Intrathecal iodinated contrast-induced transient spinal shock
- 1 Jinnah Sindh Medical University, Karachi, Sindh, Pakistan
- 2 Liaquat University of Medical and Health Sciences, Jamshoro, Sindh, Pakistan
- 3 Pulmonary and Critical Care Medicine, West Virginia University School of Medicine, Morgantown, West Virginia, USA
- 4 Internal Medicine, Western Michigan University Homer Stryker MD School of Medicine, Kalamazoo, Michigan, USA
- Correspondence to Dr Vishal Deepak; deepak.vishal@live.com
Abstract
Transient spinal shock is a previously unreported complication of intrathecal contrast. A 63-year-old man presented with the chief complaint of worsening back pain. Computed topography of lumbar spine without contrast showed a lytic lesion. After international normalized ratio (INR) correction, patient was sent for CT myelogram. After intrathecal contrast injection, the patient dropped his blood pressure profoundly and developed clinical manifestations of spinal shock. Emergent intravenous bolus fluids were initiated resulting in improvement in blood pressure. Patient’s spinal shock resolved within hours. CT myelogram was normal except previously known lytic lesion. It was concluded that the transient shock was most likely due to contrast injection. We believe that this is the first reported case of transient spinal shock following CT myelogram using water-soluble iodinated non-ionic contrast agent administered intrathecally.
Background
Contrast agents have long been used for the imaging of anatomic boundaries and to explore normal and abnormal physiologic findings. The most successful and widely applied contrast agents in use today are the iodinated contrast agents (ICAs).1 It is estimated that approximately 75 million doses of ICAs are given worldwide each year.2 Modern ICAs can be used almost anywhere in the body. Most often they are used intravenously but can be administered intra-arterially, intrathecally and intra-abdominally.3 CT myelography, a suitable alternative of MRI of spine in some patients, requires intrathecal administration of iodinated contrast. The development of non-ionic low-osmolar iodinated contrast media has greatly reduced the incidence of adverse reactions to contrast media; however, adverse reactions still occur.4
Spinal shock occurs as a result of acute spinal cord injury and is defined a state of brief physiologic reflex depression of cord function below the level of injury.5 Spinal cord injury can be either primary due to mechanical causes, metastatic disease, transection, abscess, gunshots or distraction of the nerves or secondary due to disruption or occlusion of arterial blood supply.6
Spinal shock is commonly confused but is different from neurogenic shock. The later explains the haemodynamic changes due to abrupt loss of autonomic tone due to spinal cord injury and is often seen with injury above the level of T6. Spinal shock, conversely, refers to sensation loss below the level of injury and is not circulatory in nature. However, both may coexist in a patient.5
Case presentation
A 63-year-old man presented to the emergency department (ED) with a chief complaint of left-sided lower back pain radiating to his groin for 2 days. His back pain started 1 month previously but was bearable until the last 2 days. He went to his primary care physician prior to presenting to ED. He was prescribed a tapering course of prednisone and hydrocodone–acetaminophen. His medical history was significant for chronic obstructive pulmonary disease, pulmonary embolism on lifelong anticoagulation with warfarin, sick sinus syndrome status post permanent pacemaker implantation and coronary artery disease status post percutaneous intervention.
Exam in the ED: Vital signs: blood pressure 119/71 mm Hg, heart rate 81 beats/min, temperature 98.8°F, respiratory rate of 16 breaths/min and oxygen saturation of 96% on ambient air. There was no palpable tenderness of the spine; however, the exam was done after the patient received pain medication. Patellar and achilles deep tendon reflexes were 2+. Vibration sensation was decreased in feet bilaterally. Straight leg raise test was negative ipsilaterally and contralaterally.
Laboratory investigations at the time of presentation are illustrated in table 1. CT of the lumbar spine without intravenous contrast (figure 1A–D) in the ED showed lytic type irregularity with posterior annular bulge and left foraminal disc protrusion potentially impinging L5 nerve root. In addition, CT also showed mild disc space narrowing throughout the lumbar spine.
Non-contrast CT of the lumbar spine without intravenous contrast in sagittal (A), coronal (B) and axial (C,D) views.
Laboratory investigations at the time of presentation
| Test | Results | Normal range |
| White blood cell count | 8.9x109/L | 4.5–11x109/L |
| Absolute neutrophil count | 5.5x109/L | 1.8–7.7x109/L |
| Haemoglobin | 131 g/L | 120–150 g/L |
| Platelet count | 194k/µL | 150–200k/µL |
| Serum creatinine | 0.9 mg/dL | 0.4–1.2 mg/dL |
| Serum sodium | 142 mmol/L | 135–145 mmol/L |
| Serum potassium | 4.0 mmol/L | 3.5–5.1 mmol/L |
| Serum urea nitrogen | 20 mg/dL | 8–21 mg/dL |
| Estimated glomerular filtration rate | >60 mL/min/1.73 | >60 mL/min/1.73 |
| Serum bicarbonate | 25 mmol/L | 22–32 mmol/L |
| Serum total calcium | 9.4 mg/mL | 8.4–10.3 mg/mL |
| Serum ionised calcium | 4.7 mg/mL | 4.26–4.6 mg/mL |
| Aspartate aminotransferase | 13 IU/L | 13–36 IU/L |
| Alanine aminotransferase | 21 IU/L | 6–40 IU/L |
| Alkaline phosphatase | 83 IU/L | 45–115 IU/L |
| Total bilirubin | 0.4 mg/dL | 0–1.2 mg/dL |
| Prothrombin time | 33.8 s | 10.3–13.8 s |
| International normalised ratio | 2.8 | N/A |
| Erythrocyte sediment rate | 47 mm/hour | 0–20 mm/hour |
| C reactive peptide | 8.8 mg/dL | 0.0–0.9 mg/dL |
| Blood cultures (2 sets) | No growth after 5 days | N/A |
The patient was admitted to neurology floor and neurosurgery was consulted given the CT scan findings. MRI could not be obtained as patient’s pacemaker was not compatible. Neurosurgery recommended CT myelogram for further evaluation of the lytic lesion and a bone scan while bone scan confirmed the finding of CT spine and showed abnormal uptake of radiotracer involving the endplates and posterior elements at L4-L5 and L5-S1 indicating degenerative changes.
On day 3 of admission after the international normalized ratio (INR) was corrected, the patient went for CT myelogram. After lumbar puncture and injection of contrast medium, the patient suddenly became diaphoretic with profound drop in blood pressure. A total of 15 mL of Omnipaque 180 (intended for intrathecal use) was instilled using fluoroscopic visualisation; the patient’s symptoms started while spinal needle was being removed. Of note, there was no report of bloody cerebral spinal fluid (CSF) or CSF leak during the procedure. On further evaluation, the patient was alert and oriented. He reported mild difficulty in breathing and inability to cough. He also reported his legs felt very heavy and he was unable to move them. His vital signs were: systolic blood pressure in 50 mm Hg, heart rate of 83 beats/min. He was cold and diaphoretic with weak peripheral pulses. His neurological examination revealed complete loss of: motor strength, pain and touch sensation, and deep tendon reflexes in bilateral lower extremities.
These clinical manifestations were highly concerning for neurogenic shock in the setting of recent invasive procedure involving the spinal cord. The patient was given intravenous bolus fluids with some improvement in the blood pressure. CT myelogram was completed under close observation which showed endplate irregularity and adjacent soft tissue density around L4-L5 disc with a possibility of discitis (figure 2A–C). There was no cord compression, epidural hematoma, mass or any other organic finding which could explain the patient’s acute symptoms during injection of contrast in the spine canal. Intensive care unit (ICU) team was consulted and patient was admitted to ICU for shock state.
CT myelogram of thoracolumbar spine in sagittal (A), coronal (B) and axial (C) views.
Surprisingly, soon after the admission to ICU, the patient began to regain sensation and motor strength in his lower extremities. His blood pressure returned to normal after 2 L of intravenous bolus fluids. He never required vasopressors therapy. He was kept in ICU overnight for monitoring, and then was transferred back to neurology floor. The patient also had a CT angiography of the head and neck done which did not show any flow-limiting stenosis of the head and neck vasculature.
On day 4 of admission, the patient underwent percutaneous biopsy/disc aspiration of L4-L5 for further evaluation of the CT scan findings. The aspiration tissue was sent for culture, which grew few Staphylococcus epidermidis. Infectious disease was consulted given positive cultures, and recommended repeat biopsy (because of risk of contamination of sample). Antibiotics therapy was not initiated.
On day 9, the patient underwent repeat percutaneous biopsy disc aspiration of L4-L5. Tissue culture this time did not grow any organisms. Furthermore, histology of the tissue revealed viable appearing bone with slight marrow fibrosis and chronic inflammation. Meanwhile, the patient also had work up for multiple myeloma, autoimmune disease, fungal and tubercular infection: all of which was negative as illustrated in table 2.
Additional laboratory investigations
| Test name | Results | Normal range |
| Immunology/serology | ||
| Antinuclear antibodies screen | None detected | N/A |
| Coccidiodes antibody by complement fixation | <1:2 | <1:2 |
| Histoplasma antibody by complement fixation | <1:8 | <1:8 |
| Quantiferon Tuberculois Bacilli gold | Negative | Negative |
| Serumelectrophoresis | ||
| Total protein | 6.3 | 6.00–8.30 |
| Albumin | 2.99 | 3.75–5.01 |
| Alpha 1 | 0.52 | 0.19–0.46 |
| Alpha 2 | 0.96 | 0.48–1.05 |
| Beta | 0.9 | 0.48–1.10 |
| Gamma | 0.93 | 0.62–1.51 |
| Otherchemistry | ||
| Serum kappa free light chains | 2.14 mg/dL | 0.33–1.94 mg/dL |
| Serum lambda-free chains | 1.70 mg/dL | 0.57–2.63 mg/dL |
| Serum kappa/lambda-free ratio | 1.26 | 0.26–1.65 |
Differential diagnosis
Shock was considered to be neurogenic and spinal in origin. Other differential for shock was considered but ruled out appropriately. Anaphylactic reaction to the contrast was the most important differential but the patient had received intravenous contrast in the past for CT angiography of the chest without any reaction. Furthermore, the patient received intravenous contrast during current hospitalisation for CT angiography of the head and neck and no reactions were noted.
After extensive work up including tissue biopsy, it was concluded that the patient’s back pain is most likely secondary to chronic degenerative changes and the ‘lytic lesion’ noted on multiple scans were a result of degeneration.
Outcome and follow-up
The patient was discharged home in stable condition and after improvement of symptoms with pain medications. He did not develop any complications due to transient neurogenic shock. Since the reaction, our patient experienced was not considered to be anaphylactic, there was no restriction placed on future use of intravenous contrast. In fact, 3 months after the event described in this manuscript, he received Omnipaque 350 intravenously for a CT scan to evaluate for pulmonary embolism. He suffered no ill effects from this. We suspected that he would be at risk for recurrent spinal shock and have advised that he not receive intrathecal Omnipaque (iohexol) in the future.
Discussion
Myelography is generally considered safe, with a low risk of seizures, contrast reactions and other significant complications.7 We described a patient undergoing CT myelogram with the use of intrathecal contrast agent for an improved and enhanced visualisation of spinal cord pathology. Our patient received an appropriate amount of Omnipaque 180, one of the non-ionic second-generation water-soluble iodinated agents that are considered safe and associated with very fewer adverse reactions.8 Omnipaque contains iohexol which is a non-ionic, water-soluble contrast medium. Omnipaque is available in the different concentrations: 140, 180, 240, 300, and 350 ng/mL. Omnipaque 140 (low osmolality) and Omnipaque 350 (high osmolality) are contraindicated for intrathecal use.9 The adverse neurological reactions may depend on dose, route of administration and type of procedure.10 The pathophysiology for adverse neurological reactions is not well understood but it has been linked to disturbances in osmolarity,11 lipid solubility12 or direct toxicity13 of these agents.
In our case, the patient developed clinical manifestations of shock, which were thought to be secondary to transient spinal and neurogenic shock. The Food and Drug Administration issued guidance that one brand of iodinated contrast reported less than 0.1% individual incidence of these contrast-induced reactions: feeling of heaviness, hypotension, hypertension sensation of heat, sweating, drowsiness, tinnitus, neuralgia, paresthesia, difficulty in micturition and neurological changes. All were reported to be transient and mild with no clinical sequelae. The report also includes rare central nervous system irritation with intrathecal injection manifesting as weakness, convulsion, hyperreflexia/areflexia, hypertonia/flaccidity, hemiplegia, paralysis and quadriplegia.9
In the present case, a contrast-induced adverse reaction happened even though the patient was not allergic to contrast media. This indicates that the pathophysiology for this type of reaction is different from anaphylaxis. In the survey study conducted by Sandow and Donnal to obtain information on myelography complications, 81% physician responders indicated that patients with contrast reaction did not have a history of contrast allergy.7
As mentioned above, the pathophysiology of adverse neurological reaction to intrathecal injections of ICAs is not well understood. We, however, propose a similar pathogenesis to that of contrast-induced nephropathy (CIN), that is, transient vasoconstriction of the spinal vasculature being the possible cause of shock. Changes in the renal vasculature following intravenous contrast injection are one of the well-established factors contributing to CIN. In kidneys, iodinated contrast causes transient vasodilation followed by prolonged vasoconstriction lasting 1–2 hours.14 With respect to the site of the injection during CT myelography, the iodinated material will be transported through and not metabolised in, the cerebrospinal fluid until it is reabsorbed via the arachnoid villi into the venous system.15 Thus, it may theoretically produce the same effect of transient vasoconstriction in small spinal vessels while floating through spinal CSF.
Learning points
-
Intrathecal contrast injection during CT myelography is generally safe, but rarely life-threatening adverse reactions can occur.
-
Transient spinal and neurogenic shock can happen after intrathecal contrast injection, mechanism of which can theoretically be contrast-induced vasoconstriction.
-
Physicians should be aware of adverse neurological reactions related to intrathecal contrast injections for prompt recognition and management.
Footnotes
-
Contributors ACL and SN: literature review and manuscript writing. VD: review and contribution to manuscript and changes in the revision of the manuscript. MS: review and contribution to manuscript.
-
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
-
Competing interests None declared.
-
Patient consent for publication Obtained.
-
Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.
References
Use of this content is subject to our disclaimer