| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
* From the Departments of Anesthesiology,
Neurosurgical Intensive Care Unit,* and
Neurological Surgery, University of Washington, Seattle, Washington, USA.
Address correspondence to: Dr. Irene Rozet, Assistant Professor, Harborview Medical Center, Box 359724, 325 Ninth Avenue, Seattle, Washington 98104-2499, USA. E-mail: irozet{at}u.washington.edu
 |
Abstract |
|---|
 TOP Abstract IntroductionCase reportDiscussionReferences |
|---|
Clinical features: A 57-yr-old patient was scheduled for clipping of a large unruptured basilar tip aneurysm. Abrupt bulging of the brain was observed after bone flap removal, but before dura was opened. This was associated with concurrent development of systemic hypertension to 200/120 mmHg and jugular venous bulb (SjvO2) desaturation to 13%. Rupture of aneurysm was confirmed by frank blood in cerebrospinal fluid drainage from the lumbar subarachnoid catheter.
Conclusions: Abrupt SjvO2 desaturation prior to dural opening may suggest an acute increase in intracranial pressure, which in our case followed aneurysmal rupture; the systemic response to increased intracranial pressure (Cushing’s response) may be ineffective in maintaining cerebral perfusion.
|
Introduction |
|---|
|
TOPAbstractIntroductionCase reportDiscussionReferences |
|---|
|
Case report |
|---|
|
TOPAbstractIntroductionCase reportDiscussionReferences |
|---|
A 56-yr-old male with a past medical history of stable coronary artery disease, hypertension, and heavy smoking, was transferred to our hospital for investigation of subarachnoid hemorrhage. Computed tomography of head was negative for subarachnoid hemorrhage, but angiography revealed a large aneurysm of basilar artery (Figure 1
). After unsuccessful attempts to coil the aneurysm, the patient was scheduled for surgical clipping on day 16 post-admission. Preoperatively, the patient was alert and awake with a Glasgow coma scale score of 15. After uneventful induction of anesthesia with fentanyl, propofol and rocuronium, the trachea was intubated and the patient was ventilated with a mixture of oxygen/air, and anesthesia was maintained with sevoflurane (1.5–2% end-tidal), remifentanil (infusion at 0.125 µg·kg–1··hr–1), and vecuronium as needed. In addition to routine monitoring, a 4-Fr oximetric catheter (model: 040HF4, Edwards Lifesciences, LLC, Irvine, CA, USA) was inserted into the right jugular bulb,1 and calibrated in vivo for continuous SjvO2 measurement (Vigilance Monitor, Edwards SAT-2TM computer, Irvine, CA; USA oximetry range of 0–99%). Positioning of the catheter tip was verified radiologically (Figure 2). For induction of moderate hypothermia an intravascular cooling device (Innercool Therapies, San Diego, CA, USA) was inserted into the inferior vena cava via the left femoral vein.
|
|
). The lumbar subarachnoid catheter was opened, which returned bright red blood, confirming acute rupture of the aneurysm, and then was clamped. The operation was halted, and the patient was treated with hyperventilation, iv boluses of sodium thiopental (2 g iv total), labetalol (100 mg iv), and mannitol (2 g·kg–1 iv). After approximately five minutes, SjvO2 started to increase, AP decreased to 150/70 mmHg, and HR increased to 70 beats·min–1. There was visible improvement in dural tension. At constant end-tidal CO2, SjvO2 increased progressively to 84% and remained elevated for ten minutes (Figure 3), followed by a gradual decline to 55%. The jugular venous bulb lactate was 1.8 mmol·L–1, compared to 1.0 mmol·L–1 in arterial blood. After 30 min, the brain appeared to be slack again, and with the patient hemodynamically stable, the surgical procedure was allowed to resume. The lumbar subarachnoid catheter was opened and drained 100 mL of bloody cerebrospinal fluid. Under microscopic dissection, the aneurysm was identified and found to be leaking. Temporary cardiac arrest lasting up to 25 sec was induced with escalating boluses of adenosine up to 24 mg iv, and the aneurysm was clipped successfully. Transient decrease of SjvO2 lasting five to ten seconds occurred with the two high doses of adenosine.
|
|
Discussion |
|---|
|
TOPAbstractIntroductionCase reportDiscussionReferences |
|---|
The use of SjvO2 monitoring has been described in neuroanesthesia3 and can be used to adjust mechanical ventilation and blood pressure to maintain adequate oxygen delivery to the brain. In our institution, continuous SjvO2 monitoring is a part of routine practice during clipping of basilar tip aneurysms, when transient cardiac arrest with adenosine is planned. In our patient, SjvO2 decreased abruptly from 52% to 13%, accompanied by an increase in lactate, strongly suggesting a nearly "no flow" state, confirming the diagnosis of aneurysmal rupture. Although the accuracy of oximetry at such low values has not been carefully studied (accuracy range at SatO2 = 30 to 99% is ± 2%, according to manufacturer manual), this is the lowest SjvO2 value ever reported. This was preceded by systemic hypertension, but the time lag was short, and within a minute. This is consistent with low cerebral oxygen reserve with a highly metabolically active organ requiring a high blood flow. Systemic hypertension, however, is a nonspecific sign during surgery and not diagnostic for aneurysmal rupture.
After treatment with sodium thiopental and mannitol, dural tension decreased, and SjvO2 gradually increased; both are indicative of decrease in brain compression and restoration of cerebral blood flow. Subsequent increase in SjvO2 to 84% suggests reactive hyperemia post-brain injury, or "luxury" perfusion. Had the hyperemia persisted, it would suggest that the brain might have suffered irreparable damage, and was no longer able to extract oxygen. A joint neurosurgery-anesthesia decision had been made to abandon the procedure, if the SjvO2 did not normalize within the 30 min period.
With regard to systemic blood pressure changes, SjvO2 monitoring provides some interesting insights worthy of discussion. The classical Cushing response consists of systemic hypertension and bradycardia secondary to increase in ICP.4 According to the classic hypothesis, increase of systemic BP during intracranial hypertension represents a compensatory mechanism intended to maintain cerebral perfusion pressure (CPP).5 Different mechanisms of BP elevation secondary to increased ICP had been suggested in animal studies. Systemic hypertension has been described to be a result of the reflex increase of catecholamine secretion,6–8 and a result of the sympathetic overactivity due to brainstem compression,9 or due to craniocaudal ischemia.10–13 Some animal studies suggest Cushing’s response is a late feature, when ICP approaches mean arterial pressure, signalling breakdown of cerebral autoregulation.14–17 In this situation, hypertension leads to further increase of ICP, adversely influencing cerebral perfusion.14–17 It is likely that both the level of maximal ICP, and the rate of ICP change influence the hemodynamic response. Animal studies showed "classic" Cushing’s response to be apparent and beneficial to CPP only with gradual increases in ICP, with maximal ICP staying within the limits of cerebral autoregulation.13,18 In our case, the sudden occurrence of tense dura and appearance of the bright blood from the lumbar subarachnoid catheter confirmed the diagnosis of aneurysmal rupture. In centres where subarachnoid catheters are not placed routinely, the sudden and severe SjvO2 desaturation may facilitate the diagnosis of aneurysmal rupture. Although the cranium was open, the acute profound fall of SjvO2 indicated a rapid extreme cerebral hypoperfusion secondary to increased "intraparenchymal pressure". This is the first time jugular desaturation has been recorded during acute aneurysmal rupture accompanied by the Cushing response. Although the increase in systemic blood pressure represents a compensatory mechanism to maintain CPP, the severe jugular venous desaturation in our case suggests that 1) there was cortical cerebral ischemia, 2) the Cushing response may be an ineffective compensatory mechanism.
Although not essential in routine clinical practice, the presence of SjvO2 monitoring in our case facilitated the perioperative management of unexpected aneurysmal rupture, and provided some insight regarding the mechanism and efficacy of the Cushing response.
|
Footnotes |
|---|
|
References |
|---|
|
TOPAbstractIntroductionCase reportDiscussionReferences |
|---|
2 Batjer H, Samson D. Intraoperative aneurysmal rupture: incidence, outcome, and suggestions for surgical management. Neurosurgery 1986; 18: 701–7.[Medline]
3 Matta BF, Lam AM, Mayberg TS, Shapira Y, Winn HR. A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures. Anesth Analg 1994; 79: 745–50.
4 Cushing H. Some experimental and clinical observations concerning states of increased intracranial tension. Am J Med Sci 1902; 124: 375–400.
5 Plets C. Arterial hypertension in neurosurgical emergencies. Am J Cardiol 1989; 63: 40C–2C.[Medline]
6 van Loon J, Shivalkar B, Plets C, Goffin J, Tjandra-Maga TB, Flameng W. Catecholamine response to a gradual increase of intracranial pressure. J Neurosurg 1993; 79: 705–9.[Medline]
7 Ogilvy CS, DuBois AB. Effect of increased intracranial pressure on blood pressure, heart rate, respiration and catecholamine levels in neonatal and adult rabbits. Biol Neonate 1987; 52: 327–36.[Medline]
8 Kocsis B, Fedina L, Pasztor E. Effect of preexisting brain ischemia on sympathetic nerve response to intracranial hypertension. J Appl Physiol 1991; 70: 2181–7.
9 Pasztor E, Fedina L, Kocsis B, Berta Z. Activity of peripheral sympathetic efferent nerves in experimental subarachnoid haemorrhage. Part I: observations at the time of intracranial hypertension. Acta Neurochir (Wien) 1986; 69: 125–31.
10 Rosner MJ, Newsome HH, Becker DP. Mechanical brain injury: the sympathoadrenal response. J Neurosurg 1984; 61: 76–86.[Medline]
11 Shivalkar B, Van Loon J, Wieland W, et al. Variable effects of explosive or gradual increase of intracranial pressure on myocardial structure and function. Circulation 1993; 87: 230–9.
12 Shrader H, Hall C, Zwetnow NN. Effects of prolonged supratentorial mass expansion on regional blood flow and cardiovascular parameters during the Cushing response. Acta Neurol Scand 1985; 72: 283–94.[Medline]
13 Marshman LA. Cushing’s "variant" response (acute hypotension) after subarachnoid hemorrhage. Association with moderate intracranial tensions and subacute cardiovascular collapse. Stroke 1997; 28: 1445–50.
14 Fitch W, McDowall DG, Keaney NP, Pickerodt VW. Systemic vascular responses to increased intracranial pressure. 2. The "Cushing " response in the presense of intracranial space-occupying lesions: systemic and cerebral haemodynamic studies in the dog and the baboon. J Neurol Neurosurg Psychiatry 1977; 40: 843–52.[Medline]
15 Shalit MN, Cotev S. Interrelationship between blood pressure and regional cerebral blood flow in experimental intracranial hypertension. J Neurosurg 1974; 40: 594–602.[Medline]
16 Brinker T, Seifert V, Dietz H. Cerebral blood flow and intracranial pressure during experimental subarachnoid haemorrhage. Acta Neurochir (Wien) 1992; 115: 47–52.[Medline]
17 Harris AP, Helou S, Traystman RJ, Jones MD Jr, Koehler RC. Efficacy of the Cushing response in maintaining cerebral blood flow in premature and near-term fetal sheep. Pediatr Res 1998; 43: 50–6.[Medline]
18 Barbiro-Michaely E, Mayevsky A. Effects of elevated ICP on brain function: can the multiparametric monitoring system detect the ‘Cushing Response’? Neurol Res 2003; 25: 42–52.[Medline]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
