Modern Discography

By Francisco A. Naveira, M.D.

 

Introduction

ÝÝÝÝÝÝÝÝÝÝÝÝÝÝÝ Five spinal-related pathologies are associated with syndromes involving low-back and leg pain. The five are: facet syndrome; sacroiliac joint syndrome; discogenic syndrome; central spinal stenosis; and foraminal stenosis. All may present with a common symptom complex of low-back, buttock, trochanteric, and posterior thigh pain. Most of them may also be mechanically related to radiculopathies. The spectrum of disc disease includes disc herniation, acquired spinal stenosis, myelopathy, chemical or mechanical radiculopathy, and internal disc derangement. Specific details from history, physical, and radiographic examination may allow separation of these entities, but proof of diagnosis requires data from response to treatment, facet and nerve injection, myelography, discography, nerve conduction testing, and computerized tomography (CT) or Magnetic Resonance scanning.

Discography can be performed at the cervical, thoracic, lumbar, and sacral levels. Although the basic elements of discography are the same at any level, the discogram technique and safety issues will vary with the area tested. The bulk of information available is related to cervical and lumbar discography. Crucial elements, such as Discomanometry, remain better understood at the lumbar level. Cervical, thoracic, and sacral discography should be left for discographers with 5-10 years of experience with the lumbar techniques. For the purpose of this review, we will concentrate only on Lumbar Discography.

True discography consists of several steps or elements, all of which are essential for the interpretation of the study and successful outcomes. These steps or elements must be carefully documented, and include:

1.                      Preoperative evaluation, which in turn should include

a.            VAS at its worse and prior to study

b.            Location of pain (may include a pain drawing)

c.            Aggravating factors

d.            Alleviating factors

e.            Duration of pain

f.              Onset of pain (Sudden vs. Gradual)

g.            Neurological exam

h.            Evaluation of prior films or neurological studies (EMG/PNCV)

i.              Allergies

2.                      Preoperative laboratories

a.            Coagulation parameters

b.            ESR

c.            WBC

3.                      Discogram: actual injection of radiological contrasts into the disc. There are two types:

a.            Provocative discogram

b.            Analgesic discogram

4.                      Discomanometry: monitoring and recording of the intradiscal pressures, during crucial events, related to the study.

a.            Quantitative vs. simple discomanometry

b.            Opening pressure

c.            ìPressure sensationî pressure

d.            ìPain sensationî pressure

e.            Leakage pressure

5.                      Post-discogram fluoroscopic films

a.            A-P

b.            Lateral

c.            Obliques

d.            Cephalocaudad

6.                      Post-discogram CT evaluation

7.                      Interpretation

a.            Interpretation of contrast spread:

                                                                                                       i.Real-time discogram

                                                                                                     ii.Annulogram

                                                                                                    iii.Nucleogram

                                                                                                    iv.Epidurogram

b.            Intraoperative vs. Post-discogram pain evaluation: Analgesic vs. Provocative

8.                      Decision making process

 

The discographer should have ample knowledge of the spinal anatomy, with emphasis on the neuroanatomy and disc anatomy.

These physicians should be capable of identifying and managing any complications that may arise from the procedure. Discograms should not be performed by physicians unwilling to follow up with the patient, since essential information can be lost or omitted.

 

Historical background

ÝÝÝÝÝÝÝÝÝÝÝÝÝÝÝ The first disc injection was performed in Scandinavia by Lindgren, in 1941. He presented a case of a normal disc injected with the contrast material parabordil, in a paper read before the Swedish Radiology Society. This material was not published.[1]Ý The first to report the presence of radial ruptures in the posterior and posterolateral disc annulus was Knut Lindblom. He injected discs with red lead in vitro, in 1944[2]. Carl Hirsch first used disc injections in vivo to diagnose the pathological disc level in a case of lumbago and sciatica[3]. He was the first to use pain response as a diagnostic parameter (provocative disc injections). Encouraged by Hirsch studies, Lindblom modified the technique to include the injection of radiological contrast material to visualize the radial ruptures. He expanded the diagnostic criteria to include the radiological appearance of the disc, as well as the patientís response to the injection, giving birth to ìprovocative discographyî.[4]Ý The first discography performed in the United States was done around the early 1950s[5],[6]. In 1960, Ulf Fernstrom, one of the first to note that back and leg pain occurs whether or not there is detectable nerve compression, suggested that there are both biochemical and mechanical pathophysiological mechanisms for the pain[7]. In 1962 Collins and Gardner, based on a study of 1000 patients, reported discography to be superior to myelography in the evaluation of lumbar disc disease[8]. Feinberg was one of the first to describe abnormal discogram patterns. Some of these remain valid today. He reported an evaluation of over 2000 patients. Feinberg considered that back and leg pain could not be explained by nerve compression alone and that annular tears lesions had a significant role in the pathophysiology[9].

Some of the controversy started in 1968, when Holt questioned the validity of the pain response to injection. He reported a 37% false-positive rate among asymptomatic prison inmate volunteers[10]. Holtís study, as many others, had several methodological flaws, some of which were pointed out by Simmons in 1988[11]. Some of these flaws included:

ß          All of his subjects were prisoners.

ß          He used a highly irritating contrast medium.

ß          He did not include positive pain response as criteria for positive injection.

ß          Criteria for a positive result were based primarily on radiological images.

ß          He excluded 23% of injected discs due to technical difficulties in performing the procedure.

ß          Performed a significant number of annular injections, known to be very painful.

The idea that discography was most valuable in the evaluation of patients with pain and no definite herniation was reported in a study of a large series of cases evaluated by Wiley et. al., in 1968[12]. In 1970, Henry Crock introduced the concept of an internal disc disruption syndrome with back pain as its primary symptom[13]. It was also around this time that new and safer non-ionic contrast material was developed for myelography[14]. This allowed for these radiological techniques to become safer. The addition of post-discogram CT evaluation in 1984, significantly improved the technique to image the intradiscal architecture[15]. Measurement of intradiscal pressure is not a new concept. As early as 1959, studies such as those by Nachemson have attempted to record intradiscal pressures[16]. By 1975, Nachemson had already established a clear relationship between spine position and loading, to the pressure mechanics of the discs[17].

Over the years, the procedure has undergone considerable changes to keep up with developing treatment modalities. It has also been subjected to intense scrutiny and controversy. As new orthopedic and neurosurgical technology emerges, the discography technique will also have to evolve to answer yet more questions about the area of pathology. Advances in the field of disc anatomy, algology, histology, physiology, chemistry, and pathophysiology, have helped our understanding of this complex structure. Such new understandings will continue to affect the way discography is performed and interpreted.

 

The lumbar disc

Structural Anatomy

Each lumbar intervertebral disc consists of three basic components: the central nucleus pulposus, the surrounding annulus fibrosus, and the upper and lower vertebral end-plates.

 

Microanatomy

Nucleus Pulposus ñ It is a semi-fluid mass with a consistency similar to toothpaste. The mixture of proteoglycans, aggregates, and collagen is collectively referred to as the nuclear matrix. Embryology: It is a remnant of the notochord. Histology:

    Water: 70-90% (Varies with age)[18],[19],[20] The water is mainly contained in the proteoglycans.

    Proteoglycans: 65% of nuclear dry weight. They exist in units or aggregates, with only 25% in the aggregate form18,19.

o         The water-binding capacity is mainly dependent on the chondroitin sulphate concentration.[21]

    Collagen: 15-20% of nuclear dry weight, mostly Type II (some Type III)18,[22]

    Cartilage cells: Located close to the end-plates, they are responsible for proteoglycan and collagen synthesis.[23],21

Annulus Fibrosus ñ Consists of 10 to 20 sheets[24] of highly ordered collagen fiber layers that surround the nucleus, called lamellae. They are thicker in the anterior and lateral portion of the annulus, with the posterior portion being thinner[25]. Histology:

    Water: 60-70% of its weight18,19,20.

    Collagen: 50-60% of its dry weight[26],18, mostly Type I.

    Proteoglycans: 20% of its dry weight18. (50-60% are in aggregate form[27])

    Elastic fibers: 10% of its dry weight[28].

Vertebral end-plates ñ Each of the two end-plates is a layer of cartilage 0.6-1 mm thick[29],[30]. Histology:

    Hyaline cartilage: towards vertebral body (mostly found in younger discs).

    Fibrocartilage: towards the nucleus pulposus (mostly found in older discs).

 

Functional Anatomy

Metabolism ñ The disc contains enzymes that synthesize its matrix. It also contains other enzymes such as collagenase, elastase and other proteinases, that break it down[31],[32]. The balance between the degradation and synthesis is controlled by proteinase inhibitors31. Nicotine can inhibit the synthesis of proteoglycans and type II collagen, thereby affecting this balance[33].

Weight-bearing ñ A 40 kg load is accompanied by a 0.5 mm radial expansion and a 1 mm vertical compression of the intervertebral disc.[34] It is the water content of the disc that makes the nucleus a turgid body that resists compression. Therefore, water content is of critical importance to the disc. Because water content is a function of proteoglycan content, anything that affects the proteoglycans will, in turn, affect the other.

Movement ñ These include: distraction, sliding, bending or rocking, and twisting.

Spacer ñ A normal disc maintains the distance between vertebral bodies. Disc degeneration or removal will decrease this distance, thereby causing the cephalo-caudad diameter of the neural foramen to be decreased. This anatomical change may cause significant neural foraminal stenosis and nerve root impingement. This disc degeneration will shift some of the weight-bearing from the anterior (intervertebral discs) to the posterior (zygapophysial / facet joints) elements of the spine. This will, in turn, cause degeneration and hypertrophy of the facet joints, leading to a chronic facet syndrome. Zygapophysial joint hypertrophy causes a decrease in the antero-posterior diameter of the neural foramen. This decrease in diameter will lead to foraminal stenosis and further nerve root impingement.

Creep - Defined as the time dependent part of the intervertebral disc deformation that accompanies the application of a load[35].

 

Blood and Nutrient Supply

No major arterial branches. The only vessels that supply the discs are small branches of the metaphysical arteries, which anastomose over the outer surface of the annulus and supply only the outermost fibers23. Nutrition is therefore dependent on diffusion from the vessels in the outer annulus, and from the capillary plexus to the vertebral end-plates. Although diffusion is the principal mechanism to get nutrients into the disc[36],[37], compression of the disc tends to squeeze water out. When this compression is released, water returns, carrying nutrients with it[38].

 

Neuroanatomy

Two kinds of innervation are present in the lumbar spine: one depends on the somatic nervous system and the other on the sympathetic nervous system. The sympathetic nerves are the sinu-vertebral nerves and the rami communicantes which innervate the intervertebral disc, the ventral surface of the dura mater, the longitudinal dorsal ligament and the longitudinal ventral ligament. In a healthy intervertebral disc, the outer third of the annulus contains a variety of free and complex nerve endings[39]. Most nerve endings are located in the lateral portions of the disc, with lesser concentrations in the posterior aspect, and the least located in the anterior portion of the disc39,[40],[41]. These nerve endings are supplied by branches of the lumbar ventral rami, the grey rami communicantes, and the lumbar sinuvertebral nerves[42],[43]. Each disc is innervated by the lumbar sinuvertebral nerves at its respective level and from the disc level above. There is no significant difference between endplate and annulus innervation densities. The endplate innervation is concentrated centrally adjoining the nucleus. The richest area of innervation is in the perianular connective tissue[44]. Innervation is as follows:

Lumbar ventral rami ñ Posterolateral corner of each disc.

Grey rami communicantes - Posterolateral corner and lateral aspect of each disc, and the anterior longitudinal ligament. Sympathetic nerves are likely involved in the proprioception of the spinal column[45].

Sinuvertebral nerves ñ Posterior longitudinal ligament, and most of the disc. This nerve is implicated in diffuse low back pain because of its pathway and its sympathetic component. This nerve cannot directly reach a somatic element at each level of the lumbar spine, so must first reach the L2 spinal ganglion[46]. Discogenic pain is mediated by the sinu-vertebral nerves, and through the rami communicantes reaches the L2 spinal ganglion. Anatomical and clinical features reinforce this hypothesis46.

 

A transverse section through the vertebral canal and intervertebral foramina to demonstrate the relations of the lumbar nerve roots. The roots are enclosed in their dural sleeve, which is surrounded by epidural fat in the intervertebral foramina. Radicular veins (RV) and radicular arteries (RA) run with the nerve roots. Anteriorly the roots are related to the intervertebral disc and posterior longitudinal ligament (PLL), separated from them by the sinuvertebral nerves (SVN), elements of the anterior internal vertebral venous plexus (AV), and the anterior spinal canal branches (ASCB) of the lumbar arteries (LA). Posteriorly, the roots are separated from the ligamentum flavum (LF) and zygapophysial joints (ZJ) by elements of the posterior internal vertebral venous plexus (PV), and epidural fat, which lodges in the recess between the ligamentum flavum of each side.

 

 

 

 

 

 

 

 

The nerve supply of a lumbar intervertebral disc depicted in a transverse view of the lumbar spine. Branches of the grey rami communicantes and the sinuvertebral nerves (SVN) are shown entering the disc and the anterior and posterior longitudinal ligaments (ALL, PLL). Branches from the sinuvertebral nerves also supply the anterior aspect of the dural sac and dural sleeve.

 

 

 

 

 

 

 

 

A sketch of the nerve supply of the lumbar intervertebral discs outside the vertebral canal. Laterally, the discs receive branches (1) from the grey rami communicantes of the sympathetic trunk (ST). Posterolaterally, they receive branches (2, 3) from the grey rami communicantes and the ventral rami (VR) as they emerge from the intervertebral foramina. The anterior longitudinal ligament (ALL) is innervated by recurrent branches (4) from the grey rami.

 

 

 

 

 

 

 

 

Innervation of the lumbar spine. A cross-sectional view incorporating the level of the vertebral body (VB) and its periosteum (p) on the right and intervertebral disc (IVD) on the left. PM ñ psoas major. QL ñ quadratus lumborum. IL- iliocostalis lumborum. LT ñ longissimus thoracis. M ñ multifidus. altlf ñ anterior layer of thoracolumbar fascia. pltlf ñ posterior layer of thoracolumbar fascia. esa ñ rector spinae aponeurosis. ds ñ dural sac. zj ñ zygapophysial joint. pll ñ posterior longitudinal ligament. all ñ anterior longitudinal ligament. vr ñ ventral ramus. dr ñ dorsal ramus. m ñ medial branch. i ñ intermediate branch. l ñlateral branch. svn ñ sinuvertebral nerve. grc ñ grey rami communicans. st ñ sympathetic trunk.

 

 

 

 

 

 

 

The Premise

The premise of discography is that reproduction of patientís clinical symptoms during the injection identifies the disc as a source of pain.

 

The rationale

The rationale for its use is that the results can help discriminate among the various structures that may be responsible for axial pain.

 

Validity

MRI has been found to demonstrate an abnormal disk in approximately 22-28% of subjects without back pain or sciatica[47].Ý Other studies have shown 32% of asymptomatic subjects to have ìabnormalî lumbar spines and 47% of all the subjects who had experienced LBP to have ìnormalî lumbar spines[48]. Provocative discography is the only method that directly relates a radiographic image to the patientís pain.Ý A CT/discogram is considered as positive, only if significant pain and an abnormal image are present.Ý When these two portions of the test are taken into account in asymptomatic volunteers, the study results in 100% specificity[49].Ý Discography has been found to be more sensitive than MRI in detecting annular tears[50].Ý CT/discography has an overall accuracy of 87-94%[51].Ý Discography was not found to be sensitive to lesions in the middle or outer annulus that are not contiguous with the nucleus.Ý MRI, when compared to discography, is significantly better in demonstrating posterolateral lumbar disk herniations (100% versus 86%)51,[52].Ý Discography was found to be more sensitive than myelography in detecting lateral disk herniations, especially at the L5-S1 level51,[53].Ý It is recommended that MRI be used initially in the diagnosis of low back pain.Ý In terms of surgical outcome, it has been found that when a patient has both, a positive abnormal discographic image and a painful provocative injection, there is an 88% success rate in terms of a surgery while those patients that displayed a positive image but no symptomatic pain reproduction, the success rate is only 52%[54].Ý CT/discography can identify recurrent disk herniations not visualized by Gadolinium enhanced MRI.

Lumbar discogenic pain and internal disk disruption are defined as lumbar spine pain with or without referred pain, stemming from an intervertebral disk, caused by internal disruption of the normal structural and biochemical integrity of the symptomatic disk.Ý Discogenic pain occurs in 39% of patients with severe chronic low back pain in whom the etiology has not been well defined by less invasive diagnostic testing.

Internal disk disruption was described as being different from symptomatic disk herniation.Ý In the syndrome of internal disk disruption, the primary symptom is back pain. Leg pain might be a significant part of the problem, but back pain is the dominant complaint. Provocative discography is required to establish this diagnosis. In symptomatic disk herniations, the mass effect of herniated disk material compresses neural elements causing a tissue reaction.Ý Leg pain is the dominant complaint and is always greater than back pain in the fully developed radicular syndrome. Ý

The most commonly abnormal levels are L4-5 and L5-S1 in combination, followed by L5-S1 alone, followed by the combined 3 level degeneration at L3-4, L4-5, and L5-S1.

 

Indications

1.         The primary indication for lumbar discography is chronic low-back pain with or without radicular pain in the absence of MR imaging-documented neural compression. Patients with persistent, severe back pain in whom other diagnostic tests have failed to reveal the etiology.

2.         When clinical findings suggest a level or a side different from that suggested by diagnostic imaging. (To resolve diagnostic dilemmas.)

3.         Discography should be performed only if the patient has failed conservative therapy, and other diagnostic tests have not provided sufficient diagnostic information. Generally, discography should be viewed as an invasive test to be used to seek elusive pathology, when results from other tests are equivocal or inconsistent, in a patient with symptoms severe enough to require surgical management.

4.         Not indicated or necessary to confirm the unequivocal presence of herniated discs that coincide with findings on clinical examination.

5.         Further evaluation of demonstrably abnormal discs to help assess the extent of pathology and/or correlation of the abnormality with clinical symptoms. Such may include recurrent pain from a previously operated disc and lateral disc herniation.

6.         To determine if the adjacent disks to a proposed fusion segment are symptomatic and to determine if these segments can tolerate the added stress of a nearby fusion.

7.         Further evaluation of abnormal disks or recurrent pain from a previously operated disk and lateral disk herniation.

8.         Assessment of failed surgery patients to determine if there is painful pseudoarthrosis or a symptomatic disc in a posteriorly fused segment.

9.         To determine if the patient is a candidate for IDET (Intradiscal Radiofrequency Annuloplasty / Nucleoplasty).

10.     Assessment of minimally invasive surgical candidates confirmed a contained disk herniation or to investigate dye distribution pattern prior to chemonucleolysis.

 

Anesthesia

It is recommended that short acting medications be used, since it is absolutely necessary to have an awake and responsive patient for questioning about reproduction of pain. If possible, avoid Bezodiazepines or long acting narcotics that can confuse the interpretation of the results. Intravenous sedation should be sufficient to keep the patient comfortable in the required position, but not enough to make the patient somnolent, disoriented, or uncooperative.

 

Antibiotic Coverage

           Intravenous cefazolin (2 gm) does diffuse into the human disc in detectable concentrations; and a critical time relationship exists (15-80 minutes after a bolus administration of cefazolin) for the optimal level of intradiscal antibiotics to be achieved[55].

           Prophylactic role of cefazolin administered at the time of discography. Adding the antibiotic to the intradiscal suspension or giving it intravenously 30 minutes before intradiscal inoculation of bacteria prevented any radiographic, macroscopic or histological signs of discitis; all the intervertebral disc cultures were negative. The injected contrast contained cefazolin 1 mg per ml[56].

           Intravenous cefazolin or vancomycin given within 1 hour before surgery can effectively prevent postoperative discitis[57].

           Penicillin (negatively charged) and gentamicin (positively charged) penetrated the neutrally charged annulus fibrosus, but penicillin had less ability than gentamicin to penetrate into the negatively charged nucleus pulposus. Data suggest that penetration and distribution of antibiotics into avascular intervertebral disc is significantly influenced by the charge of antibiotics[58].

           Gentamicin concentration in the rabbit nucleus pulposus does not peak until 2 hours after an intravenous bolus of drug. If gentamicin penetrates human nucleus pulposus in a similar fashion, this study could have implications for the timing of administration of this agent for prophylaxis[59].

 

Contrast Material

You should always use a water-soluble, nonirritating, non-ionic, preservative-free, hypoallergenic contrast. We currently use Isovue 300M.Ý An abnormal disk will usually accept two (2) or more ml of fluid

 

Pain Provocation hypothesis

1.ÝÝÝÝÝ The injection may increase intradiscal pressure which, in an abnormal disk, may stimulate nerve endings within the annular fibers of the disk, possible by stretching them.

2.ÝÝÝÝÝ The injection may result in some biochemical or neurochemical stimulation that causes pain.

3.                                 An injection may increase pressure at the end plates or pressure may be transferred to the vertebral body throughout the end plate resulting in an increase in intravertebral pressure and therefore pain. This hypothesis is supported by studies reporting disk injection resulting in end plate deflection and increased specimen height.

4.                                 ÝAnother hypothesis to explain the presence of pain from injection of a seemingly normal disk is that pressure from the injection is transferred to an abnormal, symptomatic adjacent disk and, thus, a positive pain response is elicited.

 

Acute-pain provocation mechanism (At the time of injection)

          Acute Pain evaluation (Provocative Discography)

-          Positive = pain above or equal to 6/10.

-          Location of pain must be described. (Back pain, leg pain) Including the side (right, left, center, bilateral) and the distribution (leg pain down to the bottom of the foot, etc.)

          Evidence

-          Stimulation of nerve endings in the outer annulus[60],[61],[62]

-          Painful endplate disruption[63]

-          Increased pressure at the endplates or within the vertebral body[64]

-          Increased Substance P and VIP in the dorsal root ganglia[65]

-          Transmission of mechanical stimulation to the facet joints.

          Problems

-          With chronic pain central sensitization occurs, and dorsal horn activity no longer depends on peripheral tissue injury. A pure stimulus response relationship no longer exists. Both previously innocuous stimuli to the dorsal horn and stimuli from outside the original receptive field cause pain. Therefore, interpretation may be inaccurate.[66],[67]

-          Psychological factors may affect results.[68]

-          Disc tears and leakage may prevent increases in intradiscal pressure, adequate enough to mimic even standing pressures.

 

Delayed-pain provocation mechanism (Hours after the injection)

          Evidence

-          Mechanism of irritation and inflammation of neural structures by exposure to nuclear material.

ß          Inflammatory glycoprotein is responsible for chemical radiculitis.[69]

          Peaks 3 weeks after acute injury to disc.

          Prolonged rest may be contraindicated because of the risk of formation of radicular adhesions.

ß          Phospholipase A2 (induced by cytokines, among others)[70]

ß          Leukotriene B4 and Thromboxane B2. (non-contained disc herniations > contained disc herniations)70

-          Pathophysiological changes

ß          Tumor necrosis factor (TNF)[71] (a cytokine) causes:

          Thrombus formation

          Intraneural edema

          Reduction of nerve conduction velocity

          Dorsal root ganglia compartment syndrome[72]

          Anti-TNF include: pentoxifylline, etanercept, and infliximab.

ß          Thromboxane A2 (TXA2) ñ induces not only potent platelet aggregation, but also blood vessel contraction.[73]

ß          Leukotriene B4 (LTB4) ñ a potent chemotactic agent, plays a role in inflammatory reactions by recruiting neutrophils and lymphocytes.73

          Problems

-          Time delay: After the exposure of the dorsal root ganglia to the nuclear matrix, it may take 2.5 to 6 hours for the spontaneous neural activity to increase.[74]

-          At this point, nobody is looking at this component of the test. Patients should be asked to keep a diary about the post-procedure pain.

          Other postulated pain mechanisms and hypothesis

Post procedure hematoma

 

Complications of discography

        Post-dural-puncture headaches (Spinal headaches)

        Meningitis

        Discitis

-            0-0.61% - Incidence based on number of patients injected.

-            0-0.03% - Incidence based on number of discs injected.

-            1.3-3% using a single needle technique and 0.35-0.7% using a double needle technique, and when prophylactic antibiotics are used, the incidence goes further than to 0.000%.

-            There is experimental evidence that prophylactic antibiotics, both intravenous and intradiscal, can prevent discitis.[75],[76]

        Intrathecal hemorrhage

        Arachnoiditis

        Severe reaction to accidental intradural injection

        Damage to the disc itself

ß                        Followed negative discogram patients for 10-20 years and found no additional abnormalities compared to those initially seen on the negative discogram.[77]

        Nerve damage

        Urticaria

        Post-injection disc herniation

        Retroperitoneal hemorrhage

        Nausea (2%)

        Convulsions (4%)

        Headaches (10%)

        Increased pain (81%)

-          Hematomas may cause significant pain and spasms.

-          Muscle and skin transgression may also cause significant pain and spasms.

-          Displacement and leakage of nuclear material during injection of contrast, may cause irritation to neural structures, which may require LESI to solve.

-          Pay attention to this pain and inquire whether or not it is different, similar, or exactly the type of pain the patient normally experiences. It may help with the diagnosis of the mechanism of the pain.

-          Consider giving patients some Klonopin or Valium for spasms.

 

Recognizing and Treating Discitis:

        Signs and symptoms

-          Worsening of pain 3 to 6 weeks after procedure.

-          May not present with fever or elevated WBC count.

        Diagnostic Tests

-          Check ESR, re-check in 24 hours if equivocal.

-          Blood culture, direct aspirate / biopsy.

-          Rule out other sources.

-          MRI with and without contrast. (Gadolinium).

-          Bone Scan

-          WBC nuclear scan

        Treatment

-          6 to 8 weeks of IV antibiotics.

-          Discectomy.

 

Clinical Symptoms

Interestingly, there are some studies to clinically evaluate discogenic pain by using a "bony vibration stimulation".Ý An attempt should be made to determine whether or not the patient can feel pain by placing a tuning fork over the spinous processes. The main symptoms are:

1.                                 Internal disk disruption - The primary symptom is back pain.

2.ÝÝÝÝÝ Symptomatic disk herniations - Leg pain is the dominant complaint and is always greater than back pain in the fully developed radicular syndrome.

 

Procedure

Prophylactic antibiotics and/or antihistamines should be considered.Ý A double needle technique should always be used.Ý The injection should be performed with contrast as previously described.Ý (Water soluble, etc.). Accurate needle placement is required to avoid annular injections, which could produce false positive results. Injection against the vertebral end plate can also cause false positive response.

ÝPressure from the discography injection could be transferred to an adjacent abnormal, symptomatic disk and thus, a positive pain response could be elicited. Due to this, it is always a good idea to monitor the pressure of the adjacent disks as contrast material is being injected and the end point pressure tested.

 

The information recorded should include:

1.     The resistance to the injection. (End-point)

2.     The amount of contrast injected. (Maximum Volume)

3.     The volume at which the patient experienced pain. (Pain Volume)

4.     The pattern of dye distribution. (Diffuse, location of fissure, extravasation, herniations, Schmorl's node etc.).

5.     Pressure at which patient experienced a "pressure sensation".

6.     Pressure at which the patient experienced "Pain".

7.     The pain response. (Location, character, distribution, intensity, and concordance or discordance with the patient's typical pain and pain pattern)

8.     Pain intensity is recorded on a 0-10 scale

 

Interpretation

Very careful attention should be paid to interpreting the pain response during the injection of each disk, including if the pain is similar to or exactly like the symptoms for which the patient seeks relief.Ý The location of the pain, and its intensity.Ý Discography should then be followed by actual CT scanning.

Pain at low pressures is most likely due to chemical irritation. .Ý Low resistance is generally associated with a tear throughout the outer annulus Pain at high pressures is possibly due to mechanical irritation, end-plate deflection, or stimulation of pressure receptors.

An intradiscal pressure of 60-70 pounds per square inch (400-500 kilopascals) is the maximum pressure that can be sustained by manual injection technique (thumb pressure on a 3.0 cc luer-lock syringe).Ý The normal intradiscal pressure of a supine patient is approximately 15-25 PSI.Ý Sitting or standing increases this normal pressure to approximately 80 PSI.

Generally, if a large volume of contrast can be injected, the disc is degenerated or there is a fissure extending through the outer annular wall.Ý Injection pressure or resistance to injection should be noted.

 

Imaging Diagnosis of Lumbar Discs[78]:

 

 

 

 

 

 

 

CT classification of Discography[79]:

 

 

 

Type 1 the discogram is normal manometrically, volume metrically, radiographically, and produced no pain.Ý The CT discogram showed contrast to be centrally located in the axial and sagittal projections.

 

 

 

 

Type 2 is identical to type 1 except that it is positive for reproduction of pain. Ý

 

 

 

 

Type 3 the annular tears lead to a radial fissure.Ý This group is further subdivided into Type 3a when the radial fissure is posterior, 3b when it radiates posterolateral, and 3c when the fissure extends lateral to a line drawn from the center of the disk tangential to the lateral border of the superior articulating process.

 

 

 

Type 4 once the radial fissure reaches the periphery of the annulus fibrosus, nuclear material may protrude causing the outer annulus to bulge

 

 

 

Type 5 when the outer annular fibers rupture, nuclear material may extrude beneath the posterior longitudinal ligament and come in direct contact with either the dura or a nerve root. Ý

 

 

 

Type 6 when the extruded fragment is no longer in continuity with the interspace it is said to beÝ sequestrated.Ý Manometrically, volumetrically, and radiographically, the discograms are always abnormal.Ý Familiar pain may only be reproduced if enough pressure is generated against the free fragment to cause stimulation of the pain sensitive structures. Ý

 

 

 

Type 7 the end stage of this degeneration is internal disk disruption, in which multiple annular tears occur.Ý The discograms are abnormal manometrically, volumetrically, and familiar pain may or may not be reproduced.ÝÝ Radiographically, the contrast usually fills the entire interspace in a chaotic fashion.Ý The CT discograms show contrast extravasation throughout multiple annular tears.

 

 

 

 

Clinical classification:

1.  No pain or pressure. (NP)

2.  Pressure (P)

3.  Pain dissimilar to clinical symptoms. (D)

4.  Pain similar to clinical symptoms. (S) (Inconsistent)

5.  Exact reproduction of symptoms. (ER) (Concordant)

6.  Pain intensity is recorded on a 0-10 scale

 

Contrast distribution[80]: (as evaluated by Fluoroscopy )

 

 

Discogram Type

 

Stage of Disk Degeneration

 

ìCotton Ballî (CB)

 

No signs of degeneration, Soft white amorphous nucleus

 

ìLobularî (L)

 

Mature disk with nucleus starting to degenerate into fibrous lumps.

 

ìIrregularî (I)

 

Degenerated disk with fissures and clefts in the nucleus and inner annulus.

 

ìFissuredî (F)

 

Degenerated disk with radio fissure leading to the outer edge of the annulus.

 

ìRupturedî (R)

 

Disk has a complete radio fissure that allows injected fluid to escape.Ý Can be in any stage of degeneration.

 

 

ìCotton Ballî

 

ìLobularî

 

ìIrregularî

 

ìFissuredî

 

ìRupturedî

 

 

 

Discomanometry

ÝÝÝÝÝÝÝÝÝÝÝÝÝÝÝ Simple discomanometry is the manual injection of fluid into the nucleus pulposus with continuous recording of the pressure as a function of time. Quantitative discomanometry is the automated injection of fluid at a constant flow rate, recording both, the volume and pressure, as a function of time.

 

Interpretation:

1.       Low resistance is generally associated with a tear throughout the outer annulus.

2.       Pain at high pressures is possibly due to mechanical irritation, end-plate deflection, or stimulation of pressure receptors.

3.       Intradiscal pressure of 60-70 pounds per square inch (PSI) is the maximum pressure that can be sustained by manual injection technique (thumb pressure on a 3.0 cc luer-lock syringe.)

4.       Generally, if a large volume of contrast can be injected, the disc is degenerated or there is a fissure extending through the outer annular wall.

5.       In general, degeneration of the intervertebral disc will cause a decrease in the mean intradiscal pressures.

6.       Opening or intrinsic pressure is defined as the pressure at which the contrast starts to enter a disc.

7.       Leakage pressure is defined as the pressure on the P-V curve, where a sudden change occurs in the curve inclination, whereby the volume increased substantially, while the pressure either stopped increasing, or changed minimally.

8.       Chemical irritation is defined as pain at or below 15 PSI above opening pressure.

9.       Mechanical irritation is defined as pain between 15 and 50 PSI above opening pressure.

10.    Indeterminate discs are defined as having pain between 51 and 90 PSI above opening pressure.

11.    Normal disc have no pain.

12.    Annular disruption ñ leaking / protrusion / annular fissuring

13.    Kpa x 0.14504 = PSI

 

Intradiscal Pressure Values for Different Positions and Exercises

Position

Pressure (PSI)

Lying supine

15

Lying on the side

17

Lying prone

16

Lying prone, extended back, supporting on elbows

36

Laughing heartily, lying laterally

22

Sneezing, lying laterally

55

Peaks by turning around

102-116

Standing, relaxed

73

Standing, performing valsalva maneuver

133

Standing, bent forward

160

Sitting relaxed, without backrest

67

Sitting actively straightening the back

80

Sitting with maximum flexion

120

Sitting bent forward with tight supporting the elbows

62

Sitting slouched into the chair

39

Standing up from a chair

160

Walking barefoot

77-94

Walking with tennis shoes

77-94

Jogging with hard street shoes

51-138

Jogging with tennis shoes

51-123

Climbing stairs, one at a time

73-102

Climbing stairs, two at a time

44-174

Walking down stairs, one stair at a time

55-87

Walking down stairs, two stairs at a time

44-131

Lifting 20Kg, bent over with round back

334

Lifting 20Kg, as taught in back school

247

Holding 20Kg close to the body

160

Holding 20Kg, 60cm away from the chest

261

Pressure increase during night (over a period of 7 hr.)

15-36

Reference: ìNew In Vivo Measurements of Pressures in the Intervertebral Disc in Daily Lifeî Wilke et al. Spine Vol.24, No 8, pp755-762, 1999.

 

 

 

Level

 

Average Volume (ml)

 

Volume Range (ml)

 

L2-3

 

0.58

 

0.4 - 0.7

 

L3-4

 

1.06

 

0.4 - 2.6

 

L4-5

 

1.09

 

0.22 - 2.4

 

L5-S1

 

0.99

 

0.42 - 2.0

 

Transition

 

0.40

 

NA

 

 

Discogram Type

 

Mean Injection Pressure (PSI)

 

Mean Injection Volume (mL)

 

1

 

34

 

0.62

 

2

 

28

 

0.71

 

3

 

26

 

1.20

 

4

 

17

 

1.54

 

5

 

19

 

More than 2.0

 

 

Disk Classification

 

Intradiscal Pressure

 

Pain Response Intensity

 

Pain Response Category

 

0-normal

 

>80 PSI

 

0

 

NA

 

1-asymptomatic

 

>50 PSI

 

Pressure, discomfort only

 

NA

 

1-asymptomatic

 

>50 PSI

 

Definite pain (>5/10)

 

Discordant

 

2-indeterminate

 

<50 PSI

 

Definite pain (>5/10)

 

Discordant

 

3-mechanical (strain)

 

30-50 PSI

 

Definite pain (>5/10)

 

Discordant

 

4-chemical (sensitized)

 

<30 PSI

 

>5/10

 

Concordant

 

Appendix A ñ Guidelines

 

Statement of purpose:

To provide guidelines to assist the Pain Physician with the performance of a discogram (discography).ÝÝ This is a diagnostic procedure used to determine the extent of involvement of a vertebral disc as a cause of the patientís pain.

 

Policy:

The following are Guidelines. Exceptions to these guidelines are up to the discretion of each physician, and shall be based on that physicianís evaluation of the case in question.

Only the trained pain physician should do this and all pain blocks. The procedure will be done under fluoroscopy. May be done in same day surgery facilities, or in clinic facilities, if fluoroscopy and a sterile environment are available.

 

Equipment:

-   ìCrash cartî must be available in the facility.

-   (2) two 10cc, luer-lock syringes

-   (1) one 3cc, luer-lock syringe

-   25-G, 1.5-in, needle (1)

-   18-G needle (1)

-   18-G, 3-inch, Quincke spinal needle (one per level to be done) (usually 3-4)

-   22-G, 7-inch, Quincke spinal needle (one per level to be done) (usually 3-4)

-   (1) one pressure manometer syringe (The kind used in angioplasties)Ý ìBasixî 25 Inflation Syringe Catalog No. IN3125 (Merit Medical 1-801-253-1600 or 1-800-356-3748) or s similar pressure-gauged (manometer) 20-60 ml syringe (Merit Medical Digital Fluid Syringe KO5-L1-L5)

-   (2) two 10cc bottles of contrast, water-soluble, non-ionic, hypoallergenic, myelogram-compatible dye/contrast. (20 ml) Either Isovue 200M or 300M, or Omnipaque 180. If patient is allergic to contrast, follow the ìProtocol for patients with Allergies to Radiological Contrastî.

-   Betadine prep or some other form of skin prep. (Alcohol or Hibiclens)

-   Prep tray

-   (4) four sterile towels

-   (1) pack of sterile 4x4

-   (1-4) one to four Band-Aids

-   Prophylactic antibiotics (as ordered by physician): Gentamicin 120mg and Ancef 1gm IV, prior to procedure. Vancomycin 1gm IV, if allergic to penicillin.

-   Fluoroscopy machine (C-Arm)

-   Fluoroscopy table (Chic table)

-   Sedation (as ordered by physician): Versed (Midazolam) 2-4mg, Fentanyl 2cc and/or propofol.

Medication:

-   Cipro (ciprofloxacin) 500 mg PO BID 24 hr prior to procedure and 5 days after.

-   Rocephin (ceftriaxone) 1-2gm. IV before the procedure

-   Another alternative is Ancef or Kefzol (cefazolin) 1-2gm. IV, before procedure.

-   Gentamicin (Garamycin) 100-200 mg IV

-   (1) one 20-30cc bottle of 2% lidocaine

-   If the patient is allergic to Penicillin, give Vancomycin 1gm. IV slowly before the procedure.

-   Ancef or Kefzol (cefazolin) 5 mg/kg to mix with contrast, only if patient is not allergic to penicillin.

Procedure:

1.       Schedule patient in Special Procedure area.

2.       Ascertain and document that the patient has a driver, has not eaten 6 hours prior to procedure, and is not taking any blood thinners.

3.       Confirm that the patient is not taking any blood thinners like Coumadin. If taking Coumadin, it most be stopped, with the consent of the prescribing physician, at least four (4) days prior to procedure.Ý ASA and ASA-containing medications should be stopped eleven (11) days prior to the procedure.

4.       Patient's Pain Clinic chart should be available at Special Procedures.

5.       Ascertain and document that female patients are not pregnant. (Question patients about possibility)

6.       The physician will review the procedure, including the risks and possible complications, and answer any questions that the patient or family may have, in the visit prior to the procedure day.

7.       Have patient or guardian sign informed consent form.

8.       Obtain baseline vital signs, which should include: BP, HR, RR, Temp, SaO2, and NAS-11(VAS).

9.       Start an IV.

10.    Place patient in position. Position: prone for lumbar or thoracic disc and supine for cervical disc.

11.    Prep: For lumbar disks, prep from the sacrum to the lower border of the scapula. For cervical, prep from the mandible to the collarbone (clavicle). Always prep wide.

12.    The following laboratory should be ordered and drawn prior to the procedure, if requested by physician: CBC (WBC and platelet count), Sedimentation rate, bleeding time, PT/PTT, INR (as felt to be necessary by physician), and pregnancy test for females in childbearing years. The procedure should never be delayed waiting for these results, except for the pregnancy test. Ideally they should have been drawn days prior to procedure.

13.    A C-Arm will be required for fluoroscopy.

14.    Schedule for IV sedation using Versed and Fentanyl IV sedation.

15.    Prophylactic antibiotics (as felt necessary by physician).
Gentamycin 120 mg IV before the procedure.

Ancef and Kefzol 1-2gm. IV, before procedure. (Except if allergic to penicillin)

16.    If patient is not allergic to penicillin, mix 1gm of powdered cefazolin (Ancef) in 10 ml of Omnipaque 180. This will give you a concentration of 100mg/ml. Take 3 ml of this solution and mix it up to a total volume of 20 ml of Omnipaque 180, in the Merit Medical Digital Fluid Syringe. This will lead to a final concentration of 15 mg/ml.

17.    If the patient is allergic to Penicillin, give Vancomycin 1gm. IV slowly before the procedure.

18.    Sedate the patient (as ordered by physician). Maintain meaningful verbal contact at all times.

19.    Assist physician as needed.

20.    At completion of the procedure, have patient return to supine position.

21.    Discard contaminated needles and equipment.

22.    Document in procedure form:
a. Name of procedure, physician, indications, date, and place where performed (Hospital, Office)
b. Vitals signs every 15 minutes
c. Post-procedure NAS-11
d. Patientís Status after procedure (Patient tolerance)
e. Any untoward effects or complications
Ýf. Intradiscal pressures
g. Injected volume
h. Pain provocation and distribution pattern
i. End point
j. Morphologic distribution of radiological contrast

23.    Observe patient for 10-15 minutes post procedure.

24.    Arrange with Radiology to have the patient taken to the CT scanner immediately after the discogram injection, and then back to Special Procedures Recovery for discharge, once the patient has met discharge criteria.

25.    Arrange for follow up appointment at the pain center in 1-2 weeks.

26.    If the patient continues to have significant pain after the discogram, then schedule the patient for an evaluation and possible epidural steroid injection, upon return to the pain clinic.

If the patient develops pain and fever, then order a sed rate and CBC. If abnormal, consider ordering a Bone Scan to rule out discitis.

 

Appendix B ñ Pressure Manometry Syringe

25 ATM Inflation Devices

 

Disposable IntelliSystemÆ 25 Inflation Syringe with 14" (35.5cm) extension tubing. Medium pressure 3-way stopcock included separately. Packaged 5 units per box, 4 boxes per case.

 

UNITED STATES
Merit Medical Systems, Inc.
1600 West Merit Parkway
South Jordan, Utah 84095 USA
Telephone: 1-800-356-3748 (Toll Free)
Telephone: 1-801-253-1600 (Direct)
Fax: 1-801-253-1652

 

 

Appendix C ñ Libman Test[81],[82],[83],[84]

 

Theory:

This test is designed to examine the patient's tolerance to pain, as an individual.

Procedure:

The test consist of the following maneuver: using the thumb of your right hand, pressure is placed for a few seconds over the anterior portion of the mastoid process towards the area of the styloid.Ý This maneuver will put pressure over a portion of the greater auricular nerve.Ý According to the degree of pain produced by this maneuver, the patient will be classified in one of three categories Libman type 1 (hyposensitive), Libman Type 2 (sensitive), or Libman Type 3 (hypersensitive).Ý The response is based on the facial and/or verbal response of the subject to the question "what do you feel when I do this?"Ý The following is a description of each one of the expected reactions. Ý

 

Libman Type 1 (hyposensitive): These are the patients who experience no pain.Ý Therefore as a consequence of this you will see no facial expression resembling that of pain, and they might vocalize that they are having no pain at all.Ý It is believed that 20% of the population belongs to this group.Ý This is variable and depends on race (in the Indian population up to 80% might be part of this group), and profession (70% of boxers).

 

Libman Type 2 (sensitive): The patients in this group will experience some pain but they will not manifest any facial expressions with it.Ý It is assumed that 40-50% of the population will be part of this group.

 

Libman Type 3 (hypersensitive): These are the patients who will not only complain of pain by vocalizing it but they will also express a facial grimace compatible with pain.Ý This group accounts for approximately 30-40% of the total population.Ý This is also influenced by the area where the patient resides (with up to 80% of the urban population being part of this group), as well as level of education (with up to 90% of the "educated" patients being part of this group), etc. (Patients that scream during local anesthetic infiltration of the skin.)

 

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