Abstract
Objective
To evaluate a new therapy of posttraumatic brain oedema, with the main concept that opening of the blood-brain barrier upsets the normal brain volume regulation, inducing oedema formation. This means that transcapillary fluid fluxes will be controlled by hydrostatic capillary and colloid osmotic pressures, rather than by crystalloid osmotic pressure. If so, brain oedema therapy should include reduction of hydrostatic capillary pressure and preservation of normal colloid osmotic pressure.
Patients
11 severely head injured comatose patients with brain swelling, raised intracranial pressure (ICP), and impaired cerebrovascular response to hyperventilation.
Interventions
To reduce capillary hydrostatic pressure the patients were given hypotensive therapy (β1-antagonist, metoprolol and α2-agonist, clonidine) and a potential precapillary vasoconstrictor (dihydroergotamine). The latter may also decrease cerebral blood volume through venous capacitance constriction. Colloid osmotic pressure was maintained by albumin infusions. The concept implies the need of a negative fluid balance with preserved normovolaemia.
Results
ICP decreased significantly within a few hours of treatment with unaltered perfusion pressure in spite of lowered blood pressure. Of 11 patients 9 survived with good recovery/moderate disability, 2 died. This was compared to outcome in a historical control group with identical entry criteria, given conventional brain oedema therapy, where mortality/vegetativity/severe disability was 100%.
Conclusion
The results indicate that the therapy should focus on extracellular rather than intracellular oedema and that ischemia is not the main triggering mechanism behind oedema formation. We suggest that our therapy is superior to conventional therapy by preventing herniation during the healing period of the blood-brain barrier.
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References
Borel C, Hanley D, Diringer MN, Rogers MC (1990) Intensive management of severe head injury. Chest 198:180–189
Fenstermacher JD (1984) Volume regulation of the central nervous system. In: Staub NC, Taylor AE (eds) Edema. Raven Press, New York, pp 383–404
Langfitt TW, Gennarelli TA (1982) Can outcome from head injury be improved? J Neurosurg 56:19–25
Jennett B, Mendelow AD (1989) Head injuries. In: Nunn JF, Utting JE, Brown Jr BR (eds) General anaesthesia. Butterworth 109, pp 1304–1317
Aldrich EF, Eisenberg HM, Saydjari C, Luerssen TG, Foulkes MA, Jane JA, Marshall LF, Marmarou A, Young HF (1992) Diffuse brain swelling in severely head-injured children. A report from the NIH traumatic coma data bank. J Neurosurg 76:450–454
Miller JD (1985) Head injury and brain ischaemia, implications for therapy. Br J Anaesth 57:120–129
Rosner MJ, Daughton S (1990) Cerebral perfusion pressure management in head injury. J Trauma 30:933–941
Marmarou A, Andersson RL, Ward JD, Choi SC, Young HF (1991) Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg 75:59–66
Miller JD, Dearden MM, Piper IR, Chan KH (1992) Control of intracranial pressure in patients with severe head injury. J Neurotrauma 9 [Suppl 1]:317–326
Messeter K, Nordström CH, Sundbärg G, Algotsson L, Ryding E (1986) Cerebral hemodynamics in patients with acute severe head trauma. J Neurosurg 64:231–237
Nordström CH, Messeter K, sundbärg G, Schalen W, Werner M, Ryding E (1988) Cerebral blood flow, vasoreactivity and oxygen consumption during barbiturate therapy in severe traumatic brain lesions. J Neurosurg 68:424–431
Schalen W, Messeter K, Nordström CH (1991) Cerebral vasoreactivity and the prediction of outcome in severe traumatic brain lesions. Acta Anaesth Scand 35:113–122
Astrup J (1991) Drug treatment in head injury. Current Opin Anaesthesiol 4:653–656
White RL, Likavec MJ (1992) The diagnosis and initial management of head injury. N Engl J Med 327:1507–1511
Chan KH, Miller JD, Dearden NM, Andrews PJD, Midgley S (1992) The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury. J Neurosurg 77:55–61
Graham DI, Adams JH, Doyle D (1987) Ischemic brain damage in fatal non-missile head injuries. J Neurol Sci 39:213–234
Cold GE (1989) Does acute hyperventilation provoke cerebral oligemia in comatose patients after head injury? Acta Neurochir 96:100–106
Obrist WD, Langfitt TW, Jaggi JL, Cruz J, Gennarelli TA (1984) Cerebral flood flow and metabolism in comatose patients with acute head injury. J Neurosurg 61:241–253
Ward JD, Becker DP, Miller JD, Choi SC, Marmarou A, Wood C, Newlon PG, Keenan R (1985) Fallure of prophylactic barbiturate coma in the treatment of severe head injury. J Neurosurg 62: 383–388
Schalen W, Messeter K, Nordström CH (1992) Complications and side-effects during thiopental therapy in patients with severe head injuries. Acta Anaesth Scand 36:369–377
Grände PO, Gustafsson D, Lindberg L (1990) Effects of thiopental on resistance vessels in cat skeletal muscle. Intensive Care Med 16:399–404
Dearden NM (1986) Management of raised ICP after severe head injury. Br J Hosp Med 36:94–103
Kaufmann AM, Cardoso ER (1992) Aggravation of vasogenic cerebral edema by multiple dose mannitol. J Neurosurg 77:584–589
Jennet B (1991) Diagnosis and management of head trauma. J Neurotrauma 8 [Suppl 1]:15–19
Grände PO, Asgeirsson B, Nordström CH (1993) A new potential therapy for treatment of posttraumatic brain oedema based on haemodynamic principles for brain volume regulation. In: Nakamura N, Hashimoto T, Yasue M (eds) Recent advances in neurotraumatology. Springer, Tokyo, pp 319–322
McClain CJ, Henning B, Ott LG, Goldblum S, Young AB (1988) Mechanisms and implications of hypoalbuminemia in head-injured patients. J Neurosurg 69:386–392
Todd NV, Graham DI (1990) Blood-brain barrier damage in traumatic brain contusions. Acta Neurochir [Suppl] 51:296–299
Grände PO (1989) The effect of dihydroergotamine in patients with head injury and raised intracranial pressure. Intensive Care Med 15:523–527
Roth B, Grände PO, Nilsson-Ehle P, Eliasson I (1993) Possible role of short-term parenteral nutrition with fat emulsions for development of haemophagocytosis with multiple organ failure in a patient with traumatic brain injury. Intensive Care Med 19:111–114
Cold GE, Taagehoj Jensen F, Malmros R (1977) The cerebrovascular CO2 reactivity during the acute phase of brain injury. Acta Anaesth Scand 21:222–231
Piatt JH, Schiff SJ (1984) High dose barbiturate therapy in neurosurgery and intensive care. Neurosurgery 15:427–444
Yada K, Nagakawa Y, Tsuru M (1973) Circulatory disturbance of the venous system during experimental intracranial hypertension. J Neurosurg 39:723–729
Grände PO (1992) New haemodynamic aspects on treatment of posttraumatic brain oedema. Svensk Förening för Anestesi och Intensivvård sept, Vol. 6; 2: pp 41–46
Simard JM, Bellefleur M (1989) Systemic arterial hypertension in head trauma. Am J Cardiol 63:32c-35c
Clifton GL, Robertson CS, Kyper K, Taylor AA, Dhekne RD, Grossman RG (1983) Cardiovascular responses to severe head injury. J Neurosurg 59:447–454
Cruickshank JM, Neil-Dwyer G, Degaute JP, Hayes Y, Kuurne T, Kytta J, Vincent JL, Carruthers ME, Patel S (1987) Reduction of stress/catecholamine-induced cardiac necrosis by β1-selective blockade. Lancet I:585–589
Schutta HS, Kassell NF, Langfitt TW (1986) Brain swelling produced by injury and aggravated by arterial hypertension. Brain 91:281–294
Gunning K, Forster A (1989) Cerebral blood flow in head injury. In: Bihari D, Holaday JW (eds) Update in intensive care and emergency medicine. Brain failure. Springer, Berlin Heidelberg New York, 9:198–205
Pappius HM (1989) Cerebral edema and the blood-brain barrier. In: Neuwelt EA (ed) Implications of the blood-brain barrier and its manipulation, vol 1. Plenum, New York, pp 293–309
McClain CJ, Cohen D, Ott L, Dinarello CA, Young B (1987) Ventricular fluid interleukin-1 activity in patients with head injury. J Lab Clin Med 110:48–54
Doczi T, Jojart I, Laszlo FA, Szerdahelyi P, Joo F, Bodosi M (1987) Significance of central vasopressin in the regulation of the water and ion balance in the central nervous system. In: Cohadon F, Baethmann A, Go KG, Miller JD (eds) Traumatic brain oedema, vol 8. Fidia Research Series, Liviana Press, Padova, pp 153–160
Obrist W, Gennarelli TA, Segawa H, Dolinskas C, Langfitt TW (1979) Relation of cerebral blood flow to neutrological status and outcome in head-injured patients. J Neurosurg 51:292–300
Bouma GJ, Muizelaar JP (1992) Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma 9 [Suppl 1]:333–348
Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B (1981) Diffuse cerebral swelling following head injuries in children: the syndrome of malignant brain oedema. J Neurosurg 54:170–178
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This manuscript was awarded the 1993 Volvo Award for CNS Injury Research by the Neurotraumatology Committee of the World Federation of Neurosurgical Societies
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Asgeirsson, B., Grände, P.O. & Nordström, C.H. A new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regulation. Intensive Care Med 20, 260–267 (1994). https://doi.org/10.1007/BF01708961
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DOI: https://doi.org/10.1007/BF01708961