Pott disease is tuberculosis of the spine, usually due to haematogenous spread from other sites, often the lungs. The lower thoracic and upper lumbar vertebrae areas of the spine are most often affected. It causes a kind of tuberculous arthritis of the intervertebral joints. The infection can spread from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients, and collapses. In a process called caseous necrosis, the disc tissue dies, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft-tissue mass often forms and superinfection is rare. Spread of infection from the lumbar vertebrae to the psoas muscle, causing abscesses, is not uncommon.The disease is named after Percivall Pott, the British surgeon who first described it in the late 18th century. Diagnosis
Blood tests– Complete blood count: leukocytosis
– Elevated erythrocyte sedimentation rate: >100 mm/hTuberculin skin test– Tuberculin skin test (purified protein derivative [PPD]) results are positive in 84–95% of patients with Pott disease who are not infected with HIV. Radiographs of the spine– Radiographic changes associated with Pott disease present relatively late. These radiographic changes are characteristic of spinal tuberculosis on plain radiography:
Lytic destruction of anterior portion of vertebral body
Increased anterior wedging
Collapse of vertebral body
Reactive sclerosis on a progressive lytic process
Enlarged psoas shadow with or without calcification
– Additional radiographic findings may include:
Vertebral end plates are osteoporotic. Intervertebral disks may be shrunken or destroyed.
Adverse effects
The most common adverse effects affecting 5 to 15% of the patients include allergic conjunctivitis, conjunctival folliculosis, conjunctival hyperemia, eye pruritus, ocular burning, and stinging. 1 to 5% of the patients in clinical trials experienced asthenia, blepharitis, corneal erosion, depression, epiphora, eye discharge, eye dryness, eye irritation, eye pain, eyelid edema, eyelid erythema, eyelid pruritus, foreign body sensation, headache, hypertension, oral dryness, somnolence, superficial punctate keratitis, and visual disturbance. Contraindications
Contraindications of Combigan include the following: reactive airway disease including bronchial asthma, a history of bronchial asthma, severe chronic obstructive pulmonary disease, sinus bradycardia, secondary or third degree atrioventricular block, overt cardiac failure, cardiogenic shock, age less than 2 years, and hypersensitivity to any component of Combigan. Pharmacology
Combigan is composed of brimonidine, a selective alpha-2 adrenergic receptor agonist, and timolol, a non-selective beta-adrenergic receptor inhibitor. Elevated IOP is considered the only modifiable risk factor in the pathogenesis of glaucoma. Brimonidine exerts its ocular hypotensive effect by decreasing aqueous humor production and increasing uveoscleral outflow, while timolol acts by reducing aqueous humor production. Combigan has a fast onset of action, and the peak IOP lowering effect occurs at two hours after administration. Preclinical studies
No carcinogenic effects were found with brimonidine tartrate in mice or rats.