1343
and other intensive-care regimens, apart from the use of CHF, with which we at least double survival time. This protocol therefore increases the chance of spontaneous recovery and helps to correctly whether liver transplantation is needed. CHF should be seriously considered in intensive care of fulminant hepatitis. FFP for plasma exchange, and filters for plasma exchange and CHF are, however, very expensive. Our protocol costs about 500 000 Japanese Yen ([2000) per day and cannot be continued
judge
indefinitely. Blood Transfusion Service,
Kyushu University Hospital, 3-1-1, Maidashi, Higashi-ku,
Fukuoka 812, Japan, Emergency Service, Kyushu University Hospital, First Department of Internal Medicine, Kyushu University, and Internal Medicine,
Fujigaoka Hospital, Yokohama
SHOICHI INABA TOSHISUKE KISHIKAWA AKINORI ZAITSU HIROMI ISHIBASHI JIRO KUDO RYUJI OGAWA MAKOTO YOSHIBA
1. Opolon P. Significance of middle molecules in the pathogenesis of hepatic encephalopathy. In: Kleinberger G, Ferenci P, Riederer P, Thuler H, eds. Advances in hepatic encephalopathy and urea cycle diseases Basel. Karger, 1984. 310-14. 2. Yoshiba M, Yamada
hepatic
coma
H, Yoshikawa Y, et al. Hemodiafiltration treatment of deep by protein passing membrane. case report. Artif Organs 1986; 10:
417-19. 3.
Chapman RW, Forman D, Peto R, Smallwood hepatic failure? Lancet 1990; 335: 32-35.
Neck
R. Liver
transplantation for
acute
injuries
SIR,-Your timely editorial (Sept 21, p 728) on neck injury brings some sanity into the whiplash controversy; too often patients are consigned to the abnormal illness behaviour category. Many doctors refuse to accept, in the absence of radiographic signs, that unhealed soft tissue injuries can cause chronic pain. Evidence is accumulating that soft tissue damage in cervical motion segments is common after neck trauma." This damage is not visible on radiography and disc injuries do not heal in two months, as is traditionally expected, because these injuries are in avascular tissues. Jonsson et aP examined 22 cervical spines from victims of road traffic accidents and found injuries in all spines, with over 200 lesions, most of which were not visible on plain radiographs. In our series of 43 deaths in trauma patients cervical spines were frozen at 70°C and sectioned in 2 mm thick sagittal slices, and almost all showed signs of injury-disc injuries in 96% and soft tissue injuries of the facet joints in 72%. Only 28% had fractures, some of which were not visible on radiographs.4 In a much larger survey of 385 -
in this motion segments were much more common than fractures of the cervical vertebrae. This cervical pattern differs from thoracolumbar injuries in which the more vertical facet orientation gives the discs greater mechanical protection from shearing forces. Osti et al5 showed in sheep that small transverse incised disc lesions close to the vertebral end-plate do not heal in 18 months, except in the outer vascular part of the anterior annulus. In magnetic resonance imaging (MRI) studies of patients with extension injuries to the neck, Davies et al6 also showed that disc tears and avulsions heal slowly. We report features of two young adult male survivors of neck injury who later died and in whom we could relate necropsy findings to clinical records. Both show a good correlation between the sites of disc injuries and the segmental distribution of pain. A 30-year-old man had an extension injury after a rear-end car accident and died 14 months later. He had had chronic right arm and shoulder pain after the injury up to the time of death. Transverse clefts were found in four discs (C4-5 to C7-Tl), adjacent to the anterior vertebral rims, all on the right side of the midline. These clefts were similar in appearance and site to the cleft consistently found in the discs of victims of trauma (figure) and their position differed from that of age-related fissures. The patient’s limb and shoulder pain had consistently been at the C5 to Tl level on the right side. In two discs there was also calcification of the injured anterior annulus, adjacent to the clefts. This change was not present initially but appeared in radiographs obtained between 7 and 14 months after injury. A 43-year-old man died 3-5 years after an extension injury to the neck, having had chronic severe pain in the neck and upper back with tingling and weakness in both arms. Examination in the months after injury showed tenderness which was greatest at the C4-5 disc; there was some sensory loss in the C6 dermatomes on both sides with decreased power in muscle groups of both upper limbs supplied by C5, 6, and 7; reflexes and muscle tone were normal. He had paraesthesia in the arms and hands, which was brought on by extension of his neck. On lumbar puncture he was thought to have a block to cerebrospinal fluid circulation when the neck was extended; traction improved his symptoms. He had no radiologically evident neck pathology, other than slight narrowing of the C4-5 disc space; an orthopaedic surgeon stated that there was "a very strong functional element in his symptoms". Findings at
spines from trauma patients, examined at necropsy department, injuries to the soft tissues of the cervical
were partial fusion across the posterior C4-5 disc space, and vascularisation of the upper part of the C5-6 disc, with an old posterior disc prolapse. The C5-6 disc had no abnormalities on radiography. There was cord damage in the form of demyelination and gliosis of the left lateral column with overlying dural fibrous thickening. It seems likely in hindsight that he had traumatic posterior prolapses of the C5-6 disc and possibly of the C4-5 disc. Traumatic disc prolapse was common in extension injuries, in both the MRI study of Davis et al6 and in our necropsy study.2 It is unreasonable to assume that chronic pain in such cases has a psychosomatic basis. Clefts in trauma patients persist for a year or more in the innervated parts of the anterior annulus, with adjacent scarring and possible calcification. Other injured parts of the disc, which have no innervation to start with, may acquire it by vascular and neural ingrowth into disc clefts.The accelerated degenerative change in the whole injured motion segment may also give rise to recurrent mechanical pain, which can sometimes be eliminated by a disc or facet block.
necropsy
Department of Neuropathology, Royal Perth Hospital, Perth, Western Australia
J. R. TAYLOR B. A. KAKULAS
JR, Twomey LT. Disc injuries in cervical trauma. Lancet 1990; 336: 1318. JR, Twomey LT Acute injuries to cervical joints an autopsy study of neck sprain. Spine (in press). 3. Jonsson H, Bring G, Rauchning W, Sahlstedt B. Hidden cervical spine injuries in traffic accident victims with skull fractures. J Spinal Disorders 1991; 4: 251-63. 4. Taylor JR. "Whiplash": the cause and the lesion. 1991 proceedings of the Australian Association of Musculo-skeletal Medicine, pl. 5 Osti OL, Vemon-Roberts B, Fraser RD. Annulus tears and invertebral disc degeneration. an experimental study using an animal model. Spine 1990; 15: 1. Taylor 2. Taylor
Sagittal section (100 pm) near midline of C6-7 disc from a 32-year-old man who died from head injuries after a car accident. Small transverse cleft containing blood (short arrow) at attachment of anterior annulus to vertebral rim and disc prolapse (long arrow) through the posterior annulus are seen. Anterior and posterior longitudinal
ligaments are not avulsed
762-67. SJ, Teresi
LM, Bradley WG, et al. Cervical spine hyperextension injuries: MR findings. Radiology 1991; 180: 245-51.
6. Davis
and other intensive-care regimens, apart from the use of CHF, with which we at least double survival time. This protocol therefore increases the chance of spontaneous recovery and helps to correctly whether liver transplantation is needed. CHF should be seriously considered in intensive care of fulminant hepatitis. FFP for plasma exchange, and filters for plasma exchange and CHF are, however, very expensive. Our protocol costs about 500 000 Japanese Yen ([2000) per day and cannot be continued
judge
indefinitely. Blood Transfusion Service,
Kyushu University Hospital, 3-1-1, Maidashi, Higashi-ku,
Fukuoka 812, Japan, Emergency Service, Kyushu University Hospital, First Department of Internal Medicine, Kyushu University, and Internal Medicine,
Fujigaoka Hospital, Yokohama
SHOICHI INABA TOSHISUKE KISHIKAWA AKINORI ZAITSU HIROMI ISHIBASHI JIRO KUDO RYUJI OGAWA MAKOTO YOSHIBA
1. Opolon P. Significance of middle molecules in the pathogenesis of hepatic encephalopathy. In: Kleinberger G, Ferenci P, Riederer P, Thuler H, eds. Advances in hepatic encephalopathy and urea cycle diseases Basel. Karger, 1984. 310-14. 2. Yoshiba M, Yamada
hepatic
coma
H, Yoshikawa Y, et al. Hemodiafiltration treatment of deep by protein passing membrane. case report. Artif Organs 1986; 10:
417-19. 3.
Chapman RW, Forman D, Peto R, Smallwood hepatic failure? Lancet 1990; 335: 32-35.
Neck
R. Liver
transplantation for
acute
injuries
SIR,-Your timely editorial (Sept 21, p 728) on neck injury brings some sanity into the whiplash controversy; too often patients are consigned to the abnormal illness behaviour category. Many doctors refuse to accept, in the absence of radiographic signs, that unhealed soft tissue injuries can cause chronic pain. Evidence is accumulating that soft tissue damage in cervical motion segments is common after neck trauma." This damage is not visible on radiography and disc injuries do not heal in two months, as is traditionally expected, because these injuries are in avascular tissues. Jonsson et aP examined 22 cervical spines from victims of road traffic accidents and found injuries in all spines, with over 200 lesions, most of which were not visible on plain radiographs. In our series of 43 deaths in trauma patients cervical spines were frozen at 70°C and sectioned in 2 mm thick sagittal slices, and almost all showed signs of injury-disc injuries in 96% and soft tissue injuries of the facet joints in 72%. Only 28% had fractures, some of which were not visible on radiographs.4 In a much larger survey of 385 -
in this motion segments were much more common than fractures of the cervical vertebrae. This cervical pattern differs from thoracolumbar injuries in which the more vertical facet orientation gives the discs greater mechanical protection from shearing forces. Osti et al5 showed in sheep that small transverse incised disc lesions close to the vertebral end-plate do not heal in 18 months, except in the outer vascular part of the anterior annulus. In magnetic resonance imaging (MRI) studies of patients with extension injuries to the neck, Davies et al6 also showed that disc tears and avulsions heal slowly. We report features of two young adult male survivors of neck injury who later died and in whom we could relate necropsy findings to clinical records. Both show a good correlation between the sites of disc injuries and the segmental distribution of pain. A 30-year-old man had an extension injury after a rear-end car accident and died 14 months later. He had had chronic right arm and shoulder pain after the injury up to the time of death. Transverse clefts were found in four discs (C4-5 to C7-Tl), adjacent to the anterior vertebral rims, all on the right side of the midline. These clefts were similar in appearance and site to the cleft consistently found in the discs of victims of trauma (figure) and their position differed from that of age-related fissures. The patient’s limb and shoulder pain had consistently been at the C5 to Tl level on the right side. In two discs there was also calcification of the injured anterior annulus, adjacent to the clefts. This change was not present initially but appeared in radiographs obtained between 7 and 14 months after injury. A 43-year-old man died 3-5 years after an extension injury to the neck, having had chronic severe pain in the neck and upper back with tingling and weakness in both arms. Examination in the months after injury showed tenderness which was greatest at the C4-5 disc; there was some sensory loss in the C6 dermatomes on both sides with decreased power in muscle groups of both upper limbs supplied by C5, 6, and 7; reflexes and muscle tone were normal. He had paraesthesia in the arms and hands, which was brought on by extension of his neck. On lumbar puncture he was thought to have a block to cerebrospinal fluid circulation when the neck was extended; traction improved his symptoms. He had no radiologically evident neck pathology, other than slight narrowing of the C4-5 disc space; an orthopaedic surgeon stated that there was "a very strong functional element in his symptoms". Findings at
spines from trauma patients, examined at necropsy department, injuries to the soft tissues of the cervical
were partial fusion across the posterior C4-5 disc space, and vascularisation of the upper part of the C5-6 disc, with an old posterior disc prolapse. The C5-6 disc had no abnormalities on radiography. There was cord damage in the form of demyelination and gliosis of the left lateral column with overlying dural fibrous thickening. It seems likely in hindsight that he had traumatic posterior prolapses of the C5-6 disc and possibly of the C4-5 disc. Traumatic disc prolapse was common in extension injuries, in both the MRI study of Davis et al6 and in our necropsy study.2 It is unreasonable to assume that chronic pain in such cases has a psychosomatic basis. Clefts in trauma patients persist for a year or more in the innervated parts of the anterior annulus, with adjacent scarring and possible calcification. Other injured parts of the disc, which have no innervation to start with, may acquire it by vascular and neural ingrowth into disc clefts.The accelerated degenerative change in the whole injured motion segment may also give rise to recurrent mechanical pain, which can sometimes be eliminated by a disc or facet block.
necropsy
Department of Neuropathology, Royal Perth Hospital, Perth, Western Australia
J. R. TAYLOR B. A. KAKULAS
JR, Twomey LT. Disc injuries in cervical trauma. Lancet 1990; 336: 1318. JR, Twomey LT Acute injuries to cervical joints an autopsy study of neck sprain. Spine (in press). 3. Jonsson H, Bring G, Rauchning W, Sahlstedt B. Hidden cervical spine injuries in traffic accident victims with skull fractures. J Spinal Disorders 1991; 4: 251-63. 4. Taylor JR. "Whiplash": the cause and the lesion. 1991 proceedings of the Australian Association of Musculo-skeletal Medicine, pl. 5 Osti OL, Vemon-Roberts B, Fraser RD. Annulus tears and invertebral disc degeneration. an experimental study using an animal model. Spine 1990; 15: 1. Taylor 2. Taylor
Sagittal section (100 pm) near midline of C6-7 disc from a 32-year-old man who died from head injuries after a car accident. Small transverse cleft containing blood (short arrow) at attachment of anterior annulus to vertebral rim and disc prolapse (long arrow) through the posterior annulus are seen. Anterior and posterior longitudinal
ligaments are not avulsed
762-67. SJ, Teresi
LM, Bradley WG, et al. Cervical spine hyperextension injuries: MR findings. Radiology 1991; 180: 245-51.
6. Davis
