Transcript for Lower back pain
Content Reviewers:Darren Miller, Evan Debevec-McKenney, Sam Gillespie, Ahmad El-Gammal, Rishi Desai, MD, MPH
Lower back pain
Back pain can originate from the spinal cord, the nerve roots, the vertebral column, the surrounding muscles and ligaments, or even extra-spinal structures such as abdominal organs.
Most lower back pain is considered non-specific musculoskeletal back pain, and is due to strained muscles and ligaments in the back. But sometimes it’s due to a specific disorder, and these can be categorized into 6 groups: degenerative disorders, mechanical disorders such as disk herniation and lumbar spinal stenosis, infections such as osteomyelitis and spinal epidural abscess, spinal epidural hematoma, inflammatory disorders such as ankylosing spondylitis, and cancers, such as multiple myeloma.
Specific disorders are often identified with a thorough history, and to help remember some common clues there’s the mnemonic: “TUNA FISH”.
“T” is for trauma. “U” is for unexplained weight loss, which may suggest a cancer. “N” is for neurological symptoms, like sensory loss, pain, or weakness in the legs, loss of sensation in the perineal area - which is called saddle anesthesia - as well as bowel, bladder, or sexual dysfunction.
“A” is for age over 50, which increases the risk of cancer.
“F” is for fever, which may indicate an infection.
“I” is for intravenous drug use or an immunocompromised state, both of which also increase the risk of infection.
“S” is for steroid use, which can cause secondary osteoporosis and vertebral fractures.
And finally, “H” is for a history of cancer.
On physical examination there might be some clues that suggest a specific disorder as well.
For example, erythema might be due to an underlying infection or and inflammatory process like psoriatic arthritis.
On palpation, if there’s a midline, point of focal tenderness then that could be due to an infection, cancer, or fracture.
Also, if there’s a problem with the straight leg test then that could be due to a radiculopathy.
If there’s no specific finding in the history or physical that suggests a specific cause, then the diagnosis is non-specific musculoskeletal pain.
Symptoms are usually unilateral, dull pain that sometimes radiates down to the thigh or buttocks but not beyond the knee.
The pain is typically worsened by movement and relieved by rest.
Often individuals can recall what triggered the pain, like lifting heavy grocery bags.
The main treatment is to increase mobility, massage, apply heat or cold, and to try physical therapy.
Non-specific musculoskeletal pain typically resolves within 4 to 6 weeks. If it doesn’t, then a specific disorder may be the underlying cause.
Now in terms of specific disorders, first up are the degenerative disorders of the spine, which are mainly due to age-related wear and tear on the spine. They include spondylosis, also called degenerative disc disease, and spondylolisthesis.
With spondylosis, the intervertebral disk and facet joints gradually degenerate with age - a bit like osteoarthritis of the spine. Over time osteophytes can sprout up and they can compress adjacent nerve roots, causing radiculopathy, or can narrow the intervertebral foramina, causing lumbar spinal stenosis.
Spondylolisthesis is slippage of one vertebral body over another due to weakness of the surrounding ligaments, and it can also cause radiculopathy and lumbar spinal stenosis.
Diagnosis is made with an MRI which shows degeneration of the intervertebral disk and bulging bony spurs called osteophytes in spondylosis, and slippage of the vertebral body in spondylolisthesis.
Treatment is usually pain management, physical therapy such as back exercises or lumbar support devices, and occasionally surgery if symptoms are severe.
Next up are the mechanical disorders - like disk herniation and lumbar spinal stenosis.
Disk herniation can happen when forces on the intervertebral disk overwhelm the intervertebral disk, called the annulus fibrosus, and the internal part of the disk, called the nucleus pulposus, herniates out of place.
The annulus fibrosus is weak in spondylosis, so those individuals are at risk for disk herniation.
But disk herniation can also occur in young, healthy individuals who lift a heavy load or have a trauma.
Usually, a herniated disc compresses the nerve roots coming out of the lumbar and sacral spine, causing lumbosacral radiculopathy, or “sciatica”, since this nerve roots also correspond to the sciatic nerve.
Now, the posterior longitudinal ligament, runs vertically along the posterior aspect of the spine, and it’s right behind the nucleus pulposus. As a result, a herniated disc often slips in a posterolateral direction - either to the left or the right of the posterior longitudinal ligament - and causes unilateral symptoms, like a shooting or electrical pain that radiates from the back down below the knee.
When a disc herniates, it compresses the nerve root below it, causing sensory or motor loss in the dermatomal and myotomal distribution of the affected nerve root.
Most commonly, intervertebral discs herniate between the L3 and L4 vertebrae, between L4 and L5, or between L5 and S1.
An L3-L4 herniated disc compresses the L4 nerve root, causing loss of sensation along the anteromedial aspect of the thigh, weakness in the quadriceps muscles causing weakness in knee extension, and a diminished quadriceps or knee jerk reflex.
An L4-L5 herniated disc compresses the L5 nerve root, causing loss of sensation along the lateral lower leg and the dorsum of the foot, and weakness in dorsiflexion of the foot. There is no reflex for L5.
An L5-S1 herniated disc compresses the S1 nerve root, causing loss of sensation along the lateral foot and ankle, weakness in plantar flexion of the foot, and a diminished achilles reflex.
Okay, a quick screening exam to test these three discs is to ask the individual to squat and rise to assess L4, heel walk to assess L5, and toe walk to assess S1. Inability to perform the movement suggests disc disease at that level.
Another test is the straight leg raise test, which is where a person lays supine, with their legs extended. Next, passively lift one leg and continue flexing the hip until the individual complains of pain.
A positive straight leg test is pain below the knee when the hip is flexed between 30 and 70 degrees. Counter-intuitively, back pain upon lifting the leg is not a positive straight leg test.
A negative straight leg test effectively rules out radiculopathy, but a positive test should be followed up with a lumbar X-ray, which may show signs of degenerative disc disease like loss of vertebral height.
However, a lumbar x-ray cannot show disc herniation, and is therefore followed by an MRI which will show evidence of a herniated disc.
Acute lumbosacral radiculopathy usually resolves with NSAIDs, but if it persists beyond 6 weeks, then surgery may be needed.
In lumbar spinal stenosis, there’s narrowing of one or more of three key anatomic structures: the central canal where spinal cord runs, the lateral recess, or the neural foramen.
The most common cause of lumbar spinal stenosis is spondylosis, but other causes are spondylolisthesis, trauma, Paget disease of the bone, and achondroplasia.
In spondylosis, osteophytes and a thickened ligamentum flavum can either cause direct mechanical compression or venous congestion which leads to edema and swelling and indirectly leads to compression.
This can lead to neurogenic claudication, also called pseudoclaudication, which is where there’s pain in the back, buttocks, and legs induced by positions that extend the spine, such as walking or standing erect, and relieved by positions that flex the spine, such as sitting, lying down or leaning forward on a shopping cart. That’s because when the spine is extended, the spinal foramina narrow, causing symptoms, and when the spine is flexed, the foramina get some breathing room, causing relief. So it’s a type of positional pain. This distinguishes it from vascular claudication, which causes exertional pain.
To make that distinction clear, a person with neurogenic claudication could ride a bike and potentially complete the Tour de France, because that position is comfortable for them. On the other hand, in vascular claudication, the exertional effort of riding a bike is painful - so they’re unlikely to get past the first few miles.
Some individuals with lumbar spinal stenosis have sensory loss or weakness - and it’s typically bilateral, and doesn’t follow a dermatomal or myotomal pattern.
The diagnosis of lumbar spinal stenosis is usually done with an MRI, which shows the narrowing of the spinal canal.
The initial treatment is with physical therapy and NSAIDs, but if that doesn’t work then corticosteroids can be injected into the epidural space to reduce edema and relieve the stenosis.
Finally, a surgical laminectomy is sometimes needed which removes the lamina; which forms the roof of the spinal canal.
Next up are infections - mainly vertebral osteomyelitis and spinal epidural abscess.
Mycobacterium tuberculosis can also cause osteomyelitis - in which case it’s specifically called Pott’s disease.
Most commonly, bacteria reach the vertebrae using the hematogenous route; which is spread through the blood from a distant site of infection, but sometimes they can be inoculated directly following trauma or surgery, or reach the vertebrae through contiguous spread from a nearby soft tissue infection, like cellulitis.
Now sometimes a focus of infection can spread from the vertebrae to the epidural space, causing a spinal epidural abscess, but sometimes epidural abscesses can develop on their own, without a history of vertebral osteomyelitis. These abscesses can grow big and compress adjacent nerve roots or even the spinal cord, causing neurological deficits.
Risk factors for vertebral osteomyelitis and spinal epidural abscess include diabetes, intravenous drug use, immunosuppression; such as HIV or chronic steroid use, presence of indwelling devices such as a central venous line, endocarditis, or urinary tract infection.
With vertebral osteomyelitis, pain is the major symptom, which may or may not be accompanied by fever.
On examination, the tenderness is pinpoint and well-localized.
Symptoms of a spinal epidural abscess include fever, back pain, and neurological deficit. However, this triad is only found in ten percent of individuals, so it’s important to keep a high index of suspicion.
Alright, laboratory investigations include a CBC to evaluate for leukocytosis, as well as an ESR and CRP levels, both of which are usually elevated.
Because the CRP rises and falls faster than the stock market, it can be used as an indicator of treatment success.
Also, blood and urine cultures should be obtained to evaluate for a potential source.
The MRI is the most sensitive imaging test for diagnosing vertebral osteomyelitis and spinal epidural abscess, and is superior to the x-ray. This is because the MRI detects abnormalities early in the course of the disease that would have otherwise been missed on an x-ray.
In vertebral osteomyelitis, the MRI shows edema of the vertebral body and destruction of the intervertebral space. Spinal epidural abscesses appear as fluid-filled sac.
Now, in vertebral osteomyelitis, the next step is a biopsy to detect the specific microorganism involved.
The biopsy can be done as an open procedure or using a needle under the guidance of CT imaging.
Individuals are usually given antibiotics for at least 6 weeks.
Empiric antibiotic therapy including a beta-lactam and vancomycin can be given if the individual is septic or if there are rapidly progressive neurological symptoms. On the other hand, when there’s a spinal epidural abscess, if there are any neurological deficits, then empiric antibiotics should be given right away. Typically, vancomycin and ceftazidime are given because they cover most of the implicated bacteria.
Additionally, surgical decompression and drainage of the abscess must be done in these individuals. That’s because the neurological deficit might progress to irreversible paralysis. However, if they have no neurological deficit, then we can obtain a sample of the abscess using CT-guided needle aspiration, and then subsequent antibiotic therapy is tailored to the results.
Finally, tuberculous osteomyelitis, or Pott’s disease is treated with the RIPE regimen: rifampin, isoniazid, pyrazinamide, and ethambutol for 2 months, followed by isoniazid and rifampin only for the remaining duration of treatment, which ranges from 9 to 12 months.