Cocaine and ketamine‑induced paraspinal muscle compartment syndrome
Thomas Saliba1, Simone Giglioli2
, Sanjiva Pather1
, Daniel DeBacker2
1Department of Imaging, CHIREC Hospitals, Université Libre de Bruxelles, Brussels, Belgium
2Department of Intensive Care, CHIREC Hospitals, Université Libre de Bruxelles, Brussels, Belgium
Keywords: Back pain, cocaine, computed tomography scan, fasciotomy, ketamine, rhabdomyolysis
Abstract
Lumbar paraspinal compartment syndrome is a rare pathology, with only 40 reported cases resulting from an increase in pressure within the muscle compartment. Symptoms typically involve pain and sometimes muscular deficits. The typical patient is a man who has undergone strenuous exercise, with few cases linked to the use of recreational drugs, such as cocaine or ketamine. We report the case of a 25 year old man presenting to the emergency room with severe diffuse back pain who had recently consumed large amounts of cocaine, ketamine, and alcohol. The patient had diffuse muscular pain, increased serum creatine kinase (CK) levels, and a negative noncontrast abdominal computed tomography (CT), leading to the suspicion of crush syndrome. Over the following days, the patient’s pain became more localized to the right paraspinal region, prompting a contrast enhanced CT. This revealed signs of muscle swelling and edema of the paraspinal muscle, leading to a suspicion of compartment syndrome, which was confirmed by an intramuscular pressure measurement. The patient underwent a surgical fasciotomy. The patient went on to have an unremarkable recovery. Lumbar paraspinal compartment syndrome is exceedingly rare. Cocaine is known to cause rhabdomyolysis both indirectly, due to behavioral disturbances, and directly due to muscle toxicity. Similarly, ketamine use has also been associated with rhabdomyolysis. The rhabdomyolysis results in greatly increased CK levels, sometimes rising up to 100 00 U/L, which should normalize over the following days. A few cases of compartment syndrome, often localized in extremities, have been reported in patients presenting cocaine or ketamine induced rhabdomyolysis. In this patient, the muscle swelling of the paraspinal muscle resulted in compartment syndrome. Patients who experience cocaine related rhabdomyolysis have a tendency for nonspecific symptoms, which would match our patient’s initial presentation. Although radiology’s contribution to the diagnosis is limited, patients suffering from back pain or nonresolving rhabdomyolysis should be submitted to imaging, which may show signs of muscle swelling and edema on CT and magnetic resonance imaging. Diagnosis of compartment syndrome should be confirmed by measurement of muscle pressure, and if elevated, the patient should be proposed for fasciotomy.
Introduction
Lumbar paraspinal compartment syndrome is a rare diagnosis, with very few cases (40) reported.[1] It is caused by an increase in pressure within the nonelastic paraspinal muscle compartments, leading to decreased perfusion and necrosis.[1] Affected patients typically present with lower back pain and, occasionally, neuromuscular deficits.[1] Men are affected in over 90% of reports, with these cases generally being linked to weightlifting and heavy physical exercise. A few cases have been linked to cocaine abuse, often associated with prolonged compression due to impaired consciousness.[2 4]
We present what is, to our knowledge, the second reported case of lumbar paraspinal compartment syndrome in a patient who had consumed drugs, including cocaine and ketamine, shortly before its onset.
Case Report
A 25 year old male patient was brought to the emergency department by ambulance for diffuse lower back pain. The patient reported diffuse, but predominantly left sided, pain in the lower back, thighs, psoitis, and renal lodges. The patient’s history revealed no known trauma, but he admitted to having consumed 10 g of ketamine, 1 g of cocaine, over five alcoholic drinks and smoking cannabis the day before. He was never unconscious and did not experience hyperkinesia or agitation.
The patient had no notable medical or surgical history except for depression and habitual consumption of ketamine, cocaine, cannabis, tobacco, and alcohol.
A blood test revealed significantly elevated creatine kinase (CK) levels of 9,842 U/L, which increased to over 20,000 U/L within the following hours. Additional findings included a lactate dehydrogenase level of 379 U/L, aspartate aminotransferase (AST) of 299 U/L, alanine aminotransferase (ALT) of 96 U/L, a slightly elevated C reactive protein of 6.9 mg/L, and a white blood cell count of 15,000/mm3 . The toxicology report showed a mildly elevated plasma ethanol level (0.37 g/L) and a positive urine test for cocaine and cannabinoids, while results were negative for amphetamines and opioids. A noncontrast abdominal computed tomography (CT) scan (NCACT) was performed due to the abdominal pain, with no notable abdominal findings.
The diagnosis of rhabdomyolysis due to intoxication by ketamine and cocaine alongside suspected crush syndrome was made. The patient received midazolam, morphine, clonidine, a drip containing crystalloids, as well as Vitamin B1, Vitamin B6, and bicarbonate.
The patient was transferred to the intensive care unit (ICU) for management of severe rhabdomyolysis by hyperhydration and urine alkalinization.
For the following days, the pain was predominantly located on the right dorsal side while the pain in the other muscles subsided.
After an initial peak of CK levels over 20,000 U/L, these decreased to 10 000 U/L and then oscillated around 19 000 U/L for the following 4 days. C reactive protein (CRP) levels continued to increase, reaching 154 U/L before stabilizing. On the 4th day, a follow up contrast enhanced abdominal CT scan (CEACT) was ordered as the patient now presented right lumbar anesthesia in addition to persistent severe back pain and increasing CRP [Figure 1]. The CEACT revealed hypodensity and swelling of the right paraspinal muscles from L1 to L5, alongside hypodermic infiltration, when compared to the contralateral side, which was interpreted as myositis.
The increasing lower back pain prompted a discussion between the radiology and ICU staff, leading to a revision of the initial NCACT CT scan, which was retrospectively found to already show slight signs of muscle hypodensity and swelling, though no hypodermic infiltration was present [Figure 2]. A comparison of the two exams did not reveal any significant increase in the degree of muscle swelling.
The combination of rhabdomyolysis, pain, and muscle swelling seen on the CT scans raised the suspicion of compartment syndrome of the lumbar paraspinal muscles, leading to an ultrasound guided needle pressure monitoring [Figure 3]. The right paraspinal compartment was found to have a pressure of 130 mmHg, compared to 22 mmHg on the contralateral side, confirming the diagnosis of compartment syndrome.
The patient underwent a right paravertebral fasciotomy the following day, and a muscle biopsy sent for pathology showed muscle inflammation and necrosis.
The patient experienced relief from his back pain in the immediate postoperative period, allowing for rapid rehabilitation The patient was able to walk 3 days later, with a blood test performed at this point showing near normal CRP and CK levels. He was discharged of the hospital 4 days after surgery.
Discussion
Compartment syndrome of lumbar paraspinal muscles is a rare diagnosis, with only 40 cases reported to date.[1,2] The most commonly affected patients are male weightlifters, patients who have been lying for prolonged periods, such as postoperative patients and athletes.[2] The patients will nearly universally present with back pain but can also have accompanying numbness or lower limb pain, amongst other rarer presentations.[2] The pain can be unilateral, but bilateral presentations are more common.[2] When taking the patient history, one should not neglect to enquire about any drugs or medication that could be responsible for myolysis. These patients should be highly suspicious of compartment syndrome. A blood test should be performed to search for signs of myolysis.
If the blood test is positive, these patients should undergo a CT scan or magnetic resonance imaging (MRI) to rule out alternative diagnoses and look for signs of compartment syndrome, followed by ultrasound guided needle pressure monitoring to confirm the diagnosis. A surgeon should be informed if there is a suspicion of compartment syndrome as surgical decompression is a mainstay treatment, resulting in better patient outcomes.
Ilyas et al. performed a review of 37 cases, with young men representing 92% of patients.[2] Most of the reported cases are linked to weightlifting (48.6%) and physical exertion (18.9%), followed by abdominal vascular surgery and bypass surgery (16.2%) [Table 1].[2] Interestingly, the mechanisms involved include extreme exercise involving these muscles or prolonged compression (eventually resulting in impaired perfusion). Sixty two percent of patients presented with bilateral compartment syndrome, and all patients who underwent a compartment pressure measurement showed increased pressures, averaging 91.8 ± 44.8 mmHg.[2] The patients with compartment syndrome also exhibited significantly increased AST, ALT, and CK levels, measured at 713 ± 331 U/L, 91 ± 117 U/L, and 66,258 ± 34,684 U/L, respectively.[2] Furthermore, patients who underwent surgical fasciotomy had far better outcomes than those who underwent conservative treatment, with 95% of operative patients reporting favorable outcomes, while only 9% of patients who underwent conservative treatment did not suffer from lingering pain and discomfort when performing physical activities.[2]
Both ketamine and cocaine are associated with rhabdomyolysis. Ketamine has been associated with rhabdomyolysis.[5 7] This rhabdomyolysis was often attributed to the severe muscular activity related to agitation.
Cocaine frequently leads to rhabdomyolysis, though few cases of compartment syndrome have been reported, often involving extremities (legs/arms) rather than paraspinal muscles.[8,9] Various mechanisms can contribute to cocaine associated rhabdomyolysis. In addition to its effects on the central nervous system, cocaine acts on the sympathetic nervous system, increasing the sensitivity of nerves to noradrenaline, blocking sodium and potassium channels, and blocking catecholamines re uptake by sympathetic nerves.[8,10] One of the likely ways in which cocaine induces muscle damage is by causing ischemia due to vasoconstriction, hyperpyrexia, thrombosis, and increased muscle activity, with 24% of cocaine users presenting at the emergency department suffering from rhabdomyolysis.[8,9,11,12] In cases of cocaine related rhabdomyolysis, CK levels have been known to increase to over 100,000 U/L.[10] Furthermore, patients who have taken cocaine often do not have the classic symptoms of nausea, vomiting, myalgia, muscle swelling, weakness, and tenderness associated with rhabdomyolysis.[10] This atypical presentation pattern is in accordance with the initially nonspecific presentation of our patient.[10] In addition to the nonspecific effects such as agitation seizures, anxiety, hyperthermia, muscle contractions, and physical restraints, cocaine also has direct toxicity both in in vitro and in vivo studies.[10,13] One potential mechanism is via the activation of caspase and p38 pathways, resulting in cytochrome C release into the cytosol and ensuing apoptosis.[13] Another mechanism is severe vasoconstriction, leading to hyperactivity of cytochrome oxidase, the final enzyme in the electron transfer chain, which causes an ischemic phase followed by reperfusion with an increase of reactive oxygen species and mitochondrial dysfunction with ensuing apoptosis.[13] Yet another mechanism may be mediated by the release of the free radical scavenger glutathione, as well as by thiobarbituric acid reactive substances.[13] The rhabdomyolysis has been shown to occur rapidly, beginning within the 1 hour half life of the cocaine, but continuing over the following days, as shown by the CK levels peak occurring around 24–72 h after consumption and only normalizing after around 5 days.[10,13] Whatever the causal mechanism, an interesting question is why the paraspinal muscles were mainly involved in this patient. This patient was never unconscious and had not been lying down for a prolonged period. It is possible that this patient had particularly developed paraspinal muscles due to his profession involving the transport of heavy loads. Paraspinal muscles also have a relatively small diameter, which, alongside the fact that this muscle group is bounded medially and posteriorly by osseous structures, prevents its expansion when the muscle swells. It therefore follows that this muscle group may be more susceptible to increases in intramuscular pressure and subsequent development of compartment syndrome.
Imagery of lumbar paraspinal compartment syndrome can include CT scans or MRIs. A CT scan may show muscle swelling and hypodensity, as was the case in our patient, though it should be noted that it cannot exclude compartment syndrome as findings may also be falsely negative in the initial stages.[3,14] MRI imaging usually shows increased T2 signal within the affected muscles, corresponding to edema, alongside muscle swelling.[4,14] Finally, the indication of surgical decompression is usually based on measurements of intramuscular pressure. To ensure that measurements are performed in the paraspinal muscle, this procedure can be guided by ultrasonography, as we did in this case.
Conclusion
Paraspinal muscle compartment syndrome is a rare diagnosis, often associated with strenuous physical exercise or prolonged compression. Cocaine and ketamine abuse may also contribute as a rare cause, as illustrated in this case. When suspected, a contrast enhanced CT should be performed before confirmation by a pressure measurement. Fasciotomy may be associated with faster recovery.
How to cite this article: Saliba T, Giglioli S, Pather S, DeBacker D. Cocaine and ketamine-induced paraspinal muscle compartment syndrome. Turk J Emerg Med 2025;25:147-51.
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
• TS:
Conceptualization
Writing – Original Draft:
Writing – Review and Editing.
• SG:
Original Draft
Methodology
Formal Analysis: Analyzed the data and interpreted the results, contributing to the statistical aspects of the research
Writing – Review and Editing.
• SP:
Original Draft
Writing – Review and Editing
Data Curation
Visualization.
• DDB:
Conceptualization
Original Draft
Writing – Review and Editing
Methodology
Supervision
Investigation
Data Curation
Visualization
Project Administration.
Thomas Saliba: none to declare, Simone Giglioli: none to declare, Sanjiva Pather: none to declare, Daniel De Backer: Edwards Lifesciences, Philips, Baxter, Viatris, Pharmazz, AOP.
None.
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