Tuberculous spondylitis and perforated peptic ulcer due to associated non-steroidal anti-inflammatory drug use

Clinical Cases 28.05.2006
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Section: Musculoskeletal system
Case Type: Clinical Cases
Patient: 78 years, female
Authors: Dr I Hagan, Dr C Corr. Cheltenham General Hospital, Sandford Rd, Cheltenham, GL53 7AN, UK
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Clinical History

A 78 year old woman with acute abdominal pain

Imaging Findings

The patient was admitted with a 12 hour history of severe upper abdominal pain. She had been taking nonsteroidal anti-inflammatory drugs (NSAIDs) for back pain for two to three months. She had a low grade pyrexia of 37.8C and a raised white cell count and C reactive protein. Contrast enhanced computed tomography (CT) of the abdomen and pelvis demonstrated a large amount of free intraperitoneal gas and a moderate amount of free fluid in keeping with a perforated viscus. A suspected site of perforation in the distal stomach was later confirmed at laparotomy as a perforated benign prepyloric ulcer, presumed secondary to NSAID use. In addition, CT showed bone destruction adjacent to the inferior endplate of the L1 vertebra with associated epidural and psoas collections. Peripheral amorphous calcification was seen in association with the psoas abscess, highly suggestive of a tuberculous aetiology.

Discussion

Although it accounts for fewer than 1% of all infections due to mycobacterium tuberculosis, tuberculous spondylitis represents the commonest site of osseous tuberculous infection. Patients usually complain of back pain of insidious onset with or without constitutional symptoms. At least half will have no radiological evidence of past or present pulmonary tuberculous infection. The vertebrae around the thoracolumbar junction are most commonly affected. Vertebral infection is a result of haematogenous seeding of the organism and infection usually begins in the anterior portion of the vertebra adjacent to the superior or inferior endplates corresponding to the presence of low flow vascular arcades at these sites. Subsequent spread may then occur to the remainder of the vertebra, through subchondral endplate into the adjacent intervertebral disc, beneath anterior or posterior longtitudinal ligaments for variable distances, or into paraspinal soft tissues, often with extensive abscess formation more dramatic than the osseous abnormalities. Complications include spinal cord compression, vertebral body collapse leading to angular kyphosis (gibbus) in adults or vertebra plana in children, and haematogenous spread of infection to other sites. Mortality may be as high as 30%. The classical description of tuberculous spondylitis by Pott involves destruction of two or more contiguous vertebral bodies and the intervening intervertebral discs. Many cases such as this one have an atypical picture, however, with involvement of only one vertebra, sparing of the intervertebral disc, and early extension into paraspinal soft tissues. Conventional radiography is insensitive in the earlier stages of infection. CT performs well in demonstrating vertebral body endplate destruction and the amorphous rim calcification often seen in association with tuberculous paraspinal abscesses but only rarely seen in pyogenic abscesses. Magnetic resonance imaging is the imaging modality of choice, however, with its superior soft tissue contrast allowing delineation of effects on neural structures and discrimination between enhancing inflammatory tissue and true abscess formation which may require drainage. The principal differential diagnosis is pyogenic spondylitis. Although it may be impossible to distinguish between pyogenic and tuberculous spondylitis on imaging criteria alone, features favouring a tuberculous aetiology are: relative sparing of the intervertebral disc; large paraspinal abscesses, especially with a thick enhancing rim or peripheral calcification; relatively little new bone formation; and a fragmentary pattern of bone destruction. This case emphasises the importance of reviewing the bones on abdominal CT even when they are not the primary reason for performing the study.

Differential Diagnosis List

Tuberculous spondylitis. NSAID-induced perforated prepyloric peptic ulcer.

Final Diagnosis

Tuberculous spondylitis. NSAID-induced perforated prepyloric peptic ulcer.

Liscense

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