Neurosurgery & Trauma

CHICAGO — An enzyme found in brain cells may become the first bedside biomarker for assessing the severity of traumatic brain injury, according to Dr. Linda Papa.

In a multicenter trial, levels of the enzyme ubiquitin C-terminal hydrolase (UCH-L1) rose significantly in severely injured brains, an increase that paralleled the rise in cerebral spinal fluid and correlated with the Glasgow Coma Scale (GCS) score, Dr. Papa told the annual meeting of the Society for Academic Emergency Medicine.

If further study confirms the value of UCH-L1 as the first clinical biomarker in traumatic brain injury (TBI), physicians will be better able to identify targets for drug therapy and guide the timing of treatment with such agents as tissue plasminogen activator, explained Dr. Papa, director of academic clinical research at Orlando Regional Medical Center.

This prospective case-control study enrolled consecutive adult patients presenting to two tertiary care teaching hospitals following severe TBIs, defined by a GCS score of less than 8 and requiring invasive intracerebral monitoring. Fourteen patients with severe TBI were enrolled over 16 months. Their mean age was 38 years, and four-fifths were men. Patients were excluded if they did not have ventriculostomy, which is necessary to obtain cerebrospinal fluid (CSF). Ventricular CSF was drained from each patient at 6, 12, 24, 48, 72, and 96 hours following TBI, and was measured by enzyme-linked immunosorbent assay for UCH-L1 levels.

Mean 12-hour UCH-L1 levels in the control group of uninjured patients with other indications for CSF drainage were 145 ng/mL for patients with GCS scores of 3–5, and 38.5 ng/mL in those with GCS scores of 6–8. Similarly, 24-hour levels were 76 and 36 ng/mL for those with GCS scores of 3–5 and 6–8, respectively. The largest increase in the experimental biomarker occurred during the first 48 hours after injury, Dr. Papa said, noting: “Then we found that patients with evolving lesions had significantly higher levels of the biomarker” than did patients with nonevolving lesions at both 48 and 72 hours.”

“There is a significant increase in CSF UCH-L1 following severe human TBI compared to uninjured controls, and there is a significant association with severity of injury as measured by GCS and the presence of evolving lesions on CT,” Dr. Papa concluded, adding that these data suggest that UCH-L1 is a potential TBI biomarker.

Levels of the enzyme in the CSF corresponded to severity of injury and to CT evidence of evolving lesions. DR. PAPA

CHICAGO — An enzyme found in brain cells may become the first bedside biomarker for assessing the severity of traumatic brain injury, according to Dr. Linda Papa.

In a multicenter trial, levels of the enzyme ubiquitin C-terminal hydrolase (UCH-L1) rose significantly in severely injured brains, an increase that paralleled the rise in cerebral spinal fluid and correlated with the Glasgow Coma Scale (GCS) score, Dr. Papa told the annual meeting of the Society for Academic Emergency Medicine.

If further study confirms the value of UCH-L1 as the first clinical biomarker in traumatic brain injury (TBI), physicians will be better able to identify targets for drug therapy and guide the timing of treatment with such agents as tissue plasminogen activator, explained Dr. Papa, director of academic clinical research at Orlando Regional Medical Center.

This prospective case-control study enrolled consecutive adult patients presenting to two tertiary care teaching hospitals following severe TBIs, defined by a GCS score of less than 8 and requiring invasive intracerebral monitoring. Fourteen patients with severe TBI were enrolled over 16 months. Their mean age was 38 years, and four-fifths were men. Patients were excluded if they did not have ventriculostomy, which is necessary to obtain cerebrospinal fluid (CSF). Ventricular CSF was drained from each patient at 6, 12, 24, 48, 72, and 96 hours following TBI, and was measured by enzyme-linked immunosorbent assay for UCH-L1 levels.

Mean 12-hour UCH-L1 levels in the control group of uninjured patients with other indications for CSF drainage were 145 ng/mL for patients with GCS scores of 3–5, and 38.5 ng/mL in those with GCS scores of 6–8. Similarly, 24-hour levels were 76 and 36 ng/mL for those with GCS scores of 3–5 and 6–8, respectively. The largest increase in the experimental biomarker occurred during the first 48 hours after injury, Dr. Papa said, noting: “Then we found that patients with evolving lesions had significantly higher levels of the biomarker” than did patients with nonevolving lesions at both 48 and 72 hours.”

“There is a significant increase in CSF UCH-L1 following severe human TBI compared to uninjured controls, and there is a significant association with severity of injury as measured by GCS and the presence of evolving lesions on CT,” Dr. Papa concluded, adding that these data suggest that UCH-L1 is a potential TBI biomarker.

Levels of the enzyme in the CSF corresponded to severity of injury and to CT evidence of evolving lesions. DR. PAPA

CHICAGO — An enzyme found in brain cells may become the first bedside biomarker for assessing the severity of traumatic brain injury, according to Dr. Linda Papa.

In a multicenter trial, levels of the enzyme ubiquitin C-terminal hydrolase (UCH-L1) rose significantly in severely injured brains, an increase that paralleled the rise in cerebral spinal fluid and correlated with the Glasgow Coma Scale (GCS) score, Dr. Papa told the annual meeting of the Society for Academic Emergency Medicine.

If further study confirms the value of UCH-L1 as the first clinical biomarker in traumatic brain injury (TBI), physicians will be better able to identify targets for drug therapy and guide the timing of treatment with such agents as tissue plasminogen activator, explained Dr. Papa, director of academic clinical research at Orlando Regional Medical Center.

This prospective case-control study enrolled consecutive adult patients presenting to two tertiary care teaching hospitals following severe TBIs, defined by a GCS score of less than 8 and requiring invasive intracerebral monitoring. Fourteen patients with severe TBI were enrolled over 16 months. Their mean age was 38 years, and four-fifths were men. Patients were excluded if they did not have ventriculostomy, which is necessary to obtain cerebrospinal fluid (CSF). Ventricular CSF was drained from each patient at 6, 12, 24, 48, 72, and 96 hours following TBI, and was measured by enzyme-linked immunosorbent assay for UCH-L1 levels.

Mean 12-hour UCH-L1 levels in the control group of uninjured patients with other indications for CSF drainage were 145 ng/mL for patients with GCS scores of 3–5, and 38.5 ng/mL in those with GCS scores of 6–8. Similarly, 24-hour levels were 76 and 36 ng/mL for those with GCS scores of 3–5 and 6–8, respectively. The largest increase in the experimental biomarker occurred during the first 48 hours after injury, Dr. Papa said, noting: “Then we found that patients with evolving lesions had significantly higher levels of the biomarker” than did patients with nonevolving lesions at both 48 and 72 hours.”

“There is a significant increase in CSF UCH-L1 following severe human TBI compared to uninjured controls, and there is a significant association with severity of injury as measured by GCS and the presence of evolving lesions on CT,” Dr. Papa concluded, adding that these data suggest that UCH-L1 is a potential TBI biomarker.

Levels of the enzyme in the CSF corresponded to severity of injury and to CT evidence of evolving lesions. DR. PAPA

BETHESDA, MD. — A growing body of research suggests dysfunction of the small-fiber axons that mediate pain sensation and autonomic function underlies complex regional pain syndrome, Dr. Anne Louise Oaklander said at a meeting sponsored by the National Institutes of Health's Pain Consortium.

Complex regional pain syndrome (CRPS) is “one of the most mysterious of the pain disorders,” said Dr. Oaklander, a neurologist at Harvard Medical School and director of the nerve injury unit at Massachusetts General Hospital, Boston. With no known cause, few physicians are willing to treat it. Others believe it to be psychosomatic. However, “we are beginning to understand the disease biology,” she said. “It's time to abandon the dichotomy between CRPS I and CRPS II [and to] consider changing the name to 'posttraumatic neuralgia.'

“Small-fiber axonopathy is what causes this,” Dr. Oaklander said.

Current diagnostic criteria for CRPS include the occurrence of a noxious event or other cause of immobilization; continuing or disproportionate pain, allodynia, or hyperalgesia; and edema, changes in skin blood flow, or abnormal sweating in the region of pain.

Most patients are classified as CRPS-I (no known nerve injury); fewer than 10% receive a diagnosis of CRPS-II (a known nerve injury). However, “a physician trained to diagnose nerve injuries can identify minor nerve injuries in most CRPS-1 patients as well,” she said.

CRPS is “what I call a focal 'pain-plus' syndrome. Patients have chronic pain but also vascular dysregulation and sometimes dystonia, contralesional 'mirror' pain … osteopenia, [and focal changes in other innervated tissues],” Dr. Oaklander said. “[The disease] reflects pathological processes, not normal pain mechanisms.”

Most patients with CRPS are young (average age 39) and female (a 4:1 ratio). Most recover spontaneously.

Skin biopsies done in Dr. Oaklander's lab of 18 CRPS-I patients show 30% fewer small-fiber nerve endings in painful CRPS-affected areas.

The identification of posttraumatic small-fiber loss in patients with CRPS was first described in 1996 and has been validated by other researchers, she noted. There is good evidence that trauma disproportionately damages small fibers, probably because they lack protective myelin and saltatory conduction. Pain results when undamaged axons within the same nerve, as well as regenerating axon spouts, malfunction, firing without cause, for instance, triggering neurogenic edema and tissue ischemia. “The problem isn't so much with the nociceptive fibers that are degenerated—it's with their neighbors, and the effects on the central nervous system,” Dr. Oaklander said. “We really can't assume that it takes a severe injury to leave someone with chronic pain—in fact, the opposite may be true.”

A swollen ankle and shallow ulcers are caused by neurogenic edema. Courtesy Dr. Anne Louise Oaklander

BETHESDA, MD. — A growing body of research suggests dysfunction of the small-fiber axons that mediate pain sensation and autonomic function underlies complex regional pain syndrome, Dr. Anne Louise Oaklander said at a meeting sponsored by the National Institutes of Health's Pain Consortium.

Complex regional pain syndrome (CRPS) is “one of the most mysterious of the pain disorders,” said Dr. Oaklander, a neurologist at Harvard Medical School and director of the nerve injury unit at Massachusetts General Hospital, Boston. With no known cause, few physicians are willing to treat it. Others believe it to be psychosomatic. However, “we are beginning to understand the disease biology,” she said. “It's time to abandon the dichotomy between CRPS I and CRPS II [and to] consider changing the name to 'posttraumatic neuralgia.'

“Small-fiber axonopathy is what causes this,” Dr. Oaklander said.

Current diagnostic criteria for CRPS include the occurrence of a noxious event or other cause of immobilization; continuing or disproportionate pain, allodynia, or hyperalgesia; and edema, changes in skin blood flow, or abnormal sweating in the region of pain.

Most patients are classified as CRPS-I (no known nerve injury); fewer than 10% receive a diagnosis of CRPS-II (a known nerve injury). However, “a physician trained to diagnose nerve injuries can identify minor nerve injuries in most CRPS-1 patients as well,” she said.

CRPS is “what I call a focal 'pain-plus' syndrome. Patients have chronic pain but also vascular dysregulation and sometimes dystonia, contralesional 'mirror' pain … osteopenia, [and focal changes in other innervated tissues],” Dr. Oaklander said. “[The disease] reflects pathological processes, not normal pain mechanisms.”

Most patients with CRPS are young (average age 39) and female (a 4:1 ratio). Most recover spontaneously.

Skin biopsies done in Dr. Oaklander's lab of 18 CRPS-I patients show 30% fewer small-fiber nerve endings in painful CRPS-affected areas.

The identification of posttraumatic small-fiber loss in patients with CRPS was first described in 1996 and has been validated by other researchers, she noted. There is good evidence that trauma disproportionately damages small fibers, probably because they lack protective myelin and saltatory conduction. Pain results when undamaged axons within the same nerve, as well as regenerating axon spouts, malfunction, firing without cause, for instance, triggering neurogenic edema and tissue ischemia. “The problem isn't so much with the nociceptive fibers that are degenerated—it's with their neighbors, and the effects on the central nervous system,” Dr. Oaklander said. “We really can't assume that it takes a severe injury to leave someone with chronic pain—in fact, the opposite may be true.”

A swollen ankle and shallow ulcers are caused by neurogenic edema. Courtesy Dr. Anne Louise Oaklander

BETHESDA, MD. — A growing body of research suggests dysfunction of the small-fiber axons that mediate pain sensation and autonomic function underlies complex regional pain syndrome, Dr. Anne Louise Oaklander said at a meeting sponsored by the National Institutes of Health's Pain Consortium.

Complex regional pain syndrome (CRPS) is “one of the most mysterious of the pain disorders,” said Dr. Oaklander, a neurologist at Harvard Medical School and director of the nerve injury unit at Massachusetts General Hospital, Boston. With no known cause, few physicians are willing to treat it. Others believe it to be psychosomatic. However, “we are beginning to understand the disease biology,” she said. “It's time to abandon the dichotomy between CRPS I and CRPS II [and to] consider changing the name to 'posttraumatic neuralgia.'

“Small-fiber axonopathy is what causes this,” Dr. Oaklander said.

Current diagnostic criteria for CRPS include the occurrence of a noxious event or other cause of immobilization; continuing or disproportionate pain, allodynia, or hyperalgesia; and edema, changes in skin blood flow, or abnormal sweating in the region of pain.

Most patients are classified as CRPS-I (no known nerve injury); fewer than 10% receive a diagnosis of CRPS-II (a known nerve injury). However, “a physician trained to diagnose nerve injuries can identify minor nerve injuries in most CRPS-1 patients as well,” she said.

CRPS is “what I call a focal 'pain-plus' syndrome. Patients have chronic pain but also vascular dysregulation and sometimes dystonia, contralesional 'mirror' pain … osteopenia, [and focal changes in other innervated tissues],” Dr. Oaklander said. “[The disease] reflects pathological processes, not normal pain mechanisms.”

Most patients with CRPS are young (average age 39) and female (a 4:1 ratio). Most recover spontaneously.

Skin biopsies done in Dr. Oaklander's lab of 18 CRPS-I patients show 30% fewer small-fiber nerve endings in painful CRPS-affected areas.

The identification of posttraumatic small-fiber loss in patients with CRPS was first described in 1996 and has been validated by other researchers, she noted. There is good evidence that trauma disproportionately damages small fibers, probably because they lack protective myelin and saltatory conduction. Pain results when undamaged axons within the same nerve, as well as regenerating axon spouts, malfunction, firing without cause, for instance, triggering neurogenic edema and tissue ischemia. “The problem isn't so much with the nociceptive fibers that are degenerated—it's with their neighbors, and the effects on the central nervous system,” Dr. Oaklander said. “We really can't assume that it takes a severe injury to leave someone with chronic pain—in fact, the opposite may be true.”

A swollen ankle and shallow ulcers are caused by neurogenic edema. Courtesy Dr. Anne Louise Oaklander

CHICAGO — Not only hypoxemia but hyperoxemia, too, is associated with increased mortality in patients with traumatic brain injury, Dr. Daniel P. Davis reported at the annual scientific sessions of the American Heart Association.

The dangers of hypoxemia in the setting of traumatic brain injury (TBI) are well documented. But the increase in bad outcomes associated with hyperoxemia hasn't previously been reported in a clinical population with TBI. The new findings suggest a need to rethink the popular practice of aggressive airway management in such patients, including intubation and ventilation with 100% fraction of inspired oxygen concentration, according to Dr. Davis of the department of emergency medicine at the University of California, San Diego.

He presented a retrospective study of 3,515 patients with TBI in the San Diego County Trauma Registry. Of them, 1,012 were hypoxemic as defined by a partial pressure of oxygen (PO₂) below 110 mm Hg, and 358 were hyperoxemic, with a PO₂ in excess of 487 mm Hg.

The Trauma and Injury Severity Score (TRISS) was used to calculate each individual's predicted survival, and the hypoxemic patients had an observed survival rate 41% lower than predicted. Hyperoxemic patients were 48% less likely to survive than was predicted by TRISS. And patients with a PO₂ in the optimal range of 110–487 mm Hg were 77% more likely to survive than was predicted. This pattern of results persisted even when intubated and nonintubated patients were analyzed separately.

The goal of aggressive airway management with hyperoxygenation is to reverse hypoxia and increase oxygen tension in an effort to counteract regional hypoperfusion and edema. But theoretic concerns exist regarding creation of a hyperoxemic state in the setting of TBI.

CHICAGO — Not only hypoxemia but hyperoxemia, too, is associated with increased mortality in patients with traumatic brain injury, Dr. Daniel P. Davis reported at the annual scientific sessions of the American Heart Association.

The dangers of hypoxemia in the setting of traumatic brain injury (TBI) are well documented. But the increase in bad outcomes associated with hyperoxemia hasn't previously been reported in a clinical population with TBI. The new findings suggest a need to rethink the popular practice of aggressive airway management in such patients, including intubation and ventilation with 100% fraction of inspired oxygen concentration, according to Dr. Davis of the department of emergency medicine at the University of California, San Diego.

He presented a retrospective study of 3,515 patients with TBI in the San Diego County Trauma Registry. Of them, 1,012 were hypoxemic as defined by a partial pressure of oxygen (PO₂) below 110 mm Hg, and 358 were hyperoxemic, with a PO₂ in excess of 487 mm Hg.

The Trauma and Injury Severity Score (TRISS) was used to calculate each individual's predicted survival, and the hypoxemic patients had an observed survival rate 41% lower than predicted. Hyperoxemic patients were 48% less likely to survive than was predicted by TRISS. And patients with a PO₂ in the optimal range of 110–487 mm Hg were 77% more likely to survive than was predicted. This pattern of results persisted even when intubated and nonintubated patients were analyzed separately.

The goal of aggressive airway management with hyperoxygenation is to reverse hypoxia and increase oxygen tension in an effort to counteract regional hypoperfusion and edema. But theoretic concerns exist regarding creation of a hyperoxemic state in the setting of TBI.

CHICAGO — Not only hypoxemia but hyperoxemia, too, is associated with increased mortality in patients with traumatic brain injury, Dr. Daniel P. Davis reported at the annual scientific sessions of the American Heart Association.

The dangers of hypoxemia in the setting of traumatic brain injury (TBI) are well documented. But the increase in bad outcomes associated with hyperoxemia hasn't previously been reported in a clinical population with TBI. The new findings suggest a need to rethink the popular practice of aggressive airway management in such patients, including intubation and ventilation with 100% fraction of inspired oxygen concentration, according to Dr. Davis of the department of emergency medicine at the University of California, San Diego.

He presented a retrospective study of 3,515 patients with TBI in the San Diego County Trauma Registry. Of them, 1,012 were hypoxemic as defined by a partial pressure of oxygen (PO₂) below 110 mm Hg, and 358 were hyperoxemic, with a PO₂ in excess of 487 mm Hg.

The Trauma and Injury Severity Score (TRISS) was used to calculate each individual's predicted survival, and the hypoxemic patients had an observed survival rate 41% lower than predicted. Hyperoxemic patients were 48% less likely to survive than was predicted by TRISS. And patients with a PO₂ in the optimal range of 110–487 mm Hg were 77% more likely to survive than was predicted. This pattern of results persisted even when intubated and nonintubated patients were analyzed separately.

The goal of aggressive airway management with hyperoxygenation is to reverse hypoxia and increase oxygen tension in an effort to counteract regional hypoperfusion and edema. But theoretic concerns exist regarding creation of a hyperoxemic state in the setting of TBI.

CHICAGO — Proton magnetic resonance spectroscopy could represent a fundamental, noninvasive diagnostic and monitoring tool for patients with brain concussions, Dr. Andre Ludovici said at the annual meeting of the Radiological Society of North America.

Current imaging with computed tomography or magnetic resonance imaging does not permit quantification of neural injury that occurs after a traumatic concussion. But proton magnetic resonance spectroscopic (1HMRS) imaging can be used to assess the neurochemical damage derived from a cerebral concussion by monitoring N-acetyl-L-aspartate (NAA) levels over time.

Current research indicates that NAA diminution appears to be linked to a general mitochondrial dysfunction, and therefore, NAA restoration can be considered a surrogate marker of metabolic recovery, said Dr. Ludovici of the University of Rome Tor Vergata.

He presented data from a pilot study in which 1HMRS was used to measure the levels of NAA and choline (Cho) relative to creatine (Cr) in the brains of 32 male contact sport players. Of these, 14 had suffered concussions, and had Glasgow Coma Scale scores between 13 and 15. The 1HMRS signal was collected from a single voxel placed bilaterally in the subcortical frontal white matter. Scans were performed after a 3-month period of inactivity, until the third day following a match, and at the 10th and 30th day after the injury had occurred.

The patients were boxers and kick boxers, with a mean age of 21 years. Three patients did not complete the study, and one was excluded because of a cerebral bleed.

The average NAA/Cr ratio was significantly lower at the first time point among concussive patients compared with healthy patients (1.83 vs. 2.11), he said. At 10 days, the NAA/Cr ratio showed a trend toward normalization, and at 30 days there was a complete recovery of baseline NAA values.

From baseline, there was a 35% reduction in NAA levels among concussive patients. There was no significant difference in the NAA/Cho ratio between groups at the three time points, he said. All patients were held back from sports until their NAA values normalized.

CHICAGO — Proton magnetic resonance spectroscopy could represent a fundamental, noninvasive diagnostic and monitoring tool for patients with brain concussions, Dr. Andre Ludovici said at the annual meeting of the Radiological Society of North America.

Current imaging with computed tomography or magnetic resonance imaging does not permit quantification of neural injury that occurs after a traumatic concussion. But proton magnetic resonance spectroscopic (1HMRS) imaging can be used to assess the neurochemical damage derived from a cerebral concussion by monitoring N-acetyl-L-aspartate (NAA) levels over time.

Current research indicates that NAA diminution appears to be linked to a general mitochondrial dysfunction, and therefore, NAA restoration can be considered a surrogate marker of metabolic recovery, said Dr. Ludovici of the University of Rome Tor Vergata.

He presented data from a pilot study in which 1HMRS was used to measure the levels of NAA and choline (Cho) relative to creatine (Cr) in the brains of 32 male contact sport players. Of these, 14 had suffered concussions, and had Glasgow Coma Scale scores between 13 and 15. The 1HMRS signal was collected from a single voxel placed bilaterally in the subcortical frontal white matter. Scans were performed after a 3-month period of inactivity, until the third day following a match, and at the 10th and 30th day after the injury had occurred.

The patients were boxers and kick boxers, with a mean age of 21 years. Three patients did not complete the study, and one was excluded because of a cerebral bleed.

The average NAA/Cr ratio was significantly lower at the first time point among concussive patients compared with healthy patients (1.83 vs. 2.11), he said. At 10 days, the NAA/Cr ratio showed a trend toward normalization, and at 30 days there was a complete recovery of baseline NAA values.

From baseline, there was a 35% reduction in NAA levels among concussive patients. There was no significant difference in the NAA/Cho ratio between groups at the three time points, he said. All patients were held back from sports until their NAA values normalized.

CHICAGO — Proton magnetic resonance spectroscopy could represent a fundamental, noninvasive diagnostic and monitoring tool for patients with brain concussions, Dr. Andre Ludovici said at the annual meeting of the Radiological Society of North America.

Current imaging with computed tomography or magnetic resonance imaging does not permit quantification of neural injury that occurs after a traumatic concussion. But proton magnetic resonance spectroscopic (1HMRS) imaging can be used to assess the neurochemical damage derived from a cerebral concussion by monitoring N-acetyl-L-aspartate (NAA) levels over time.

Current research indicates that NAA diminution appears to be linked to a general mitochondrial dysfunction, and therefore, NAA restoration can be considered a surrogate marker of metabolic recovery, said Dr. Ludovici of the University of Rome Tor Vergata.

He presented data from a pilot study in which 1HMRS was used to measure the levels of NAA and choline (Cho) relative to creatine (Cr) in the brains of 32 male contact sport players. Of these, 14 had suffered concussions, and had Glasgow Coma Scale scores between 13 and 15. The 1HMRS signal was collected from a single voxel placed bilaterally in the subcortical frontal white matter. Scans were performed after a 3-month period of inactivity, until the third day following a match, and at the 10th and 30th day after the injury had occurred.

The patients were boxers and kick boxers, with a mean age of 21 years. Three patients did not complete the study, and one was excluded because of a cerebral bleed.

The average NAA/Cr ratio was significantly lower at the first time point among concussive patients compared with healthy patients (1.83 vs. 2.11), he said. At 10 days, the NAA/Cr ratio showed a trend toward normalization, and at 30 days there was a complete recovery of baseline NAA values.

From baseline, there was a 35% reduction in NAA levels among concussive patients. There was no significant difference in the NAA/Cho ratio between groups at the three time points, he said. All patients were held back from sports until their NAA values normalized.

BUENOS AIRES — Treatment of orthopedic injuries in patients with traumatic brain injury should not be delayed, Dr. Ivan Rubel said at the annual conference of the International Society of Orthopaedic Surgery and Traumatology.

A population-based study conducted in the Twin Cities area of Minnesota found that most patients who were seen in an emergency department for traumatic brain injury had received the injury from sports and recreational activities (Minn. Med. 2006;89:40–4). The traumatic brain injuries that trauma surgeons are more likely to encounter, however, come from falls or car accidents, said Dr. Rubel, director of the orthopedics and traumatology department at FLENI Institute in Buenos Aires.

Pelvic and extremity fractures are common in patients with traumatic brain injury. Many skeletal injuries are not given priority, or might even be missed. However, as the survival rate of patients with traumatic brain injury has increased, there is a greater emphasis on minimizing dysfunction and disability in these patients, particularly when the dysfunction and disability arise from concomitant orthopedic trauma.

In a study of health-related quality of life in pediatric patients during the first year following a traumatic brain injury, the treatment of associated injuries was shown to have a greater impact than other factors such as patient or family characteristics (Arch. Pediatr. Adolesc. Med. 2006;160:252–60). “With the recent advances in intensive care medicine, most of these patients survive,” said Dr. Rubel. “We have to focus on minimizing the dysfunction and disability.”

The main question concerns when to operate on orthopedic injuries in a patient with traumatic brain injury, explained Dr. Rubel. Early fracture fixation in blunt trauma patients is generally recommended, but many doctors are hesitant to perform early fixation in patients with severe brain trauma. There is a widespread view that fracture fixation should be postponed to protect the injured brain.

This view was challenged by a study examining the timing of fracture fixation in blunt trauma patients with severe head injuries (Am. J. Surg. 1998;176:324–9). Investigators reviewed records of 47 consecutive blunt trauma patients with both severe head injuries and long bone fractures requiring surgical fixation. Twenty-two patients had undergone early fracture fixation within 24 hours of hospital admission (mean time 17 hours), and 25 patients had undergone delayed treatment (mean time 143 hours). Review of patient records revealed that there were no significant differences between the two groups in terms of neurologic or orthopedic complications, length of hospital stay, or mortality. Thus, delay of fracture fixation did not protect the injured brain in this study population.

Dr. Rubel described a young patient who was treated at FLENI Institute for a severe traumatic head injury and multiple fractures. The head injury required decompression with a wide craniotomy. The patient remained in a coma for 6 weeks, and CT scans showed cerebral edema. Radiography revealed a huge intrapelvic calcification affecting the bladder and rectum, malunion of the pelvis, malunion of the tibia, and a radio-ulnar synostosis. She was placed in long arm and leg casts and was told that she could not have pelvic surgery because of the likelihood that she would die during the procedure.

“Once at our institution, the malunion of the tibia was corrected upon admission, and she was allowed to exercise on a rehabilitation bicycle,” said Dr. Rubel. The second step was resection of the forearm synostosis, which improved the position of the hand for daily activities and allowed her to rehabilitate her writing capabilities, he said. As the brain edema resolved, the patient gradually improved both in cognition and in function. Restoration of the pelvic malunion with serial osteotomies was the last surgical intervention.

“It's hard for patients to understand not to put weight on the leg, since the brain is still inflamed,” said Dr. Rubel. Rehabilitation was performed in a pool with chest-deep water. At 6 months from the accident, she returned to her normal activities.

Immediately after trauma, there is a window of opportunity when treatment of orthopedic injuries is optimal. Use that window of opportunity around trauma and start helping the patients right away to minimize their skeletal and psychological and cognitive dysfunction, advised Dr. Rubel.

BUENOS AIRES — Treatment of orthopedic injuries in patients with traumatic brain injury should not be delayed, Dr. Ivan Rubel said at the annual conference of the International Society of Orthopaedic Surgery and Traumatology.

A population-based study conducted in the Twin Cities area of Minnesota found that most patients who were seen in an emergency department for traumatic brain injury had received the injury from sports and recreational activities (Minn. Med. 2006;89:40–4). The traumatic brain injuries that trauma surgeons are more likely to encounter, however, come from falls or car accidents, said Dr. Rubel, director of the orthopedics and traumatology department at FLENI Institute in Buenos Aires.

Pelvic and extremity fractures are common in patients with traumatic brain injury. Many skeletal injuries are not given priority, or might even be missed. However, as the survival rate of patients with traumatic brain injury has increased, there is a greater emphasis on minimizing dysfunction and disability in these patients, particularly when the dysfunction and disability arise from concomitant orthopedic trauma.

In a study of health-related quality of life in pediatric patients during the first year following a traumatic brain injury, the treatment of associated injuries was shown to have a greater impact than other factors such as patient or family characteristics (Arch. Pediatr. Adolesc. Med. 2006;160:252–60). “With the recent advances in intensive care medicine, most of these patients survive,” said Dr. Rubel. “We have to focus on minimizing the dysfunction and disability.”

The main question concerns when to operate on orthopedic injuries in a patient with traumatic brain injury, explained Dr. Rubel. Early fracture fixation in blunt trauma patients is generally recommended, but many doctors are hesitant to perform early fixation in patients with severe brain trauma. There is a widespread view that fracture fixation should be postponed to protect the injured brain.

This view was challenged by a study examining the timing of fracture fixation in blunt trauma patients with severe head injuries (Am. J. Surg. 1998;176:324–9). Investigators reviewed records of 47 consecutive blunt trauma patients with both severe head injuries and long bone fractures requiring surgical fixation. Twenty-two patients had undergone early fracture fixation within 24 hours of hospital admission (mean time 17 hours), and 25 patients had undergone delayed treatment (mean time 143 hours). Review of patient records revealed that there were no significant differences between the two groups in terms of neurologic or orthopedic complications, length of hospital stay, or mortality. Thus, delay of fracture fixation did not protect the injured brain in this study population.

Dr. Rubel described a young patient who was treated at FLENI Institute for a severe traumatic head injury and multiple fractures. The head injury required decompression with a wide craniotomy. The patient remained in a coma for 6 weeks, and CT scans showed cerebral edema. Radiography revealed a huge intrapelvic calcification affecting the bladder and rectum, malunion of the pelvis, malunion of the tibia, and a radio-ulnar synostosis. She was placed in long arm and leg casts and was told that she could not have pelvic surgery because of the likelihood that she would die during the procedure.

“Once at our institution, the malunion of the tibia was corrected upon admission, and she was allowed to exercise on a rehabilitation bicycle,” said Dr. Rubel. The second step was resection of the forearm synostosis, which improved the position of the hand for daily activities and allowed her to rehabilitate her writing capabilities, he said. As the brain edema resolved, the patient gradually improved both in cognition and in function. Restoration of the pelvic malunion with serial osteotomies was the last surgical intervention.

“It's hard for patients to understand not to put weight on the leg, since the brain is still inflamed,” said Dr. Rubel. Rehabilitation was performed in a pool with chest-deep water. At 6 months from the accident, she returned to her normal activities.

Immediately after trauma, there is a window of opportunity when treatment of orthopedic injuries is optimal. Use that window of opportunity around trauma and start helping the patients right away to minimize their skeletal and psychological and cognitive dysfunction, advised Dr. Rubel.

BUENOS AIRES — Treatment of orthopedic injuries in patients with traumatic brain injury should not be delayed, Dr. Ivan Rubel said at the annual conference of the International Society of Orthopaedic Surgery and Traumatology.

A population-based study conducted in the Twin Cities area of Minnesota found that most patients who were seen in an emergency department for traumatic brain injury had received the injury from sports and recreational activities (Minn. Med. 2006;89:40–4). The traumatic brain injuries that trauma surgeons are more likely to encounter, however, come from falls or car accidents, said Dr. Rubel, director of the orthopedics and traumatology department at FLENI Institute in Buenos Aires.

Pelvic and extremity fractures are common in patients with traumatic brain injury. Many skeletal injuries are not given priority, or might even be missed. However, as the survival rate of patients with traumatic brain injury has increased, there is a greater emphasis on minimizing dysfunction and disability in these patients, particularly when the dysfunction and disability arise from concomitant orthopedic trauma.

In a study of health-related quality of life in pediatric patients during the first year following a traumatic brain injury, the treatment of associated injuries was shown to have a greater impact than other factors such as patient or family characteristics (Arch. Pediatr. Adolesc. Med. 2006;160:252–60). “With the recent advances in intensive care medicine, most of these patients survive,” said Dr. Rubel. “We have to focus on minimizing the dysfunction and disability.”

The main question concerns when to operate on orthopedic injuries in a patient with traumatic brain injury, explained Dr. Rubel. Early fracture fixation in blunt trauma patients is generally recommended, but many doctors are hesitant to perform early fixation in patients with severe brain trauma. There is a widespread view that fracture fixation should be postponed to protect the injured brain.

This view was challenged by a study examining the timing of fracture fixation in blunt trauma patients with severe head injuries (Am. J. Surg. 1998;176:324–9). Investigators reviewed records of 47 consecutive blunt trauma patients with both severe head injuries and long bone fractures requiring surgical fixation. Twenty-two patients had undergone early fracture fixation within 24 hours of hospital admission (mean time 17 hours), and 25 patients had undergone delayed treatment (mean time 143 hours). Review of patient records revealed that there were no significant differences between the two groups in terms of neurologic or orthopedic complications, length of hospital stay, or mortality. Thus, delay of fracture fixation did not protect the injured brain in this study population.

Dr. Rubel described a young patient who was treated at FLENI Institute for a severe traumatic head injury and multiple fractures. The head injury required decompression with a wide craniotomy. The patient remained in a coma for 6 weeks, and CT scans showed cerebral edema. Radiography revealed a huge intrapelvic calcification affecting the bladder and rectum, malunion of the pelvis, malunion of the tibia, and a radio-ulnar synostosis. She was placed in long arm and leg casts and was told that she could not have pelvic surgery because of the likelihood that she would die during the procedure.

“Once at our institution, the malunion of the tibia was corrected upon admission, and she was allowed to exercise on a rehabilitation bicycle,” said Dr. Rubel. The second step was resection of the forearm synostosis, which improved the position of the hand for daily activities and allowed her to rehabilitate her writing capabilities, he said. As the brain edema resolved, the patient gradually improved both in cognition and in function. Restoration of the pelvic malunion with serial osteotomies was the last surgical intervention.

“It's hard for patients to understand not to put weight on the leg, since the brain is still inflamed,” said Dr. Rubel. Rehabilitation was performed in a pool with chest-deep water. At 6 months from the accident, she returned to her normal activities.

Immediately after trauma, there is a window of opportunity when treatment of orthopedic injuries is optimal. Use that window of opportunity around trauma and start helping the patients right away to minimize their skeletal and psychological and cognitive dysfunction, advised Dr. Rubel.

NEW ORLEANS — Abusive head trauma is misdiagnosed in almost a third of children who are brought to the emergency department, Dr. Denis R. Pauzé said at the annual meeting of the American College of Emergency Physicians.

A missed diagnosis of abusive head trauma (AHT), also known as inflicted head trauma or shaken baby syndrome, can have tragic consequences, he said. Most infant homicides are caused by AHT, with the highest incidence occurring in babies less than 6 months old, said Dr. Pauzé of Inova Fairfax Hospital, Falls Church, Va.

“Failure to diagnose these infants and children leaves them at high risk for repeat abuse, which can lead to learning disabilities, permanent brain damage, or death. Just 5–20 seconds of shaking can kill,” Dr. Pauzé said. But making the diagnosis can be difficult. A child who has been shaken often presents with nonspecific symptoms, such as poor feeding, vomiting, diarrhea, irritability, and fever. “We therefore must have a high index of suspicion in order to diagnose inflicted head trauma,” he said.

An article published in the Journal of the American Medical Association (1999;281:621–6) is “must reading” for emergency department physicians, he said.

In a chart review, the researchers studied the characteristics of unrecognized AHT in children less than 3 years old. They found that nearly one-third of abused children who presented after AHT had their initial diagnosis missed. The average delay in diagnosis was 7 days.

The most common erroneous diagnoses made were gastroenteritis, influenza, accidental head injury, rule-out sepsis, increasing head size, otitis media, seizure disorder, reflux, and apnea. Misinterpretation of the CT scan or radiograph also caused a delay in diagnosis, which ranged from 1 to 174 days.

On the horizon to help emergency physicians make the right diagnosis in a timely manner are traumatic brain markers. Many organs, including the liver, pancreas, kidney, and heart, have serum biomarkers that act as guides to organ injury. The hope is that a biomarker for brain injury will become a bedside test for AHT in the future.

Until then, a complete and thorough history and physical exam are needed to diagnose AHT, Dr. Pauzé said.

Conflicting histories, delay in seeking medical care, or repetitive injuries should make physicians suspicious. Other red flags include injuries that are not consistent with the history given or with the developmental age of the infant or child.

A head-to-toe physical exam must be done, including checking for macrocephaly and inspecting for scalp, facial, or neck bruises. Examine the ribs and extremities for signs of tenderness or deformity and, if possible, perform a funduscopic exam for retinal hemorrhages.

'We … must have a high index of suspicion in order to diagnose inflicted head trauma.' DR. PAUZÉ

NEW ORLEANS — Abusive head trauma is misdiagnosed in almost a third of children who are brought to the emergency department, Dr. Denis R. Pauzé said at the annual meeting of the American College of Emergency Physicians.

A missed diagnosis of abusive head trauma (AHT), also known as inflicted head trauma or shaken baby syndrome, can have tragic consequences, he said. Most infant homicides are caused by AHT, with the highest incidence occurring in babies less than 6 months old, said Dr. Pauzé of Inova Fairfax Hospital, Falls Church, Va.

“Failure to diagnose these infants and children leaves them at high risk for repeat abuse, which can lead to learning disabilities, permanent brain damage, or death. Just 5–20 seconds of shaking can kill,” Dr. Pauzé said. But making the diagnosis can be difficult. A child who has been shaken often presents with nonspecific symptoms, such as poor feeding, vomiting, diarrhea, irritability, and fever. “We therefore must have a high index of suspicion in order to diagnose inflicted head trauma,” he said.

An article published in the Journal of the American Medical Association (1999;281:621–6) is “must reading” for emergency department physicians, he said.

In a chart review, the researchers studied the characteristics of unrecognized AHT in children less than 3 years old. They found that nearly one-third of abused children who presented after AHT had their initial diagnosis missed. The average delay in diagnosis was 7 days.

The most common erroneous diagnoses made were gastroenteritis, influenza, accidental head injury, rule-out sepsis, increasing head size, otitis media, seizure disorder, reflux, and apnea. Misinterpretation of the CT scan or radiograph also caused a delay in diagnosis, which ranged from 1 to 174 days.

On the horizon to help emergency physicians make the right diagnosis in a timely manner are traumatic brain markers. Many organs, including the liver, pancreas, kidney, and heart, have serum biomarkers that act as guides to organ injury. The hope is that a biomarker for brain injury will become a bedside test for AHT in the future.

Until then, a complete and thorough history and physical exam are needed to diagnose AHT, Dr. Pauzé said.

Conflicting histories, delay in seeking medical care, or repetitive injuries should make physicians suspicious. Other red flags include injuries that are not consistent with the history given or with the developmental age of the infant or child.

A head-to-toe physical exam must be done, including checking for macrocephaly and inspecting for scalp, facial, or neck bruises. Examine the ribs and extremities for signs of tenderness or deformity and, if possible, perform a funduscopic exam for retinal hemorrhages.

'We … must have a high index of suspicion in order to diagnose inflicted head trauma.' DR. PAUZÉ

NEW ORLEANS — Abusive head trauma is misdiagnosed in almost a third of children who are brought to the emergency department, Dr. Denis R. Pauzé said at the annual meeting of the American College of Emergency Physicians.

A missed diagnosis of abusive head trauma (AHT), also known as inflicted head trauma or shaken baby syndrome, can have tragic consequences, he said. Most infant homicides are caused by AHT, with the highest incidence occurring in babies less than 6 months old, said Dr. Pauzé of Inova Fairfax Hospital, Falls Church, Va.

“Failure to diagnose these infants and children leaves them at high risk for repeat abuse, which can lead to learning disabilities, permanent brain damage, or death. Just 5–20 seconds of shaking can kill,” Dr. Pauzé said. But making the diagnosis can be difficult. A child who has been shaken often presents with nonspecific symptoms, such as poor feeding, vomiting, diarrhea, irritability, and fever. “We therefore must have a high index of suspicion in order to diagnose inflicted head trauma,” he said.

An article published in the Journal of the American Medical Association (1999;281:621–6) is “must reading” for emergency department physicians, he said.

In a chart review, the researchers studied the characteristics of unrecognized AHT in children less than 3 years old. They found that nearly one-third of abused children who presented after AHT had their initial diagnosis missed. The average delay in diagnosis was 7 days.

The most common erroneous diagnoses made were gastroenteritis, influenza, accidental head injury, rule-out sepsis, increasing head size, otitis media, seizure disorder, reflux, and apnea. Misinterpretation of the CT scan or radiograph also caused a delay in diagnosis, which ranged from 1 to 174 days.

On the horizon to help emergency physicians make the right diagnosis in a timely manner are traumatic brain markers. Many organs, including the liver, pancreas, kidney, and heart, have serum biomarkers that act as guides to organ injury. The hope is that a biomarker for brain injury will become a bedside test for AHT in the future.

Until then, a complete and thorough history and physical exam are needed to diagnose AHT, Dr. Pauzé said.

Conflicting histories, delay in seeking medical care, or repetitive injuries should make physicians suspicious. Other red flags include injuries that are not consistent with the history given or with the developmental age of the infant or child.

A head-to-toe physical exam must be done, including checking for macrocephaly and inspecting for scalp, facial, or neck bruises. Examine the ribs and extremities for signs of tenderness or deformity and, if possible, perform a funduscopic exam for retinal hemorrhages.

'We … must have a high index of suspicion in order to diagnose inflicted head trauma.' DR. PAUZÉ

BUENOS AIRES — Glucocorticoid steroids are widely used to treat acute spinal cord injuries, but there is no clear consensus on their use, reported Dr. Keith D.K. Luk at the annual conference of the International Society of Orthopaedic Surgery and Traumatology.

The initial spinal cord injury triggers a complex cascade of molecular and cellular events. Lipid peroxidation of cellular membranes occurs as a secondary effect of spinal cord injuries and results in irreversible damage, said Dr. Luk, chair professor and head of the department of orthopedics and traumatology at the University of Hong Kong.

The National Acute Spinal Cord Injury Study (NASCIS) group conducted the first randomized, multicenter clinical study to examine the efficacy of methylprednisolone for acute spinal cord injury. The prevailing assumption of the benefits of methylprednisolone precluded the inclusion of a placebo group in the study design, as it was considered unethical to deny patients a treatment considered to be the standard of care. Thus, all patients in NASCIS I received methylprednisolone.

NASCIS I, initiated in 1979, compared functional outcome in 330 patients randomized to receive a 10-day regimen of methylprednisolone by intravenous bolus of either a low dosage of 100 mg per day or a high dosage of 1,000 mg per day (JAMA 1984;251:45–52). Outcome was assessed at 6 months and 12 months. Unexpectedly, the results showed no significant differences in neurologic benefit. The higher dose of methylprednisolone was associated with increased risk of infection, with no apparent increase in neurologic benefit.

A second clinical study (NASCIS II) was undertaken in which 162 patients were given a higher dose of methylprednisolone over a shorter period of time, and 171 patients received a placebo (N. Engl. J. Med. 1990;322:1405–11). The methylprednisolone regimen consisted of an intravenous bolus of 30 mg/kg, followed by a 23-hour infusion of methylprednisolone at 5.4 mg/kg per hour. A third treatment group of 154 patients received 24-hour dosing with naloxone, an opiate receptor antagonist.

High-dose methylprednisolone treatment initiated within 8 hours showed significant neurologic benefit, and the functional benefits were sustained at 6 weeks, 6 months, and 1 year. Treatment had to be given within an 8-hour window after the initial injury, before the onset of lipid peroxidation.

Conclusions of NASCIS II were controversial. The study analyses were criticized, particularly regarding the issue of post hoc stratification based on time of treatment (J. Neurosurg. 2000;93[Suppl 1]:1–7).

A third randomized, controlled clinical trial, known as NASCIS III, compared three treatments in 499 patients with acute spinal cord injury (JAMA 1997;277:1597–604). The methylprednisolone regimen in NASCIS II served as the active control. All patients were treated within 8 hours of the initial injury. Before randomization, all patients received an initial intravenous bolus of high-dose methylprednisolone (30 mg/kg). Patients in the methylprednisolone treatment groups then were given methylprednisolone infusion at 5.4 mg/kg per hour for 24 hours (active control group) or for 48 hours. The third treatment group received infusions of tirilazad mesylate over a 48-hour period.

The results showed that all treatment regimens were comparable in patients treated within 3 hours of injury. Those treated within 3 hours who received methylprednisolone for 48 hours had significantly better neurologic recovery, although the 48-hour treatment group experienced more side effects associated with steroid use. Controversy over data analysis in NASCIS II and NASCIS III remains.

A summary statement from the Spine Focus Panel suggested indications for methylprednisolone use in acute nonpenetrating spinal cord injury (Spine 2001;26[Suppl 24]:55). Treatment initiated within 3 hours should follow the methylprednisolone regimen used in NASCIS II (24 hours), and treatment initiated after 3 hours but before 8 hours should follow the high-dose regimen used in NASCIS III (48 hours). Methylprednisolone treatment should not be started after 8 hours, nor is it recommended in acute penetrating spinal cord injury, according to the Spine Focus Panel statement.

The Canadian Association of Emergency Physicians issued a position statement in 2003 declaring that “methylprednisolone for acute spinal cord injury is not a standard of care; it is only a treatment option.”

BUENOS AIRES — Glucocorticoid steroids are widely used to treat acute spinal cord injuries, but there is no clear consensus on their use, reported Dr. Keith D.K. Luk at the annual conference of the International Society of Orthopaedic Surgery and Traumatology.

The initial spinal cord injury triggers a complex cascade of molecular and cellular events. Lipid peroxidation of cellular membranes occurs as a secondary effect of spinal cord injuries and results in irreversible damage, said Dr. Luk, chair professor and head of the department of orthopedics and traumatology at the University of Hong Kong.

The National Acute Spinal Cord Injury Study (NASCIS) group conducted the first randomized, multicenter clinical study to examine the efficacy of methylprednisolone for acute spinal cord injury. The prevailing assumption of the benefits of methylprednisolone precluded the inclusion of a placebo group in the study design, as it was considered unethical to deny patients a treatment considered to be the standard of care. Thus, all patients in NASCIS I received methylprednisolone.

NASCIS I, initiated in 1979, compared functional outcome in 330 patients randomized to receive a 10-day regimen of methylprednisolone by intravenous bolus of either a low dosage of 100 mg per day or a high dosage of 1,000 mg per day (JAMA 1984;251:45–52). Outcome was assessed at 6 months and 12 months. Unexpectedly, the results showed no significant differences in neurologic benefit. The higher dose of methylprednisolone was associated with increased risk of infection, with no apparent increase in neurologic benefit.

A second clinical study (NASCIS II) was undertaken in which 162 patients were given a higher dose of methylprednisolone over a shorter period of time, and 171 patients received a placebo (N. Engl. J. Med. 1990;322:1405–11). The methylprednisolone regimen consisted of an intravenous bolus of 30 mg/kg, followed by a 23-hour infusion of methylprednisolone at 5.4 mg/kg per hour. A third treatment group of 154 patients received 24-hour dosing with naloxone, an opiate receptor antagonist.

High-dose methylprednisolone treatment initiated within 8 hours showed significant neurologic benefit, and the functional benefits were sustained at 6 weeks, 6 months, and 1 year. Treatment had to be given within an 8-hour window after the initial injury, before the onset of lipid peroxidation.

Conclusions of NASCIS II were controversial. The study analyses were criticized, particularly regarding the issue of post hoc stratification based on time of treatment (J. Neurosurg. 2000;93[Suppl 1]:1–7).

A third randomized, controlled clinical trial, known as NASCIS III, compared three treatments in 499 patients with acute spinal cord injury (JAMA 1997;277:1597–604). The methylprednisolone regimen in NASCIS II served as the active control. All patients were treated within 8 hours of the initial injury. Before randomization, all patients received an initial intravenous bolus of high-dose methylprednisolone (30 mg/kg). Patients in the methylprednisolone treatment groups then were given methylprednisolone infusion at 5.4 mg/kg per hour for 24 hours (active control group) or for 48 hours. The third treatment group received infusions of tirilazad mesylate over a 48-hour period.

The results showed that all treatment regimens were comparable in patients treated within 3 hours of injury. Those treated within 3 hours who received methylprednisolone for 48 hours had significantly better neurologic recovery, although the 48-hour treatment group experienced more side effects associated with steroid use. Controversy over data analysis in NASCIS II and NASCIS III remains.

A summary statement from the Spine Focus Panel suggested indications for methylprednisolone use in acute nonpenetrating spinal cord injury (Spine 2001;26[Suppl 24]:55). Treatment initiated within 3 hours should follow the methylprednisolone regimen used in NASCIS II (24 hours), and treatment initiated after 3 hours but before 8 hours should follow the high-dose regimen used in NASCIS III (48 hours). Methylprednisolone treatment should not be started after 8 hours, nor is it recommended in acute penetrating spinal cord injury, according to the Spine Focus Panel statement.

The Canadian Association of Emergency Physicians issued a position statement in 2003 declaring that “methylprednisolone for acute spinal cord injury is not a standard of care; it is only a treatment option.”

BUENOS AIRES — Glucocorticoid steroids are widely used to treat acute spinal cord injuries, but there is no clear consensus on their use, reported Dr. Keith D.K. Luk at the annual conference of the International Society of Orthopaedic Surgery and Traumatology.

The initial spinal cord injury triggers a complex cascade of molecular and cellular events. Lipid peroxidation of cellular membranes occurs as a secondary effect of spinal cord injuries and results in irreversible damage, said Dr. Luk, chair professor and head of the department of orthopedics and traumatology at the University of Hong Kong.

The National Acute Spinal Cord Injury Study (NASCIS) group conducted the first randomized, multicenter clinical study to examine the efficacy of methylprednisolone for acute spinal cord injury. The prevailing assumption of the benefits of methylprednisolone precluded the inclusion of a placebo group in the study design, as it was considered unethical to deny patients a treatment considered to be the standard of care. Thus, all patients in NASCIS I received methylprednisolone.

NASCIS I, initiated in 1979, compared functional outcome in 330 patients randomized to receive a 10-day regimen of methylprednisolone by intravenous bolus of either a low dosage of 100 mg per day or a high dosage of 1,000 mg per day (JAMA 1984;251:45–52). Outcome was assessed at 6 months and 12 months. Unexpectedly, the results showed no significant differences in neurologic benefit. The higher dose of methylprednisolone was associated with increased risk of infection, with no apparent increase in neurologic benefit.

A second clinical study (NASCIS II) was undertaken in which 162 patients were given a higher dose of methylprednisolone over a shorter period of time, and 171 patients received a placebo (N. Engl. J. Med. 1990;322:1405–11). The methylprednisolone regimen consisted of an intravenous bolus of 30 mg/kg, followed by a 23-hour infusion of methylprednisolone at 5.4 mg/kg per hour. A third treatment group of 154 patients received 24-hour dosing with naloxone, an opiate receptor antagonist.

High-dose methylprednisolone treatment initiated within 8 hours showed significant neurologic benefit, and the functional benefits were sustained at 6 weeks, 6 months, and 1 year. Treatment had to be given within an 8-hour window after the initial injury, before the onset of lipid peroxidation.

Conclusions of NASCIS II were controversial. The study analyses were criticized, particularly regarding the issue of post hoc stratification based on time of treatment (J. Neurosurg. 2000;93[Suppl 1]:1–7).

A third randomized, controlled clinical trial, known as NASCIS III, compared three treatments in 499 patients with acute spinal cord injury (JAMA 1997;277:1597–604). The methylprednisolone regimen in NASCIS II served as the active control. All patients were treated within 8 hours of the initial injury. Before randomization, all patients received an initial intravenous bolus of high-dose methylprednisolone (30 mg/kg). Patients in the methylprednisolone treatment groups then were given methylprednisolone infusion at 5.4 mg/kg per hour for 24 hours (active control group) or for 48 hours. The third treatment group received infusions of tirilazad mesylate over a 48-hour period.

The results showed that all treatment regimens were comparable in patients treated within 3 hours of injury. Those treated within 3 hours who received methylprednisolone for 48 hours had significantly better neurologic recovery, although the 48-hour treatment group experienced more side effects associated with steroid use. Controversy over data analysis in NASCIS II and NASCIS III remains.

A summary statement from the Spine Focus Panel suggested indications for methylprednisolone use in acute nonpenetrating spinal cord injury (Spine 2001;26[Suppl 24]:55). Treatment initiated within 3 hours should follow the methylprednisolone regimen used in NASCIS II (24 hours), and treatment initiated after 3 hours but before 8 hours should follow the high-dose regimen used in NASCIS III (48 hours). Methylprednisolone treatment should not be started after 8 hours, nor is it recommended in acute penetrating spinal cord injury, according to the Spine Focus Panel statement.

The Canadian Association of Emergency Physicians issued a position statement in 2003 declaring that “methylprednisolone for acute spinal cord injury is not a standard of care; it is only a treatment option.”

BOSTON — Long-term outcomes of hand transplant patients show that recipients can have good graft functionality and quality of life if they comply with immunosuppressive regimens, according to speakers at the 2006 World Transplant Congress.

Worldwide experience with hand transplants now includes 24 hands in 18 patients with “excellent results,” said Dr. Suzanne T. Ildstad, director of the Institute for Cellular Therapeutics at the University of Louisville (Ky.).

Patients are reluctant to undertake a hand transplant “until we modify or reduce the intensity of immunosuppression,” said Dr. Ildstad. “There are discussions right now with our group and other groups of using steroid-sparing protocols as well as attempts to induce tolerance,” she noted.

Dr. Ildstad presented the 7-year results of a 37-year-old, left-hand-dominant man (patient No. 1, currently the recipient of the longest-surviving hand transplant in the world) and the 4-year results of a 36-year-old, right-hand-dominant man (patient No. 2). Both men lost their left hands in fireworks accidents.

On measurements with the United Kingdom Medical Research Council strength scale, patient No. 1 had an excellent return of function of intrinsic muscles whereas patient No. 2 had an improved, but somewhat delayed, return of function because of a period of noncompliance with his immunosuppressive regimen.

Sensation gradually improved in patient No. 1 to the point where it has become “essentially normal” after 7 years of follow-up, Dr. Ildstad said. Patient No. 2 also experienced gradual improvement in sensation, but it was slightly delayed in comparison with patient No. 1.

In skin biopsy specimens from both patients, low-grade cellular infiltrates have been detected. The patients did not have rejections treated unless they were severe, she said.

When patient No. 2 decided to stop taking his immunosuppressive medications, he subsequently had a grade 3 rejection episode that was “relatively readily reversed” with antithymocyte globulins (Thymoglobulin), increased doses of tacrolimus (Prograf), and corticosteroid boluses, which is contrary to what Dr. Ildstad and many transplant immunologists would have predicted because of the presumed antigenicity of the skin.

In a study of two men who received bilateral hand transplants, improvement in function was accompanied by changes in brain function and good quality of life, reported Dr. Palmina Petruzzo of the department of transplantation at Hôpital Edouard Herriot, Lyon, France.

Functional MRI shows that the patients' representation of their hands in their brains progressively shifted from lateral to medial regions of the motor cortex.

By 2 years following transplantation, hand motor coordination had improved in both patients to the point where they could perform complex movements involving intersegmental coordination, which were assessed while the patients wore a CyberGlove containing 22 sensors that monitor hand movement, according to Dr. Ildstad.

A recipient of a transplant of a left hand demonstrated his manual dexterity and control by tying his shoe at his 4-year checkup. Courtesy Jewish Hospital/Kleinert, Kutz and Associates Hand Care Center/University of Louisville

BOSTON — Long-term outcomes of hand transplant patients show that recipients can have good graft functionality and quality of life if they comply with immunosuppressive regimens, according to speakers at the 2006 World Transplant Congress.

Worldwide experience with hand transplants now includes 24 hands in 18 patients with “excellent results,” said Dr. Suzanne T. Ildstad, director of the Institute for Cellular Therapeutics at the University of Louisville (Ky.).

Patients are reluctant to undertake a hand transplant “until we modify or reduce the intensity of immunosuppression,” said Dr. Ildstad. “There are discussions right now with our group and other groups of using steroid-sparing protocols as well as attempts to induce tolerance,” she noted.

Dr. Ildstad presented the 7-year results of a 37-year-old, left-hand-dominant man (patient No. 1, currently the recipient of the longest-surviving hand transplant in the world) and the 4-year results of a 36-year-old, right-hand-dominant man (patient No. 2). Both men lost their left hands in fireworks accidents.

On measurements with the United Kingdom Medical Research Council strength scale, patient No. 1 had an excellent return of function of intrinsic muscles whereas patient No. 2 had an improved, but somewhat delayed, return of function because of a period of noncompliance with his immunosuppressive regimen.

Sensation gradually improved in patient No. 1 to the point where it has become “essentially normal” after 7 years of follow-up, Dr. Ildstad said. Patient No. 2 also experienced gradual improvement in sensation, but it was slightly delayed in comparison with patient No. 1.

In skin biopsy specimens from both patients, low-grade cellular infiltrates have been detected. The patients did not have rejections treated unless they were severe, she said.

When patient No. 2 decided to stop taking his immunosuppressive medications, he subsequently had a grade 3 rejection episode that was “relatively readily reversed” with antithymocyte globulins (Thymoglobulin), increased doses of tacrolimus (Prograf), and corticosteroid boluses, which is contrary to what Dr. Ildstad and many transplant immunologists would have predicted because of the presumed antigenicity of the skin.

In a study of two men who received bilateral hand transplants, improvement in function was accompanied by changes in brain function and good quality of life, reported Dr. Palmina Petruzzo of the department of transplantation at Hôpital Edouard Herriot, Lyon, France.

Functional MRI shows that the patients' representation of their hands in their brains progressively shifted from lateral to medial regions of the motor cortex.

By 2 years following transplantation, hand motor coordination had improved in both patients to the point where they could perform complex movements involving intersegmental coordination, which were assessed while the patients wore a CyberGlove containing 22 sensors that monitor hand movement, according to Dr. Ildstad.

A recipient of a transplant of a left hand demonstrated his manual dexterity and control by tying his shoe at his 4-year checkup. Courtesy Jewish Hospital/Kleinert, Kutz and Associates Hand Care Center/University of Louisville

BOSTON — Long-term outcomes of hand transplant patients show that recipients can have good graft functionality and quality of life if they comply with immunosuppressive regimens, according to speakers at the 2006 World Transplant Congress.

Worldwide experience with hand transplants now includes 24 hands in 18 patients with “excellent results,” said Dr. Suzanne T. Ildstad, director of the Institute for Cellular Therapeutics at the University of Louisville (Ky.).

Patients are reluctant to undertake a hand transplant “until we modify or reduce the intensity of immunosuppression,” said Dr. Ildstad. “There are discussions right now with our group and other groups of using steroid-sparing protocols as well as attempts to induce tolerance,” she noted.

Dr. Ildstad presented the 7-year results of a 37-year-old, left-hand-dominant man (patient No. 1, currently the recipient of the longest-surviving hand transplant in the world) and the 4-year results of a 36-year-old, right-hand-dominant man (patient No. 2). Both men lost their left hands in fireworks accidents.

On measurements with the United Kingdom Medical Research Council strength scale, patient No. 1 had an excellent return of function of intrinsic muscles whereas patient No. 2 had an improved, but somewhat delayed, return of function because of a period of noncompliance with his immunosuppressive regimen.

Sensation gradually improved in patient No. 1 to the point where it has become “essentially normal” after 7 years of follow-up, Dr. Ildstad said. Patient No. 2 also experienced gradual improvement in sensation, but it was slightly delayed in comparison with patient No. 1.

In skin biopsy specimens from both patients, low-grade cellular infiltrates have been detected. The patients did not have rejections treated unless they were severe, she said.

When patient No. 2 decided to stop taking his immunosuppressive medications, he subsequently had a grade 3 rejection episode that was “relatively readily reversed” with antithymocyte globulins (Thymoglobulin), increased doses of tacrolimus (Prograf), and corticosteroid boluses, which is contrary to what Dr. Ildstad and many transplant immunologists would have predicted because of the presumed antigenicity of the skin.

In a study of two men who received bilateral hand transplants, improvement in function was accompanied by changes in brain function and good quality of life, reported Dr. Palmina Petruzzo of the department of transplantation at Hôpital Edouard Herriot, Lyon, France.

Functional MRI shows that the patients' representation of their hands in their brains progressively shifted from lateral to medial regions of the motor cortex.

By 2 years following transplantation, hand motor coordination had improved in both patients to the point where they could perform complex movements involving intersegmental coordination, which were assessed while the patients wore a CyberGlove containing 22 sensors that monitor hand movement, according to Dr. Ildstad.

A recipient of a transplant of a left hand demonstrated his manual dexterity and control by tying his shoe at his 4-year checkup. Courtesy Jewish Hospital/Kleinert, Kutz and Associates Hand Care Center/University of Louisville

HALIFAX, N.S. — Emergency physicians don't miss many clinically significant findings on computerized axial tomography scans of the head.

Neuroradiologists agreed with the CT interpretations made by emergency department physicians almost all of the time, Dr. Abdullah Al-Reesi reported in a poster presented at the 11th International Conference on Emergency Medicine.

Dr. Al-Reesi, of the University of Ottawa, reviewed 442 consecutive CT head scans done in an emergency department over a 5-month period, comparing the interpretations done by both groups of physicians.

Indications for CT were head injury, headache, seizure, confusion, decreased consciousness, cerebrovascular accident, transient ischemic attack, and dizziness.

ED physicians missed three clinically significant lesions: two nontraumatic and one traumatic subarachnoid hemorrhages. They also missed six clinically nonsignificant findings, which included one small (less than 5 mm) cerebral contusion, three cases of fluid in the sinuses, one small lacunar infarct, and one patchy hypodensity later identified as a multiple sclerosis lesion. A patient with an intraventricular hemorrhage was discharged home. Once the error was recognized, he was referred for emergency neurosurgical consult.

HALIFAX, N.S. — Emergency physicians don't miss many clinically significant findings on computerized axial tomography scans of the head.

Neuroradiologists agreed with the CT interpretations made by emergency department physicians almost all of the time, Dr. Abdullah Al-Reesi reported in a poster presented at the 11th International Conference on Emergency Medicine.

Dr. Al-Reesi, of the University of Ottawa, reviewed 442 consecutive CT head scans done in an emergency department over a 5-month period, comparing the interpretations done by both groups of physicians.

Indications for CT were head injury, headache, seizure, confusion, decreased consciousness, cerebrovascular accident, transient ischemic attack, and dizziness.

ED physicians missed three clinically significant lesions: two nontraumatic and one traumatic subarachnoid hemorrhages. They also missed six clinically nonsignificant findings, which included one small (less than 5 mm) cerebral contusion, three cases of fluid in the sinuses, one small lacunar infarct, and one patchy hypodensity later identified as a multiple sclerosis lesion. A patient with an intraventricular hemorrhage was discharged home. Once the error was recognized, he was referred for emergency neurosurgical consult.

HALIFAX, N.S. — Emergency physicians don't miss many clinically significant findings on computerized axial tomography scans of the head.

Neuroradiologists agreed with the CT interpretations made by emergency department physicians almost all of the time, Dr. Abdullah Al-Reesi reported in a poster presented at the 11th International Conference on Emergency Medicine.

Dr. Al-Reesi, of the University of Ottawa, reviewed 442 consecutive CT head scans done in an emergency department over a 5-month period, comparing the interpretations done by both groups of physicians.

Indications for CT were head injury, headache, seizure, confusion, decreased consciousness, cerebrovascular accident, transient ischemic attack, and dizziness.

ED physicians missed three clinically significant lesions: two nontraumatic and one traumatic subarachnoid hemorrhages. They also missed six clinically nonsignificant findings, which included one small (less than 5 mm) cerebral contusion, three cases of fluid in the sinuses, one small lacunar infarct, and one patchy hypodensity later identified as a multiple sclerosis lesion. A patient with an intraventricular hemorrhage was discharged home. Once the error was recognized, he was referred for emergency neurosurgical consult.

The use of 64-slice multidetector computed tomography (64-MDCT) offers a number of advantages in the evaluation of head and neck trauma in the emergency department—as in the case of the 37-year-old woman imaged above—according to Dr. Osamu Sakai, director of head and neck imaging at Boston Medical Center where 64-MDCT is used in the level I trauma center.

Several images can be acquired simultaneously with 64-MDCT, allowing for faster scans in trauma cases and resulting in earlier therapy and reduced mortality. In addition, 64-MDCT reduces motion artifacts, sharpening multiplanar images and 3D reconstructions.

Thinner slices can be achieved with 64-MDCT, meaning that voxels approach the same size in all dimensions (isotropy). Isotropic voxels allow cross-sectional images to be reconstructed in arbitrary planes, allowing physicians to choose the best views. In addition, spatial resolution with 64-MDCT is in the submillimeter range. Increased resolution decreases partial volume effect caused by having more than one tissue type within the voxel. Partial volume effect results in voxels with average radiodensities of all of the tissue types present in the voxel and may thus be hard to interpret.

For CT angiography (CTA), 64-MDCT's faster scans result in less venous contamination, the superimposition of venous structures on the image that can occur when scanning times are slower because contrast material has time to reach the veins. While scan delay time after intravenous contrast injection is unchanged, the total dose of contrast may be reduced. Requests for CTA have increased dramatically since the introduction of 64-MDCT, according to Dr. Sakai, also of Boston University. CTA using 64-MDCT is now a first-line study for patients with suspected vascular injury and subarachnoid hemorrhage because faster scan times reduce artifacts, such as venous contamination.

The woman imaged above was ejected from her vehicle as the result of a collision, resulting in multiple skull base fractures. Volume-rendering CTA demonstrates an intact circle of Willis (images g and h). Volume-rendering CT venography reveals thrombosed distal right transverse and sigmoid sinuses and jugular bulb/vein (left image).

“Almost all stable patients with penetrating injuries, fractures of skull base and cervical spine, or other clinically suspected vascular injuries undergo CTA with 64-MDCT at our institution,” wrote Dr. Sakai and his colleagues in a poster presented at the 2006 annual meeting of the American Society of Neuroradiology.

Finally, 64-MDCT can “unfuse” or retrospectively produce thinner axial images provided there are sufficient raw data. Abnormalities that aren't picked up on routine 5-mm sections can pop out when reviewed at 1.25-mm or 0.625-mm thickness and spacing, providing additional information to physicians and can be crucial when trauma is not clinically suspected, according to Dr. Sakai.

The use of 64-slice multidetector computed tomography (64-MDCT) offers a number of advantages in the evaluation of head and neck trauma in the emergency department—as in the case of the 37-year-old woman imaged above—according to Dr. Osamu Sakai, director of head and neck imaging at Boston Medical Center where 64-MDCT is used in the level I trauma center.

Several images can be acquired simultaneously with 64-MDCT, allowing for faster scans in trauma cases and resulting in earlier therapy and reduced mortality. In addition, 64-MDCT reduces motion artifacts, sharpening multiplanar images and 3D reconstructions.

Thinner slices can be achieved with 64-MDCT, meaning that voxels approach the same size in all dimensions (isotropy). Isotropic voxels allow cross-sectional images to be reconstructed in arbitrary planes, allowing physicians to choose the best views. In addition, spatial resolution with 64-MDCT is in the submillimeter range. Increased resolution decreases partial volume effect caused by having more than one tissue type within the voxel. Partial volume effect results in voxels with average radiodensities of all of the tissue types present in the voxel and may thus be hard to interpret.

For CT angiography (CTA), 64-MDCT's faster scans result in less venous contamination, the superimposition of venous structures on the image that can occur when scanning times are slower because contrast material has time to reach the veins. While scan delay time after intravenous contrast injection is unchanged, the total dose of contrast may be reduced. Requests for CTA have increased dramatically since the introduction of 64-MDCT, according to Dr. Sakai, also of Boston University. CTA using 64-MDCT is now a first-line study for patients with suspected vascular injury and subarachnoid hemorrhage because faster scan times reduce artifacts, such as venous contamination.

The woman imaged above was ejected from her vehicle as the result of a collision, resulting in multiple skull base fractures. Volume-rendering CTA demonstrates an intact circle of Willis (images g and h). Volume-rendering CT venography reveals thrombosed distal right transverse and sigmoid sinuses and jugular bulb/vein (left image).

“Almost all stable patients with penetrating injuries, fractures of skull base and cervical spine, or other clinically suspected vascular injuries undergo CTA with 64-MDCT at our institution,” wrote Dr. Sakai and his colleagues in a poster presented at the 2006 annual meeting of the American Society of Neuroradiology.

Finally, 64-MDCT can “unfuse” or retrospectively produce thinner axial images provided there are sufficient raw data. Abnormalities that aren't picked up on routine 5-mm sections can pop out when reviewed at 1.25-mm or 0.625-mm thickness and spacing, providing additional information to physicians and can be crucial when trauma is not clinically suspected, according to Dr. Sakai.

The use of 64-slice multidetector computed tomography (64-MDCT) offers a number of advantages in the evaluation of head and neck trauma in the emergency department—as in the case of the 37-year-old woman imaged above—according to Dr. Osamu Sakai, director of head and neck imaging at Boston Medical Center where 64-MDCT is used in the level I trauma center.

Several images can be acquired simultaneously with 64-MDCT, allowing for faster scans in trauma cases and resulting in earlier therapy and reduced mortality. In addition, 64-MDCT reduces motion artifacts, sharpening multiplanar images and 3D reconstructions.

Thinner slices can be achieved with 64-MDCT, meaning that voxels approach the same size in all dimensions (isotropy). Isotropic voxels allow cross-sectional images to be reconstructed in arbitrary planes, allowing physicians to choose the best views. In addition, spatial resolution with 64-MDCT is in the submillimeter range. Increased resolution decreases partial volume effect caused by having more than one tissue type within the voxel. Partial volume effect results in voxels with average radiodensities of all of the tissue types present in the voxel and may thus be hard to interpret.

For CT angiography (CTA), 64-MDCT's faster scans result in less venous contamination, the superimposition of venous structures on the image that can occur when scanning times are slower because contrast material has time to reach the veins. While scan delay time after intravenous contrast injection is unchanged, the total dose of contrast may be reduced. Requests for CTA have increased dramatically since the introduction of 64-MDCT, according to Dr. Sakai, also of Boston University. CTA using 64-MDCT is now a first-line study for patients with suspected vascular injury and subarachnoid hemorrhage because faster scan times reduce artifacts, such as venous contamination.

The woman imaged above was ejected from her vehicle as the result of a collision, resulting in multiple skull base fractures. Volume-rendering CTA demonstrates an intact circle of Willis (images g and h). Volume-rendering CT venography reveals thrombosed distal right transverse and sigmoid sinuses and jugular bulb/vein (left image).

“Almost all stable patients with penetrating injuries, fractures of skull base and cervical spine, or other clinically suspected vascular injuries undergo CTA with 64-MDCT at our institution,” wrote Dr. Sakai and his colleagues in a poster presented at the 2006 annual meeting of the American Society of Neuroradiology.

Finally, 64-MDCT can “unfuse” or retrospectively produce thinner axial images provided there are sufficient raw data. Abnormalities that aren't picked up on routine 5-mm sections can pop out when reviewed at 1.25-mm or 0.625-mm thickness and spacing, providing additional information to physicians and can be crucial when trauma is not clinically suspected, according to Dr. Sakai.