Professional Documents
Culture Documents
v- 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 hyperten-
sion 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 13"and 30* 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~ than
at 0* (84.3 _+ 14.5 rata Hg vs. 895 _ 14.6 ram Hg), as was the mean ICP ( 14.1 _ 6.7 rata 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~significantly reduced ICP in the majority of the 22 patients without
reducing CPP or CBF.
LEVATED intracranial pressure (ICP) or inade- dence suggesting that CPP is maximum when patients
TABLE 2
Effects of head elevation on cerebral and systemic pkysiologicat parameters in 22 patients*
Parameter 30~Head Elevation 0~Head Elevation MeanDifference P Value
mean carotid pressure (mm Hg) 84.3 _+14.5 89.5 -+ 14.6 -5.2 --. 8.1 0.0062
intracranialpressure(ram Hg) 14.1 + 6.7 19.7 __.8.3 -5.7 _-X5.6
- 0.0001
cerebral perfusionpressure(CPP) (mm Hg) 70.2 +__18.1 69.7 _+ 18.7 0.45 - 8.8 0.8
cerebral blood flow(CBF)(ml/100gm/min) 47.8 _+ 16.9 48.9 ---20.4 -1.03 + 10.8 0,657
cerebrovascularresistance(CPP/CBF) 1.72 _ 0.8 1.72 + 0.9 -0.0014 ---0.356 0.9844
cerebral metabolicrate of oxygen(zmol/100gm/min) 1.35 "- 0.59 1.28 + 0.53 0.075 _+0.23 0.14
arteriovenousoxygendifference(umol/ml) 1.81 _+0.63 1.72 _+0.73 0.093 + 0.35 0.23
PaCO2(mm Hg) 32.34 _+5.89 32.46 -+ 6.4 -0.1 + 1.9 0.77
arteriovenousdifferenceof lactate (umol/ml) -0.05 + 0.05 -0.05 _+0.06 -0.0002+ 0.06 0.18
oxygensaturationin jugularbulb (%) 69.9 _+9 70.3 + 10.2 -0.0043_+0.042 0.63
* Values representmean _+standarddeviation.
FIG. 1. Graph showing cerebral and systemic physiological parameters at head elevations of 0~ and 30~ in
22 patients with head injury. At 30", the intracranial pressure (ICP) was lower in 77% of patients, higher in
14%, and the same in 9%; mean carotid pressure (MCP) was lower in 59%, higher in 23%, and the same in
18%; cerebral perfusion pressure (CPP) was lower in 55% and higher in 45%; and cerebral blood flow (CBF)
was lower in 36%, higher in 36%, and the same in 14%. See text for analysis of the significance of the
differences.
Results
The effects of head elevation on ICP, MCP, CPP,
and CBF are illustrated in Fig. 1 and are given in Table
2 for all parameters measured. The mean values (+
standard deviation) for the MCP and ICP were signifi-
cantly lower at 30 ~ head elevation than at 0": 84.3 +
14.5 m m Hg versus 89.5 + 14.6 m m Hg for MCP, and
14.1 + 6.7 mm Hg versus 19.7 + 8.3 m m Hg for ICP.
The mean values for CPP and CBF were unaffected by
head elevation: 70.2 ___ 18.1 m m Hg at 30 ~ and 69.7 +
18.7 m m Hg at 0 ~ for CPP, and 47.8 _+ 16.9 ml/100
gm/min at 30* and 48.9 _+ 20.4 ml/100 gm/min at 0 ~
for CBF. None of the other parameters showed a statis-
tically significant difference between head elevations at
30* and at 0 ~ The results were not affected by whether
the head was at 30* or at 0* for the initial measurements.
Correlation analysis revealed a significant relation-
ship between the ICP level at 0* head elevation and the
amount of change in ICP after 30* head elevation (r = FIG. 2. Correlation between the level of intracranial pres-
sure (ICP) at 0 ~ head elevation and the amount of change in
-0.5890). The higher the ICP with the patient in the ICP after head elevation to 30~ The higher the ICP level in
horizontal position (0*), the greater the reduction in the horizontal position (0~ the greater was the reduction in
ICP at head elevation of 30* (Fig. 2). The effect of head ICP at 30~ of head elevation (r = -0.5890).
TABLE 3
Effects of head elevation on cerebra! and systemic physiological parameters" in six patients with ICP greater than 25 mm Hg*
after head elevation may depend upon the relative size 9. Magnaes B: Movement of cerebrospinal fluid within the
of each intracranial compartment at the time of head craniospinal space when sitting up and lying down. Surg
elevation, m.~vIn patients with raised ICP, the intracra- Neurol 10:45-49, 1978
10. Marmarou A, Shulman K, LaMorgese J: Compartmental
nial compliance decreases, t~ 12,20 and smaller changes
analysis of compliance and outflow resistance of the
in intracranial volume, such as those produced by CSF cerebrospinal fluid system. 3 Neurosurg 43:523-534, 1975
displacement, will produce greater changes in ICP. 11. Maser AL, Marmarou A, Ward JD, et al: Pressure-volume
Although the overall results of the present study show index in head injury. 3 Neurosurg 67:832-840, 1987
no effect of head elevation on CBF, one must bear in 12. Miller JD: Significance and management of intracranial
mind that our measurements are of global CBF and hypertension in head injury, in Ishii S, Nagai H, Brock
M (eds): Intracranial Pressure V. Berlin: Springer-Verlag,
that regional areas of decreased CBF may exist in the
1983, pp 44-53
presence of normal global blood flow measurements. 13. Narayan RK: Head injury, in Grossman RG, Hamilton
Only in one patient did the CBF fall to ischemic levels WJ (eds): Principles of Neurosurgery. New York: Raven
after head elevation, and the vasodilatory cascade sug- Press, 1991, pp 235-291
gested by Rosner t<~7 seemed to be demonstrable. In 14. Paulson OB, Strandgaard S, Edvinsson L: Cerebral auto-
this patient, the low CPP (59 m m Hg) emphasizes once regulation. Cerebrovasc Brain Metab Rev 2:161-192, 1990
more the importance of maintaining adequate levels of 15. Ports DG, Deonarine V: Effect of positional changes and
jugular vein compression on the pressure gradient across
CPP. The results of the present study suggest that, in the arachnoid villi granulations of the dog. J Neurosurg
general, head-injured patients with raised ICP should 38:722-728, 1973
be maintained with the head elevated to 30 ~ which will 16. Rosner MJ: Cerebral perfusion pressure: link between
produce a fall in ICP without a significant decrease in intracranial pressure and systemic circulation, in Wood
CBF in the majority of these patients. JH (ed): Cerebral Blood Flow. Physiologic and Clinical
Aspects. New York: McGraw-Hill, 1987, pp 425-448
17. Rosner M J: Vasodilatatory cascade and intracranial pres-
References
sure waves: theory, physiology and therapy, in Miller JD,
1. Davenport A, Will EJ, Davison AM: Effect of posture on Teasdale GM, Rowan JO, et al (eds): Intracranial Pressure
intracranial pressure and cerebral perfusion pressure in VI. New York: Springer-Verlag, 1986, pp 137-141
patients with fulminant hepatic and renal failure after 18. Rosner MJ, Coley IB: Cerebral perfusion pressure, intra-
acetaminophen self-poisoning. Crit Care Med 18: cranial pressure, and head elevation. J Neurosnrg 65:
286-289, 1990 636-641, 1986
2. Durward QJ, Amacher AL, Del Maestro RF, et at: Cere- 19. Rosner MJ, Daughton S: Cerebral perfusion pressure
bral and cardiovascular responses to changes in head management in head injury. J Trauma 30:933-941, 1990
elevation in patients with intracranial hypertension. J 20. Shapiro K, Marmarou A, Shulman K: Characterization
Neurosurg 59:938-944, 1983 of clinical CSF dynamics and neural axis compliance
3. Eisenberg HM, Frankowski RF, Contant CF, et at: High- using the pressure-volume index: I. The normal pressure-
dose barbiturate control of elevated intracranial pressure volume index. Ann Neurol 7:508-514, 1980
in patients with severe head injury. J Neurosurg 69: 2l. Toole JF: Effects of change of head, limb and body
15-23, 1988 position on cephalic circulation. N Engl J Med 279:
4. Kenning JA, Toutant SM, Saunders RL: Upright patient 307-311, 1968
positioning in the management of intracranial hyperten- 22. Woischneck D, Gaab MR, Rickels E, et al: Correct meas-
sion. Surg Neurol 15:148-152, 1981 urements of cerebral perfusion pressure, in Hoff JT, Betz
5. Kety SS: The theory and applications of the exchange of AL (eds): Intracranial Pressure VII. Berlin: Springer-
inert gas at the lungs and tissues. Pharmaeol Rev 3:1-41, Verlag, 1989, pp 850-852
1951
6. Kety SS, Schmidt CF: The determination of cerebral
blood flow in man by the use of nitrous oxide in low
Manuscript received May 19, 1991.
concentrations. Am J Physiol 143:53-66, 1945 This study was supported in part by National Institutes of
7. Kety SS, Schmidt CF: The nitrous oxide method for the Health Grant PO 1-NS27616.
quantitative determination of cerebral blood flow in man: Some portions of this paper were presented at the Eighth
theory, procedure, and normal values. J Clin Invest 27: International Symposium on Intracranial Pressure, in Rotter-
476-483, 1948 dam, The Netherlands, in June, 1991.
8. Magnaes B: Body position and cerebrospinal fluid pres- Address reprint requests to: Robert G. Grossman, M.D.,
sure. Part l: clinical studies on the effect of rapid postural Department of Neurosurgery, Baylor College of Medicine,
changes. J Neurosurg 44:687-697, 1976 One Baylor Plaza, Houston, Texas 77030.