Presentation on theme: "BY: RUTH EMBAIE PRESENTED BY DR ZOZIK FATTAH CENTRAL MIDDLESEX HOSPITAL Back Pain."— Presentation transcript:
BY: RUTH EMBAIE PRESENTED BY DR ZOZIK FATTAH CENTRAL MIDDLESEX HOSPITAL Back Pain
Introduction Extremely common problem that is often poorly managed. Challenge because it is so common demanding of medical resources and, a major cause of physical, psychological and social disability. 85-90% are simple low back pain (or 'mechanical low back pain') in which the symptoms by definition cannot be ascribed to a particular pathology. vary with posture, activity, time and treatment. Radicular (or nerve root pain) may occur with low back pain.
Introduction Radicular (or nerve root pain) may occur with low back pain. Sciatica is a lay term for pain extending into the leg (buttock, thigh, calf or heel). Classification: acute (less than 6 weeks), sub-acute (6-12 weeks) and chronic (more than 12 weeks) but is less useful clinically because of the variable and recurrent nature of symptoms. Recurrent low back pain has been defined as a new episode of pain after a symptom-free period of 6 months.
Epidemiology 80%-90% of adult men and women between the ages of 30 and 50 years. Smoking and obesity increase risk. Second only to the common cold as a cause of lost days at work. In 2005, the Trades Union Congress (TUC) estimated 4.9 million working days per year are lost Both high physical workload and job dissatisfaction increase the risk of absence due to back pain.
Back pain is expensive NICE (2009) reported that: Treating all types of back pain costs the NHS more than £1000 million per year. Lost production as a result of low back pain costs at least £3500 million per year
RED FLAGS BACK PAIN Red flags for possible serious spinal pathology from the history are: 1 1 History of: Cancer Drug abuse HIV Immunosuppression Prolonged use of corticosteroids Constitutional symptoms, e.g. fever, chills, unexplained weight lossunexplained weight loss Recent violent trauma (such as vehicle accident or fall from a height) Minor trauma, or even just strenuous lifting, in people with osteoporosisosteoporosis Age at onset less than 20 or over 50 years (new back pain) Recent bacterial infection, e.g. urinary tract infection Pain that is: Worse when supine Severe at night time Thoracic Constant and progressive Non-mechanical without relief from bed rest or postural modification Unchanged despite treatment for 2-4 weeks Accompanied by severe morning stiffness (rheumatoid arthritis and ankylosing spondylitis)morning stiffnessrheumatoid arthritisankylosing spondylitis Severe and leaves patients unable to walk or self-care Accompanied by saddle anaesthesia or recent onset of difficulty with bladder or bowels
Important to recognise those that are not The aims of back pain assessment are: 1 1 To recognise serious pathology. To relieve pain. To improve function. To recognise and assess level of disability. To identify barriers to recovery. To prevent recurrence or persistence of symptoms
PATHOPHYSIOLOGY The pathophysiology of mechanical LBP remains complex and multifaceted. Multiple anatomic structures and elements of the lumber spine (eg, bones, ligaments, tendons, disks, muscle) are all suspected to have a role. (See the images below.) Many of these components of the lumber spine have sensory innervation that can generate nociceptive signals representing responses to tissue-damaging stimuli. Other causes could be neuropathic (eg, sciatica). Most chronic LBP cases most likely involve mixed nociceptive and neuropathic etiologies.
Biomechanically, the movements of the lumbar spine consist of the cumulative motions of the vertebrae, with 80-90% of the lumbar flexion/extension occurring at the L4-L5 and L5- S1 intervertebral disks. The lumbar spine position most at risk for producing LBP is forward flexion (bent forward), rotation (trunk twisted), and attempting to lift a heavy object with out- stretched hands. Axial loading of short duration is resisted by annular collagen fibers in the disk. Axial loading of a longer duration creates pressure to the annulus fibrosis and increased pressure to the endplates. If the annulus and endplate are intact, the loading forces can be adequately resisted. However, compressive muscular forces may combine with the loading forces to increase intradiskal pressure that exceeds the strength of the annular fibers.
Repetitive, compressive loading of the disks in flexion (eg, lifting) puts the disks at risk for an annular tear and internal disk disruption. Likewise, torsional forces on the disks can produce shear forces that may induce annular tears. (Degenerative disk forces are demonstrated in the image below.) The contents of the annulus fibrosis (nucleus pulposus) may leak through these tears. Central fibers of the disk are pain free, so early tears may not be painful.
Glutamate, a neuroexcitatory transmitter, has been identified in degenerated disk proteoglycan and has been found to diffuse to the dorsal root ganglion (DRG) affecting glutamate receptors. Substance P (pain) is present in afferent neurons, including the DRG, and is released in response to noxious stimuli, such as vibration and mechanical compression of the nerve. Steady, cyclic, or vibratory loading induces laxity and creep in the viscoelastic structures of the spinal elements. This creep does not recover fully in the in vivo cat model, even when rest periods are equal in duration to the loading period.
The concept of a biomechanical degenerative spiral has an appealing quality and is gaining wider acceptance. This concept postulates the breakdown of the annular fibers allows PLA2 and glutamate, and possibly other as-yet unknown compounds, to leak into the epidural space and diffuse to the DRG. The weakened vertebra and disk segment become more susceptible to vibration and physical overload, resulting in compression of the DRG and stimulating release of substance P. Substance P, in turn, stimulates histamine and leukotriene release, leading to an altering of nerve impulse transmission. The neurons become sensitized further to mechanical stimulation, possibly causing ischemia, which attracts polymorphonuclear cells and monocytes to areas that facilitate further disk degeneration and produce more pain