Endoscopic endocrine neck surgery with carbon dioxide insufflation: the effect on intracranial pressure in a large animal model

BACKGROUND: Endoscopic endocrine neck surgery requires insufflation with carbon dioxide (CO(2)) at 10 to 15 mm Hg, which may decrease the cerebral venous return and increase intracranial pressure. This study evaluated the effect of CO(2) neck insufflation on intracranial pressure (ICP) and hemodynamic parameters. METHODS: Fifteen pigs underwent endoscopic thyroid dissection. Insufflation was performed with CO(2) at 0 (sham), 10, 15, and 20 mm Hg and with helium at 20 mm Hg with 3 pigs in each group. ICP, mean arterial pressure, central venous pressure (CVP), cardiac output, and blood gas were measured at baseline, 30, 60, and 120 minutes. RESULTS: There were no differences in mean ICP between the sham group and CO(2) insufflation at 10 mm Hg. Mean ICP increased significantly with CO(2) at 15 and 20 mm Hg and with helium at 20 mm Hg. A significant increase in CVP occurred in pigs operated with CO(2) at 20 mm Hg. We observed jugular vein collapse under all insufflation pressures; however, pigs operated at 10 mm Hg were able to maintain an intermittent blood flow. CONCLUSIONS: A severe increase in ICP occurs with insufflation pressures higher than 15 mm Hg, possibly as a result of decreased cervical venous blood flow. Carbon dioxide insufflation up to 10 mm Hg does not alter ICP and is recommended for clinical application in endoscopic neck surgery.     

The effects of pipecuronium bromide on intracranial pressure and cerebral perfusion pressure

Twenty patients with expansive pathologic intracranial lesions, who were anesthetized with thiopental, nitrous oxide in oxygen, and fentanyl and mechanically ventilated to ensure normocarbia, received pipecuronium bromide 70 microg/kg i.v. Intracranial pressure (ICP), heart rate, arterial pressure, central venous pressure (CVP), EKG, and end-tidal CO2 were simultaneously recorded for 5 min before and for 15 min after administration of the muscle relaxant. No statistically significant changes in ICP and cerebral perfusion pressure were observed after administration of pipecuronium bromide. Cardiovascular stability was maintained during the study period except for a small, although significant, decrease of the CVP from 5.7 +/- 2.5 (SEM) to 5.0 +/- 2.5 mm Hg. These results, together with the long-lasting muscular effect of pipecuronium bromide, suggest that this new neuromuscular blocking agent may be used for muscle relaxation during neurosurgical operations in patients who have normal intracranial pressure at the time of administration of the drug.     

Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.     

The influence of some inhalation anaesthetics on the intracranial pressure with special reference to nitrous oxide (author's transl)]

The influence of inhalation anaesthetics on intracranial pressure (ICP), arterial blood pressure and cerebral perfusion pressure (CPP) was investigated on 12 unconscious patients with head injury having an initial ICP of about 20 mm Hg. Halothane, enflurane and nitrous oxide induced a considerable rise of ICP during a 15 to 25 minute period of observation. The moderate fall in blood pressure caused by halothane and enflurane enhanced the reduction of the calculated CPP. Besides, a regular fall in blood pressure of about 16% was observed under the influence of nitrous oxide, subsequently reducing the CPP in some cases under 40 mm Hg. Inhalation anaesthetics, including nitrous oxide, should therefore not be used in patients with decreased intracranial compliance before the increased ICP is treated.     

The relation between intracranial pressure,mean arterial pressure and cerebral blood flow in patients with severe head injury

In patients with severe head injuries ICP, MAP and CBF were measured continuously. In most patients there was a positive vasopressor response to increasing ICP, but the ICP/MAP ratio varied considerably in individual cases. CBF was diminished either by increasing ICP or by decreasing MAP. This effect was more marked with ICP above 40 mm Hg or MAP below 110 mm Hg. In terminal stages there was often a negative MAP/ICP ratio accompanied by massive cerebral hyperaemia. Key words: Severe head injury--intracranial pressure--mean arterial pressure--cerebral blood flow--cerebral perfusion pressure--critical limit of ICP and CBF. Abbreviations: ICP equals intracranial pressure (mm Hg); CBF, Flow equals cerebral blood flow (ml/min); MAP equals mean arterial pressure (mm Hg); CPP equals cerebral perfusion pressure (mm Hg) (difference between MAP and ICP); BP equals blood pressure.     

Reverse Trendelenburg position reduces intracranial pressure during craniotomy.

Cerebral swelling and herniation pose serious surgical obstacles during craniotomy for space-occupying lesions. Positioning patients head-up has been shown previously to reduce intracranial pressure (ICP) in neurotraumatized patients, but has not been investigated during intracranial surgery. The current study examined the effects of 10-deg reverse Trendelenburg position (RTP) on ICP and cerebral perfusion pressure (CPP). Forty adult patients subjected to craniotomy for supratentorial tumors were given standardized propofol-fentanyl-cisatracurium general anesthesia and were moderately hyperventilated. In 26 of 40 patients with expected poor clinical outcome, an additional catheter was placed in the internal jugular bulb to determine internal jugular bulb pressure (JBP). ICP was determined by subdural measurement using a 22-gauge needle advanced through the dura after removal of the bone flap. ICP was referenced to the level of the dural incision. ICP, mean arterial blood pressure, and CPP were compared with repeat measurements 1 minute after RTP. The tension of the dura was graded qualitatively by the surgeon by digital palpation and was compared to post-RTP. ICP decreased from 9.5 mm Hg to 6.0 mm Hg ( P <.001; all values are median) within 1 minute after 10-deg RTP. Mean arterial blood pressure decreased from 82.0 mm Hg to 78.5 mm Hg ( P <.001). CPP was unchanged (70.5 mm Hg versus 71 mm Hg after RTP), whereas JBP decreased from 8 mm Hg to 4 mm Hg ( P <.001). High initial ICP was correlated to the greatest magnitude of decrease in ICP. No significant correlation was found between change in ICP and change in JBP. Intracranial pressure after RTP resulted in decreased tension of the dura. RTP appears to be an effective means of reducing ICP during craniotomy, thereby reducing the risk of cerebral herniation. CPP is not affected. Studies over longer periods of time are warranted, however.     

The effect of propofol sedation on the intracranial pressure of patients with an intracranial space-occupying lesion

The fear of producing CO(2) retention and a secondary increase of intracranial pressure (ICP) sometimes precludes the use of sedation for the spontaneously breathing patient in the presence of an intracranial space-occupying lesion. In this study we assessed the effect of moderately deep propofol sedation on the ICP of patients undergoing stereotactic brain tumor biopsy under regional anesthesia. Thirty patients were randomized into 2 groups to receive propofol titrated to a level of 2 on the Observer's Assessment of Alertness/Sedation Scale or no sedation. ICP was measured via the biopsy needle. Preoperative data were similar in both groups. During surgery, patients receiving propofol had a higher arterial Pco(2) (48 +/- 8 mm Hg versus 41 +/- 3 mm Hg; P = 0.005) (95% confidence interval, 43-53 mm Hg and 39-43 mm Hg, respectively), resulting in a lower arterial pH (P = 0.002) than patients in the no-sedation group. The median ICP (95% confidence interval) for both groups was similar-13 mm Hg (8.2-16.2 mm Hg) and 15 mm Hg (8.3-21.7 mm Hg)-for the propofol and no-sedation groups, respectively (P = 0.66). Cerebral perfusion pressure was lower in the propofol group (76 +/- 18 mm Hg versus 89 +/- 18 mm Hg; P = 0.003). Moderately deep propofol sedation does not result in a higher ICP than no sedation in patients undergoing stereotactic brain tumor biopsy. Further studies are needed to assess the effect on ICP of other sedative medications.     

Experimental evaluation of the Spiegelberg intracranial pressure and intracranial compliance monitor. Technical note

The goal of this study was to compare the Spiegelberg intraventricular intracranial pressure (ICP)/intracranial compliance monitoring device, which features an air-pouch balloon catheter, with existing gold-standard methods of measuring ICP and intracranial compliance. A Spiegelberg intraventricular catheter, a standard intraventricular catheter, and a Codman intraparenchymal ICP microsensor were placed in five sheep, which previously had been given anesthetic and paralytic agents, to allow comparative measurement of ICP at incremental levels (range 5-50 mm Hg). Intracranial pressure measured using the Spiegelberg intraventricular air-pouch balloon catheter displayed a linear correlation with ICP measured using the standard intraventricular fluid-filled catheter (r2 = 0.9846, p < 0.001; average bias -0.74 mm Hg), as well as with ICP measured using the Codman intraparenchymal strain-gauge sensor (r2 = 0.9778, p < 0.001; average bias 0.01 mm Hg). Automated measurements of intraventricular compliance obtained using the Spiegelberg compliance device were compared with compliance measurements that were made using the gold-standard manual cerebrospinal fluid bolus injection technique at ICPs ranging from 5 to 50 mm Hg, and a linear correlation was demonstrated between the two methods (r2 = 0.7752, p < 0.001; average bias -0.019 ml/mm Hg). The Spiegelberg air-pouch ICP/compliance monitor provides ICP and compliance data that are very similar to those obtained using both gold-standard methods and an intraparenchymal ICP monitor over a range of pathophysiological ICPs. The automated closed Spiegelberg system offers practical advantages for the measurement of intraventricular compliance. Assessment of the clinical utility and robustness of the Spiegelberg system, together with the development of an intraparenchymal device, would enhance the clinical utility of automated compliance measurement and expand the range of its applications.     

Adverse impact of a calcium entry-blocker (verapamil) on intracranial pressure in patients with brain tumors

In order to examine the effects of verapamil on intracranial pressure (ICP) in patients with compromised intracranial compliance, five hypertensive patients with supratentorial tumors were given verapamil, 5 mg intravenously, at the time of anesthesia induction. Within 4 minutes, ICP increased 67% from 18 +/- 4 mm Hg (standard error) to 27 +/- 5 mm Hg (p less than 0.05), whereas mean arterial pressure decreased 20% from 111 +/- 7 mm Hg to 89 +/- 4 mm Hg (p less than 0.05), and cerebral perfusion pressure (CPP) decreased 33% from 93 +/- 11 mm Hg to 62 +/- 6 mm Hg (p less than 0.05). The increases in ICP responded promptly to hyperventilation and intravenous lidocaine (1.5 mg/kg). A control group of five hypertensive patients with supratentorial tumors received the same anesthetic agents without verapamil. In this group, ICP and CPP were unchanged. The authors conclude that calcium entry-blockers, such as verapamil, should be avoided in patients with compromised intracranial compliance unless ICP is being monitored and proper therapy for intracranial hypertension can be rapidly instituted.     

Cerebral perfusion pressure, intracranial pressure, and head elevation

Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20 degrees to 30 degrees, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10 degrees of head elevation from 0 degree to 50 degrees. For every 10 degrees of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 +/- 3.4 mm Hg (mean +/- standard error of the mean] always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0 degree head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.     

Desflurane increases intracranial pressure more and sevoflurane less than isoflurane in pigs subjected to intracranial hypertension

Desflurane and sevoflurane may have advantages over isoflurane in neuroanesthesia, but this is still under debate. A porcine model with experimental intracranial hypertension was used for paired comparison of desflurane, sevoflurane, and isoflurane with respect to the effects on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and intracranial pressure (ICP). The agents, given in sequence to each of six pigs, were compared at 0.5 and 1.0 minimal alveolar concentrations (MAC) and three mean arterial blood pressure (MAP) levels (50, 70, and 90 mm Hg) at normocapnia and one MAP level (70 mm Hg) at hypocapnia. MAC for each agent had been previously determined in a standardized manner for comparison reliability. CBF was measured with Xe. MAP was lowered by inflation of a balloon catheter in the inferior caval vein and raised by inflation of a balloon catheter in the descending aorta. ICP was measured intraparenchymally. Two Fogarty catheters positioned extradurally were inflated to a baseline ICP of 20 to 22 mm Hg at 0.2 MAC of each agent. CBF and ICP with the three agents at normocapnia and MAP 70 and 90 mm Hg at both 0.5 and 1.0 MAC were as follows (P < 0.05): desflurane > isoflurane > sevoflurane. None of the agents abolished CO2 reactivity. High-dose desflurane resulted in a higher CBF at hypocapnia than corresponding doses of sevoflurane or isoflurane, but there were no significant differences between the agents in ICP at hypocapnia. The present study showed that desflurane increased ICP more and sevoflurane less than isoflurane during normoventilation, but the differences disappeared with hyperventilation.     

Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury

During 1977-1978, 127 patients with severe head injury were admitted and underwent intracranial pressure (ICP) monitoring. All patients had Glasgow Coma Scale (GCS) scores of 7 or less. All received identical initial treatment according to a standardized protocol. The patients' average age was 29 years; 60% had multiple trauma, and 35% needed emergency intracranial operations. Treatment for elevations of ICP was begun when ICP rose to 20 to 25 mm Hg, and included mannitol therapy and drainage of cerebrospinal fluid (CSF) when possible. Forty-three patients (34%) had ICP greater than or equal to 25 mm Hg; of these, 36 (84%) died. The mortality rate of the entire group was 46%. During 1979-1980, 106 patients with severe head injury were admitted and underwent ICP monitoring. Their average ager was 29 years; 51% had multiple trauma, and 31% underwent emergency intracranial surgery. All patients received the same standardized protocol as the previous series, with the exception of the treatment of ICP. In this present series: if ICP was 15 mm Hg or less (normal ICP), patients were continued on hyperventilation, steroids, and intensive care; if ICP was 16 to 24 mm Hg, mannitol was administered and CSF was drained; if ICP was 25 mm Hg or greater, the patients were randomized into a controlled barbiturate therapy study. Twenty-six patients (25%) had ICP's of 25 mm Hg or greater, compared to 34% in the previous series (p less than 0.05), and 18 of these 26 patients (69%) died. The overall mortality for this current series was 28% compared to 46% in the previous series (p less than 0.0005). This study reconfirms the high mortality rate if ICP is 25 mm Hg or greater; however, the data also document that early aggressive treatment based on ICP monitoring significantly lessens the incidence of ICP of 25 mm Hg or greater and reduces the overall mortality rate of severe head injury.     

Short-term lack of cerebral perfusion with good outcome. Advantages of early intracranial pressure monitoring

A 21-year-old man was injured by a tailboard of a truck. He suffered a severe head injury with bilateral depressed skull fractures necessitating surgical decompression. On admission to the hospital the patient showed bending to pain stimuli (Glasgow Coma Score 5). Anisocoria was noticed from the beginning. Initial intracranial pressure (ICP), measured 3 hours after injury, was 30 mm Hg, and the cerebral perfusion pressure (CPP) was 70 mm Hg. During surgical elevation of the skull fracture on the right side an unexplainable rise of ICP to values of 100 mm Hg occurred, which corresponded to the mean arterial blood pressure (MAP). At the same time both pupils were dilated and fixed indicating a lack of cerebral perfusion. Due to immediate trephination of the opposite side, the ICP was lowered to values below 20 mm Hg, and sufficient cerebral perfusion (above 50 mm Hg) was regained. The patient showed a good recovery and was transferred to a rehabilitation center 5 weeks after injury.This case report emphasizes the importance of early and continuous intracranial pressure monitoring for adequate therapy in neurosurgical emergencies.     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients.

The traditional practice of elevating the head in order to lower intracranial pressure (ICP) in head-injured patients has been challenged in recent years. Some investigators argue that patients with intracranial hypertension should be placed in a horizontal position, the rationale being that this will increase the cerebral perfusion pressure (CPP) and thereby improve cerebral blood flow (CBF). However, ICP is generally significantly higher when the patient is in the horizontal position. This study was undertaken to clarify the issue of optimal head position in the care of head-injured patients. The effect of 0 degree and 30 degrees head elevation on ICP, CPP, CBF, mean carotid pressure, and other cerebral and systemic physiological parameters was studied in 22 head-injured patients. The mean carotid pressure was significantly lower when the patient's head was elevated at 30 degrees than at 0 degrees (84.3 +/- 14.5 mm Hg vs. 89.5 +/- 14.6 mm Hg), as was the mean ICP (14.1 +/- 6.7 mm Hg vs. 19.7 +/- 8.3 mm Hg). There was no statistically significant change in CPP, CBF, cerebral metabolic rate of oxygen, arteriovenous difference of lactate, or cerebrovascular resistance associated with the change in head position. The data indicate that head elevation to 30 degrees significantly reduced ICP in the majority of the 22 patients without reducing CPP or CBF.     

Effect of decompressive craniectomy on intracranial pressure and cerebrospinal compensation following traumatic brain injury

OBJECTIVE: Decompressive craniectomy is an advanced treatment option for intracranial pressure (ICP) control in patients with traumatic brain injury. The purpose of this study was to evaluate the effect of decompressive craniectomy on ICP and cerebrospinal compensation both within and beyond the first 24 hours of craniectomy. METHODS: This study was a retrospective analysis of the physiological parameters from 27 moderately to severely head-injured patients who underwent decompressive craniectomy for progressive brain edema. Of these, 17 patients had undergone prospective digital recording of ICP with estimation of ICP waveform-derived indices. The pressure-volume compensatory reserve (RAP) index and the cerebrovascular pressure reactivity index (PRx) were used to assess those parameters. The values of parameters prior to and during the 72 hours after decompressive craniectomy were included in the analysis. RESULTS: Decompressive craniectomy led to a sustained reduction in median (interquartile range) ICP values (21.2 mm Hg [18.7; 24.2 mm Hg] preoperatively compared with 15.7 mm Hg [12.3; 19.2 mm Hg] postoperatively; p = 0.01). A similar improvement was observed in RAP. A significantly lower mean arterial pressure (MAP) was needed after decompressive craniectomy to maintain optimum cerebral perfusion pressure (CPP) levels, compared with the preoperative period (99.5 mm Hg [96.2; 102.9 mm Hg] compared with 94.2 mm Hg [87.9; 98.9 mm Hg], respectively; p = 0.017). Following decompressive craniectomy, the PRx had positive values in all patients, suggesting acquired derangement in pressure reactivity. CONCLUSIONS: In this study, decompressive craniectomy led to a sustained reduction in ICP and improvement in cerebral compliance. Lower MAP levels after decompressive craniectomy are likely to indicate a reduced intensity of treatment. Derangement in cerebrovascular pressure reactivity requires further studies to evaluate its significance and influence on outcome.     

Effects of PEEP on the intracranial system of patients with head injury and subarachnoid hemorrhage: the role of respiratory system compliance

BACKGROUND: Positive end-expiratory pressure (PEEP) can be effective in improving oxygenation, but it may worsen or induce intracranial hypertension. The authors hypothesized that the intracranial effects of PEEP could be related to the changes in respiratory system compliance (Crs). METHODS: A prospective study investigated 21 comatose patients with severe head injury or subarachnoid hemorrhage receiving intracranial pressure (ICP) monitoring who required mechanical ventilation and PEEP. The 13 patients with normal Crs were analyzed as group A and the 8 patients with low Crs as group B. During the study, 0, 5, 8, and 12 cm H2O of PEEP were applied in a random sequence. Jugular pressure, central venous pressure (CVP), cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral compliance, mean velocity of the middle cerebral arteries, and jugular oxygen saturation were evaluated simultaneously. RESULTS: In the group A patients, the PEEP increase from 0 to 12 cm H2O significantly increased CVP (from 10.6 +/- 3.3 to 13.8 +/- 3.3 mm Hg; p < 0.001) and jugular pressure (from 16.6 +/- 3.1 to 18.8 +/- 3.2 mm Hg; p < 0.001), but reduced mean arterial pressure (from 96.3 +/- 6.7 to 91.3 +/- 6.5 mm Hg; p < 0.01), CPP (from 82.2 +/- 6.9 to 77.0 +/- 6.2 mm Hg; p < 0.01), and mean velocity of the middle cerebral arteries (from 73.1 +/- 27.9 to 67.4 +/- 27.1 cm/sec; F = 7.15; p < 0.001). No significant variation in these parameters was observed in group B patients. After the PEEP increase, ICP and cerebral compliance did not change in either group. Although jugular oxygen saturation decreased slightly, it in no case dropped below 50%. CONCLUSIONS: In patients with low Crs, PEEP has no significant effect on cerebral and systemic hemodynamics. Monitoring of Crs may be useful for avoiding deleterious effects of PEEP on the intracranial system of patients with normal Crs.     

Elevated intracranial pressure stimulates gastric contractility in the rat

The gastric contractile response to elevated intracranial pressure (ICP) was studied in conscious rats. Elevation of intracranial pressure to 20 mm Hg was associated with a marked increase in the amplitude of gastric contractions (70-90% over baseline) without any change in contractile frequency (5.2 +/- .5 contractions per min). The increase in contractility continued for 45 min following release of the pressure. Vagotomy completely blocked the increase in gastric contractility seen with elevation in ICP. We conclude that acute elevation of intracranial pressure in rats results in increased force of gastric contractions. The forceful contractions persist despite release of the pressure and the increased contractile force is vagally mediated.     

Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension

To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15 degrees, 30 degrees, and 60 degrees. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15 degrees (a fall of -4.5 +/- 1.6 mm Hg, p less than 0.001) and 30 degrees (a fall of -6.1 +/- 3.5 mm Hg, p less than 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60 degrees, the mean ICP increased to -3.8 +/- 9.3 mm Hg of baseline, while the CPP decreased -7.9 +/- 9.3 mm Hg (p less than 0.02), and the cardiac index also fell -0.25 +/- 0.28 liters/min/sq m (p less than 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15 degrees or 30 degrees) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0 degrees) or higher (60 degrees) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.     

Efficacy of hyperventilation,blood pressure elevation,and metabolic suppression therapy in controlling intracranial pressure after head injury

OBJECT: Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. METHODS: Thirty-three patients with a mean age of 33 +/- 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 +/- 5 to 27 +/- 5 mm Hg and in ICP from 20 +/- 11 to 13 +/- 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 +/- 5 mm Hg and ICP increased from 16 +/- 9 to 19 +/- 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 +/- 10 to 16 +/- 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. CONCLUSIONS: Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.     

Chronic cerebral arterial spasm. The role of intracranial pressure.

The author used isolated rabbit common carotid and femoral arteries perfused at a constant pressure of 90 mm Hg to examine the variation of flow (F) with transmural pressure (TMP). When the TMP was reduced below 50 to 60 mm Hg in arteries with normal smooth muscle tone, arterial resistance increased significantly causing a reduction in flow. It is suggested that the diffuse arterial narrowing that occurs in patients with severe intracranial hypertension may be the result of a similar reduction in TMP. In the presence of active vasoconstriction, any increase in extraluminal (intracranial) pressure (ICP) resulted in a substantial increase in arterial resistance and subsequent reduction of flow. This F-TMP relationship depended only on the initial degree of constriction and was independent of the vasoconstrictor used to achieve this constriction and of the artery in which this constriction was produced. A review of the literature suggests that human cerebral arteries normally exhibit only mild constrictions in response to subarachnoid blood during the chronic phase of spasm. In the present study, a mild constriction in the absence of increased ICP or a moderate increase in ICP (45 mm Hg) in the absence of constriction produced minor reductions in arterial diameter and an average flow reduction of only 5% to 10%. However, when ICP was increased to 45 mm Hg in the presence of a mild constriction, severe arterial narrowing resulted and flow was reduced by 50%. Therefore, it is suggested that chronic arterial spasm is the result of a mild constriction which is amplified by the simultaneous occurrence of increased ICP. Phenoxybenzamine was found to be effective in reversing and preventing these contractions. The improvement in flow produced by phenoxybenzamine decreased as the TMP was reduced below 60 mm Hg. The effects of both diffuse and local spasm on cerebral blood flow are discussed.