Acute Lumbar Paraspinal Myonecrosis in Football Players with Sickle Cell Trait: A Case Series : Medicine & Science in Sports & Exercise

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Acute Lumbar Paraspinal Myonecrosis in Football Players with Sickle Cell Trait

A Case Series


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Medicine & Science in Sports & Exercise 49(4):p 627-632, April 2017. | DOI: 10.1249/MSS.0000000000001167
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The first case report of the lumbar paraspinal compartment syndrome was in 1985, a young white man in Vermont who presented to an emergency room with severe, unrelenting low back pain (LBP) and paraspinal muscle spasm after a day of downhill skiing (2). In the three decades since then, this compartment syndrome has been reported occasionally, mainly in the spine and emergency medicine literature and in recreational or weekend athletes after, for example, snow skiing, water skiing, surfboarding, weight lifting, or intense gym workouts (1,3,4,8–12,17,18). In these reports, the emphasis has largely been on recognition of this uncommon syndrome of severe, exertional LBP that can be confused with more common conditions.

It is key to distinguish this unique syndrome from, for example, lumbar muscle strain, disc herniation, vertebral fracture, or even inflammatory LBP or renal colic. Early diagnosis enables early weighing of the need for fasciotomy and in general facilitates proper therapy that can mitigate or prevent long-term sequelae and allow elite athletes to return soon to their sport.

Lumbar paraspinal compartment syndrome, however, is rarely reported in elite team athletes, is not featured in major sports medicine textbooks, and is little known in football. We believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to this uncommon syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, we believe that SCT may represent an additional risk factor for LPSMN. Accordingly, we present six cases of LPSMN in elite African American football players with SCT. All six athletes (cases 1–6) were informed that the particulars of their cases would be included in a manuscript for possible publication and/or in presentations at national sports medicine meetings, and all six consented to this.

Case Presentations

Case 1

This athlete developed this syndrome four times. First, as a college freshman, age 18 yr, a skilled-position player, he developed LBP in a conditioning run on day 1 of summer training, doing incremental serial sprints on a track. He ran 110 yd, then 220 yd, and then 440 yd. However, during the next sprint, aiming for 660 yd, he developed severe LBP, greater on the left, ran ever slower and in a more lordotic running posture, and finally stopped short of the goal, disabled by the LBP.

He was hospitalized for 4 d, where on admission he had tenderness along the lumbar paraspinal muscles bilaterally (with swelling on the left), required narcotic medication for pain control and had a peak serum creatine kinase (CK) of 55,400 IU·L−1, and a computerized tomography (CT) scan read as “marked swelling and decreased tissue attenuation throughout paraspinal muscles, more on the left, mainly in the longissimus and iliocostalis lumborum.” No magnetic resonance imaging (MRI) was conducted. He was back to training in approximately 2 wk.

As a college senior, again in conditioning, serial sprints, in the eighth 100-yd sprint, he was again limited by LBP, again worse on the left. He was seen in an emergency department, where he seemed clinically to have a milder version of LPSMN. Serum CK was 4300 IU·L−1 (and later peaked at 42,000 IU·L−1). No scan was conducted, and he was not hospitalized. He returned to full training in 7–10 d.

His third bout of apparent LPSMN occurred soon after college graduation while training for professional football. We are told the course was even milder this time, but we have no details.

His fourth bout of LPSMN, however, was as disabling as his first. By then, age 30 yr, he was a football coach. On the day of the event, he lifted weights then played in a competitive basketball game. He noticed LBP in the second quarter, had to sit some because of increasing LBP in the fourth quarter, but pushed through the pain to finish the game. Then he sat in his car, fighting LBP, for 20 min, before driving home. At home, he went to the floor, on hands and knees, “screaming” from LBP. His wife felt his back muscles and described them as “rigid as a board.” She called 911, and he was hospitalized for 5–6 d, on narcotic medications for pain control. His serum CK peaked at >50,000 IU·L−1, and his MRI showed swelling and diffuse edema in the same paraspinal muscles involved (by CT) in his first bout. Because of mild fever and one positive blood culture (likely a contaminant), he had needle biopsy of an involved paraspinal muscle, which showed no abscess, only myonecrosis and some sickling. He slowly recovered as an outpatient. We again emphasized SCT exercise precautions to him—and to his wife—and to our knowledge, he has done well.

Case 2

This athlete, a defensive end, age 19 yr, developed LPSMN at least twice. He suffered his first diagnosed bout during a 90-min lower-body drill in January, day 1 after a winter break. The drill comprised thrusts, squats, and pushing a weighted sled. Near the end, he “cramped up” in legs and low back and asked an athletic trainer to “stretch him out.” He then tried to walk to the locker room but collapsed outside, saying his legs were “locked up,” and in severe LBP. He lay prone for 2–3 min, until he was carted inside. After 20 min of rest and supplemental oxygen, his legs felt better, but he still had major LBP on the left. He recalled that the previous summer, after doing one-leg squats, he had similar acute LBP, mainly on the left. He “fought through it” then, did not report it, and it resolved in a week. This time, likely his second bout, he was seen by a team physician, the working diagnosis was LPSMN, and he was managed as an outpatient. The next day, serum CK was 10,648 IU·L−1. The next day, a CT scan (Fig. 1) showed swelling and signal intensity in lumbar paraspinal muscles, worse on the left, and CK was 4738 IU·L−1. Two days later, an MRI scan showing diffuse edema in the same muscles was read as consistent with LPSMN, involving the deep multifidus and rotares (Figs. 2 and 3). He was back to full training in 1–2 wk.

Case 2, axial CT. Note swelling and signal intensity in multifidus and rotares.
Case 2, axial MRI. Compare with CT. Note edema in multifidus and rotares.
Case 2, coronal MRI. Note edema in multifidus and rotates compartments.

In February the next year, during a similar drill comprising squats and sled pushing, he felt his low back and thighs “tighten up” and begin to hurt, felt he should rest, but finished the drill upon urging by the coach. He then sat in the cold tub a long time and finally managed to get home (on a Friday evening). Three days later, a team physician evaluated him in the training room, with LBP and stiffness, with paraspinal tenderness, more on the left, and CK 8010 IU·L−1. He was held out and seen again in 2 d; his low back was still stiff and weak, but improving, and CK was 1919 IU·L−1. An MRI scan was similar to that of his first bout, involving the same paraspinal muscles, but the changes were milder. He resumed full training in 1–2 wk. He was told to stop any drill at the onset of any undue leg or back symptoms. He completed his football career—and had a stellar senior season—with no further bouts of LPSMN.

Case 3

This lineman, age 20 yr, developed acute LBP, more on the right, while undergoing lower-body drills similar to those in case 2. For a span of 1 wk, the LBP began in bear-crawl, sled-pushing drills, peaked a few days later in one-leg squat drills with leg weights, then continued to limit him, so he quit early in repeat bear-crawl, sled-pushing drills, 1 wk after his LBP began. He described the pain as similar to pain—along with “wobbly legs”—the previous year in repeat sprints or ramp runs. Serum CK 4 d after the peak LBP was 2136 IU·L−1, and an MRI scan was read as consistent with LPSMN, with edema and possible myonecrosis of the erector spinae, more on the right. His clinical course was mild enough that he resumed full training 2 wk after the onset of his LBP.

Case 4

This lineman, age 19 yr, developed acute LBP not during lower-body, strength-power drills as in cases 2 and 3, but rather approximately 45 min into a strenuous practice including a one-on-one contact drill where he repeatedly took his stance and then burst up and into his opponent. This was his first full practice in nearly 2 wk because of an upper-extremity injury. The LBP was severe, without radicular pain, but with discomfort in the right buttock and thigh. He was seen by a team physician in the training room, where he denied previous similar pain. There was paraspinal tenderness bilaterally, limited range of motion at the lumbar spine, exacerbation of LBP by flexion, and an equivocal straight leg–raising test on the right.

He was hospitalized because of intractable LBP that, for control, required intravenous and oral narcotics and help from pain management services. A slightly elevated serum creatinine (2.05 mg·dL−1) soon normalized after hydration. The initial serum CK of 2038 IU·L−1 peaked at 10,000 IU·L−1 on hospital day 5. An MRI scan showed extensive edema and inflammation in erector spinae, read as consistent with rhabdomyolysis, the right spinalis severely affected (Fig. 4). A pyrophosphate bone scan showed irreversible cell injury in the left iliocostalis lumborum muscle.

Case 4, MRI. Extensive edema and inflammation in erector spinae, consistent with rhabdomyolysis; right spinalis severely affected.

After 15 d, he went home in a wheelchair and began rehabilitation. He required narcotics and other medications for LBP that resolved for 8 wk. Repeat MRI at 8 wk showed improvement overall, but with a focal area of evolving myonecrosis of the right erector spinae at L5. He then walked without a cane and resumed light workouts, but even after 24 wk, with improved flexibility, strength, and fitness, he sat out spring practice. He returned to football in the fall and earned a starting position but then had a season-ending lower-extremity injury. He played football for two more years; he had other orthopedic injuries but no further limitations from his low back.

Case 5

This rising senior skilled-position player, age 22 yr, developed acute, severe LBP, mainly on the left, while weight lifting, a series of cleans and jerks, supervised by a new strength coach. He started a conditioning run right afterward but “looked terrible trying to run,” running slowly and awkwardly “tilting” to the right. An athletic trainer pulled him out; he had severe LBP with radiation of pain to his testicles. He was sent to an emergency room (approximately 6:00 p.m.), where testicular ultrasound examination was normal and a spine radiograph showed only a left curvature of the lumbar spine, thought maybe from left paraspinal muscle spasm. No other laboratory testing was conducted. He was sent home with a diagnosis of back strain. Early the next morning, still in great pain, he was sent for an MRI scan by the team physician who had seen the evolution of case 4. The athlete was in so much pain that the radiologist could not finish the MRI scan, but the images showed swelling, edema, and blood product breakdown of left paraspinal muscles from T12 to the sacrum, suggesting myonecrosis and raising concern for compartment syndrome. The player was hospitalized. An orthopedic surgeon decided against measuring compartment pressures, judging no need for fasciotomy. Renal output and function remained normal. Serum CK was 7387 IU·L−1 on admission and rose to 14,797 IU·L−1 on day 4, but by then he was walking, showering, and feeling better. He was soon off parenteral narcotics for pain and was discharged home on day 6. This bout of LPSMN occurred in January, not long after returning from a break after a bowl game. After 4 wk, the player was cleared for all training, including spring practice, and played in all games that fall season without problems from his low back. Despite this good clinical recovery, a follow-up MRI scan at 3 months showed some residual changes (Fig. 5).

Case 5, MRI at 3 months. Residual changes of acute LPSMN.

Case 6

This National Football League defensive end, age 25 yr, deconditioned from previous surgery, was returning to training in July. He took part in a preseason lift and run session, 16 sprints of 110 yd each. Approximately 1 h later, he reported to an athletic trainer with acute LBP thought maybe a muscle strain. The team physician saw him. The pain was lumbar, with mild limitation in range of motion in all planes, and lumbar muscle spasm. Straight leg–raising tests were negative, there was no radicular pain, and ambulation was fairly normal. The next day, he felt worse, an MRI scan was conducted, and he was hospitalized. The MRI scan showed posterior central disc herniation at L4–L5 and diffuse edema in paraspinal muscles from L2 to L3 through the lumbosacral region. Serum CK on day 4 was just more than 40,000 IU·L−1, and 3 d later it was less than 10,000 IU·L−1. The final diagnosis was LPSMN. He required oral narcotics for pain and was hospitalized for a week. He missed 2 wk of activity and then returned slowly in a limited capacity. It took him 4 months to feel “back to 100%.”

Table 1 summarizes the cardinal features of LPSMN in our football players with SCT: settings, pain patterns, physical examination, scan findings, and clinical course.

Cardinal features of LPSMN in football players with SCT.


We present six cases of a novel syndrome of acute, disabling LBP in football players with SCT. This syndrome, which involves LPSMN, is not widely known in football conditioning and might be confused with other conditions, such as muscle strain (as in two of our cases), lumbar disc herniation, pars stress fracture or other fractures, lumbar facet syndrome, or even inflammatory LBP or renal colic. As our cases show, LPSMN can strike during serial sprinting, lower-body drills such as sled pushing, one-on-one contact drills, or weight lifting. It can recur, as in two of our cases, and as in our case 1, it can occur in college football during sprinting and later in life during basketball.

We believe SCT is a potential risk factor for LPSMN in intense conditioning or training for football. These paraspinal muscles are large and well developed in our athletes. They are in tight compartments with fascial and bony confinement, and their blood supply is from small branches of segmental arteries from the aorta and iliac arteries. They may be “overdeveloped” for their blood supply and so prone to claudication syndromes. All-out exertion may lead to swelling and congestion of the muscle, may increase the pressure in the compartment, and may further limit blood supply, causing ischemia. With SCT, these conditions can also trigger exertional sickling by creating, in concert, 1) hypoxemia, 2) lactic acidosis, 3) hyperthermia of working muscle, and 4) dehydration of red cells coursing through this milieu. Sickling can “log-jam” the microcirculation of the muscle and hence increase ischemia in the compartment. We think the net effect can be local sickling sufficient to cause acute LPSMN—and the threat of compartment syndrome needing fasciotomy.

The only other case of acute paraspinal compartment syndrome (or LPSMN) in college football that we find in the literature was an African American player, age 23 yr, who developed acute, severe LBP during weight lifting. His MRI also showed swelling and diffuse edema of the lumbar paraspinal muscles. He had “negative sickle cell screening,” but the SCT screening test was not defined (7). Two cases of LPSMN have occurred recently in African American men in the US military. One was from a gym workout; it required fasciotomy (15). Both military men had SCT. We note that myonecrosis can also occur in sickle cell anemia (16).

We should clarify how we interpret the MRI scans, arguably the “gold standard” for diagnosing this syndrome. First, several team physicians with several decades of combined experience have seen this unique syndrome only in football players with SCT. Second, we admit that MRI scans are nonspecific and do not yield “cellular” diagnoses. Rhabdomyolysis is largely a clinical diagnosis (along with rising serum CK levels), and myonecrosis is a cellular diagnosis. However, third, our diagnostic radiologists are impressed by these unique MRI scans. When asked for a differential diagnosis without clinical information, they lean toward a diffuse vascular injury, including maybe diabetic myositis or septic emboli. When they hear the clinical context, they agree that the MRI is consistent with acute exertional LPSMN and that sickling could produce such a diffuse vascular injury. Finally, we saw muscle uptake of diphosphonate in a bone scan that suggests rhabdomyolysis (case 4); we found myonecrosis by needle biopsy (case 1); and in some follow-up MRI scans, we saw residual changes, including cysts, that almost surely reflect myonecrosis. All considered, we are confident in our diagnosis of LPSMN.

We do not claim, however, that SCT is requisite for LPSMN in football or other sports. In fact, for the past three decades, as we mentioned in our introduction, acute lumbar paraspinal compartment syndrome—likely with some myonecrosis in most cases—has been reported on occasion in patients without SCT or unlikely to have SCT. Two early patients were Caucasian downhill skiers (2,4). Another was an Australian skier who got fasciotomy (8). Another was a Japanese surfboarder who got fasciotomy (9). Then came the case of an Austrian rugby player after weight lifting; he too got fasciotomy (10). Another was a man who began gym workouts, similar to the previously mentioned case of an African American military man (3). Three more cases were in weight lifters. Two cases got fasciotomy; two cases were African American, one negative for SCT (11,12,18). Another case was a boy, 16 yr old, presumably Caucasian, a new “fitness fanatic”; he got fasciotomy (17). Of these 10 nonfootball cases, 6 got fasciotomy.

By contrast, none of our six football cases got fasciotomy. However, we lack enough information to adjudicate the role or timing of fasciotomy in LPSMN. It may or may not be needed, and this decision is best left to physicians on the scene. Our case 5, for example, still has loss of lumbar muscle mass on the left, and any long-term sequelae of severe LPSMN are unclear.

A recent article augments this field (14). It presents a man, age 30 yr, who lifted weights—a session targeting lumbar muscles—and the next day went to an emergency room with severe loin pain, radiating to his groin, which he thought was a “trapped nerve.” Physicians considered it to be renal colic, but that workup was negative, and serum CK was 42,000 IU·L−1. An MRI scan showed “erector spinae rhabdomyolysis” and lumbar paraspinal “compartment syndrome.” He was hospitalized and treated conservatively. His CK peaked at 68,000 IU·L−1. He was discharged after 2 wk. One week later his CK was 224 IU·L−1, and his lumbar pain was gone.

On the basis of this case, the authors say that acute lumbar paraspinal compartment syndrome should be in the differential diagnosis of loin pain. The same might be said for testicular pain, as in our case 5. The authors review 15 cases in the literature, missing a few cases that we found, but adding (to our list) five more cases from weight lifting, two requiring fasciotomy. All cases they found were young men, with an average age of 28 yr (14).

There is, however, one case report of a Caucasian woman, age 20 yr, who water skied for hours 1 d and developed acute LBP on the right. The next day, she played ultimate Frisbee, before presenting to an emergency room with severe LBP. Her serum CK was 19,000 IU·L−1 (it peaked at 38,000 IU·L−1). An MRI scan showed swollen right lumbar paraspinal muscles and edema or hematoma. She was hospitalized. Her LBP was treated with intravenous narcotics until she became unresponsive, required intubation, and recovered after naloxone. Despite 3 months of physical therapy, some pain continued, limiting her activity to biking. Repeat MRI scan at 4 months showed mild atrophy and some necrosis in the right lumbar paraspinal muscles. The final diagnosis was LPSMN and compartment syndrome (1).

Finally, the disabling pain of LPSMN may save lives by stopping SCT football players before they exert to the point of full-blown collapse (known as exercise collapse associated with sickle cell trait, or ECAST) that—in football and in the military—has too often been fatal (5,6,13). Or LPSMN may be a harbinger that a given SCT athlete may be at risk for ECAST. Further research may clarify these issues. With the National Collegiate Athletic Association program of SCT screening, we can better correlate acute LBP and cases of LPSMN with SCT status. Also of note is that the National Collegiate Athletic Association program for SCT has sharply reduced ECAST deaths in Division-1 football (6).


We report a syndrome of acute, exertional, severe LBP in football, from LPSMN, in elite African American players with SCT. The diagnostic hallmarks and clinical course of this novel syndrome are summarized in Table 1. We believe SCT is a potential risk factor for LPSMN in football. However, SCT is not requisite to LPSMN, which likely contributes to the lumbar paraspinal compartment syndrome occasionally reported after skiing, surfboarding, intense gym workouts, or weight lifting. In football, LPSMN occurs not in the play of the game but in serial sprinting, lower-body drills, one-on-one contact drills, or weight lifting that targets lumbar muscles. It tends to occur early in conditioning/training, sometimes after deconditioning. Acute LPSMN can be confused with muscle strain (as in two of our cases), lumbar disc or facet syndromes, or even renal colic or testicular trauma. LPSMN can require narcotics, which can be problematic. Although it can resolve in 1–2 wk, it can also be far more severe, requiring fasciotomy (not conducted in our cases) or leading to sequelae and/or lengthy rehabilitation. LPSMN can also recur, as in two of our athletes. It is conceivable that LPSMN may save lives by preventing ECAST. We still have gaps in knowledge and work to do, for example, on the role of compartment pressure testing and fasciotomy and on how best to prevent sequelae and speed return to play. Increasing our knowledge of LPSMN will enable those of us in sports medicine to diagnose it early, treat it properly, lessen its effect, and learn how to prevent it.

The authors have received no funding for these case studies and have no conflict of interest to declare. Their results and conclusion do not constitute endorsement by the American College of Sports Medicine. The authors affirm that they present their results clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.


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