CASE REPORT
Exercise-induced Pediatric Lumbar Paravertebral Compartment Syndrome: A Case Report Verena M. Schreiber, MD and W. Timothy Ward, MD
Abstract: Acute compartment syndrome is described as an elevation of interstitial pressure in a closed fascial compartment that can lead to damage of the microvasculature with subsequent tissue necrosis. Although paravertebral compartment syndrome has been described there is no case of paravertebral compartment syndrome that has been described in the pediatric population. We report the case of a 17-year-old boy who presented at our institution with severe, acute-onset low back pain that started shortly after a rigorous 4-hour workout. He was diagnosed with acute lumbar paravertebral compartment syndrome and underwent emergent fasciotomy with 2 more debridements. Key Words: compartment syndrome, paraspinal, paravertebral, lumbar, fasciotomy (J Pediatr Orthop 2015;35:e49–e51)
A
cute compartment syndrome is described as an elevation of interstitial pressure in a closed fascial compartment that can lead to damage of the microvasculature with subsequent tissue necrosis. Although compartment syndrome has been mainly described in extremities, multiple authors have reported case examples of paravertebral compartment syndrome.1–4 To our knowledge no case of paravertebral compartment syndrome has been described in the pediatric population.
HISTORY A 17-year-old boy presented to our emergency department with an 18-hour history of severe, acute-onset low back pain that started shortly after a rigorous 4-hour workout consisting of a myriad of calisthenics. This was not a common workout routine for this adolescent. The pain was primarily confined to a right lumbar paravertebral location and was so severe that the patient was not comfortable standing up. The pain was exacerbated by movement or sitting. He also reported numbness and tingling in the lumbar region. No radicular symptoms were reported. The patient had initially presented to an outpatient urgent care center the same day of the workout and was prescribed a muscle relaxant as well as acetaminophen and ibuprofen. That evening his urine appeared brown in color, From the Department of Orthopaedic Surgery, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA. The authors declare no conflicts of interest. Reprints: W. Timothy Ward, MD, Division of Pediatric Orthopaedic Surgery, Children’s Hospital of Pittsburgh of UPMC, 4401 Penn Avenue, 4th Floor, Pittsburgh, PA 15224. E-mail: [email protected]. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Pediatr Orthop
Volume 35, Number 6, September 2015
and the severe back pain persisted despite using narcotic medication. On presentation to his primary care provider the following day a urine dipstick revealed large amounts of protein and blood for which he was then referred to our emergency department for concern about rhabdomyolysis. His vital signs were stable. Blood tests a revealed a creatinine phosphokinase level of 116,000 IU/L (normal range, 33 to 145 IU/ L) as well as an elevated alanine aminotransferase (364 IU/L; normal range, 17 to 63 IU/L) and aspartate transaminase (1330 IU/L; normal range, 25 to 55 IU/L). Creatinine and blood urea nitrogen were within normal limits. Urinalysis revealed >100 red blood cells per high power field. Glomerulonephritis workup was negative, however, microscopic findings were consistent with acute tubular necrosis. Renal ultrasound failed to show any abnormalities. The patient was felt to have rhabdomyolysis in the face of acute-onset severe low back pain. A gadolinium contrast lumbar magnetic resonance imaging (MRI) study revealed significant diffuse heterogenous hypofusion and hyperperfusion signal changes in the lumbar paravertebral muscles consistent with swelling, inflammation, and early necrosis (Fig. 1). The elevated muscle enzymes, MRI findings, and clinical presentation of acute-onset severe low back pain supported a tentative diagnosis of acute paralumbar compartment syndrome or possible paraspinal abscess. Repeat creatinine phosphokinase drawn a few hours after the first test showed an increase to 170,000 IU/L. A decision was made to proceed with emergent paraspinal muscle fasciotomies. The paralumbar muscles appeared swollen under the exposed paraspinal fascia on visualization. The rightsided fascia was incised and a small but definitive area of ischemic muscle was appreciated at the L4 level. No purulence was observed. The pale and ischemic looking muscle did not contract to electrocautery stimulation in contrast to good contractility of the surrounding viable muscle (Fig. 2). Muscle tissue was sent to pathology and a diagnosis of necrotic muscle was confirmed. The left-sided paraspinal fascia was also released and the muscle appeared to be swollen but displayed good stimulation to electrocautery and was felt to be uniformly viable. The wound was covered with a vacuum-assisted device. The patient reported immediate relief of his back pain in the recovery room. An additional debridement was performed 2 days later and on day 6 the wound was closed with an estimation that about 15% of the right-sided lumbar musculature was removed at the L4 level. Liver enzymes as well as creatinine phosphokinase trended down appropriately and the patient was discharged to home on hospital day 7. He has remained pain free at 4 months’ follow-up and has returned to full activities.
DISCUSSION Acute compartment syndrome has been mainly described in the extremities and is caused by increasing pressure in a closed fibrous-osseous space. This can lead www.pedorthopaedics.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
e49
J Pediatr Orthop
Schreiber and Ward
Volume 35, Number 6, September 2015
FIGURE 1. Axial T2 with contrast magnetic resonance imaging showing edema and necrosis in lumbar paravertebral musculature.
to necrosis and irreversible injury of muscle and surrounding tissues. Multiple studies using magnetic resonance for determination of pH, tissue oxygenation, and energy stores, as well as histochemistry, electron microscopy, and Doppler flow have identified changes in muscle tissue in the setting of ischemia. Muscle exposed to complete ischemia remains electrically responsive for up to 3 hours and survives for up to 4 hours without undergoing irreversible damage. However, complete ischemic time of 8 hours leads to irreversible damage.5–10 Rhabdomyolysis is caused by an increase in free ionized calcium in the cytoplasm and damages the skeletal muscle, which causes toxic intracellular material to be released into the systemic circulation. The most common complications of rhabdomyolysis are renal failure, myoglobin cast formation, and direct renal toxic effects; however, the development of compartment syndrome has been described as well.11 Muscle cells are impaired by calcium and sodium influx, which promote the accumulation of extracellular fluid into the cells. This will then lead to an increase in intramuscular pressure.12,13 Treatment of rhabdomyolysis includes the prevention of acute renal failure, treatment of metabolic acidosis, early correction of potentially lethal electrolyte disorders, and the management of other coexisting complication.13 Paravertebral compartment syndrome is a rare condition that has been reported in adults after exercise and after certain sports such as downhill skiing as well as a reperfusion injury after abdominal aortic surgery.1–3,14 The paravertebral muscles, that is, the erector spinae muscles, are described as curved tubes parallel to the spine and are enclosed by the posterior and middle lamellae of the lumbodorsal fascia. The posterior lamellae arise medially at the
e50 | www.pedorthopaedics.com
FIGURE 2. Intraoperative view of lumbar paravertebral compartment with decompression of the right compartment. Asterisk marks the area of necrosis.
spinous process and interspinous ligaments dorsally and then caudally the sacral fascia is formed by the posterior and middle layer. The fascial septa laterally arise from the 3 abdominal muscles and ventrally the fascia attaches to the transverse processes.1,15,16 Paravertebral compartment syndrome usually presents with acute onset of severe pain after exercise with unresponsiveness to pain medicine. High creatinine phosphokinase levels and myoglobinuria consistent with rhabdomyolysis can be found. MRI will confirm heterogenous signal changes consistent with swelling or necrosis. Loss of sensation in the paravertebral region may or may not be found and is caused by damage to the lateral branch of the posterior primary ramus at multiple levels.17 Nathan and colleagues performed a systematic review on paravertebral compartment syndrome and defined criteria to distinguish acute from chronic compartment syndrome including but not limited to the acute onset of excruciating pain, rigidity of the paravertebral muscles, elevation of creatinine phosphokinase, no history of back pain, localized sensory loss in the paravertebral region, urine myoglobinuria, and changes on MRI. All of these parameters were present in our patient. The authors also concluded that as in other muscle compartments in the body surgical decompression should be performed as early as possible in the majority of cases to avoid functional sequelae. This Copyright
r
2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Pediatr Orthop
Volume 35, Number 6, September 2015
should be combined with conservative measure, for example, adequate fluid resuscitation.18 Given the findings on clinical examination and MRI we decided to forego intracompartmental pressure measurements. Wik and colleagues reported a case of exertional paraspinal compartment syndrome in a 30-year-old male with clinical presentation of paraspinal compartment syndrome and rhabdomyolysis. The patient was treated conservatively as it was felt that the prolonged time to diagnosis in this case (about 48 to 72 h) would have led to irreversible muscle damage. The rhabdomyolysis resolved after 21 days, however, the patient continued to experience significant lower back pain that led to the author’s conclusion that surgical decompression would most likely have been a more prudent choice.19 In our case the patient presented within 24 hours after onset of back pain and surgical decompression was performed within 36 hours after onset of back pain with dramatic improvement of renal function. At the 3 months follow-up the patient was doing very well with no complaints in the lower back. Our case report, while very similar to those cases already reported in the adult literature, is the first such report in the pediatric population. The marked severity of the back pain was in excess of that typically seen in other adolescent back disorders. The unusually dramatic amount of acute-onset low back pain in association with the history of excessive exercise, abnormal MRI, and abnormal muscle enzymes in conjunction with the immediate alleviation of symptoms after paralumbar fasciotomy makes us confident that this report is that of an acute-onset paralumbar compartment syndrome. Had fasciotomy been performed several hours sooner it is possible that no muscle necrosis would have been found. In conclusion, paravertebral compartment syndrome should be considered in the differential diagnosis in adolescents who have recently undergone high-demand activities presenting with unusually severe acute-onset low back pain. Diagnosis is made by weighing the history, clinical examination, MRI findings, and muscle/urine enzyme levels. Compartment measurements can be performed in addition. Surgical decompression in conjunction with supportive management is the optimal treatment for this rare condition. REFERENCES 1. Carr D, Gilbertson L, Frymoyer J, et al. Lumbar paraspinal compartment syndrome. A case report with physiologic and anatomic studies. Spine. 1985;10:816–820.
Copyright
r
2015 Wolters Kluwer Health, Inc. All rights reserved.
Pediatric Lumbar Paravertebral Compartment Syndrome
2. Mattiassich G, Larcher L, Leitinger M, et al. Paravertebral compartment syndrome after training causing severe back pain in an amateur rugby player: report of a rare case and review of the literature. BMC Musculoskelet Disord. 2013;14:259. 3. Khan RJ, Fick DP, Guier CA, et al. Acute paraspinal compartment syndrome. A case report. J Bone Joint Surg Am. 2005;87: 1126–1128. 4. Kitajima I, Tachibana S, Hirota Y, et al. Acute paraspinal muscle compartment syndrome treated with surgical decompression: a case report. Am J Sports Med. 2002;30:283–285. 5. Heckman MM, Whitesides TE Jr, Grewe SR, et al. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma. 1993;7: 199–210. 6. Heckman MM, Whitesides TE Jr, Grewe SR, et al. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg Am. 1994;76:1285–1292. 7. Heppenstall RB, Sapega AA, Izant T, et al. Compartment syndrome: a quantitative study of high-energy phosphorus compounds using 31 P-magnetic resonance spectroscopy. J Trauma. 1989;29:1113–1119. 8. Heppenstall RB, Sapega AA, Scott R, et al. The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop Relat Res. 1988;226:138–155. 9. Heppenstall RB, Scott R, Sapega A, et al. A comparative study of the tolerance of skeletal muscle to ischemia. Tourniquet application compared with acute compartment syndrome. J Bone Joint Surg Am. 1986;68:820–828. 10. Matava MJ, Whitesides TE Jr, Seiler JG III, et al. Determination of the compartment pressure threshold of muscle ischemia in a canine model. J Trauma. 1994;37:50–58. 11. Vanholder R, Sever MS, Erek E, et al. Rhabdomyolysis. J Am Soc Nephrol. 2000;11:1553–1561. 12. Better OS, Rubinstein I, Reis DN. Muscle crush compartment syndrome: fulminant local edema with threatening systemic effects. Kidney Int. 2003;63:1155–1157. 13. Chatzizisis YS, Misirli G, Hatzitolios AI, et al. The syndrome of rhabdomyolysis: complications and treatment. Eur J Intern Med. 2008;19:568–574. 14. DiFazio FA, Barth RA, Frymoyer JW. Acute lumbar paraspinal compartment syndrome. A case report. J Bone Joint Surg Am. 1991; 73:1101–1103. 15. Peck D, Nicholls PJ, Beard C, et al. Are there compartment syndromes in some patients with idiopathic back pain? Spine. 1986; 11:468–475. 16. Fairbank JC, O’Brien JP. The abdominal cavity and thoracolumbar fascia as stabilizers of the lumbar spine in patients with lowback pain. I Mech E Conf Proc. 1980:73–78. 17. Bogduk N. A reappraisal of the anatomy of the human lumbar erector spinae. J Anat. 1980;131(pt 3):525–540. 18. Nathan ST, Roberts CS, Deliberato D. Lumbar paraspinal compartment syndrome. Int Orthop. 2012;36:1221–1227. 19. Wik L, Patterson JM, Oswald AE. Exertional paraspinal muscle rhabdomyolysis and compartment syndrome: a cause of back pain not to be missed. Clin Rheumatol. 2010;29:803–805.
www.pedorthopaedics.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
e51
Exercise-induced Pediatric Lumbar Paravertebral Compartment Syndrome: A Case Report Verena M. Schreiber, MD and W. Timothy Ward, MD
Abstract: Acute compartment syndrome is described as an elevation of interstitial pressure in a closed fascial compartment that can lead to damage of the microvasculature with subsequent tissue necrosis. Although paravertebral compartment syndrome has been described there is no case of paravertebral compartment syndrome that has been described in the pediatric population. We report the case of a 17-year-old boy who presented at our institution with severe, acute-onset low back pain that started shortly after a rigorous 4-hour workout. He was diagnosed with acute lumbar paravertebral compartment syndrome and underwent emergent fasciotomy with 2 more debridements. Key Words: compartment syndrome, paraspinal, paravertebral, lumbar, fasciotomy (J Pediatr Orthop 2015;35:e49–e51)
A
cute compartment syndrome is described as an elevation of interstitial pressure in a closed fascial compartment that can lead to damage of the microvasculature with subsequent tissue necrosis. Although compartment syndrome has been mainly described in extremities, multiple authors have reported case examples of paravertebral compartment syndrome.1–4 To our knowledge no case of paravertebral compartment syndrome has been described in the pediatric population.
HISTORY A 17-year-old boy presented to our emergency department with an 18-hour history of severe, acute-onset low back pain that started shortly after a rigorous 4-hour workout consisting of a myriad of calisthenics. This was not a common workout routine for this adolescent. The pain was primarily confined to a right lumbar paravertebral location and was so severe that the patient was not comfortable standing up. The pain was exacerbated by movement or sitting. He also reported numbness and tingling in the lumbar region. No radicular symptoms were reported. The patient had initially presented to an outpatient urgent care center the same day of the workout and was prescribed a muscle relaxant as well as acetaminophen and ibuprofen. That evening his urine appeared brown in color, From the Department of Orthopaedic Surgery, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA. The authors declare no conflicts of interest. Reprints: W. Timothy Ward, MD, Division of Pediatric Orthopaedic Surgery, Children’s Hospital of Pittsburgh of UPMC, 4401 Penn Avenue, 4th Floor, Pittsburgh, PA 15224. E-mail: [email protected]. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Pediatr Orthop
Volume 35, Number 6, September 2015
and the severe back pain persisted despite using narcotic medication. On presentation to his primary care provider the following day a urine dipstick revealed large amounts of protein and blood for which he was then referred to our emergency department for concern about rhabdomyolysis. His vital signs were stable. Blood tests a revealed a creatinine phosphokinase level of 116,000 IU/L (normal range, 33 to 145 IU/ L) as well as an elevated alanine aminotransferase (364 IU/L; normal range, 17 to 63 IU/L) and aspartate transaminase (1330 IU/L; normal range, 25 to 55 IU/L). Creatinine and blood urea nitrogen were within normal limits. Urinalysis revealed >100 red blood cells per high power field. Glomerulonephritis workup was negative, however, microscopic findings were consistent with acute tubular necrosis. Renal ultrasound failed to show any abnormalities. The patient was felt to have rhabdomyolysis in the face of acute-onset severe low back pain. A gadolinium contrast lumbar magnetic resonance imaging (MRI) study revealed significant diffuse heterogenous hypofusion and hyperperfusion signal changes in the lumbar paravertebral muscles consistent with swelling, inflammation, and early necrosis (Fig. 1). The elevated muscle enzymes, MRI findings, and clinical presentation of acute-onset severe low back pain supported a tentative diagnosis of acute paralumbar compartment syndrome or possible paraspinal abscess. Repeat creatinine phosphokinase drawn a few hours after the first test showed an increase to 170,000 IU/L. A decision was made to proceed with emergent paraspinal muscle fasciotomies. The paralumbar muscles appeared swollen under the exposed paraspinal fascia on visualization. The rightsided fascia was incised and a small but definitive area of ischemic muscle was appreciated at the L4 level. No purulence was observed. The pale and ischemic looking muscle did not contract to electrocautery stimulation in contrast to good contractility of the surrounding viable muscle (Fig. 2). Muscle tissue was sent to pathology and a diagnosis of necrotic muscle was confirmed. The left-sided paraspinal fascia was also released and the muscle appeared to be swollen but displayed good stimulation to electrocautery and was felt to be uniformly viable. The wound was covered with a vacuum-assisted device. The patient reported immediate relief of his back pain in the recovery room. An additional debridement was performed 2 days later and on day 6 the wound was closed with an estimation that about 15% of the right-sided lumbar musculature was removed at the L4 level. Liver enzymes as well as creatinine phosphokinase trended down appropriately and the patient was discharged to home on hospital day 7. He has remained pain free at 4 months’ follow-up and has returned to full activities.
DISCUSSION Acute compartment syndrome has been mainly described in the extremities and is caused by increasing pressure in a closed fibrous-osseous space. This can lead www.pedorthopaedics.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
e49
J Pediatr Orthop
Schreiber and Ward
Volume 35, Number 6, September 2015
FIGURE 1. Axial T2 with contrast magnetic resonance imaging showing edema and necrosis in lumbar paravertebral musculature.
to necrosis and irreversible injury of muscle and surrounding tissues. Multiple studies using magnetic resonance for determination of pH, tissue oxygenation, and energy stores, as well as histochemistry, electron microscopy, and Doppler flow have identified changes in muscle tissue in the setting of ischemia. Muscle exposed to complete ischemia remains electrically responsive for up to 3 hours and survives for up to 4 hours without undergoing irreversible damage. However, complete ischemic time of 8 hours leads to irreversible damage.5–10 Rhabdomyolysis is caused by an increase in free ionized calcium in the cytoplasm and damages the skeletal muscle, which causes toxic intracellular material to be released into the systemic circulation. The most common complications of rhabdomyolysis are renal failure, myoglobin cast formation, and direct renal toxic effects; however, the development of compartment syndrome has been described as well.11 Muscle cells are impaired by calcium and sodium influx, which promote the accumulation of extracellular fluid into the cells. This will then lead to an increase in intramuscular pressure.12,13 Treatment of rhabdomyolysis includes the prevention of acute renal failure, treatment of metabolic acidosis, early correction of potentially lethal electrolyte disorders, and the management of other coexisting complication.13 Paravertebral compartment syndrome is a rare condition that has been reported in adults after exercise and after certain sports such as downhill skiing as well as a reperfusion injury after abdominal aortic surgery.1–3,14 The paravertebral muscles, that is, the erector spinae muscles, are described as curved tubes parallel to the spine and are enclosed by the posterior and middle lamellae of the lumbodorsal fascia. The posterior lamellae arise medially at the
e50 | www.pedorthopaedics.com
FIGURE 2. Intraoperative view of lumbar paravertebral compartment with decompression of the right compartment. Asterisk marks the area of necrosis.
spinous process and interspinous ligaments dorsally and then caudally the sacral fascia is formed by the posterior and middle layer. The fascial septa laterally arise from the 3 abdominal muscles and ventrally the fascia attaches to the transverse processes.1,15,16 Paravertebral compartment syndrome usually presents with acute onset of severe pain after exercise with unresponsiveness to pain medicine. High creatinine phosphokinase levels and myoglobinuria consistent with rhabdomyolysis can be found. MRI will confirm heterogenous signal changes consistent with swelling or necrosis. Loss of sensation in the paravertebral region may or may not be found and is caused by damage to the lateral branch of the posterior primary ramus at multiple levels.17 Nathan and colleagues performed a systematic review on paravertebral compartment syndrome and defined criteria to distinguish acute from chronic compartment syndrome including but not limited to the acute onset of excruciating pain, rigidity of the paravertebral muscles, elevation of creatinine phosphokinase, no history of back pain, localized sensory loss in the paravertebral region, urine myoglobinuria, and changes on MRI. All of these parameters were present in our patient. The authors also concluded that as in other muscle compartments in the body surgical decompression should be performed as early as possible in the majority of cases to avoid functional sequelae. This Copyright
r
2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Pediatr Orthop
Volume 35, Number 6, September 2015
should be combined with conservative measure, for example, adequate fluid resuscitation.18 Given the findings on clinical examination and MRI we decided to forego intracompartmental pressure measurements. Wik and colleagues reported a case of exertional paraspinal compartment syndrome in a 30-year-old male with clinical presentation of paraspinal compartment syndrome and rhabdomyolysis. The patient was treated conservatively as it was felt that the prolonged time to diagnosis in this case (about 48 to 72 h) would have led to irreversible muscle damage. The rhabdomyolysis resolved after 21 days, however, the patient continued to experience significant lower back pain that led to the author’s conclusion that surgical decompression would most likely have been a more prudent choice.19 In our case the patient presented within 24 hours after onset of back pain and surgical decompression was performed within 36 hours after onset of back pain with dramatic improvement of renal function. At the 3 months follow-up the patient was doing very well with no complaints in the lower back. Our case report, while very similar to those cases already reported in the adult literature, is the first such report in the pediatric population. The marked severity of the back pain was in excess of that typically seen in other adolescent back disorders. The unusually dramatic amount of acute-onset low back pain in association with the history of excessive exercise, abnormal MRI, and abnormal muscle enzymes in conjunction with the immediate alleviation of symptoms after paralumbar fasciotomy makes us confident that this report is that of an acute-onset paralumbar compartment syndrome. Had fasciotomy been performed several hours sooner it is possible that no muscle necrosis would have been found. In conclusion, paravertebral compartment syndrome should be considered in the differential diagnosis in adolescents who have recently undergone high-demand activities presenting with unusually severe acute-onset low back pain. Diagnosis is made by weighing the history, clinical examination, MRI findings, and muscle/urine enzyme levels. Compartment measurements can be performed in addition. Surgical decompression in conjunction with supportive management is the optimal treatment for this rare condition. REFERENCES 1. Carr D, Gilbertson L, Frymoyer J, et al. Lumbar paraspinal compartment syndrome. A case report with physiologic and anatomic studies. Spine. 1985;10:816–820.
Copyright
r
2015 Wolters Kluwer Health, Inc. All rights reserved.
Pediatric Lumbar Paravertebral Compartment Syndrome
2. Mattiassich G, Larcher L, Leitinger M, et al. Paravertebral compartment syndrome after training causing severe back pain in an amateur rugby player: report of a rare case and review of the literature. BMC Musculoskelet Disord. 2013;14:259. 3. Khan RJ, Fick DP, Guier CA, et al. Acute paraspinal compartment syndrome. A case report. J Bone Joint Surg Am. 2005;87: 1126–1128. 4. Kitajima I, Tachibana S, Hirota Y, et al. Acute paraspinal muscle compartment syndrome treated with surgical decompression: a case report. Am J Sports Med. 2002;30:283–285. 5. Heckman MM, Whitesides TE Jr, Grewe SR, et al. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma. 1993;7: 199–210. 6. Heckman MM, Whitesides TE Jr, Grewe SR, et al. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg Am. 1994;76:1285–1292. 7. Heppenstall RB, Sapega AA, Izant T, et al. Compartment syndrome: a quantitative study of high-energy phosphorus compounds using 31 P-magnetic resonance spectroscopy. J Trauma. 1989;29:1113–1119. 8. Heppenstall RB, Sapega AA, Scott R, et al. The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop Relat Res. 1988;226:138–155. 9. Heppenstall RB, Scott R, Sapega A, et al. A comparative study of the tolerance of skeletal muscle to ischemia. Tourniquet application compared with acute compartment syndrome. J Bone Joint Surg Am. 1986;68:820–828. 10. Matava MJ, Whitesides TE Jr, Seiler JG III, et al. Determination of the compartment pressure threshold of muscle ischemia in a canine model. J Trauma. 1994;37:50–58. 11. Vanholder R, Sever MS, Erek E, et al. Rhabdomyolysis. J Am Soc Nephrol. 2000;11:1553–1561. 12. Better OS, Rubinstein I, Reis DN. Muscle crush compartment syndrome: fulminant local edema with threatening systemic effects. Kidney Int. 2003;63:1155–1157. 13. Chatzizisis YS, Misirli G, Hatzitolios AI, et al. The syndrome of rhabdomyolysis: complications and treatment. Eur J Intern Med. 2008;19:568–574. 14. DiFazio FA, Barth RA, Frymoyer JW. Acute lumbar paraspinal compartment syndrome. A case report. J Bone Joint Surg Am. 1991; 73:1101–1103. 15. Peck D, Nicholls PJ, Beard C, et al. Are there compartment syndromes in some patients with idiopathic back pain? Spine. 1986; 11:468–475. 16. Fairbank JC, O’Brien JP. The abdominal cavity and thoracolumbar fascia as stabilizers of the lumbar spine in patients with lowback pain. I Mech E Conf Proc. 1980:73–78. 17. Bogduk N. A reappraisal of the anatomy of the human lumbar erector spinae. J Anat. 1980;131(pt 3):525–540. 18. Nathan ST, Roberts CS, Deliberato D. Lumbar paraspinal compartment syndrome. Int Orthop. 2012;36:1221–1227. 19. Wik L, Patterson JM, Oswald AE. Exertional paraspinal muscle rhabdomyolysis and compartment syndrome: a cause of back pain not to be missed. Clin Rheumatol. 2010;29:803–805.
www.pedorthopaedics.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
e51
