1145
7. Kreusser KL, Schmidt RE, Shackleford GD, Volpe JJ. Value of ultrasound for identification of acute hemorrhagic necrosis of thalamus and basal ganglia in an asphyxiated term infant. Ann Neurol 1984: 16: 361-63. 8. Voit T, Lemburg P. Damage of thalamus and basal ganglia in asphyxiated full-term neonates. Neuropediatrics 1987; 18: 176-181. 9. Cabanas F, Pellicer A. Perez-Higueras A, Garica-Alix A, Roche C, Quero J. Ultrasonographic findings in thalamus and basal ganglia in term asphyxiated infants. Pediatric Neurology 1991; 7: 211-15. 10. DiMario FJ, Clancy R. Symmetrical thalamic degeneration with calcifications of infancy. Am J Dis Child 1989; 143: 1056-60. 11. Shen EY, Lin JCT, Shih CC. Pathological echogenicity of the thalamus in newborn and young infants. J Formosan Med Assoc 1988; 87: 891-97. 12. Steinlin M, Dirr R, Martin E, et al. MRI following severe perinatal asphyxia: preliminary experience. Pediatr Neurol 1991; 7: 164-70. 13. Pasternak JF, Predey TA, Mikhael MA. Neonatal asphyxia: vulnerability of basal ganglia, thalamus and brainstem. Pediatr Neurol 1991; 7: 147-49. 14. Babcock DS, Ball W. Postasphyxial encephalopathy in full-term infants: ultrasound diagnosis. Radiology 1983; 148: 417-23. 15. Shewmon DA, Fine M, Masdeu JC, Palacios E. Postischemic hypervascularity of infancy: a stage in the evolution of ischemic brain damage with characteristic CT scan. Ann Neurol 1981; 9: 358-65. 16. Levene MI, Williams JL, Fawer C-L. Ultrasound of the infant brain. Oxford: Blackwell, 1985. 17. Volpe JJ. Neurology of the newborn. 2nd ed. Philadelphia: WB Saunders, 1987. 18. Trounce JQ, Dodd KL, Fawer C-L, Fielder AR, Punt J, Levene MI. Primary thalamic haemorrhage in the newborn: a new clinical entity. Lancet 1985; i: 190-92. 19. Adams C, Hochhauser L, Logan WJ. Primary thalamic and caudate hemorrhage in term neonates presenting with seizures. Pediatr Neurol
1988; 4: 175-77. 20. Roland EH, Flodmark O, Hill A. Thalamic hemorrhage with intraventricular hemorrhage in the full-term newborn. Pediatrics 1990; 85: 737-42. 21. Teele RL, Hernanz-Schulman M, Sotrel A. Echogenic vasculature in the basal ganglia of neonates: a sonographic sign of vasculopathy. Radiology 1988; 169: 423-27. 22. Hughes P, Weinberger E, Shaw DWW. Linear areas of echogenicity in the thalami and basal ganglia of neonates: an expanded association.
Radiology 1991; 179: 103-05. 23. Abuelo DN, Barsel-Bowers G, Tutschka BG, Ambler M, Singer DB. Symmetrical infantile thalamic degeneration in two sibs. J Med Genet 1981; 18: 448-50. 24. Aicardi J, Goutieres F. A progressive familial encephalopathy in infancy with calcifications of the basal ganglia and chronic cerebrospinal fluid lymphocytosis. Ann Neurol 1984; 15: 49-54. 25. Mehta L, Trounce JQ, Moore JR, Young ID. Familial calcification of the basal ganglia with cerebrospinal fluid pleocytosis. J Med Genet 1986; 23: 157-60.
Endoprostheses for bony metastases
Bony metastases
seldom
kill, but they
can
weaken
the skeleton and cause severe pain.12 If they replace enough bone, the skeleton fails by pathological fracture. The principles behind the management of bony metastases have not changed substantially over the past twenty years, but there has been a transformation in the means by which they are realised as implant design has improved. Surgical intervention should be considered if metastatic bone pain cannot be relieved by other means; if fracture is likely, as indicated by the loss of more than half the cortical bone thickness;3 or if a fracture has already occurred. The extent to which the skeleton is involved can be mapped by plain radiographs and radionuclide scans; computed tomography and magnetic resonance imaging are occasionally needed to plan an operation in greater
detail. Methods that restore mechanical stability must be used to ensure that full weightbearing is possible immediately after the operation. Implants of insufficient strength will eventually fracture and those that fail to stabilise the skeleton will loosen unless supported by new bone formation or by the use of polymethyhnethacrylate (PMMA) cement.44 If a patient has multiple metastases, any theoretical concern about spreading tumour further by intramedullary nailing is virtually dispelled. Most diaphyseal pathological fractures of proximal limb bones should be stabilised by use of a modem interlocking nail system, with PMMA cement if the lesion is extensive. Adjunctive radiotherapy, chemotherapy, or hormonal manipulation may be started once the wounds have healed. Some lesions defy nailing: they may lie too near a joint to permit restoration of stability, or may present in smaller bones such as radius and ulna for which intramedullary nailing is inappropriate. Most of these lesions can be stabilised with a combination of plates, screws, and PMMA cement. Deposits around the hip or shoulder cannot be treated satisfactorily by either method, but may be amenable to replacement with a standard hip or shoulder prosthesis. Endoprosthetic replacement, with implants originally designed for the treatment of primary bone tumours, has a clearly defined place in the treatment of secondary deposits; this approach was lately reviewed by Chan and co-workers.5 These researchers restricted their use of endoprostheses to compliant patients with an anticipated survival of more than six months who could not be treated by other methods, or in whom alternative methods had failed. Local infection and previous radiotherapy of a dose likely to wound were other healing prejudice contraindications. Two-thirds of the patients had solitary metastases, and more than three-quarters had femoral deposits. This work suggests that solitary metastases, especially from a hypernephroma, should be excised with wide margins and an intact covering of normal tissue as for a primary malignant bone tumour. Patients with solitary deposits from breast or prostate tumours may be treated in the same way but will not survive as long. The extent and location of the resultant defect will determine the method of reconstruction,6but endoprosthetic replacement is needed for large metaphyseal lesions. 1.
Portenoy
RK. Cancer
pain: pathophysiology
and
syndromes. Lancet
1992; 339: 1026-31. 2. Hanks GW, Justins DM. Cancer pain: management. Lancet 1992; 339: 1031-36. 3. Fidler M. Prophylactic internal fixation of secondary neoplastic deposits in long bones. Br Med J 1973; i: 341-43. 4. Harrington KD, Sim FH, Enis JE, Johnston JO, Dick HM, Gristina AG. Methylmethacrylate as an adjunct in the internal fixation of pathological fractures. J Bone Joint Surg 1976; 58A: 1047-55. 5. Chan D, Carter SR, Grimer RJ, Sneath RS. Endoprosthetic replacement for bony metastases. Ann R Coll Surg Engl 1992; 74: 13-18. 6. Editorial. Bridging the gap: reconstructing large defects in the skeleton. Lancet 1990; 336: 1101-03.
7. Kreusser KL, Schmidt RE, Shackleford GD, Volpe JJ. Value of ultrasound for identification of acute hemorrhagic necrosis of thalamus and basal ganglia in an asphyxiated term infant. Ann Neurol 1984: 16: 361-63. 8. Voit T, Lemburg P. Damage of thalamus and basal ganglia in asphyxiated full-term neonates. Neuropediatrics 1987; 18: 176-181. 9. Cabanas F, Pellicer A. Perez-Higueras A, Garica-Alix A, Roche C, Quero J. Ultrasonographic findings in thalamus and basal ganglia in term asphyxiated infants. Pediatric Neurology 1991; 7: 211-15. 10. DiMario FJ, Clancy R. Symmetrical thalamic degeneration with calcifications of infancy. Am J Dis Child 1989; 143: 1056-60. 11. Shen EY, Lin JCT, Shih CC. Pathological echogenicity of the thalamus in newborn and young infants. J Formosan Med Assoc 1988; 87: 891-97. 12. Steinlin M, Dirr R, Martin E, et al. MRI following severe perinatal asphyxia: preliminary experience. Pediatr Neurol 1991; 7: 164-70. 13. Pasternak JF, Predey TA, Mikhael MA. Neonatal asphyxia: vulnerability of basal ganglia, thalamus and brainstem. Pediatr Neurol 1991; 7: 147-49. 14. Babcock DS, Ball W. Postasphyxial encephalopathy in full-term infants: ultrasound diagnosis. Radiology 1983; 148: 417-23. 15. Shewmon DA, Fine M, Masdeu JC, Palacios E. Postischemic hypervascularity of infancy: a stage in the evolution of ischemic brain damage with characteristic CT scan. Ann Neurol 1981; 9: 358-65. 16. Levene MI, Williams JL, Fawer C-L. Ultrasound of the infant brain. Oxford: Blackwell, 1985. 17. Volpe JJ. Neurology of the newborn. 2nd ed. Philadelphia: WB Saunders, 1987. 18. Trounce JQ, Dodd KL, Fawer C-L, Fielder AR, Punt J, Levene MI. Primary thalamic haemorrhage in the newborn: a new clinical entity. Lancet 1985; i: 190-92. 19. Adams C, Hochhauser L, Logan WJ. Primary thalamic and caudate hemorrhage in term neonates presenting with seizures. Pediatr Neurol
1988; 4: 175-77. 20. Roland EH, Flodmark O, Hill A. Thalamic hemorrhage with intraventricular hemorrhage in the full-term newborn. Pediatrics 1990; 85: 737-42. 21. Teele RL, Hernanz-Schulman M, Sotrel A. Echogenic vasculature in the basal ganglia of neonates: a sonographic sign of vasculopathy. Radiology 1988; 169: 423-27. 22. Hughes P, Weinberger E, Shaw DWW. Linear areas of echogenicity in the thalami and basal ganglia of neonates: an expanded association.
Radiology 1991; 179: 103-05. 23. Abuelo DN, Barsel-Bowers G, Tutschka BG, Ambler M, Singer DB. Symmetrical infantile thalamic degeneration in two sibs. J Med Genet 1981; 18: 448-50. 24. Aicardi J, Goutieres F. A progressive familial encephalopathy in infancy with calcifications of the basal ganglia and chronic cerebrospinal fluid lymphocytosis. Ann Neurol 1984; 15: 49-54. 25. Mehta L, Trounce JQ, Moore JR, Young ID. Familial calcification of the basal ganglia with cerebrospinal fluid pleocytosis. J Med Genet 1986; 23: 157-60.
Endoprostheses for bony metastases
Bony metastases
seldom
kill, but they
can
weaken
the skeleton and cause severe pain.12 If they replace enough bone, the skeleton fails by pathological fracture. The principles behind the management of bony metastases have not changed substantially over the past twenty years, but there has been a transformation in the means by which they are realised as implant design has improved. Surgical intervention should be considered if metastatic bone pain cannot be relieved by other means; if fracture is likely, as indicated by the loss of more than half the cortical bone thickness;3 or if a fracture has already occurred. The extent to which the skeleton is involved can be mapped by plain radiographs and radionuclide scans; computed tomography and magnetic resonance imaging are occasionally needed to plan an operation in greater
detail. Methods that restore mechanical stability must be used to ensure that full weightbearing is possible immediately after the operation. Implants of insufficient strength will eventually fracture and those that fail to stabilise the skeleton will loosen unless supported by new bone formation or by the use of polymethyhnethacrylate (PMMA) cement.44 If a patient has multiple metastases, any theoretical concern about spreading tumour further by intramedullary nailing is virtually dispelled. Most diaphyseal pathological fractures of proximal limb bones should be stabilised by use of a modem interlocking nail system, with PMMA cement if the lesion is extensive. Adjunctive radiotherapy, chemotherapy, or hormonal manipulation may be started once the wounds have healed. Some lesions defy nailing: they may lie too near a joint to permit restoration of stability, or may present in smaller bones such as radius and ulna for which intramedullary nailing is inappropriate. Most of these lesions can be stabilised with a combination of plates, screws, and PMMA cement. Deposits around the hip or shoulder cannot be treated satisfactorily by either method, but may be amenable to replacement with a standard hip or shoulder prosthesis. Endoprosthetic replacement, with implants originally designed for the treatment of primary bone tumours, has a clearly defined place in the treatment of secondary deposits; this approach was lately reviewed by Chan and co-workers.5 These researchers restricted their use of endoprostheses to compliant patients with an anticipated survival of more than six months who could not be treated by other methods, or in whom alternative methods had failed. Local infection and previous radiotherapy of a dose likely to wound were other healing prejudice contraindications. Two-thirds of the patients had solitary metastases, and more than three-quarters had femoral deposits. This work suggests that solitary metastases, especially from a hypernephroma, should be excised with wide margins and an intact covering of normal tissue as for a primary malignant bone tumour. Patients with solitary deposits from breast or prostate tumours may be treated in the same way but will not survive as long. The extent and location of the resultant defect will determine the method of reconstruction,6but endoprosthetic replacement is needed for large metaphyseal lesions. 1.
Portenoy
RK. Cancer
pain: pathophysiology
and
syndromes. Lancet
1992; 339: 1026-31. 2. Hanks GW, Justins DM. Cancer pain: management. Lancet 1992; 339: 1031-36. 3. Fidler M. Prophylactic internal fixation of secondary neoplastic deposits in long bones. Br Med J 1973; i: 341-43. 4. Harrington KD, Sim FH, Enis JE, Johnston JO, Dick HM, Gristina AG. Methylmethacrylate as an adjunct in the internal fixation of pathological fractures. J Bone Joint Surg 1976; 58A: 1047-55. 5. Chan D, Carter SR, Grimer RJ, Sneath RS. Endoprosthetic replacement for bony metastases. Ann R Coll Surg Engl 1992; 74: 13-18. 6. Editorial. Bridging the gap: reconstructing large defects in the skeleton. Lancet 1990; 336: 1101-03.
