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.     

Circadian rhythm of cerebral perfusion pressure and intracranial pressure in head injury

The aim of the study was to determine if Cerebral Perfusion Pressure CPP and Intracranial Pressure ICP, in patients with head injury, has a circadian rhythm. CPP and ICP data of 13 patients were analysed using the Regressive and Iterative Cosinor methods. The Regressive Cosinor method did not detect a strong 24 hour rhythm. Therefore, the Iterative Cosinor method was used to seek rhythms with period not necessarily equal to 24 hours. Studying consecutive patient days by the Iterative cosinor method showed that rhythm is present but the rhythm period was often not 24 hours. A significant rhythm in the range of 20-30 hours was detected in eight patients for CPP 62 and in six patients for ICP 46. To validate the results real and surrogate time series were compared. The clinical implications of rhythmic data analysis are discussed.     

The importance of brain temperature in patients after severe head injury: relationship to intracranial pressure,cerebral perfusion pressure,cerebral blood flow,and outcome

Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. The temperature difference between brain and rectal temperature was also calculated. Mild hypothermia (34-36 degrees C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean brain temperature ranged from 36.9 +/- 0.4 degrees C in the normothermic group to 38.2 +/- 0.5 degrees C in the hyperthermic group, 35.3 +/- 0.5 degrees C in the mild therapeutic hypothermia group, and 34.3 +/- 1.5 degrees C in the hypothermia group without active cooling. The mean DeltaT(br-rect) was positive for patients with a T(br) above 36.0 degrees C (0.0 +/- 0.5 degrees C) and negative for patients during mild therapeutic hypothermia (-0.2 +/- 0.6 degrees C) and also in those with a brain temperature below 36 degrees C without active cooling (0.8 +/- -1.4 degrees C) - the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a brain temperature between 36.0 degrees C and 37.5 degrees C was 37.8 +/- 14.0 mL/100 g/min. The lowest CBF was measured in patients with a brain temperature <36.0 degrees C and a negative brain-rectal temperature difference (17.1 +/- 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.     

The effect of mannitol on cerebral blood flow

The objective of this study was to evaluate the effects of mannitol, given over different time periods, on regional cerebral blood flow (rCBF) in patients with intracranial aneurysms. Seven patients with unruptured aneurysms (Group I) and 16 patients with Grade I and II subarachnoid hemorrhage (SAH) (Group II) received 1.5 gm/kg/8 hrs of 20% mannitol intravenously over a 24-hour period. Seven other patients with unruptured aneurysms (Group III) received 1.5 gm/kg of mannitol over 8 hours only. The last seven patients with unruptured aneurysms (Group IV) received the same dose, but as an intravenous bolus. Over a period of 24 hours, the patients underwent serial measurements of rCBF, intracranial pressure (ICP), mean blood pressure (MBP), cardiac output, and cerebral metabolic rate of oxygen consumption (CMRO2). Mannitol, when given as a continuous intravenous infusion, increased rCBF significantly without increasing MBP or decreasing ICP. This increase was more pronounced in SAH patients. The effects of mannitol lasted for 18 hours when given over an 8-hour period only; however, when it was given as a bolus, the increase in rCBF lasted for 24 hours, cardiac output tended to increase, and the effect on CMRO2 was variable.     

Effect of mannitol on cerebral blood flow and microcirculation during experimental middle cerebral artery occlusion

Regional cerebral blood flow (rCBF) was measured during and after a 2-3 hour occlusion period of the middle cerebral artery (MCA) in cats with the hydrogen clearance technique. The effects of mannitol upon rCBF were studied. Transient hypotension during occlusion dropped the blood flow to near zero on the occluded side, leading to postischemic hypoperfusion. Mannitol failed to modify blood flow during the occlusion period, but was effective in preventing any further decrease of blood flow during hypotension. Animals receiving mannitol had an improved postischemic recovery of blood flow. The correlation of ischemic severity and postischemic brain damage and the effects of mannitol on these parameters are discussed.     

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.     

Continuous cerebral compliance monitoring in severe head injury: its relationship with intracranial pressure and cerebral perfusion pressure

Summary Background. Cerebral compliance expresses the capability to buffer an intracranial volume increase while avoiding a rise in intracranial pressure (ICP). The autoregulatory response to Cerebral Perfusion Pressure (CPP) variation influences cerebral blood volume which is an important determinant of compliance. The direction of compliance change in relation to CPP variation is still under debate. The aim of the study was to investigate the relationship between CPP and compliance in traumatic brain injured (TBI) patients by a new method for continuous monitoring of intracranial compliance as used in neuro-intensive care (NICU).Method. Three European NICU’s standardised collection of CPP, compliance and ICP data to a joint database. Data were analyzed using an unpaired student t-test and a multi-level statistical model.Results. For each variable 108,263 minutes of data were recorded from 21 TBI patients (19 patients GCS≤8; 90% male; age 10–77 y). The average value for the following parameters were: ICP 15.1±8.9 mmHg, CPP 74.3±14 mmHg and compliance 0.68±0.3 ml/mmHg. ICP was ≥20 mmHg in 20% and CPP<60 mmHg for 10.7% of the time. Compliance was lower (0.51±0.34 ml/mmHg) at ICP≥20 than at ICP<20 mmHg (0.73±0.37 ml/mmHg) (p<0.0001). Compliance was significantly lower at CPP<60 than at CPP≥60 mmHg: 0.56±0.36 and 0.70±0.37 ml/mmHg respectively (p<0.0001). The CPP – compliance relationship was different when ICP was above 20 mmHg compared with below 20 mmHg. At ICP<20 mmHg compliance rose as CPP rose. At ICP≥20 mmHg, the relation curve was convexly shaped. At low CPP, the compliance was between 0.20 and 0.30 ml/mmHg. As the CPP reach 80 mmHg average compliance was 0.55 ml/mmHg., but compliance fell to 0.40 ml/mmHg when CPP was 100 mmHg.Conclusions. Low CPP levels are confirmed to be detrimental for intracranial compliance. Moreover, when ICP was pathological, indicating unstable intracranial equilibrium, a high CPP level was also associated with a low volume-buffering capacity.     

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.     

Effect of cerebral perfusion pressure on contusion volume following impact injury

OBJECT: Although it is generally acknowledged that a sufficient cerebral perfusion pressure (CPP) is necessary for treatment of severe head injury, the optimum CPP is still a subject of debate. The purpose of this study was to investigate the effect of various levels of blood pressure and, thereby, CPP on posttraumatic contusion volume. METHODS: The left hemispheres of 60 rats were subjected to controlled cortical impact injury (CCII). In one group of animals the mean arterial blood pressure (MABP) was lowered for 30 minutes to 80, 70, 60, 50, or 40 mm Hg 4 hours after contusion by using hypobaric hypotension. In another group of animals the MABP was elevated for 3 hours to 120 or 140 mm Hg 4 hours after contusion by administering dopamine. The MABP was not changed in respective control groups. Intracranial pressure (ICP) was monitored with an ICP microsensor. The rats were killed 28 hours after trauma occurred and contusion volume was assessed using hematoxylin and eosin-stained coronal slices. No significant change in contusion volume was caused by a decrease in MABP from 94 to 80 mm Hg (ICP 12+/-1 mm Hg), but a reduction of MABP to 70 mm Hg (ICP 9+/-1 mm Hg) significantly increased the contusion volume (p < 0.05). A further reduction of MABP led to an even more enlarged contusion volume. Although an elevation of MABP to 120 mm Hg (ICP 16+/-2 mm Hg) did not significantly affect contusion volume, there was a significant increase in the contusion volume at 140 mm Hg MABP (p < 0.05; ICP 18+/-1 mm Hg). CONCLUSION: Under these experimental conditions, CPP should be kept within 70 to 105 mm Hg to minimize posttraumatic contusion volume. A CPP of 60 mm Hg and lower as well as a CPP of 120 mm Hg and higher should be considered detrimental.     

Effect of mannitol on local cerebral blood flow after temporary complete cerebral ischemia in rats.

The effects of pretreatment with mannitol on local cerebral blood flow (CBF) after permanent or temporary global cerebral ischemia were evaluated with 14C-iodoantipyrine autoradiography in rats under halothane-N2O endotracheal anesthesia. Blood pressure, pulse rate, arterial blood gas levels, and electroencephalographic (EEG) tracings were monitored throughout the experiments. After permanent occlusion of the basilar artery and both external carotid and pterygopalatine arteries, severe global ischemia was induced by permanent occlusion of the common carotid arteries (CCA's) or by a 30-minute temporary CCA occlusion followed by 5 minutes of reperfusion. Intravenous mannitol (25%, 1 gm/kg) or saline solution was administered 5 minutes before occlusion of the CCA's. Cerebral blood flow was measured in 24 anatomical regions. The EEG tracings flattened within 2 to 3 minutes after the onset of ischemia, and no recovery was observed during reperfusion. In the mannitol-treated rats and the saline-treated controls, autoradiographic studies after permanent occlusion showed no CBF in the forebrain or cerebellum, although brain-stem and spinal cord CBF values were normal. After 5 minutes of reperfusion, CBF in the cortex, basal ganglia, and white matter was 100% to 200% higher in mannitol-treated rats and 50% to 100% higher in saline-injected rats than in the nonischemic anesthetized control group. Heterogeneously distributed areas of no-reflow were seen in all saline-injected rats but were observed in none of the mannitol-treated rats. Pretreatment with mannitol prevented postischemic obstruction of the microcirculation during 5 minutes of recirculation after 30 minutes of severe temporary ischemia, but the EEG signals did not recover. Further studies of the functional and morphological responses to longer periods of postischemic recirculation are needed to verify the extent to which these mannitol-induced effects are protective.     

Cerebral perfusion pressure management in head injury

A method of ICP management is presented based upon maintenance of cerebral perfusion pressure ( CPP = SABP - ICP) at 70-88 mm Hg or in some cases greater. To do this, we have employed volume expansion, nursed patients in the flat position, and actively used catecholamine infusions to maintain the SABP side of the CPP equation at levels necessary to obtain the target CPP. CSF drainage and mannitol have freely been used to maintain the ICP portion of the equation. Thirty-four consecutive patients with GCS less than or equal to 7 were admitted to the Neurosurgical Intensive Care Unit (GCS = 5.1 +/- 1.4) and managed with this protocol. CPP was maintained at 84 +/- 11 mm Hg, ICP was 23 +/- 9.8 mm Hg, and SABP averaged 106 +/- 11 mm Hg. CVP was 8.0 +/- 3.7 mm Hg and average fluid intake was approximately 5.4 +/- 3.9 liters/d. Output averaged 5.0 +/- 4.0 liters/d; additionally, albumin (25%) (33 +/- 44 gm/d) and PRBCs were used for vascular expansion and hemoglobin was maintained (11.5 +/- 1.4 gm/dl). Three patients died of uncontrolled ICP (all protocol errors). Four other patients succumbed, none secondary to ICP and all secondary to potentially avoidable complications. Morbidity (GOS = 4.2 +/- 0.87) appeared to be as good or superior to previous methods of therapy. Overall, mortality was 21% and that from uncontrollable ICP was 8%. This approach to the management of intracranial hypertension proved safe, rational, and greatly enhanced the therapeutic options available. It was also consistent with optimal care of other organ systems. The results bring into question many of the standard tenets of neurosurgical ICP management and suggest new avenues of investigation.     

Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow.

Increased brain tissue stiffness following severe traumatic brain injury is an important factor in the development of raised intracranial pressure (ICP). However, the mechanisms involved in brain tissue stiffness are not well understood, particularly the effect of changes in systemic blood pressure. Thus, controversy exists as to the optimum management of blood pressure in severe head injury, and diverging treatment strategies have been proposed. In the present study, the effect of induced alterations in blood pressure on ICP and brain stiffness as indicated by the pressure-volume index (PVI) was studied during 58 tests of autoregulation of cerebral blood flow in 47 comatose head-injured patients. In patients with intact autoregulation mechanisms, lowering the blood pressure caused a steep increase in ICP (from 20 +/- 3 to 30 +/- 2 mm Hg, mean +/- standard error of the mean), while raising blood pressure did not change the ICP. When autoregulation was defective, ICP varied directly with blood pressure. Accordingly, with intact autoregulation, a weak positive correlation between PVI and cerebral perfusion pressure was found; however, with defective autoregulation, the PVI was inversely related to cerebral perfusion pressure. The various blood pressure manipulations did not significantly alter the cerebral metabolic rate of oxygen, irrespective of the status of autoregulation. It is concluded that the changes in ICP can be explained by changes in cerebral blood volume due to cerebral vasoconstriction or dilatation, while the changes in PVI can be largely attributed to alterations in transmural pressure, which may or may not be attenuated by cerebral arteriolar vasoconstriction, depending on the autoregulatory status. The data indicate that a decline in blood pressure should be avoided in head-injured patients, even when baseline blood pressure is high. On the other hand, induced hypertension did not consistently reduce ICP in patients with intact autoregulation and should only be attempted after thorough assessment of the cerebrovascular status and under careful monitoring of its effects.     

Monitoring of cerebrospinal dynamics using continuous analysis of intracranial pressure and cerebral perfusion pressure in head injury

Summary Cerebrospinal dynamics has been investigated by statistical analysis of results of computerised monitoring of 80 head injured patients admitted to the Intensive Care Unit at Pinderfields General Hospital. One minute average values of intracranial pressure (ICP), systemic arterial pressure (ABP), cerebral perfusion pressure (CPP), amplitude of the fundamental component of the intracranial pressure pulse wave and the short-term moving correlation coefficient between that amplitude and mean ICP (RAP) were recorded. It was found that reduction of CPP down to 40mmHg was more often caused by decrease in ABP than increase in ICP. Further falls in CPP below 40mmHg were caused by substantial increases in ICP above 25 mmHg. The relationship between the ICP pulse wave amplitude and CPP showed a significant gradual increase in amplitude with CPP decreasing from 75 to 30 mmHg. For CPP below 30 mmHg there is a sharp decrease in amplitude followed by a change in the coefficient RAP from positive to negative values. This was interpreted as a sign of critical disturbance in cerebral circulation.     

The effects of indomethacin on intracranial pressure,cerebral blood flow and cerebral metabolism in patients with severe head injury and intracranial hypertension

Summary In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control intracranial pressure (ICP) (ICP>20 mmHg) by artificial hyperventilation (PaCO₂ level 3.5–4.0 kPa) and barbiturate sedation, indomethacin was used as a vasoconstrictor drug. In all patients, indomethacin (a bolus injection of 30 mg, followed by 30 mg/h for seven hours) reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in CBF at 2h. After 7h, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In the other patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. These results suggest that indomethacin due to its cerebral vasoconstrictor and antipyretic effect should be considered as an alternative for treatment of ICP-hypertension in head-injured patients.Presented at the Fifth Nordic CBF Symposium, Lund, Sweden, 21–22 May 1990.     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and regional cerebral oxygen saturation in patients with cerebral hemorrhage

OBJECTIVE: To study the effects on cerebral dynamics and regional oxygenation (rSO2) of the semi-sitting position, with the head at either 30 degrees or 45 degrees, in surgery for cerebral hemorrhage. PATIENTS AND METHODS: We performed a prospective study of 10 patients undergoing surgery for cerebral hemorrhage under sedation and analgesia and with mechanical ventilation. Intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and rSO2 measured using near-infrared spectroscopy were recorded with the head in the supine position (0 degrees) and elevated to an angle of 30 degrees and then 45 degrees, following a stabilization period of 5 minutes. RESULTS: Mean (SD) ICP values were significantly lower in both semi-sitting positions than in the supine position: 2.8 (1.4) mm Hg lower at 30 degrees and 4.4 (1.4) mm Hg lower at 45 degrees. Mean CPP values were fell slightly when the head was elevated to 30 degrees (3.5 [3.1] mm Hg, P=.048); a greater reduction was achieved when the head was elevated 45 degrees (7.1 [4.8] mm Hg, P<.01). The greatest reduction in mean MAP values also occurred with the head elevated to 45 degrees (11.8 [4.6] mm Hg, P<.001). Mean rSO2 values fell when the head was elevated to 30 degrees and 45 degrees; the greatest reduction occurred when the head was elevated to 45 degrees (7% [2%], P<.001). There was a moderate correlation between CPP values and changes in rSO2 (r2=0.45, P<.001). CONCLUSION: Head elevation significantly reduces ICP and CPP in patients with cerebral hemorrhage. Head elevation also reduces rSO2, to a greater or lesser extent depending on the degree to which the head is elevated.     

Effects of perfusion pressure on cerebral blood flow and oxygenation during normothermic cardiopulmonary bypass

BACKGROUND: Central nervous system dysfunction after cardiopulmonary bypass (CPB) is an important cause of morbidity and mortality after cardiac surgery. Perfusion pressure (PP) during CPB could be one of the important determinants of cerebral blood flow (CBF). The objective of the present study was to determine the effect of PP on CBF and cerebral oxgenation during normothermic CPB. METHODS: Twelve adult patients undergoing coronary artery bypass graft surgery were randomly assigned to one of two groups based on PP (High and Low group). Patients in High group received phenylephrine immediately after the onset of CPB to maintain PP between 60 and 80 mmHg. Oxyhemoglobin (O2Hb), deoxyhemoglobin (HHb), tissue oxygenation index (TOI), and oxidized cytochrome aa3 (CtOx) were measured by near-infrared spectroscopy, and internal jugular venous bulb blood oxygen saturation (SjvO2) was measured simultaneously. S-100 beta protein concentrations were also measured before and after CPB. RESULTS: SjvO2 in High group increased significantly during CPB. CtOx in Low group decreased significantly during CPB, whereas TOI was unchanged. Although S-100 beta increased significantly at the end of CPB, there was no difference between the groups. CONCLUSIONS: These results suggest that maintaining high PP is benefical for CBF during normothermic CPB.