Effect of sufentanil on intracranial pressure in neurosurgical patients

The effects of sufentanil on intracranial pressure, mean arterial pressure, cerebral perfusion pressure and heart rate were studied in 20 neurosurgical intensive care unit patients. Epidural intracranial pressure probes were implanted in patients who suffered head injury, intracerebral haemorrhage or underwent tumour resection. Sufentanil was given intravenously in sequential doses of 0.5, 1.0 and 2.0 micrograms/kg. Fifteen minutes elapsed after each dose. The patients were allocated to either group 1 (baseline intracranial pressure less than 20 mmHg) or group 2 (baseline intracranial pressure greater than 20 mmHg). Intracranial pressure did not change significantly in either group. Therefore the falls in mean arterial pressure with the highest dose in both groups and with 1.0 micrograms/kg in group 2, closely reflect corresponding reductions in cerebral perfusion pressure. As sufentanil in itself exerts no effects on intracranial pressure, concomitant haemodynamic changes are the critical factor for an adequate cerebral perfusion pressure.     

Outcomes of blunt head trauma without intracranial pressure monitoring

Although guidelines exist for intracranial pressure (ICP)-guided treatment after head trauma, no conclusive data exist that support routine ICP monitoring. A retrospective case series was reviewed of all patients admitted to the intensive care unit with a diagnosis of blunt head trauma between January 1, 1999 and December 31, 2004. None of the patients in the final analysis had ICP monitoring. Data collected included age, sex, mechanism of injury, Glasgow Coma Score (GCS) at admission, injury severity score, disposition, and length of stay. One hundred thirty-one patients with a median age of 41 years were included. There were 104 men (79%). The median GCS at admission was 12. There were 22 deaths (17% mortality). Stepwise logistic regression analysis identified older age, higher injury severity score, and lower GCS to be predictors of death. The mortality rate was higher in patients with GCS < or =8 compared with GCS >8 (33% vs 8%, respectively; P < 0.001). Ten of 23 patients with a GCS of 3 died (43% mortality). The median time to death for patients with a GCS of 3 was 2 days. Although the Brain Trauma Foundation has published guidelines advocating routine ICP monitoring, no large randomized prospective studies are available to determine its effect on outcome. None of the patients in this study had ICP monitoring. Our overall survival rate of 83 per cent is relatively high. Patients with a low GCS and, specifically, those with a GCS of 3 may not benefit from ICP monitoring because of early and irreversible trauma. Variability in the use of ICP monitoring will remain until ICP monitoring can be conclusively proven to improve outcome.     

Complications of intracranial pressure monitoring in trauma patients

A retrospective review of 175 intracranial pressure (ICP) monitors placed in 140 trauma patients over a recent 3-year period showed a 10.3% infection rate. Factors that were related to the development of an ICP monitor-related infection included: 1) duration of monitoring; 2) requirement for serial monitors; and 3) concurrent infection at other sites. These findings are discussed in light of the related literature concerning ICP monitoring and recommendations made to decrease the incidence of infection-related complications.     

Hypertonic saline lowers raised intracranial pressure in children after head trauma

Eighteen pediatric patients who sustained traumatic brain injury were enrolled in a double-blind, crossover study comparing the effects of 3% saline and 0.9% saline infusions on raised intracranial pressure (ICP). After resuscitation, each patient received a bolus of each saline concentration, and ICP was monitored for 2 h. Initial mean ICP before 0.9% saline infusions equaled 19.3 mm Hg and averaged 20.0 mm Hg during the subsequent 2-h trials (p = 0.32). Baseline mean ICP before 3% saline administration equaled 19.9 mm Hg and averaged 15.8 mm Hg for 2 h postinfusion (p = 0.003). Central venous pressure did not change significantly in either group, nor did measurements of renal function. Serum sodium concentrations increased in all 18 trials of 3% saline. Maximal concentrations of serum sodium occurred 30 min after bolus administration of 3% saline. Three percent saline significantly reduces raised ICP after traumatic brain injury when compared with normal saline. Intravascular dehydration, as measured by central venous pressure, did not occur during the study period.     

Effect of remifentanil on intracranial pressure and cerebral blood flow velocity in patients with head trauma

BACKGROUND: Remifentanil, an ultra-short-acting opioid, is used as an on-top analgesic in head trauma patients during transient painful procedures, e.g. endotracheal suctioning, physiotherapy, on the intensive care unit. However, previous studies have shown that opioids may increase intracranial pressure and decrease cerebral blood flow. METHODS: The present study investigates the effect of remifentanil on mean arterial blood pressure, intracranial pressure measured with intraparenchymal or epidural probes, and on cerebral blood flow velocity assessed by transcranial Doppler flowmetry in 20 head trauma patients sedated with propofol and sufentanil. Ventilation was adjusted for a target PaCO2 of 4.7-5.1 kPa. After baseline measurements a bolus of remifentanil (0.5 microg x kg(-1) i.v.) was administrated followed by a continuous infusion of remifentanil (0.25 microg x kg(-1) x min(-1) i.v.) for 20 min. RESULTS: There was no change in mean arterial blood pressure, intracranial pressure, and cerebral blood flow velocity in response to remifentanil infusion over time. Statistical analysis was performed using the Wilcoxon Signed Rank test. CONCLUSIONS: These data suggest that remifentanil can be used for on-top analgesia in head trauma patients without adverse effects on cerebrovascular haemodynamics, cerebral perfusion pressure or intracranial pressure.     

The relationship of intracranial pressure Lundberg waves to electroencephalograph fluctuations in patients with severe head trauma

Summary Lundberg (or B) waves, defined as repetitive changes in intracranial pressure (ICP) occurring at frequencies of 0.5 to 2 waves/min, have been attributed to cerebral blood flow fluctuations induced by central nervous system pace-makers or cerebral pressure autoregulation. We prospectively recorded and digitalized at a frequency rate of 10Hz (AcqKnowledge^TM software) the following parameters in 6 brain injured patients: mean arterial pressure, heart rate, ICP, mean flow velocity of the middle cerebral artery (MFV_MCA) (transcranial Doppler WAKI^TM) and left and right spectral edge frequency (SEFl, SEFr) of continuous electroencephalogram (EEG) recordings (Philips^TM technologies). All patients were sedated using a combination of sufentanil and midazolam and mechanically ventilated. Cerebral electrical activity (oscillations of SEF at a mean frequency of 26±9mHz) and MFV_MCA fluctuations were found strongly correlated with the intracranial Lundberg B waves (mean frequency 23±7mHz). These result support the existence of a neuropacemaker at the origin of the Lundberg B waves. The change in cerebral electrical activity, resulting from cerebral pacemakers, could increase cerebral metabolic rate of oxygen (CMRO₂) and thus lead to an increase in cerebral blood flow and secondarily of ICP through a change in cerebral blood volume.     

Changes in intracranial pressure in severe head injured patients in hemodialysis

Two cases of acute post-traumatic renal failure in severely head injured patients are reported. An increase in intracranial pressure (ICP) was shown up by continuous monitoring during haemodialysis: it was more important during conventional haemodialysis than during continuous arteriovenous haemofiltration. Although this effect is well known experimentally, few cases of continuous ICP pressure monitoring have been reported in head injury patients undergoing haemodialysis. The increase in ICP is explained in the dog as a result of blood-brain differences in urea concentration and osmolality leading to an increase in cerebral spinal fluid volume and cerebral tissue swelling. If dialysis is necessary in these patients, it should be carried out early and progressively, the patient's ICP being monitored continuously.     

An increase in intracranial pressure following fentanyl

We report an unusual fentanyl-induced reaction in an 8-year-old boy who had to be sedated and hyperventilated because of a severe head injury. Following the intravenous administration of a bolus of fentanyl, the intracranial pressure rose markedly for about 10 min. Simultaneously, the arterial blood pressure fell and heart rate increased, critically reducing the cerebral perfusion pressure temporarily. This reaction could be due to histamine-induced vasodilation.     

Relationship between hyperventilation and intracranial pressure in patients with severe head injury

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Opioid sedation does not alter intracranial pressure in head injured patients

Purpose

This study aimed to examine the effects of sedative doses of morphine, fentanyl and sufentanil on intracranial pressure (ICP) in head-injured patients in whom changes in mean artenal pressure (MAP) were minimized.

Methods

Fifteen severely head-injured patients (G5C of ≤8) were randomly assigned to receive either fentanyl. sufentanil or morphine, titrating the drug to a maximal 10% decrease in MAP. The patients were subsequently given an infusion of the same opioid. For four hours, ICP MAP and heart rate were recorded. Results: In all groups, there were no increases in ICP. There was a decrease in MAP in the sufentanil group at 10 min (P < 0.05) and 45 min after the initial opioid bolus. These decreases in MAP were not associated with increases in ICP.

Conclusion

The study suggests that when opioids are titrated in head-injured patients, worsening intracranial pressure can be avoided.     

Long-term intracranial pressure monitoring in comatose patients suffering from head injuries. A critical survey

Summary On the basis of a series of 75 patients, the practical use of ICP continuous long-term recording in severe head injuries without mass lesions or remaining deeply comatose after surgical procedures is critically analyzed. ICP monitoring alone seems to be not essential for prognosis. Conversely it is of much greater use as a guide to management (respirator treatment, osmotics, CSF drainage). If the pros and cons of the procedure are carefully weighed, it would appear that, for the time being, ICP long-term monitoring is justified only in comatose patients on intensive care.     

Computed tomographic brain density measurement as a predictor of elevated intracranial pressure in blunt head trauma

There are no independent computed tomography (CT) findings predictive of elevated intracranial pressure (ICP). The purpose of this study was to evaluate brain density measurement on CT as a predictor of elevated ICP or decreased cerebral perfusion pressure (CPP). A prospectively collected database of patients with acute traumatic brain injury was used to identify patients who had a brain CT followed within 2 hours by ICP measurement. Blinded reviewers measured mean density in Hounsfield Units (HU) within a 100-mm2 elliptical region at four standardized positions. Brain density measurement was compared for patients with an ICP of 20 or greater versus less than 20 mm Hg and CPP of 70 or greater versus less than 70 mm Hg. During a 2-year period, 47 patients had ICP monitoring after brain CT. Average age was 40 +/- 18 years old; 93.6 per cent were male; mean Injury Severity Score was 25 +/- 10; and Glasgow Coma Scale was 6 +/- 4. There was no difference in brain density measurement for observer 1, ICP less than 20 (26.3 HU) versus ICP 20 or greater (27.4 HU, P = 0.545) or for CPP less than 70 (27.1 HU) versus CPP 70 or greater (26.2, P = 0.624). Similarly, there was no difference for observer 2, ICP less than 20 (26.8 HU) versus ICP 20 or greater (27.4, P = 0.753) and CPP less than 70 (27.6 HU) versus CPP 70 or greater (26.2, P = 0.436). CT-measured brain density does not correlate with elevated ICP or depressed CPP and cannot predict patients with traumatic brain injury who would benefit from invasive ICP monitoring.     

Gangrene and renal failure caused by dihydroergotamine used to treat raised intracranial pressure following head trauma

A case of peripheral gangrene and renal failure following the use of dihydroergotamine (DHE) for treatment of raised intracranial pressure (ICP) is reported. There have been several reports of vasospasm and peripheral gangrene caused by DHE used in combination with heparin for prevention of deep venous thrombosis. Clinical experience with the use of DHE in head trauma is limited. This case report emphasises the seriousness of the adverse effects associated with the use of this drug.     

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.     

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.     

Management of head injury. Treatment of abnormal intracranial pressure.

Intracranial hypertension is recognized as a fundamental pathophysiologic process in brain injury. Although the exact pressure level defining intracranial hypertension remains to be firmly established, the majority of evidence available currently suggests that ICP should generally be treated when it exceeds 20 mm Hg. We suggest that lesions in the temporal lobe be treated at 15 mm Hg owing to the special relationship of this region to the brain stem. Along with the individual intracranial pressure reading, however, the course of the pressure over time and the status of the intracranial compliance as reflected in the ICP waveform must be considered when evaluating the intracranial dynamics. There is mounting evidence that patients with intracranial hypertension may comprise a heterogeneous group and that subgroups differ in their optimal treatment strategies. Although we cannot as yet identify such groups, factors such as age, CT diagnosis, responsiveness to hyperventilation, pressure-volume index, and ICP waveform are emerging as important differentiating factors. In particular, young patients with absent perimesencephalic cisterns and a tight brain on CT scan who manifest intracranial hypertension may comprise a group more suitable for treatment with hyperventilation and hypnotics than with osmotic agents. Although this is yet to be firmly established, currently it should be considered when such a patient responds poorly early in the course of conventional therapy for raised ICP. Treatment of intracranial hypertension remains rooted in the conventional therapeutic maneuvers. Maintenance of the basic homeostatic state of the patient is to be supplemented with head elevation, sedation, pharmacologic paralysis, hyperventilation, CSF drainage, and osmotic therapy as indicated. Outside of the special considerations discussed earlier, barbiturates should only be considered in patients with refractory intracranial hypertension without preexisting cardiovascular contraindications. Although several other agents have shown promise, currently the most exciting agent appears to be etomidate, which may prove quite useful. As ICP is better defined and understood, many significant and experimentally approachable questions are recognized. The basic mechanisms of raised ICP are slowly becoming elucidated. Clinical clues with which to subdivide patients with intracranial hypertension are being defined. New agents with efficacy in lowering raised ICP are appearing, and determination of their mechanisms of action may provide insight into the underlying disorder.