Pott Disease D/D Spinal tumors Mycobacterium kansasii Nocardiosis Paracoccidioidomycosis Septic arthritis Spinal cord abscess Lab studies for confirmation Tuberculin skin test (PPD) - Results are positive in 84-95% of patients with Pott disease who are not infected with HIV Erythrocyte sedimentation rate (ESR) - May be markedly elevated (>100 mm/h) Microbiologic studies - Used to confirm the diagnosis With regard to the above-mentioned microbiologic studies, bone tissue or abscess samples are obtained to stain for acid-fast bacilli (AFB), and organisms are isolated for culture and susceptibility.
CASE UPDATE. I am thankful to each and every one of you who answed the case. All of you have given the appropriate answers. Esr was 40mm/ hr. All tumor markers were - ve.xray chest , us abdomen were normal. Pt was transferred to spinal surgeon . Posreolateral decompression laminectomy with stabilization & screw fixation done .Drained the impending abcess. BIOPDY REPOR TUBERCULOUS DISCITIS. 2nd post op day the pt became unresponsive inn the icu with rapid AF. SEEN BY cardiologist, intensivist , tried resuscitation but unfortunately the patient passed away. MRI report;Intervertebral disc appears irregular with T2 hyperintense & T1 hypointense signal at D11-12 level..Area if heterogeneous marrow signals seen in the vertebral bodies at D11& D12 with reduced vertebral heights.The intervening end plateappears irregular with STIR hyperintensities.The ID disc appears mildly hyperintense in DW1 .Milf gibbus deformity causing spinalcord compression.Minimal AP diameter measures 6.5mm. Subtle T2 hyperintense signals seen in the cord atthis level.Small T2 and STIR hyperintense signal with no enhancement noted in prevertebral & left paravertebral location of D11. Imp: MRI of the spine show area of heterogeneous marrow signals at D11-12 with endplate irregularity and enhancing signals in the IV disc .Small prevertebral, left paravertebral and epidural collection at D11. Findings suggestive of SPONDYLODISCITIS .TUBERCULOSIS.
Looks like infective process with collapse and compression Needs posterior predisposition screw stabilisation and posterolateral decompression under cover of AKT and antibiotics prior to surgery with HPE, Culture for MDR. If patient is not willing for surgery then AKT with antibiotics, DVT prophylactic dose heparin to improve perfusion, chymeral forte, vitamin C with graduated PELVIC TRACTION, organic raw food
Paradiscal TB with cold abscess anteriorly and extradural compression posterioly UMN features in lower limbs Anterolateral decompression? Other options are laminectomy and pedicle screw fixation spanning the lesion ATT and fusion once lesion heals
Destruction of Vertebral Structure and collapse with loss of Intervertebral space and cold abscess anteriorly compressing upon the spinal cord developing Paraparesis due to Compressive Myelopathy...
No significant psychological factor seems to contribute in the present condition. This appears to be agerelated organic condition
?TB spine/metastasis into spine- cb nat test, CT guided biopsy, ant decompression &fusion/corprorraphy/bone grafting.
Looks like spondylodiscitis ...needs contrast study for better characterisation and to look for abcess
As patient is having Diabetes chances are there that patient is having potts spine.
Probably Potts spine Other pathological fractures has to be ruled out
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What are the DD for this patient. How to Approach? What Investigation to be doneDr. Alfaz Lakhani1 Like13 Answers
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New Case 16 yr ,F ,student, Presented with back pain 2 months ,evaluated by the local hospital with xray taken at lumbosacral spine and was reported as normal . The girl was unable to localize the pain. Since 1week she has difficulty to walk and not going to school due to pain and sitting in the chair and sleeping. Denied having any motor or sensory symptoms.No bowel or bladder symptoms. On Exam ,no neurocutaneous markers Gr5/ 5 power .DTRs normally elicitable. Normal abdominal reflexes and downgoing plantars. Intact sensations. yesterday OPD case,After MRI she was ref to spinal surgeon who suggested Surgery. In the night itself the family insisted for discharge and discharged at request.All blood work up normal. ESR 20mm/ hr. Normal peripheral smear . What abnormality in the spine MRI , Possible diagnosis and managementDr. Manorama Rajan2 Likes13 Answers
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Hi Doctors, I treating a male patient age 60 yr, he is k/c/o addiction of Inj Daiclofenac 3ml and Inj Dexa 80mg IM daily from last 20yrs. Also he is recently diagnosis DM Vital parameters are within normal limits. ECG Normal . HB:7 nld WBC : 14800 Plt. : Normal LFT: Abnormal RFT: Normal Serology: Negative BSL: F-180 PP- 204 Urine-R: Abnormal Pus culture not done. Now he is suffering severe pain all joints. Rx Inj Piptaz 4.5 TDS Inj Pan40mg OD Inj Eldervit stat Inj Dynapar AQ 1ml SOS Inj Lasix Inj Ferinject with NS Tab Ampachakwati Tab Udliv Tab Enzomac Fort Can you give me your valuable opinion???. What is the Diagnosis in your view ???.Amardeep Ebhate1 Like9 Answers
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51 yrs lady menopause since 3-4 yrs.teacher by profession. No H/O Koch's ,DM ,any operative H/O recurrent UTI 2yrs before took treatment and renal scaring was there so started on olmesartan 20 od which is stopped since June 2016. H/O zyloric 300 od for 2 yrs. At present uric acid and BP are normal. C/ O Low backache since Nov. 2015 which started while she was taking Root canal treatment. Took pain killers and physiotherapy but no result.so went to orthopaedic who advised MRI which was done which revealed ?TB L2 spine. So CT scan L2 done which ruled out TB. Again in Dec.2015 and Jan 2016 two MRI done which revealed L4 spondylolisthesis and no Koch's . So opinion of spine surgeon taken who advised biopsy which is negative for Koch's and malignancy. Diagnosis was compression # L2 So vertebroplasty done. Treated with calcium vit d3 and parathyroid hormone injection .inj.to continue for 6 months started in July 2016. Now some questions 1 Can it be a case of Koch's spine? 2 Can it be malignancy? 3 How to rule out above two ? 4 why there is degeneration ? as new scan is showing ?compression # L1 . 5 is there any relation to hormones ? 6 how to proceed further ? 7 can empirically start anti Koch's treatment ?Dr. Aniruddha Lele3 Likes9 Answers
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RHEUMATOID ARTHRITIS RA is a type of inflammatory arthritis. Other examples include seronegative spondyarthritides, reactive arthritis, lyme arthritis, crystal arthritis and postviral arthritis. Features of inflammatory arthritis : ●Pain and stiffness worse in the morning and after rest. ●Early morning pain and stiffness may last several hours (in OA, duration is much shorter). ●Inflammatory markers (ESR, CRP)usually raised. ●Often accompanied by normochromic, normocytic anaemia. This is a chronic symmetrical arthritis. When we say it is symmetrical, we don’t necessarily mean a mirror image, just that the same joints are affected on both sides of the body. it is also important to remember that RA is a systemic condition, with many extra-articular manifestations. This is a chronic symmetrical arthritis. When we say it is symmetrical, we don’t necessarily mean a mirror image, just that the same joints are affected on both sides of the body. it is also important to remember that RA is a systemic condition, with many extra-articular manifestations. Typically it affects the peripheral joints, and there is inflammation of the joint (synovitis). Deformity is common and the course is extremely variable. Epidemiology and Aetiology : ●Affects 0.5-3% of the population worldwide. ●Can present at any age (from childhood to old age), but the peak incidence is between 30-50 years. ●women affected more than men (M:F – 1:2). ■before the menopause, risk is 3x higher for women . ■after the menopause it is equal. ■suggests sex hormones involved in some way. ■the contraceptive pill can delay the onset, but does not reduce the risk. ●Genetic factors are involved. Certain HLA variants are implicated, especially in severe forms of the disease:. ●HLA-DR4 – occurs in 50-75% of patients, and is associated with a particularly poor prognosis. ●HLA-DR1 is another variant associated with RA, and poor prognosis. ●Environmental factors: ¤Smoking ¤Stress ¤Infection Clinical features : Most commonly, the condition will present as progressive over weeks to months. These patients have the worse prognosis. But in some cases it can come on in days, or even overnight. Also, it is almost always a polyarthritis, but some cases do present as monoarthritis, most commonly of the knee or shoulder, or with carpal tunnel syndrome. ●symmetrical swollen distal joints. ●Often warm and tender joints. ●sometimes presents as a sudden onset of widespread arthritis, but this is rare. ●Typically the joint of the hand (MCP, DIP and PIP’s)and the distal metatarsals of the foot. ●Sometimes it affects the wrists, elbows, shoulders, knees and ankles. ●Hips are very rarely affected. ●Limitation of movement. ●Muscle wasting. ●Pain and stiffness – worse in the morning, may improve with activity. It is often described as an ache type pain. ●Disturbed sleep. ●Nodules – in the early and mild stages of the disease, there are relatively few inflammatory cells in the joints. As the disease progresses, these increase in number and there may be nodular masses of inflammatory cells within the joint. Rheumatoid nodules occur when these inflammatory cells form similar inflammatory structures outside of the joint capsules. The nodules are usually pink/red and have a rubbery texture. They are painless. You should always check the elbows in a hand exam, looking for rheumatoid nodules!. ●Osteoporosis – often occurs in the bones immediately around the affected joints, particularly in the fingers. This may be the first sign of RA. ●Secondary Osteoarthritis. ●Deformity – as the joint capsule is destroyed, and the articular surface damaged, deformity occurs. Specific examples include ●Hands ¤Swan necking – the fingers become hyperextended at the PIP, and flexed at the DIP. ¤Z-thumb. ¤Subluxation of the MCP –not that this is not swelling!. ¤Muscle wasting – “guttering” – ‘gutters’ seen between the extensor tendons on the back of the hand. ●Why do the muscles waste so quickly in joint disease? – In a normal individual, if you don’t use a muscle, it will waste at a rate of about 1% of its mass/day. However, in joint disease, the rate of wasting in much greater. This is because in joint disease, there is inhibition of nerve afferents, for nerves that innervate the muscles around a joint. This alters the muscle tone/reflex feedback loop, leading to decreased innervation of the muscle, and as a result, wasting occurs very quickly. ●Inflamed flexor tendon sheaths – these serious impair function. ●Carpal tunnel syndrome is common. ●Ulnar deviation – the fingers point towards the ulnar side. ●Fixed flexion deformity – aka buttonhole or boutonniere deformity. ●Shoulders – Shoulders are commonly affected, and at first it may mimic rotator cuff tendonitis. Later, the joint becomes stiffened. Rotator cuff tears can occur late on. ●Elbows – less commonly affected. Flexion may be lost, which makes eating very difficult. ●Knees – massive synovitis and effusion. These respond well to steroid injection and aspiration. A persistent effusion may increase the risk of cyst formation, and these can rupture. Varus or valgus deformity can occur, and there may be joint space narrowing and secondary OA.Knee replacement can restore much of the function, and relieve pain. ●Cervical spine – pain in the neck is more commonly muscular, but you can get joint disease itself in the cervical spine. There can be bone destruction, which poses a risk to the spinal cord.Be wary loss of sphincter control, or unexplained weakness in late RA – could be due to cord compression!. ●Feet – often the first signs of the disease may only be in the feet. The patient may describe an uncomfortable sensation that feels like walking on marbles. This is due to subluxation of the heads of the metatarsals in the feet. Presentations : ■Palindromic – monoarticular attacks, last 24-48 hours. 50% of cases will progress to other types of RA. ■Transient – lasts <12 months, then permanently remits. Usually seronegative. No lasting damage. ■Remitting – may be active for several years at a time, before remitting. Lasting damage is minimal. ■Chronic, persistent – the most common form. May be seronegative or seropositive. Follows a relapsing remitting course over many years. Seropositive patients have worse joint disease and higher risk of long-term disability. ■Rapidly progressive – rapid progression occurs over several years. Severe joint damage, disability and high rate of complications. Normal initial investigations : ■Blood count: ●Anaemia. ●ESR/CRP raised due to inflammation. Monitoring levels of these can be used to assess treatment . ■Serology – check for rheumatoid factor – only present in 70% of cases. ¤ANA’s – anti-nuclear antibodies – these are also regularly tested for, and show up in 30% of cases. ¤Anti-CCP – testing for this is becoming more common. ■X-ray – useful to get a baseline reading at the start of the disease. Normally only soft tissue swellings initially. Later there may be:¤Boney erosions. ¤Osteopenia (lower than normal bone density). ■Joint aspiration – in the presence of effusion. Aspirate will appear cloudy due to the presence of white cells. If the joint is suddenly painful, always aspirate to check for septic arthritis, as this can rapidly destroy joints. ■MRI – very rarely used, but can show early bone erosions. Also used in widespread disease to assess the extent of the joint damage.Dr. Girish Dahake10 Likes9 Answers