem cell transplantation, diabetes mellitus, or glucocorticoid therapy. Approximately one-third of infected patients are immunocompetent.
Systemic nocardiosis (two or more sites involved) accounts for 32 percent of cases with a mortality rate varying from seven percent to 44 percent. It is uncommon to obtain a positive blood culture during the first several days, and blood cultures should be held for about four weeks. Patients with systemic nocardia may develop retroperitoneal and psoas abscesses. The mean time of diagnosis ranges from 42 days to 12 months; this case took 31 days. Two-drug therapy is recommended, and three-drug therapy if life-threatening infection is present. For a severe infection not involving the central nervous system, Bactrim plus Amikacin or Imipenem plus Amikacin is recommended. The duration of treatment depends on the patient's response, severity of the disease, and the relapsing nature of nocardia, but a prolonged course for at least a year is recommend. Some suggest indefinite suppressive therapy.
Interestingly, this patient's last chemotherapy treatment was more than a year earlier, his TB infection was 20 years earlier, and he was not on steroids or calcitonin inhibitors. He was erroneously diagnosed with a mass on chest x-ray approximately a year before presentation, which was attributed to his CLL. The patient did admit to symptoms consistent with the disease such as fever, fatigue, anorexia, weight loss, and cough. He denied night sweats, dyspnea, hemoptysis, or pleuritic chest pain. This is usually misdiagnosed as TB because upper lobe involvement is common. The first case of nocardia spondylodiscitis accompanied by a psoas abscess secondary to spread from pulmonary nocardiosis was described in January 2007. Fortunately in that case, the patient's clinical condition improved after one year of treatment.
Back pain is a common complaint in the emergency department, and it is often rapidly diagnosed and treated in fast tracks. Occasionally the etiology, though, is secondary to significant pathology, as in this case. It is prudent for tthe physician to routinely perform a detailed history and physical, and maintain a high level of suspicion for the uncommon.
Dr. Keehn, left, is a second-year emergency medicine resident; Dr. Weinstein, second from left, is an attending in infectious disease; Dr. Levy, second from right, is the director of the emergency medicine residency, and Dr. Zimmerman, far right, is an emergency medicine attending, all at Good Samaritan Hospital in West Islip, NY.
1. Handad, F. Nocardia nova as the causative agent in spondylodiscitis and psoas abscess. J Clin Microbiol
2. Lerner PI. Nocardiosis. Clin Infect Dis
© 2010 Lippincott Williams & Wilkins, Inc.
3. Torres OH, et al. Infection caused by Nocardia farcinica
: Case report and review. Euro J Clin Microbiol Infect Dis