Medida da diferença artério-venosa de oxigênio na monitorização de pacientes com hemorragia subaracnóidea por aneurisma cerebral

Pereira, Ronaldo Sérgio Santana; Ramalho, Márcio Robertti; Viscardi, Renato Camargo; Motta, Luiz Augusto Casulari Roxo da; Carvalho, Márcio Vinhal de; Suzuki, Kunio; Mello, Paulo Andrade de

doi:10.1590/S0004-282X1997000100006

Resumos

A diferença artério-venosa de oxigênio (DAVO2), pelo fato de estar relacionada com o metabolismo cerebral, reflete alterações que ocorrem em determinadas situações patológicas, entre elas as causadas pela hemorragia subaracnóidea espontânea (HSAE). Com a finalidade de avaliar a relação entre alterações na DAVO2 com o quadro clínico e a evolução de pacientes com HSAE, devido à ruptura de aneurisma cerebral, este método foi utilizado em 30 pacientes portadores desta patologia, admitidos na Unidade de Neurocirurgia do HBDF. A HSAE foi confirmada por CT de crânio em 17 pacientes e por punção lombar em 13. Dezoito pacientes foram admitidos com Hunt & Hess (H&H) I ou II, sete com H&H III e cinco com H&H IV ou V. A medida da DAVO2 baseou-se na equação de Fick e os resultados clínicos foram avaliados pela escala de seqüelas de Glasgow. Dezenove pacientes apresentaram DAVO2 normais (inicialmente e durante a evolução), sendo que três faleceram; cinco tiveram valores de DAVO2 sempre baixos e três faleceram; os restantes seis pacientes tiveram valores da DAVO2 sempre elevados e dois faleceram. Os pacientes com DAVO2 normais tiveram melhor evolução clínica e índice de mortalidade menor, quando comparados com os pacientes com valores anormais da DAVO2 (p<0,05). O diagnóstico de vasoespasmo foi feito, em sua maioria, pela avaliação clínica, sendo confirmado radiologicamente em oito pacientes, mas estes últimos tiveram DAVO2 normais. A medida isolada da DAVO2 não foi suficiente para o diagnóstico do vasoespasmo, porém refletiu alterações metabólicas precoces. Baseada nestes resultados, a DAVO2 pode ser usada como parâmetro importante na monitorização da evolução dos pacientes com HSAE.

hemorragia subaracnóidea espontânea; aneurisma cerebral; vasoespasmo cerebral; fluxo sanguíneo cerebral; diferença artério-venosa de oxigênio (DAV02)

The arterious venous oxygen difference (AVDO2) due to the close relationship with cerebral metabolic rate of oxygen and cerebral blood flow shows metabolic alterations that occur in some pathological situations in the brain including subarachnoid haemorrhage. The AVDO2 was calculated by the Fick equation and the results evaluated by the Glasgow outcome scale. Measurements of arteriojugular oxygen difference were carried out in 30 patients with subarachnoid haemorrhage due to rupture of intracranial aneurysms, as an attempt to monitor the relationship between changes in AVDO2, clinical picture, and evolution of the patients. The subarachnoid haemorrhage was diagnosed by CT scan in 17 patients and by lumbar punction in 13 and the diagnosis of arterial vasospasm was carried out by clinical evaluation and confirmed by four vessels angiogram in only eight patients. Eighteen patients were admitted with Hunt & Hess (H&H) I/II, seven with H&H III and five with H&H IV/V. Nineteen patients had AVDO2 normal and this group had three deaths; five patients had AVD02 continuously low with three deaths; and six patients had AVDO2 continuously high with two deaths. The patients with normal AVDO2 had better prognosis and clinical evolution than the patients with abnormal values of AVDO2. In conclusion, AVDO2 measurements could not be correlated with the diagnosis of vasospasm, but was useful in the early identification of metabolic changes that occur after subarachnoid haemorrhage and could be used as an supplementary monitoring in the clinical evaluation of patients with this pathology.

subarachnoid haemorrhage; cerebral aneurysm; arterial vasospasm; cerebral blood flow; arterious venous oxygen difference (AVDO2)

Medida da diferença artério-venosa de oxigênio na monitorização de pacientes com hemorragia subaracnóidea por aneurisma cerebral

Measurement of arteriovenous oxygen difference in the monitoring of patients with subarachnoid haemorrhage due to cerebral aneurysm

Ronaldo Sérgio Santana Pereira^I; Márcio Robertti Ramalho^III; Renato Camargo Viscardi^II; Luiz Augusto Casulari Roxo da Motta^I; Márcio Vinhal de Carvalho^III; Kunio Suzuki^I; Paulo Andrade de Mello^IV

^IMédico da UNC do HBDF

^IIMédico da UTI do HBDF

^IIIEx-Médico Residentede Neurocirurgia do HBDF

^IVProfessor Titular de Neurocirurgia da Universidade de Brasília

RESUMO

A diferença artério-venosa de oxigênio (DAVO2), pelo fato de estar relacionada com o metabolismo cerebral, reflete alterações que ocorrem em determinadas situações patológicas, entre elas as causadas pela hemorragia subaracnóidea espontânea (HSAE). Com a finalidade de avaliar a relação entre alterações na DAVO2 com o quadro clínico e a evolução de pacientes com HSAE, devido à ruptura de aneurisma cerebral, este método foi utilizado em 30 pacientes portadores desta patologia, admitidos na Unidade de Neurocirurgia do HBDF. A HSAE foi confirmada por CT de crânio em 17 pacientes e por punção lombar em 13. Dezoito pacientes foram admitidos com Hunt & Hess (H&H) I ou II, sete com H&H III e cinco com H&H IV ou V. A medida da DAVO2 baseou-se na equação de Fick e os resultados clínicos foram avaliados pela escala de seqüelas de Glasgow. Dezenove pacientes apresentaram DAVO2 normais (inicialmente e durante a evolução), sendo que três faleceram; cinco tiveram valores de DAVO2 sempre baixos e três faleceram; os restantes seis pacientes tiveram valores da DAVO2 sempre elevados e dois faleceram. Os pacientes com DAVO2 normais tiveram melhor evolução clínica e índice de mortalidade menor, quando comparados com os pacientes com valores anormais da DAVO2 (p<0,05). O diagnóstico de vasoespasmo foi feito, em sua maioria, pela avaliação clínica, sendo confirmado radiologicamente em oito pacientes, mas estes últimos tiveram DAVO2 normais. A medida isolada da DAVO2 não foi suficiente para o diagnóstico do vasoespasmo, porém refletiu alterações metabólicas precoces. Baseada nestes resultados, a DAVO2 pode ser usada como parâmetro importante na monitorização da evolução dos pacientes com HSAE.

Palavras-chave: hemorragia subaracnóidea espontânea, aneurisma cerebral, vasoespasmo cerebral, fluxo sanguíneo cerebral, diferença artério-venosa de oxigênio (DAV02).

ABSTRACT

The arterious venous oxygen difference (AVDO2) due to the close relationship with cerebral metabolic rate of oxygen and cerebral blood flow shows metabolic alterations that occur in some pathological situations in the brain including subarachnoid haemorrhage. The AVDO2 was calculated by the Fick equation and the results evaluated by the Glasgow outcome scale. Measurements of arteriojugular oxygen difference were carried out in 30 patients with subarachnoid haemorrhage due to rupture of intracranial aneurysms, as an attempt to monitor the relationship between changes in AVDO2, clinical picture, and evolution of the patients. The subarachnoid haemorrhage was diagnosed by CT scan in 17 patients and by lumbar punction in 13 and the diagnosis of arterial vasospasm was carried out by clinical evaluation and confirmed by four vessels angiogram in only eight patients. Eighteen patients were admitted with Hunt & Hess (H&H) I/II, seven with H&H III and five with H&H IV/V. Nineteen patients had AVDO2 normal and this group had three deaths; five patients had AVD02 continuously low with three deaths; and six patients had AVDO2 continuously high with two deaths.

The patients with normal AVDO2 had better prognosis and clinical evolution than the patients with abnormal values of AVDO2. In conclusion, AVDO2 measurements could not be correlated with the diagnosis of vasospasm, but was useful in the early identification of metabolic changes that occur after subarachnoid haemorrhage and could be used as an supplementary monitoring in the clinical evaluation of patients with this pathology.

Key words: subarachnoid haemorrhage, cerebral aneurysm, arterial vasospasm, cerebral blood flow, arterious venous oxygen difference (AVDO2).

Texto completo disponível apenas em PDF.

Full text available only in PDF format.

Aceite: 3-setembro-1996.

Estudo realizado na Unidade de Neurocirurgia (UNC) e Unidade de Terapia Intensiva (UTI) do Hospital de Base do Distrito Federal (HBDF).

Dr. Ronaldo Sérgio Santana Pereira - Unidade de Neurocirurgia, Hospital de Base do Distrito Federal - SMHS Q 101 Asa Sul - 70335-900 Brasília DF - Brasil.

1. Bouma GJ, Muizelaar JP, Choi SC, Newlon PG, Young HE Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg 1991 ;75:685-693.
2. Cruz J. Monitorização hemodinâmica e metabólica cerebral em humanos. Arq Bras Neurocirurg 1993;11:209-215.
3. Cruz J. Combined continuous monitoring of systemic and cerebral oxygenation in acute brain injury: preliminary observations. Crit Care Med 1993;21:1225-1232.
4. Cruz J. An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake. J Neurosurg 1995;82:379-385.
5. Cruz J, Jaggi JL, Hoffstad OJ. Cerebral blood flow and oxygen consumption in acute brain injury with acute anemia: an alternative for the cerebral metabolic rate of oxygen consumption? Crit Care Med 1993;21:1218-1224.
6. Cruz J, Jaggi JL, Hoffstad OJ. Cerebral blood flow, vascular resistance, and oxygen metabolism in acute brain trauma: redefining of cerebral perfusion pressure? Crit Care Med 1995;23:1412-1417.
7. Cruz J, Raps EC, Hoffstad OJ, Jaggi JL, Gennarelli TA. Cerebral oxygenation monitoring. Crit Care Med 1993;21:1242-1243.
8. Fein JM. Cerebral energy metabolism after subarachnoid haemorrhage. Stroke 1975 ;6:1 -8.
9. Garlick R, Bihari D. The use of intermittent and continuous recordings of jugular venous bulb oxygen saturation in the unconscious patient. Scand J Clin Lab Invest 1987;47(Suppl 188):47-52.
10. Grubb RL, Raichle ME, Eichling JO, Gado MH. Effects of subarachnoid haemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans. J Neurosurg 1977;46:446-453.
11. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968;28:14-20.
12. Jakobsen M, Enevoldsen EM, Bjerre P. Cerebral blood flow and metabolism following subarachnoid haemorrhage: cerebral oxygen uptake and global blood flow during the acute period in patients with SAH. Acta Neurol Scand 1990; 82:174-182.
13. Jakobsen M, Enevoldsen EM, Dalager T. Spasm index in subarachnoid haemorrhage: consequences of vasospasm upon cerebral blood flow and oxygen extraction. Acta Neurol Scand 1990;82:311-320.
14. Jakobsen M, Overgaard J, Marcussen E, Enevoldsen EM. Relation between angiographic cerebral vasospasm and regional CBF in patients with SAH. Acta Neurol Scand 1990;82:109-115.
15. Jakobsen M, Skjodt T, Enevoldsen EM. Cerebral blood flow and metabolism following subarachnoid haemorrhage: effect of subarachnoid blood. Acta Neurol Scand 1991;83:226-233.
16. Jennett B, Bond M. Assesment of outcome after severe brain damage: a practical scale. Lancet 1975;1:480-484.
17. Kaminogo M, Ichikura A, Shibata S, Toba T, Yonekura M. Effect of acetazolamide on regional cerebral oxygen saturation and regional cerebral blood flow. Stroke 1995;26:2358-2360.
18. Knuckey NW, Fox RA, Surveyor I, Strokes BAR. Early cerebral blood flow and computarized tomography in predicting ischemia after cerebral aneurysm rupture. J Neurosurg 1985;62:850-855.
19. Lassen NA, Lane MH. Validity of internal jugular blood for study of cerebral blood flow and metabolism. J Appl Physiol 1961;16:313-320.
20. Mathew NT, Meyer JS, Hartmann A. Diagnosis and treatment of factors complicating subarachnoid haemorrhage. Neuroradiology 1974;6:237-245.
21. Meyer CHA, Lowe D, Meyer M, Richardson PL, Neil-Dwyer G. Progressive change in cerebral blood flow during the three weeks after subarachnoid haemorrhage. Neurosurgery 1983; 12:58-76.
22. Muizelaar JP, Marmarou A, Ward JD, Kontos HA, Choi SC, Becker DP, Gruemer H, Young HF. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurgery 1991:75:731-739.
23. Pulsinelli WA, Levy DE. Cerebrovascular disease. In Wyngaarden JB, Smith LH, Bennett JC (eds.). Cecil textbook of medicine. Ed. 19. Philadelphia; Saunders;1992:2145-2162.
24. Ritter AM, Robertson CS. Intensive care management of the neurosurgical patients. Contemp Neurosurg 1994; 16:1 -8.
25. Robertson CS, Narayan RK, Gokaslan ZL, Pahwa R, Grossman RG, Caram P, Allen E. Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatose patients. J Neurosurg 1988;70:222-230.
26. Sheinberg M, Kanter MJ, Robertson CS, Contant CF, Narayan RK, Grossman RG. Continuous monitoring of jugular venous oxygen saturation in head-injured patients. J Neurosurg 1992;76:212-217.
27. Sutton LN, McLaughlin AC, Dante S. Cerebral venous oxygen content as a measure of brain energy metabolism with increased intracranial pressure and hyperventilation. J Neurosurg 1990;73:927-932.
28. Teardale G, Jennett B. Assesment of coma and impaired consciousness: a practical scale. Lancet 1974;2:81-84.
29. Voldby B, Enevoldsen EM. Intracranial pressure changes following aneurysm rupture: Part 3. Recurrent haemorrhage. J Neurosurg 1982;56:784-789.
30. Voldby B, Enevoldsen EM, Jensen FT. Regional cerebral blood flow, intraventricular pressure and cerebral metabolism in patients with ruptured intracranial aneurysms. J Neurosurg 1985; 62:48-58.

Datas de Publicação

Publicação nesta coleção
10 Nov 2010
Data do Fascículo
1997

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. Bouma GJ, Muizelaar JP, Choi SC, Newlon PG, Young HE Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg 1991 ;75:685-693.

[2] 2. Cruz J. Monitorização hemodinâmica e metabólica cerebral em humanos. Arq Bras Neurocirurg 1993;11:209-215.

[3] 3. Cruz J. Combined continuous monitoring of systemic and cerebral oxygenation in acute brain injury: preliminary observations. Crit Care Med 1993;21:1225-1232.

[4] 4. Cruz J. An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake. J Neurosurg 1995;82:379-385.

[5] 5. Cruz J, Jaggi JL, Hoffstad OJ. Cerebral blood flow and oxygen consumption in acute brain injury with acute anemia: an alternative for the cerebral metabolic rate of oxygen consumption? Crit Care Med 1993;21:1218-1224.

[6] 6. Cruz J, Jaggi JL, Hoffstad OJ. Cerebral blood flow, vascular resistance, and oxygen metabolism in acute brain trauma: redefining of cerebral perfusion pressure? Crit Care Med 1995;23:1412-1417.

[7] 7. Cruz J, Raps EC, Hoffstad OJ, Jaggi JL, Gennarelli TA. Cerebral oxygenation monitoring. Crit Care Med 1993;21:1242-1243.

[8] 8. Fein JM. Cerebral energy metabolism after subarachnoid haemorrhage. Stroke 1975 ;6:1 -8.

[9] 9. Garlick R, Bihari D. The use of intermittent and continuous recordings of jugular venous bulb oxygen saturation in the unconscious patient. Scand J Clin Lab Invest 1987;47(Suppl 188):47-52.

[10] 10. Grubb RL, Raichle ME, Eichling JO, Gado MH. Effects of subarachnoid haemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans. J Neurosurg 1977;46:446-453.

[11] 11. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968;28:14-20.

[12] 12. Jakobsen M, Enevoldsen EM, Bjerre P. Cerebral blood flow and metabolism following subarachnoid haemorrhage: cerebral oxygen uptake and global blood flow during the acute period in patients with SAH. Acta Neurol Scand 1990; 82:174-182.

[13] 13. Jakobsen M, Enevoldsen EM, Dalager T. Spasm index in subarachnoid haemorrhage: consequences of vasospasm upon cerebral blood flow and oxygen extraction. Acta Neurol Scand 1990;82:311-320.

[14] 14. Jakobsen M, Overgaard J, Marcussen E, Enevoldsen EM. Relation between angiographic cerebral vasospasm and regional CBF in patients with SAH. Acta Neurol Scand 1990;82:109-115.

[15] 15. Jakobsen M, Skjodt T, Enevoldsen EM. Cerebral blood flow and metabolism following subarachnoid haemorrhage: effect of subarachnoid blood. Acta Neurol Scand 1991;83:226-233.

[16] 16. Jennett B, Bond M. Assesment of outcome after severe brain damage: a practical scale. Lancet 1975;1:480-484.

[17] 17. Kaminogo M, Ichikura A, Shibata S, Toba T, Yonekura M. Effect of acetazolamide on regional cerebral oxygen saturation and regional cerebral blood flow. Stroke 1995;26:2358-2360.

[18] 18. Knuckey NW, Fox RA, Surveyor I, Strokes BAR. Early cerebral blood flow and computarized tomography in predicting ischemia after cerebral aneurysm rupture. J Neurosurg 1985;62:850-855.

[19] 19. Lassen NA, Lane MH. Validity of internal jugular blood for study of cerebral blood flow and metabolism. J Appl Physiol 1961;16:313-320.

[20] 20. Mathew NT, Meyer JS, Hartmann A. Diagnosis and treatment of factors complicating subarachnoid haemorrhage. Neuroradiology 1974;6:237-245.

[21] 21. Meyer CHA, Lowe D, Meyer M, Richardson PL, Neil-Dwyer G. Progressive change in cerebral blood flow during the three weeks after subarachnoid haemorrhage. Neurosurgery 1983; 12:58-76.

[22] 22. Muizelaar JP, Marmarou A, Ward JD, Kontos HA, Choi SC, Becker DP, Gruemer H, Young HF. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurgery 1991:75:731-739.

[23] 23. Pulsinelli WA, Levy DE. Cerebrovascular disease. In Wyngaarden JB, Smith LH, Bennett JC (eds.). Cecil textbook of medicine. Ed. 19. Philadelphia; Saunders;1992:2145-2162.

[24] 24. Ritter AM, Robertson CS. Intensive care management of the neurosurgical patients. Contemp Neurosurg 1994; 16:1 -8.

[25] 25. Robertson CS, Narayan RK, Gokaslan ZL, Pahwa R, Grossman RG, Caram P, Allen E. Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatose patients. J Neurosurg 1988;70:222-230.

[26] 26. Sheinberg M, Kanter MJ, Robertson CS, Contant CF, Narayan RK, Grossman RG. Continuous monitoring of jugular venous oxygen saturation in head-injured patients. J Neurosurg 1992;76:212-217.

[27] 27. Sutton LN, McLaughlin AC, Dante S. Cerebral venous oxygen content as a measure of brain energy metabolism with increased intracranial pressure and hyperventilation. J Neurosurg 1990;73:927-932.

[28] 28. Teardale G, Jennett B. Assesment of coma and impaired consciousness: a practical scale. Lancet 1974;2:81-84.

[29] 29. Voldby B, Enevoldsen EM. Intracranial pressure changes following aneurysm rupture: Part 3. Recurrent haemorrhage. J Neurosurg 1982;56:784-789.

[30] 30. Voldby B, Enevoldsen EM, Jensen FT. Regional cerebral blood flow, intraventricular pressure and cerebral metabolism in patients with ruptured intracranial aneurysms. J Neurosurg 1985; 62:48-58.