Академический Документы
Профессиональный Документы
Культура Документы
Pathophysiology
Intracranial Compliance. The MonroeKellie
doctrine dictates that the cranial vault is a xed
space that contains three compartments: blood,
cerebrospinal uid (CSF), and brain tissue. In the
average adult, the brain volume is 1400 ml, the
blood volume is 150 ml, and the CSF volume is 150
ml. CSF is produced by the choroid plexus in the
ventricles at a rate of approximately 20 ml/hr, and
drains into the venous system via the arachnoid villi
and granulations [1]. This outow is normally of low
resistance; hence jugular venous pressure is the
chief determinant of ICP in healthy patients. Normal
ICP ranges from 50 to 200 mmH2O or 315 mmHg.
In routine intensive care unit (ICU) practice, the
goal of ICP management is to maintain levels below
20 mmHg.
In pathologic states characterized by increased
ICP (Table 1), additional volume is added to the
intracranial compartment. This can result from the
addition of an extrinsic mass lesion or from an
increase in the volume of CSF (hydrocephalus),
brain tissue (cytotoxic edema), or blood (vasogenic
edema). To maintain ICP within normal limits, these
increases in intracranial volume are initially counterbalanced by volume reductions in the other
compartments. CSF is displaced through the foramen magnum into the paraspinal space, blood is
displaced from the intracranial to the extracranial
venous system, and the brain parenchyma is compressed. After these mechanisms are exhausted,
Copyright 2002 Blackwell Science, Inc. 55
56
57
Fig 4. Pathologic ICP elevations. (A) Lundberg A (plateau) waves. (B) Lundberg B waves. (Reprinted from
Mayer SA. Management of increased intracranial pressure. In: Wijdicks EFM, Diringer MN, Bolton CF, et al.
Continuum: Critical Care. Minneapolis, MN: American
Academy of Neurology, 1997:4761.)
Fig 5. Plateau waves followed by sustained ICP elevation in a patient with traumatic brain injury. Early in the
course of the recording, plateau waves exceeding 90
mmHg are associated with ``mirror'' reductions in CPP
below 50 mmHg. At the end of the recording, ICP remains
elevated between 40 and 60 mmHg, MAP falls below 75
mmHg, and CPP drops to 20 mmHg. At this point the
patient became clinically brain dead.
58
cerebral vessels to return to normal caliber, restoring CBV and ICP to normal levels.
ICP Monitoring
Indications. Invasive monitoring of ICP is generally indicated in patients who meet all three of the
following criteria:
1. The patient is suspected to be at risk for elevated
ICP.
2. The patient is comatose (Glasgow coma scale
score 8).
3. The prognosis is such that aggressive ICU treatment is indicated.
Suspicion of increased ICP is usually based on
clinical signs (Tables 2 and 3) and the results of a
computed tomography (CT) scan showing signicant intracranial mass effect with midline shift or
effacement of the basal cisterns. However, in
comatose patients with TBI, intracranial hypertension occurs in approximately 10% of patients with
normal CT scans; this risk is even higher in patients
more than 40 years old, with motor posturing, or
with hypotension (systolic blood pressure < 90
mmHg) [12].
If a patient is awake and can follow commands, it
is unlikely that ICP is dangerously elevated [13], and
the benets of ventricular drainage or ICP monitoring probably do not outweigh the risks. Careful
monitoring of mental status in an ICU will usually
sufce in these cases.
Invasive ICP monitoring devices. Empiric therapy for increased ICP (i.e., standing doses of mannitol) without invasive monitoring is a distressingly
common practice. This approach is unsatisfactory
Clinical hallmark
Causes
Ipsilateral CN 3 palsy
Contralateral motor posturing
Central transtentorial
Subfalcine
Cerebellar
(upward or downward)
59
60
BRAIN TISSUE PO2 (PBTO2) MONITORING. SjvO2 monitoring assesses the adequacy of global cerebral
oxygen delivery, whereas PbtO2 monitoring measures regional oxygen tension. Both emerging
technologies provide continuous information regarding the adequacy of CPP and CBF at the tissue
level [2931]. SjvO2 is measured with a 5-French
beroptic oxygen saturation catheter placed retrograde in the internal jugular vein so that the tip is
positioned in the jugular bulb; PbtO2 is measured
with a miniaturized Clark electrode embedded in
the tip of a thin catheter inserted 34 cm into the
cerebral white matter (the Licox or Neurotrend
device). Both techniques can detect inadequate
CBF (i.e., ischemia), which may occur even in
patients with relatively normal CPP [32], and
excessive CBF (i.e., hyperemia), which can aggravate ICP related to vasogenic edema and breakthrough of autoregulation [33]. Accordingly these
monitors can be used to optimize therapy: mannitol
and vasopressor infusion reduce ICP and improve
cerebral oxygenation when SjvO2 or PbtO2 values
fall below critical levels [3032], whereas hyperventilation reduces ICP and tissue oxygenation
when it is supranormal due to relative hyperperfusion [31] (Table 4). The depth and duration of
ischemia detected by either device is highly correlated with poor clinical outcome in patients with
severe TBI [30,31]. Since neither monitor alone can
detect all episodes of ischemia [34], selection of
which type to use depends on the specic clinical
circumstances at hand. PbtO2 monitoring is generally easier to use, and is most desirable when
detection of ischemia in a specic brain region is the
Normal valuea
Critical upper limit
(indicates hyperemia)
Critical lower limit
(indicates ischemia)
Average value in severe TBIa
SjvO2
(%)
PbtO2
(mm Hg)
62
80
37
NA
50
73 10
32 19
predominant concern, whereas SjvO2 is less inuenced by high FiO2 levels and hence may be a more
reliable measure of relative hyperperfusion [34].
CEREBRAL MICRODIALYSIS. This adjunctive monitoring
technique is labor intensive and has yet to gain
widespread acceptance. A probe is placed through
the skull and levels of different substances may be
measured using high-performance liquid chromatography (HPLC). Lactate, glutamate, and more
recently extracellular potassium have been measured using this microdialysis. These levels correlate
with cerebral ischemia and poor outcome [35].
MULTIMODAL MONITORING. Finally, a combination of
multiple monitoring techniques may soon be
possible. Various prototypes are in development
that can allow simultaneous monitoring of ICP,
PbtO2, PbtCO2, pH, brain temperature, laser Doppler ow, and even microdialysis.
61
ow, and have been shown to exacerbate hypoxicischemic neuronal injury in experimental animals
[45]. As a general standard, acetaminophen and
cooling blankets should be given to all patients with
sustained fevers in excess of 38.3C (101.0F), but
evidence for their efcacy in neurologic patients is
scant [46,47]. Endovascular cooling with the use of
closed-circuit water-circulating intravenous catheters is a promising new approach that is currently
under development.
Recent studies suggest that indomethacin may be
the ideal antipyretic to use in patients with
increased ICP. Indomethacin has been shown to
decrease CBF and ICP in animal models and
patients with TBI [48]. The mechanism of action is
not known, but may involve vasoconstriction of
cerebral vessels and inhibition of prostaglandin
synthesis [48].
SEIZURE PROPHYLAXIS. Seizures can lead to profound
elevations of CBF, CBV, and ICP, even in patients
who are sedated or paralyzed [49]. This is secondary
to the increased cerebral metabolic demand that
occurs with seizures. Intravenous fosphenytoin
(1520 mg/kg loading dose, 35 mg/kg/day) is
the preferred agent for seizure prophylaxis while in
the ICU.
STEROIDS. Dexamethasone and other steroids
should not be used as a standard treatment for ICP
because they are ineffective against cytotoxic
edema [50]. There is generally no role for steroids
in the treatment of mass effect related to cerebral
infarction [51], intracerebral hemorrhage [52], or TBI
[53]. By contrast, vasogenic edema related to
neoplasm or abscess is steroid responsive, and
dexamethasone 420 mg every 6 hours can lead to
dramatic reductions in lesion volume [54].
62
63
Pharmacology
Dosage Range
Morphine sulfate
Fentanyl
0.53.0 lg/kg/hr
Sufentanil
0.10.6 lg/kg/hr
Propofol
0.66 mg/kg/hr
Midazolam
0.050.1 mg/kg/hr
Sedative-analgesic agents
Sedative-hypnotic agents
Dosages are approximate and should be titrated to the patient's level of agitation and ICP. A combination of a sedative-analgesic and
sedative-hypnotic agent may be more effective than the use of a single agent.
64
Pharmacology
Dosage Range
Nicardipine
210 lg/kg/min
65
References
1. Ropper AH, Rockoff MA. Physiology and clinical aspects of
raised intracranial pressure. In: Ropper AH, ed. Neurological
66
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
severe head injury; lactated Ringer's solution versus hypertonic saline. Crit Care Med 1998;26:12651270
Busto R, Dietrich WD, Globus MY, et al. Small differences in
intraischemic brain temperature critically determine the extent of ischemic injury. J Cereb Blood Flow Metab
1987;7:129138
O'Donnell J, Axelrod P, Fisher C, et al. Use and effectiveness
of hypothermia blankets for febrile patients in the intensive
care unit. Clin Infect Dis 1996;24:12081213
Mayer SA, Commichau C, Scarmeas N, et al. Clinical trial of
an air-circulating cooling blanket for fever control in critically-ill neurologic patients. Neurology 2001;56:292298
Slavik R, Rhoney D. Indomethacin: a review of its cerebral
blood ow effects and potential use for controlling intracranial pressure in traumatic brain injury patients. Neurol Res
1999;21:491499
Lassen NA. Control of the cerebral circulation in health and
disease. Circ Res 1974;34:749760
Fishman RA. Brain edema. N Engl J Med 1975;293:706711
Anderson DC, Cranford RE. Corticosteroids in ischemic
stroke. Stroke 1979;10:6871
Pourgvarin H, Bhoopat TW, Viriyavejakul A, et al. Effects of
dexamethasone in primary supratentorial intracerebral
hemorrhage. N Engl J Med 1987;316:12291233
Cooper PR, Moody S, Clark WK, et al. Dexamethasone and
severe head injury: a prospective double-blind trial. J Neurosurg 1979;51:307331
Galich JM, French LA. Use of dexamethasone in the treatment
of cerebral edema resulting from brain tumors and brain
surgery. Am Pract 1961;12:169174
McKinley B, Parmley C, Tonneson A. Standardized management of intracranial pressure: a preliminary clinical trial. J
Trauma 1999;46:271279
Munch EC, Bauhuf C, Horn P, et al. Therapy of malignant
intracranial hypertension by controlled lumbar cerebrospinal uid drainage. Crit Care Med 2001;29:976981
Schwab S, Steiner T, Aschoff A, et al. Early hemicraniectomy
in patients with complete middle cerebral artery infarction.
Stroke 1998;29:18881893
Schwab S, Junger E, Spranger M, et al. Craniectomy: an
aggressive treatment approach in severe encephalitis.
Neurology 1997;48:412417
Guerra WK, Gaab MR, Dietz H, et al. Surgical decompression for traumatic brain swelling: indications and results. J
Neurosurg 1999;90:187196
Mayer SA, Connolly ES, Bates J, et al. Decompressive hemicraniectomy for massive cerebral hemorrhage [abstract].
Stroke 2001;32:357
Kress JP, Pohlman AS, O'Connor MF, et al. Daily interruption of sedative infusions in critically ill patients
undergoing mechanical ventilation. N Engl J Med 2000;
342:14711477
Albanese J, Viviand X, Potie F, et al. Sufentanil, fentanyl, and
alfentanil in head trauma patients: a study on cerebral
hemodynamics. Crit Care Med 1999;27:407411
de Nadal M, Ausina A, et al. Effects on intracranial pressure of
fentanyl in severe head injured patients. Neurochirurgia
1998;71(suppl):1012
Kelly D, Goodale D, Williams J, et al. Propofol in the treatment of moderate and severe head injury: a randomized,
prospective double-blinded pilot trial. J Neurosurg
1999;90:10421051
67