According to the American Society of Interventional Pain Physicians (ASIPP), interventional pain management (IPM) is a 'discipline of medicine devoted to the diagnosis and treatment of pain related disorders.' IPM utilizes a multidisciplinary approach in which a team of health care professionals works together to provide a full range of treatments and services for patients suffering from chronic and/or acute pain. The goals of IPM are to relieve, reduce, or manage pain and improve a patient's overall quality of life through minimally invasive techniques specially designed to diagnose and treat painful conditions. The discipline also strives to help patients return to their everyday activities quickly and without heavy reliance on medications. The team members of IPM include a physiatrist (physical medicine and rehabilitation specialist), anesthesiologist, general surgeon, internist, and psychiatrist [1]. Interventional physiatry is a branch of physical medicine and rehabilitation that treats pain using precisely placed anti-inflammatory injections into the spine and pelvis, guided by specially equipped X-ray machines [2,3]. Interventional pain physicians may perform selective nerve root blocks, facet joint procedures, spinal cord stimulation, epidural injections, intrathecal pump placement, trigger point procedures, and vertebroplasty. They can also perform disc procedures such as discography, provocative discography, intradiscal electrothermaltherapy (IDET), etc. [3,4]. In 1998, the American Board of Physical Medicine and Rehabilitation joined the American Board of Anesthesiology in recognition of pain management as an interdisciplinary subspecialty [4,5]. In Bangladesh, however, the situation is completely different, with some limited spinal and peripheral joint procedures being performed by different specialists (physiatrists, orthopedists, anesthesiologists, neurologists, etc.) in their private practices. The subspecialty of interventional pain management does not exist, and there are no institutes devoted solely to IPM. In this article, we focus on the current practice of IPM in a tertiary medical college hospital in Bangladesh.

Patients who visited and received treatment through a pain clinic in the Department of Physical Medicine and Rehabilitation (PMR) at Chittagong Medical College Hospital over a period of 3 years (2006-2008) were enrolled in the study. Sources of patients were the outpatient department (PMR OPD), and the rheumatology follow up clinic, spondylarthropathy (SpA) clinic, and rheumatoid arthritis (RA) clinic, conducted in the department on separate days. Data were collected and recorded on a formulated data sheet containing each patient's particular and clinico-radiological information. To facilitate description, patients were categorized into the following 4 groups:

G-A: Degenerative peripheral joint disorders

G-B: Inflammatory rheumatological disorders

G-C: Non-infectious and non-inflammatory soft tissue rheumatism (STR)

G-D: Radicular and referred lower back pain (LBP)

Inflammatory joint disorders were classified according to the following clinical criteria: 1987 revised American College of Rheumatology (ACR) criteria for RA; modified New York criteria for ankylosing spondylitis (AS); and European Spondylarthropathy Study Group criteria for SpA [6-8]. Degenerative knee conditions were diagnosed according to clinical findings, with recommended clinical criteria used in some cases (ACR criteria for knee osteoarthritis, OA) [9]. Radiological corroboration was done where necessary. Pain in between the 12^th rib and the inferior gluteal folds is known as LBP [10], and the common musculoskeletal sources of LBP are lumbar spondylosis, lumbar spinal stenosis, prolapsed lumbar intervertebral disc (PLID), myofascial pain syndrome (MPS), fibromyalgia (FMS), lumbar ligamentous sprain, piriformis syndrome, sacroiliac joint dysfunction, AS, vertebral body fracture, and spondylodiscitis. The term lumbar spinal stenosis is used to describe abnormal narrowing of the central part, lateral recesses, or intervertebral foramen of the lumbar spine to the point where the neural elements are compromised and signs or symptoms develop in the lower limbs. Common causes of lumbar spinal stenosis are lumbar spondylosis, lumbar spondylolisthesis, ligamentum flavum hypertrophy, facet joint arthropathy, PLID, and spondylodiscitis [10,11]. All of these clinical conditions except infective discitis were treated with interventional procedures in the pain clinic. Ligamentum flavum hypertrophy/facet hypertrophy was diagnosed with lumbar spine MRI. Soft tissue lesions can be due to trauma, overuse, infection, inflammation, or endocrinopathy, or may be idiopathic. In this paper, non-infectious and non-inflammatory soft tissue rheumatism are discussed separately.

During the study period, a total of 45,842 patients were treated in the PMR OPD. Out of these patients, 1,260 (2.8%) with different articular and non-articular clinical conditions underwent intervention in the pain clinic. The patients' demographic profile is presented in Table 1. The greatest number of patients came from the PMR OPD (500, 39.7%), followed by the rheumatology follow up clinic (280, 22.2%), RA clinic (130, 10.3%), and SpA clinic (110, 8.7%). 240 patients (19.0%) were referred from different departments of the facility for better management, including rehabilitative support. Among the 1260 patients, degenerative peripheral joint disorders were the most common diagnosis (600, 46.0%), followed by inflammatory rheumatological conditions (300, 23.0%), non-infectious/non-inflammatory soft-tissue rheumatism (300, 23.0%), and radicular/referred LBP (100, 8.0%) (Fig. 1). These are discussed separately below.

Common inflammatory rheumatological conditions include SpA, RA, vasculitis, systemic lupus erythematosus, and mixed connective tissue disease, where along with spinal and peripheral joints, periarticular soft tissues also can be involved. Soft tissue lesions in the form of enthesitis are more common in SpA than in other inflammatory joint disorders, and are mostly distributed in the Achilles tendon and plantar fascia. It also can be seen in the head/base of the metatarsal bone, origin of the adductor muscle of the thigh, extensor tendon, anterior superior iliac spine, iliac crest, symphysis pubis, or de Quervain's tenosynovial sheath, etc. [17]. Compressive neuropathy due to soft tissue inflammation at the nerve tunnel is common in RA [18]. In inflammatory rheumatological conditions, spine and peripheral joints respond well to steroids/NSAIDs (non-steroidal anti-inflammatory drugs) and DMARDs (disease modifying anti-rheumatic drugs) [19,20]. Pulsed steroid (375-1,000 mg) in 5% dextrose aqua is a treatment option in acute flare-ups of RA/SpA, usually practiced for 3-5 consecutive days [21]. Osteoarthritis predominantly affects the weight bearing lower extremity joints and is more common in the knee than in the hip, ankle, or foot joints. In the upper extremity, OA usually involves the acromioclavicular joint. Along with oral medications, I/A steroids and local anesthetics can be effective in both inflammatory and degenerative joint disorders [20]. I/A injection of sodium hyaluronate (20 mg/2 ml) is a treatment option in OA of the knee responding poorly to available conservative approaches [22]. To reduce joint pain and repair damaged cartilage, at least 3 injections should be given in each joint for three successive weeks [22]. I/A ozone prolotherapy is also effective in knee OA, as described in some research articles [23,24]. After aspiration, bandaging can be done to prevent recurrent effusion, followed by restriction of knee weight bearing activities for the next 24-48 hours. Common complications during and after joint injection are aspiration pain, recurrent effusion, transient rise of blood pressure (steroid-induced), acute flare-up, injection site pain, overlying skin depigmentation, joint infection, or avascular necrosis. Aspiration pain is more common if joint procedures are done without local anesthesia. Acute flare-up is possible within the first 24-72 hours following the procedure, and generally resolves spontaneously, but can be managed with local application of ice/cold compresses. Recurrent effusion is more common in deformed joints. Overlying skin depigmentation has been reported following triamcinolone-mediated joint/soft tissue intervention [25]. In this recent study, a total of 300 cases of different inflammatory rheumatological conditions and 600 cases of degenerative peripheral joint disorders were treated in the pain clinic. In both of these conditions, the most common site of peripheral joint intervention was the knee. Soft tissue rheumatism (STR), soft tissue lesion, and compressive neuropathy were common in inflammatory rather than degenerative peripheral joint disorders. Inflammatory soft tissue lesions were commonly distributed in the plantar fascia (30), de Quervain's tenosynovial sheath (10), and trigger finger (6). Heel enthesitis (plantar fasciitis and Achilles tendinitis) was common in SpA. All compressive neuropathy in the form of CTS was classified as RA. I/A steroids were given to reduce joint pain, and the knee joint received a maximum dose (80 mg) of methylprednisolone among all peripheral joints. Injection of sodium hyaluronate 20 mg/2 ml was given in 10 cases of OA of the knee. Of these patients, only 2 received the recommended dose (at least 3 injections for 3 consecutive weeks). Pulsed steroids were given only in 10 cases (3.3%) of RA and SpA during acute flare-ups. To avoid development of avascular necrosis, we did not perform any steroidal intervention in the hip joint. During and following joint procedures, reported complications were aspiration pain, recurrent effusion, flare-ups, and skin depigmentation. Recurrent effusion was common in deformed knee joints (58). Flare-ups were documented within the first 24 hours. Aspiration pain was more common in the knee joint at the midpoint of the procedure, as we didn't use local anesthetic before joint injection. Skin depigmentation was found more frequently with triamcinolone acetonide preparation.

Non-infectious and non-inflammatory STR [26] has two basic patterns: compressive neuropathy and soft tissue lesion proper. Compressive neuropathy is commonly distributed in the carpal tunnel, tarsal tunnel, fibular neck (compression of the common peroneal nerve at the fibular neck), Guyon's canal (ulnar border of the wrist compressing the ulnar nerve) [27], anterior superior iliac spine (meralgia paresthetica), and interdigital nerve (Morton's nerve). Compressive neuropathy can also sometimes be associated with cervical and lumbar spinal stenosis, termed double crush phenomenon [27]. On the other hand, soft tissue lesion proper is usually distributed in the wrist/hand (de Quervain's tenosynovial sheath, flexor tendon), shoulder girdle (bicipital tendon, supraspinatus tendon), elbow (lateral and medial epicondyle), heel (plantar fascia, Achilles tendon), extensor tendon of hand/foot dorsum, knee (anserine bursa), and shoulder joint capsule [28, 29]. All of these soft tissues can be involved in different localized or systemic musculoskeletal disorders. In addition to inflammatory/degenerative rheumatological conditions, STR can also be found in endocrine disorders, overuse, and trauma, or it may be idiopathic [18,29,30]. Adhesive capsulitis is the leading presentation of idiopathic STR in some co-morbid conditions, such as DM, hypo- or hyperthyroidism, stroke, dyslipidemia, or ischemic heart disease. Patients usually complain of shoulder/arm pain with restricted movements impairing daily activities [27]. Other than adhesive capsulitis, MPS is another common pattern of idiopathic STR [30]. In overuse syndrome, it commonly involves the shoulder girdle (bicipital tendinitis, supraspinatus tendinitis), elbow (tennis and golfer's elbow), and wrist/hand (de Quervain's tenosynovitis, trigger finger/trigger thumb) [31-33]. All of these soft tissues can also be involved in DM, hypothyroidism, acromegaly, or postmenopausal women, due to associated hormonal imbalance [27,34]. Along with oral medications (NSAIDs, analgesic or neuropathic agents), physical interventions (therapeutic pulsed ultrasound), therapeutic exercise, and IL steroid/ozone or prolotherapy can also be effective in managing this, a common rheumatological manifestation. When all of these approaches have failed, then surgery can be done to release soft tissues [27,28]. Following local steroid injection, common complications are skin depigmentation, soft tissue injury, injection site pain, flare-ups, and infection. Rupture of the plantar fascia is also possible after local steroid injection. In our study, idiopathic soft tissue lesions were treated in 190 cases (63.3%), and the most common presentation was adhesive capsulitis (90). MPS was diagnosed in 50 cases. Soft tissue lesions due to overuse and blunt trauma were seen in 50 cases, and most common (15) in the elbow region. In the lower back, pain was due to lumbar ligamentous sprain and MPS. Anserine bursitis was diagnosed in 5 cases of OA of the knee. STR in the form of trigger finger/trigger thumb (35) and compressive neuropathy (15) was diagnosed in 50 patients having endocrine problems. Traumatic compressive neuropathy was seen in 10 cases. Other than trauma/overuse or endocrinopathy, compressive neuropathy can also be seen in cervical and lumbar spondylosis, and in our recent study all 5 cases of TTS were found in lumbar spinal stenosis, with a final diagnosis of double crush phenomenon. Idiopathic compressive neuropathy was also seen in 20 patients. Following IL steroid injection, reported complications were skin depigmentation, recurrence, acute flare-up, and failure. Skin depigmentation was seen in 20 cases (69.0%) following triamcinolone injection.

The basic patterns of LBP are localized, radicular, and referred. Localized and radicular LBP occur due to spine degeneration, inflammation, infection, trauma, tumor, or disc herniation. Radiculopathy can be both dermatomal and non-dermatomal; dermatomal pain follows the corresponding nerve root, whereas in non-dermatomal radiculopathy, the pain is due to involvement of multiple nerve roots or a single nerve, and doesn't follow a single nerve root [35]. One of the common but rarely considered causes of non-dermatomal radicular LBP is piriformis syndrome, which may develop following low back trauma, and in which the patient may feel discomfort in sitting for long periods, standing, walking, and even in forward bending [36]. Along with NSAIDs, muscle relaxants, and neuropathic agents, radiculopathy can be treated with physical interventions (therapeutic ultrasound, transcutaneous electrical nerve stimulation) and therapeutic exercises [37]. For radicular lower back pain, epidural injections using methylprednisolone and local anesthetics may be helpful. Lumbar epidural injections can be performed using anatomical landmarks (LOR, loss of resistance), and also with C-arm fluoroscopy, and are commonly performed at the L3-4/L4-5 level [14, 15]. This treatment is effective in spinal stenosis, PLID, and degenerative disc disease, but less effective in spondylolisthesis [38,39]. On the other hand, in piriformis syndrome, respective muscle intervention can be done with steroids and local anesthetics using anatomical landmarks, motor stimulation, C-arm fluoroscopy, and ultrasound guidance [40]. After steroidal intervention, recurrence of piriformis muscle pain is common, requiring botulinum toxin injection [41]. Piriformis injection followed by piriformis muscle stretching exercises may provide the maximum benefit. Referred LBP is mostly due to sacroiliac and facet arthropathy, but it can also be viscerogenic in source. Facet and sacroiliac arthropathy can be treated with I/A steroid injections or radiofrequency ablation of the respective joint/nerve supplying the joint [42,43]. Radiculopathy due to disc prolapse not responding to epidural steroids can be managed with ozone nucleolysis [44]. IDET is a good option for internal disc disruption, and non-traumatic vertebral body fracture can be managed with vertebroplasty [45,46]. During and after epidural/facet joint injection, common complications are headache, neurogenic shock, thecal sac puncture, temporary dizziness, multiple pricks, vasovagal reaction, infection, potential weight gain, transient rise of blood pressure/hyperglycemia (steroid-induced), and failure, among others [47,48]. In the current study, a total of 60 patients with radicular LBP were treated in the pain clinic by IPM. A common presentation of dermatomal radiculopathy was lumbar spinal stenosis (50, 83.3%), due to degenerative disc disease, PLID, spondylolisthesis, spondylodiscitis, and vertebral body fracture. All cases of dermatomal radiculopathy except only one infectious lumbar spondylodiscitis were treated with lumbar epidural injection using the LOR technique. The majority of lumbar interlaminar epidural injections were performed at L3-4 (35, 71.4%). It takes about 1 week (mean 5 days) to initiate pain reduction, and a patients' reported 70% reduction of pain was sustained in 27 patients even after 6 months following the intervention. This pain reduction was sustained for only 4 months in another 13 patients, with a repeated epidural injection necessary by this time. Numerical pain reduction score was below 50% in 4 cases of spondylolisthesis. In piriformis syndrome, the average duration between intervention and at least 50% pain improvement was 5 days. Out of 10 patients, 6 obtained 70% reported pain reduction, which was maintained for an average of 3 months with NSAIDs (diclofenac sodium) and muscle relaxants (tolperison and/or cyclobenzaprine). Common post-procedural complications were multiple pricks in lumbar epidural injections, headache, flare-ups, and partial recovery.

It can be concluded that IPM is gaining popularity throughout the world in the management of painful musculoskeletal conditions. Along with anesthesiologists, physiatrists have a definitive role in IPM. To better serve pain sufferers, the physiatrist must work hand-in-hand with other specialties. In this article, we describe a few procedures performed in the PMR department of a tertiary medical college hospital in Bangladesh using only anatomical landmarks, so accuracy was not ensured. We did not perform any intervention in a facet joint, sacroiliac joint, sympathetic ganglion, vertebral body, or intervertebral disc using radiofrequency ablation, IDET, ozone nucleolysis, or steroid injection because of: (1) Lack of a C-arm facility in the PMR department; (2) Greater reliance on oral medications; (3) Lack of knowledge of diagnostic musculoskeletal ultrasonogram or fluoroscopy; (4) Lack of exposure to interventional pain procedures; and (5) Poor knowledge about the spectrum of IPM. Therefore, we recommend: (1) Development of an IPM unit in the PMR department; (2) Greater emphasis on IPM as a separate entity; (3) Increased collaboration with other institutes/departments dealing with interventional procedures both at home and abroad; (4) Development of skills in IPM through special training; and (5) Training in diagnostic musculoskeletal ultrasonogram/electrodiagnosis to ensure a safe and accurate interventional approach, with an ultimate goal of serving pain sufferers to ensure them a better quality of life.