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Increasing Back Pain in a Young Man
roentgenogram of the month Increasing Back Pain in a Young Man* Manus M. Hoeper, M.D .; Michael Blauth , M .D .; and Hans J Schaefers, M.D.
A
(Chest 1993; 104:925-26)
29-year-old man was referred for evaluation for liver transplantation. Alcoholic cirrhosis had been diagnosed 3 years previously, and he had discontinued alcohol consumption since that time. There was no history of previous liver failure, encephalopathy, or esophageal variceal bleeding. Aside from a left-sided pleuropneumonia due to Staphylococcus aureus infection 18 months prior to his present admission, his medical history was unremarkable. The patient had been in stable condition until 6 weeks prior to presentation, when he first experienced dull pain in the back that was aggravated by motion. There was no fever, cough, night sweats, or weight loss. When his symptoms increased, a chest radiograph was obtained elsewhere (Fig 1), which was read as normal. The pain persisted, and nonsteroidal antiinflammatory agents were prescribed , with little subjective improvement. One week before admission, the patient experienced left-sided chest pain, which resolved spontaneously during the following days. At the time of admis sion, the patient was still suffering from back pain but appeared otherwise well . Physical examination revealed a diffuse tenderness to percussion over the thoracic vertebral column. Breath sounds were normal over the right lung and diminished over the dorsal aspect of the left lung without crackles or rales. Laboratory studies disclosed a white blood cell count of 4.4 x lQ9!L with 54 percent neutrophils, 36 percent lymphocytes, 6 percent monocytes, and 2 percent eosinophils. The C-reactive protein level was less than 6 mgIL. The erythrocyte sedimentation rate was elevated to 45 mmlh . Hepatic function was well preserved, with normal result s for serum albumin, bilirubin, and prothrombin time. The aminotransferase levels were not elevated . Abdominal ultrasound *From the Department of Pneumology (Dr. Hoeper); the Trauma Department (Dr. Blauth), and the Division of Thoracic and Cardiovascular Surgery (Dr. Schaefers), Hannover Medic al School, Hannover, Germany.
FIG URE
I
FIG URE
2
disclosed moderate portal hypertension with splenic enlargement and minimal ascites. Pulmonary function tests demonstrated a mild decrease in the vital capacity without obstructive patterns, and arterial blood gas values were normal. A purified protein derivative test was negative. Another chest radiograph was obtained (Fig 2).
CHEST I 104 I 3 I SEPTEMBER , 1993
925
Diagnosis: Chronic osteomyelitis with thoracic disk space infection at T4-5 to T8-9 with a paravertebral abscess and a left -sided pleural empyema The chest radiograph (Fig 2) revealed an opacification of the left middle and lower lung fields and mild bilateral mediastinal widening. Lateral projection and tomography demonstrated spontaneous fusion of disk spaces T4-5 to 1'8-9 with sclerosis of the adjacent vertebrae. A thoracic ultrasound examination confirmed the suspected diagnosis of a pleural effusion, and diagnostic thoracentesis revealed pus. On microbiologic examination, S aureus was isolated. Acid-fast bacilli were not found . Transesophageal echocardiography gave no evidence of bacterial endocarditis but demonstrated pre- and paravertebral liquid structures. A computed tomographic scan of the thorax (Fig 3) revealed a paravertebral soft-tissue mass with liquid portions descending from the level of the aortic arch to the level of the suprarenal glands. There was marginal enhancement after intravenous administration of contrast material, indicating a paravertebral abscess . There were multiple destructive lesions in the vertebral column. Left-sided pleural empyema was found communicating with the paravertebral abscess. The patient was treated with intravenous antibiotics and underwent surgery a few days later. Decortication of the pleural empyema was performed via a left posterolateral thoracotomy followed by wide incision, debridement and irrigation of both paravertebral spaces, and drainage with chest tubes. The postoperative course was uneventful, and after a 6-week course of antibiotic treatment, there was no further evidence of ongoing infection. In summary, this patient suffered from a paravertebral abscess with communicating left-sided pleural empyema. We believe that the primary source of infection was hematogenous vertebral osteomyelitis, most likely a sequela of the previous staphylococcal pleuropneumonia. The prominent feature of the first chest radiograph (Fig 1) was marked bilateral mediastinal widening due to the paravertebral inflammatory process. In addition, the second chest radiograph showed a left-sided pleural empyema. At this time, the mediastinal widening was still detectable but less apparent, which was probably due to spontaneous perforation of the abscess into the left pleural space . Mediastinal processes, as in this case , are not often encountered and are usually attributed to lymphoma, thymoma, germ cell tumors, neurogenic tumors, esophageal lesions, or vascular enlargements. Paraver-
FIGURE
3
tebral abscesses are an additional cause of mediastinal masses but may not be included in the differential diagnosis in the absence of fever or an elevated white blood cell count. Nevertheless, the lack of clinical and laboratory signs of inflammation is not unusual in this disorder, I and in some instances, an elevated erythrocyte sedimentation rate may be the only clue that backache is due to something other than an orthopedic disorder." Computed tomography and magnetic resonance imaging are the most appropriate diagnostic means to establish the diagnosis and to determine the extension of paravertebral soft-tissue involvement, abscess formation , and bone erosions." Almost any microorganism may be identified as the cause of vertebral osteomyelitis, although S aureus is the most common pathogen.' The detection of vertebral osteomyelitis and paravertebral abscesses should lead to a careful search for tuberculosis, which is well known to produce paravertebral abscesses," but as this case demonstrates, large abscesses due to classic pyogenic microorganisms may also appear without apparent signs of infection . REFERENCES 1 Mankin HJ, Back and neck pain. In: Wilson JD . et al, eds. Harrison's principles of internal medicine, 12th ed . New York: McGraw-Hili , 1991; 116-24 2 Baldwin N, Scott AR, Heller SR. O'Donoghue 0, Tottersall RB. Vertebral and paravertebral sepsis in diabetes: an easily missed cause of backache . Diabetic Med 1985; 2:395-97 3 Colimba C . Firoonznia H , Rani M. CT of osteomyelitis in the spine . AJR 1984; 142:159-63 4 Musher OM , Thorsteinsson SB, Minuth SN. Luchi RS. Vertebral osteomyelitis: still a diagnostic pitfall. Arch Intern Med 1976; 136:105-10 5 Gorse GJ, Pais MJ. Kusske JA. Cesario TC . Tuberculous spondylitis: a report of six cases and a review of the literature. Medicine (Baltimore) 1983; 62:178-93
Roentgenogram of the Month (Hoeper, Blauth, SChaefers)
A
(Chest 1993; 104:925-26)
29-year-old man was referred for evaluation for liver transplantation. Alcoholic cirrhosis had been diagnosed 3 years previously, and he had discontinued alcohol consumption since that time. There was no history of previous liver failure, encephalopathy, or esophageal variceal bleeding. Aside from a left-sided pleuropneumonia due to Staphylococcus aureus infection 18 months prior to his present admission, his medical history was unremarkable. The patient had been in stable condition until 6 weeks prior to presentation, when he first experienced dull pain in the back that was aggravated by motion. There was no fever, cough, night sweats, or weight loss. When his symptoms increased, a chest radiograph was obtained elsewhere (Fig 1), which was read as normal. The pain persisted, and nonsteroidal antiinflammatory agents were prescribed , with little subjective improvement. One week before admission, the patient experienced left-sided chest pain, which resolved spontaneously during the following days. At the time of admis sion, the patient was still suffering from back pain but appeared otherwise well . Physical examination revealed a diffuse tenderness to percussion over the thoracic vertebral column. Breath sounds were normal over the right lung and diminished over the dorsal aspect of the left lung without crackles or rales. Laboratory studies disclosed a white blood cell count of 4.4 x lQ9!L with 54 percent neutrophils, 36 percent lymphocytes, 6 percent monocytes, and 2 percent eosinophils. The C-reactive protein level was less than 6 mgIL. The erythrocyte sedimentation rate was elevated to 45 mmlh . Hepatic function was well preserved, with normal result s for serum albumin, bilirubin, and prothrombin time. The aminotransferase levels were not elevated . Abdominal ultrasound *From the Department of Pneumology (Dr. Hoeper); the Trauma Department (Dr. Blauth), and the Division of Thoracic and Cardiovascular Surgery (Dr. Schaefers), Hannover Medic al School, Hannover, Germany.
FIG URE
I
FIG URE
2
disclosed moderate portal hypertension with splenic enlargement and minimal ascites. Pulmonary function tests demonstrated a mild decrease in the vital capacity without obstructive patterns, and arterial blood gas values were normal. A purified protein derivative test was negative. Another chest radiograph was obtained (Fig 2).
CHEST I 104 I 3 I SEPTEMBER , 1993
925
Diagnosis: Chronic osteomyelitis with thoracic disk space infection at T4-5 to T8-9 with a paravertebral abscess and a left -sided pleural empyema The chest radiograph (Fig 2) revealed an opacification of the left middle and lower lung fields and mild bilateral mediastinal widening. Lateral projection and tomography demonstrated spontaneous fusion of disk spaces T4-5 to 1'8-9 with sclerosis of the adjacent vertebrae. A thoracic ultrasound examination confirmed the suspected diagnosis of a pleural effusion, and diagnostic thoracentesis revealed pus. On microbiologic examination, S aureus was isolated. Acid-fast bacilli were not found . Transesophageal echocardiography gave no evidence of bacterial endocarditis but demonstrated pre- and paravertebral liquid structures. A computed tomographic scan of the thorax (Fig 3) revealed a paravertebral soft-tissue mass with liquid portions descending from the level of the aortic arch to the level of the suprarenal glands. There was marginal enhancement after intravenous administration of contrast material, indicating a paravertebral abscess . There were multiple destructive lesions in the vertebral column. Left-sided pleural empyema was found communicating with the paravertebral abscess. The patient was treated with intravenous antibiotics and underwent surgery a few days later. Decortication of the pleural empyema was performed via a left posterolateral thoracotomy followed by wide incision, debridement and irrigation of both paravertebral spaces, and drainage with chest tubes. The postoperative course was uneventful, and after a 6-week course of antibiotic treatment, there was no further evidence of ongoing infection. In summary, this patient suffered from a paravertebral abscess with communicating left-sided pleural empyema. We believe that the primary source of infection was hematogenous vertebral osteomyelitis, most likely a sequela of the previous staphylococcal pleuropneumonia. The prominent feature of the first chest radiograph (Fig 1) was marked bilateral mediastinal widening due to the paravertebral inflammatory process. In addition, the second chest radiograph showed a left-sided pleural empyema. At this time, the mediastinal widening was still detectable but less apparent, which was probably due to spontaneous perforation of the abscess into the left pleural space . Mediastinal processes, as in this case , are not often encountered and are usually attributed to lymphoma, thymoma, germ cell tumors, neurogenic tumors, esophageal lesions, or vascular enlargements. Paraver-
FIGURE
3
tebral abscesses are an additional cause of mediastinal masses but may not be included in the differential diagnosis in the absence of fever or an elevated white blood cell count. Nevertheless, the lack of clinical and laboratory signs of inflammation is not unusual in this disorder, I and in some instances, an elevated erythrocyte sedimentation rate may be the only clue that backache is due to something other than an orthopedic disorder." Computed tomography and magnetic resonance imaging are the most appropriate diagnostic means to establish the diagnosis and to determine the extension of paravertebral soft-tissue involvement, abscess formation , and bone erosions." Almost any microorganism may be identified as the cause of vertebral osteomyelitis, although S aureus is the most common pathogen.' The detection of vertebral osteomyelitis and paravertebral abscesses should lead to a careful search for tuberculosis, which is well known to produce paravertebral abscesses," but as this case demonstrates, large abscesses due to classic pyogenic microorganisms may also appear without apparent signs of infection . REFERENCES 1 Mankin HJ, Back and neck pain. In: Wilson JD . et al, eds. Harrison's principles of internal medicine, 12th ed . New York: McGraw-Hili , 1991; 116-24 2 Baldwin N, Scott AR, Heller SR. O'Donoghue 0, Tottersall RB. Vertebral and paravertebral sepsis in diabetes: an easily missed cause of backache . Diabetic Med 1985; 2:395-97 3 Colimba C . Firoonznia H , Rani M. CT of osteomyelitis in the spine . AJR 1984; 142:159-63 4 Musher OM , Thorsteinsson SB, Minuth SN. Luchi RS. Vertebral osteomyelitis: still a diagnostic pitfall. Arch Intern Med 1976; 136:105-10 5 Gorse GJ, Pais MJ. Kusske JA. Cesario TC . Tuberculous spondylitis: a report of six cases and a review of the literature. Medicine (Baltimore) 1983; 62:178-93
Roentgenogram of the Month (Hoeper, Blauth, SChaefers)