Lower back pain in Surgery

1. Dr. Ssentamu Timothy
MBChB, MMED ORTHO

2. 1. Introduction
LBP is defined as pain located between
the lower 12nd rib and the gluteal folds
This pain may occasionally extend down
to the level of the knee but not beyond
LBP affects up to 80% of the adult pop. at
some time
LBP is the most common reason for
patient visits to physicians offices

3. Introduction (cont.)
 The precise cause of LBP is poorly known and
only 10-20% of all pts have their pain attributed
to an accepted, definable dx.
 In majority of cases LBP tends to disappear
with time.
 In about 90% of patients symptoms tend to
resolve within 3months of onset.

4. 2. Epidemiology
 LBP is one of the top 10 reasons patients seek
care from physicians
 The prevalence of LBP has varied from 7.6-
37% worldwide
 The prev. of LBP in US ranges from 15-20%
and from 25-45% in European countries
 The prev.of LBP in Mulago(2002) was
17%(Galukande)

5. Epid. (cont.)
 LBP is more prevalent in industrialized
societies; however, clear genetic factors which
make a specific ethnicity or race more prone to
experience this disorder have not been
identified to date
 Men and women are affected equally, but
women more often report low back symptoms
after age 60 years.

6. Epid. (cont.)
 The incidence of LBP peaks in the middle years
of life and declines in old age when
degenerative changes of the spine are universal.
 Sciatica usually occurs in patients during the
fourth and fifth decades of life; the average age
of patients who undergo lumbar discectomy is
42 years.

7. 3. Aetiology
Aetiologically LBP can be classified in the
following ways:-
3:1 Intrinsic causes ( i.e. causes within
the back)
3:1:1 Congenital
 Spina bifida
 Hemivertebra
 Split vertebra

8. Aetiology (cont.)
3:1:2 Traumatic
 Lumboscral strain
 Injuries to the intervertebral disc, ligaments
and muscles
 Spondylolisthesis
 Compression #
 Vertebral process #
 Ruptured disc

9. Aetiology (cont.)
3:1:3 Functional defects
 Anteroposterior imbalance e.g.
 Pregnancy
 Fixed flexion deformity
 Etc
 Lateral imbalance
 Scoliosis
 Leg length discrepancy
 Etc

10. Aetiology (cont.)
3:1:4 Inflammatory
 Pyogenic osteomyelitis
 Tuberculosis
 Rheumatoid arthritis
 Brucellosis
 Ankylosing spondylosis
 Myositis
 Fibrositis

11. Aetiology (cont.)
3:1:5 Degenerative
 Osteoarthritis
 Senile osteoporosis
 Degenerative disc disease
3:1:6 Neoplastic
 Primary tumor
 Multiple myeloma
 Osteoid osteoma etc

12. Aetiology (cont.)
 Metastatic tumors from:-
 Breast
 Bronchus
 Kidney
 Suprarenal
 Prostate
 Thyroid
 GIT

13. Aetiology (cont.)
3:2 Extrinsic causes
 These include:-
3:2:1 Abdominal disorders
 Pancreatitis
 Cholecystitis
 Biliary calculus
 Peptic ulcer
 Hiatus hernia

14. Aetiology (cont.)
3:2:2 Pelvic disorders
 Pelvic inflammatory disease
 Intrapelvic tumors
3:2:3 Genito-urinary disorders
 Renal infection
 Ureteric calculus
 Prostatitis
 Prostatic carcinoma

15. Aetiology (cont.)
3:2:4 Vascular disorders
Aortic aneurysm
Ischaemic pain from occlusion of the
aorta or iliac arteries

16. 4. Pathophysiology
 The lumbar spine is a flexible portion of the vertebral
column that supports the head, upper extremities, and
internal organs over a bipedal stance
 The sacrum forms the foundation of the spine through
which it articulates with the pelvis at the sacroiliac
joints.

17. Pathophysiology (cont.)
 The lumbar spine is capable of supporting
heavy loads in relation to its cross-sectional
area.
 It resists anterior gravitational movement by
maintaining lordosis in a neutral posture
 The lumbar spine is unsupported laterally and
displays considerable mobility in both the
sagittal and coronal planes

18. Pathophysiology (cont.)
 The bony vertebrae act as specialized structures for
transmitting loads through the spine
 Vertebral bodies are progressively larger in cross-
sectional area because gravitational loads increase
from cephalad to caudal segments

19. Pathophysiology (cont.)
 Bony projections from the lumbar vertebra (i.e.
transverse processes and spinous processes) maintain
ligamentous and muscular connections to the
segments above and below
 The intervertebral disc is composed of the outer
annulus fibrosus and the inner nucleus pulposus.

21. Pathophysiology (cont.)
 The outer portion of the annulus inserts into the
vertebral body and accommodates nociceptors and
proprioceptive nerve endings.
 The inner portion of the annulus encapsulates the
nucleus, providing the disc with extra strength during
compression

22. Pathophysiology (cont.)
The nucleus pulposus constitutes two
thirds of the surface area of the disc and
supports more than 70% of the
compressive load.
 The nucleus is composed of proteoglycan
megamolecules

23. Pathophysiology (cont.)
 Animal studies have demonstrated that trauma to
discs increases concentrations of neuropeptides e.g.
substance P (SP) and vasoactive intestinal peptide
(VIP) in the dorsal root ganglion, suggesting that they
may play a role in the transmission or modulation of
pain

24. Pathophysiology (cont.)
 Until the third decade of life, the gel of the inner
nucleus pulposus is composed of approximately
90% water; however, water content gradually
diminishes over the next 4 decades to
approximately 65%.
 Repeated loading and recurrent microtrauma
results in circumferential and radial tears in
annular fibers.

25. Pathophysiology (cont.)
 Coalescence of circumferential tears into radial
tears may allow nuclear material to migrate out
of the annular containment into the epidural
space and cause nerve root compression or
irritation.
 Over time, hypertrophy of the facets and bony
overgrowth of the vertebral endplates
contribute to progressive foraminal and central
canal narrowing

26. Pathophysiology (cont.)
 Spinal stenosis reaches a peak later in life and may
produce radicular, myelopathic, or vascular syndromes
such as pseudoclaudication and spinal cord ischemia.
 LBP is most common in the early stages of disc
degeneration.

27. Pathophysiology (cont.)
 Neuropeptides such as SP, VIP, and calcitonin-gene
related peptides (CRGP) also have been found in
capsular- and joint-nerve fibers of the facets.
 These neuropeptides may be released in response to
noxious chemical or physical stimulation and are
capable of mediating neurogenic inflammation

28. Pathophysiology (cont.)
 Recently, some investigators have proposed that
release of these neuropeptides stimulate the synthesis
of inflammatory agents (eg, cytokines, prostaglandin
E) and degradation enzymes (eg, protease,
collagenase), which cause progressive deterioration of
the motion-segment structures, especially the
intervertebral disc.

29. Pathophysiology (cont.)
 Furthermore, injury and the consequential
neurochemical influences may initiate
degenerative, inflammatory, and reciprocal
biochemical changes, which modify or prolong the
pain stimulus
 Phospholipase A2 plays a role in numerous models
of inflammation and has been found to be
elevated in surgically extracted samples of human
herniated discs

30. Pathophysiology (cont.)
 Also, PL A2 play a dual role, inciting disc degeneration
and sensitizing annular fibers.
 Inflammatory and other chemical factors may
sensitize tissues within the spinal segment to perceive
and translate biomechanical stresses into various
degrees and character of axial and limb pain..

31. Pathophysiology (cont.)
 In some cases, inflammatory factors may be
primarily responsible for causing pain, which is
relieved by epidural steroid injections.
 Structures within the lumbar spine that are pain
sensitive include the nerve roots, dura,
posterior and anterior longitudinal ligaments,
external annular fibers of the disc, facet
joints, joint capsules, and cancellous bone.

32. Pathophysiology (cont.)
 Intraspinal structures without proven nociceptive
capacity include the ligamentum flavum, inner
annulus, and nucleus pulposus
 Spinal nerve roots have unique characteristics,
which may contribute to radicular symptoms.
 Nerve roots lack epineurium and perineurium, and
therefore lack a well-developed intraneural blood-
nerve barrier.

33. Pathophysiology (cont.)
 This anatomical characteristic engenders nerve roots
more susceptible to compression injury than
peripheral nerves and more vulnerable to endoneural
edema formation.

34. 5. Clinical presentation
5:1 Symptoms
 In pts who present with LBP, an enquiry must be made
about:-
5:1:1 The mode of onset ( i.e. sudden or gradual)
Sudden onset after lifting weight in a stooping position
may be due to disc prolapse

35. Clinical presentation (cont.)
5:1:2 Nature of pain (i.e. dull, sharp, throbbing
5:1:3 Exact site
5:1:4 Any radiation
5:1:4 Aggrev.& relieving factors
5:1:5 Presence of any referred pain
5:1:6 ROS
5:1:7 PMHx
5:1:8 SFHx

36. Clinical presentation (cont.)
5:2 Physical exam.
5:2:1 General exam
5:2:2 Local exam.
a. Inspection i.e. look for:-
 Attitude and deformity
 Gait
 Swelling
 Paraplegia

37. Clinical presentation (cont.)
b. Palpation i.e. feel for:-
 Tenderness
 Swelling
 Wasting and rigidity of the erector spinae muscle

38. Clinical presentation (cont.)
c. Percussion
 Percussion over the spine is sometimes performed to
elicit tenderness

39. Clinical presentation (cont.)
d. Movements
 Movs. of the spine i.e. Lumboscral
e. Measurements
 The lengths of the lower limbs must be measured to
exclude shortening of any limb as the cause of scoliosis
f. Straight leg rising test
 Active and passive

40. Clinical presentation (cont.)
5:2:3 Systemic exam.
 Rectal and vagina exam. to exclude pelvic masses

41. 6. Investigations
6:1 Lab investigations
 CBC
 ESR
 Urinalysis
6:2 Imaging investigations
 Plain Lumboscral x-rays- AP&lateral

42. Investigations (cont.)
 CT scan
 Myelogram
 MRI
6:3 Procedures
Histopathology

43. 7. Treatment
7:1 Non-operative therapy
7:1:1 Pharmacologic therapy
 Nonsteroidal ant-inflammatory agents e.g.
ibuprofen
 Narcotics
 Epidural steroid

44. Treatment (cont)
 Muscle relaxants
E.g. Cyclobenzaprine
 Corticosteroids
 Cyclooxygenase II inhibitors e.g. Celecoxib
7:1:2 Bed rest

45. Treatment (cont.)
7:1:3 Physiotherapy
7:2 Surgical therapy

46. Read about;
Mechanical low back pain
Disorders of the sacrum and coccyx