This document summarizes evaluation and management of elevated intracranial pressure in adults. It discusses causes of increased intracranial pressure including brain masses, edema, hydrocephalus, and venous obstruction. It covers monitoring of intracranial pressure, indications for monitoring, and types of monitors. It also provides an overview of general management strategies and specific therapies to lower intracranial pressure such as osmotic therapy, glucocorticoids, hyperventilation, barbiturates, and decompressive craniectomy.

1. Intracranial
Pressure
CAUSES , PHYSIOLOGY , HISTORY , CLINICAL FINDINGS ,
MONITORING ,INVESTIGATIONS AND TREATMENT.

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3. Evaluation and
management of elevated
intracranial pressure
in adults
Intracranial pressure is normally ≤15 mmHg in adults, and
pathologic intracranial hypertension (ICH) is present at
pressures ≥20 mmHg. ICP is normally lower in children
than adults, and may be subatmospheric in newborns [2].
Homeostatic mechanisms stabilize ICP, with occasional
transient elevations associated with physiologic events,
including sneezing, coughing, or Valsalva maneuvers

4. Intracranial components
 In adults, the intracranial compartment is protected
by the skull, a rigid structure with a fixed internal
volume of 1400 to 1700 mL.
 ●Brain parenchyma — 80 percent
 ●Cerebrospinal fluid — 10 percent
 ●Blood — 10 percent
 ITs SIMPLE , just ask yourself how the above three can
be increased .

5. major causes of increased
intracranial pressure include:
 ●Intracranial mass lesions (eg, tumor, hematoma)
 ●Cerebral edema (such as in acute hypoxic ischemic
encephalopathy, large cerebral infarction, severe
traumatic brain injury)
 ●Increased cerebrospinal fluid (CSF) production, eg,
choroid plexus papilloma
 ●Decreased CSF absorption, eg, arachnoid granulation
adhesions after bacterial meningitis
 ●Obstructive hydrocephalus
 ●Obstruction of venous outflow, eg, venous sinus
thrombosis, jugular vein compression, neck surgery
 ●Idiopathic intracranial hypertension (pseudotumor
cerebri)

6. Cerebral Compliance

7. Cerebral Blood flow

12. One notable false localizing
syndrome seen following
neurologic injury, referred
to as Kernohan's notch
phenomenon, consists of
the combination of
contralateral pupillary
dilatation and ipsilateral
weakness

13. ICP MONITORING
 The purpose of monitoring ICP is to improve the clinician's ability to
maintain adequate CPP and oxygenation. The only way to reliably
determine CPP (defined as the difference between MAP and ICP) is to
continuously monitor both ICP and blood pressure (BP). In general,
these patients are managed in intensive care units (ICUs) with an ICP
monitor and arterial line. The combination of ICP monitoring and
concomitant management of CPP may improve patient outcomes,
particularly in patients with closed head trauma

14. INDICATIONS (In who should
we monitor ?)
 Since ICP monitoring is associated with a small risk of
serious complications, including CNS infection and
intracranial hemorrhage, it is reasonable to try to limit
its use to patients most at risk of elevated ICP [25]. In
general, invasive monitoring of ICP is indicated in
patients who are [26]:
 ●Suspected to be at risk for elevated ICP
 ●Comatose (Glasgow Coma Scale <8) (table 2)
 ●Diagnosed with a process that merits aggressive
medical care

15. 7490638
21
PubMed
TI
Intracranial pressure monitoring and outcomes after traumatic brain injury.
AU
Lane PL, Skoretz TG, Doig G, Girotti MJ
SO
Can J Surg. 2000;43(6):442.

17. Eisenberg HM, Gary HE Jr, Aldrich EF, et al. Initial CT findings in 753 patients
with severe head injury. A report from the NIH Traumatic Coma Data Bank. J
Neurosurg 1990; 73:688. O'Sullivan MG, Statham PF, Jones PA, et al. Role of
intracranial pressure monitoring in severely head-injured patients without signs of
intracranial hypertension on initial computerized tomography. J Neurosurg 1994;
80:46.
Lobato RD, Sarabia R, Rivas JJ, et al. Normal computerized tomography scans in
severe head injury. Prognostic and clinical management implications. J Neurosurg
1986; 65:784.
Although CT scans may suggest elevated ICP based on the presence of mass
lesions, midline shift, or effacement of the basilar cisterns (image 1), patients
without these findings on initial CT may have elevated ICP. This was
demonstrated in a prospective study of 753 patients treated at four major head
injury research centers in the United States, which found patients whose initial CT
scan did not show a mass lesion, midline shift, or abnormal cisterns had a 10 to
15 percent chance of developing elevated ICP during their hospitalization
other studies have shown that up to one-third of patients with initially normal scans
developed CT scan abnormalities within the first few days after closed head injury [28,29
Together, these findings demonstrate that ICP can be elevated even in the setting of a
normal initial CT, demonstrating the importance of invasive monitoring in high-risk patien
and the role of follow-up imaging in patients who develop clinical evidence of increased
during hospitalization.

18. •ICP MONITORING
•Types of monitors
• - Intraventricular
• - Intraparenchymal
• - Subarachnoid
• - Epidural
•Waveform analysis
•Noninvasive systems
•Advanced neuromonitoring

24. Noninvasive systems — A number of devices designed to record ICP noninvasively
have been studied, but most have not demonstrated reproducible clinical success or
have been studied in large clinical trials. We do not use these in clinical practice.
Transcranial Doppler (TCD) measures the velocity of blood flow in the proximal
cerebral circulation. TCD can be used to estimate ICP based on characteristic changes
in waveforms that occur in response to increased resistance to cerebral blood flow
[43,44]. Generally, TCD is a poor predictor of ICP, although in trauma patients TCD
findings may correlate with outcome at six months [45-48].
Tissue resonance analysis (TRA), an ultrasound-based method, has shown some
promise. In one trial 40 patients underwent both invasive and TRA ICP monitoring,
with good correlation between concomitant invasive and TRA measurements [49].
Ocular sonography can provide a noninvasive measure of optic nerve sheath
diameter, which has been found to correlate with intracranial pressure. A
number of studies have found that diameters of 5 to 6 mm have the ability to
discriminate between normal and elevated ICP in patients with intracranial
hemorrhage and traumatic brain injury [50-56].

25. Intraocular pressure can be assessed noninvasively using an
ultrasonic handheld optic tonometer. While some evidence
suggests that intraocular pressure correlates with ICP in the
absence of oculofacial trauma or glaucoma [57], most other
studies' findings disagree [58-60].
Tympanic membrane displacement (measured using an impedance
audiometer) has been compared to direct monitoring, based on the
hypothesis that increased ICP will transmit a pressure wave to the
tympanic membrane via the perilymph [61,62].

29. GENERAL MANAGEMENT
Resuscitation
Urgent situations
Monitoring and the decision to treat
Fluid management
Sedation
Blood pressure control
Position
Fever
Antiseizure therapy
SPECIFIC THERAPIES
Osmotic therapy and diuresis
- Mannitol
- Hypertonic saline bolus
- Other agents
Glucocorticoids
Hyperventilation
Barbiturates
Therapeutic hypothermia
Removal of CSF
Decompressive craniectomy

33. Who needs urgent intervention ?
●A history that suggests elevated ICP (eg, head trauma, sudden severe headache
typical of subarachnoid hemorrhage)
●An examination that suggests elevated ICP (unilateral or bilaterally fixed and dilated
pupil(s), decorticate or decerebrate posturing, bradycardia,
hypertension and/orrespiratory depression)
●A Glasgow coma scale (GCS) ≤8
●Potentially confounding, reversible causes of depressed mental status, hypotension
(SBP <60 mmHg in adults), hypoxemia (PaO2 <60 mmHg), hypothermia (<36ºC), or
obvious intoxication are absent
WHAT are the urgent interventions ?
In such patients osmotic diuretics may be used urgently (see 'Mannitol' below).
In addition, standard resuscitation techniques should be instituted as soon as possible:
●Head elevation
●Hyperventilation to a PCO2 of 26 to 30 mmHg ( contraindicated in traumatic injury and
acute stroke patients )( discussed later on )
●Intravenous mannitol (1 to 1.5 g/kg)

37. Blood pressure control
 In general, BP should be sufficient to maintain CPP >60
mmHg.
 Hypertension should generally only be treated when
CPP >120 mmHg and ICP >20 mmHg.
 Caution should be taken to avoid CPP <50 mmHg or,
as noted above, normalization of blood pressure in
patients with chronic hypertension in whom the
autoregulatory curve has shifted to the right

38. Position
 Patients with elevated ICP should be positioned to
maximize venous outflow from the head.
 Important maneuvers include reducing excessive flexion
or rotation of the neck, avoiding restrictive neck taping,
and minimizing stimuli that could induce Valsalva
responses, such as endotracheal suctioning.
 Patients with elevated ICP have historically been
positioned with the head elevated above the heart
(usually 30 degrees) to increase venous outflow. It should
be noted that head elevation may lower CPP [20,74];
however, given the proven efficacy of head elevation in
lowering ICP, most experts recommend raising the
patient's head as long as the CPP remains at an
appropriate level [75].

40. Fever
 Elevated metabolic demand in the brain results in
increased cerebral blood flow (CBF), and can elevate
ICP by increasing the volume of blood in the cranial
vault. Conversely, decreasing metabolic demand can
lower ICP by reducing blood flow.
 Therefore, aggressive treatment of fever,
including acetaminophen and mechanical cooling, is
recommended in patients with increased ICP.

42. Antiseizure therapy
 Seizures can both complicate and contribute to
elevated ICP
Anticonvulsant therapy should be instituted if seizures
are suspected; prophylactic treatment may be warranted
in some cases.

44. SPECIFIC THERAPIES
 Osmotic therapy and diuresis
Mannitol-Osmotic diuretics reduce brain volume by
drawing free water out of the tissue and into the
circulation, where it is excreted by the kidneys, thus
dehydrating brain parenchyma
It is prepared as a 20 percent solution, and given as a
bolus of 1 g/kg.
Repeat dosing can be given at 0.25 to 0.5 g/kg as
needed,

45. Mannitol
 The effects are usually present within minutes, peak at
about one hour, and last 4 to 24 hours
 Some have reported a "rebound" increase in ICP; this
probably occurs when mannitol, after repeated use, enters
the brain though a damaged blood-brain barrier and
reverses the osmotic gradient [85,86].
 Useful parameters to monitor in the setting of mannitol
therapy include serum sodium, serum osmolality, and
renal function.
 Concerning findings associated with the use
of mannitol include serum sodium >150 meq, serum
osmolality >320 mOsm, or evidence of evolving acute
tubular necrosis (ATN).

48. Hypertonic saline bolus
 Mannitol and hypertonic saline have been compared
in at least eight randomized trials of patients with
elevated ICP from a variety of causes (traumatic brain
injury, stroke, tumors)
 Meta-analyses of these trials have found that
hypertonic saline appears to have greater efficacy in
managing elevated ICP, but clinical outcomes have
not been systematically examined

51. Other agents-Furosemide
 Furosemide, 0.5 to 1.0 mg/kg intravenously, may be
given with mannitol to potentiate its effect. However,
this effect can also exacerbate dehydration and
hypokalemia [105-107].
 Glycerol and urea were used historically to control ICP
via osmoregulation; however, use of these agents has
decreased because equilibration between brain and
plasma levels occurs more quickly than
with mannitol.

52. Glucocorticoids
 Glucocorticoids — Glucocorticoids were associated
with a worse outcome in a large randomized clinical
trial of their use in moderate to severe head injury
[110,111]. They should not be used in this setting.
 In contrast, glucocorticoids may have a role in the
setting of intracranial hypertension caused by brain
tumors and CNS infections.

54. Hyperventilation
 Use of mechanical ventilation to lower PaCO2 to 26
to 30 mmHg has been shown to rapidly reduce ICP
through vasoconstriction and a decrease in the
volume of intracranial blood; a 1 mmHg change in
PaCO2 is associated with a 3 percent change in CBF
The effect of hyperventilation on ICP is short-lived (1 to
24 hours)
Following therapeutic hyperventilation, the patient's
respiratory rate should be tapered back to normal over
several hours to avoid a rebound effect
Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in
adults with head injury-outcomes at 6 months. Edwards P et al Lancet 2005.

55. Therapeutic hyperventilation should be considered as an urgent
intervention when elevated ICP complicates cerebral edema,
intracranial hemorrhage, and tumor. Hyperventilation should not be
used on a chronic basis, regardless of the cause of increased ICP.
Hyperventilation should be minimized in patients with traumatic brain
injury or acute stroke. In these settings, vasoconstriction may cause a
critical decrease in local cerebral perfusion and worsen neurologic injury,
particularly in the first 24 to 48 hours

56. Barbiturates
 The use of barbiturates is predicated on their ability to
reduce brain metabolism and cerebral blood flow, thus
lowering ICP and exerting a neuroprotective effect
 Pentobarbital is generally used, with a loading dose of 5
to 20 mg/kg as a bolus, followed by 1 to 4 mg/kg per hr
 Continuous EEG monitoring is generally used; EEG burst
suppression is an indication of maximal dosing.
 The therapeutic value of this maneuver is somewhat
unclear. In a randomized trial of 73 patients with
elevations in ICP refractory to standard therapy, patients
treated with pentobarbital were 50 percent more likely
to have their ICP controlled.
TI
High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury.
AU
Eisenberg HM, Frankowski RF, Contant CF, Marshall LF, Walker MD
SO
J Neurosurg. 1988;69(1):15.

57. Therapeutic hypothermia
 Given the uncertainties surrounding the appropriate
use of therapeutic hypothermia in patients with
elevated ICP, this treatment should be limited to
clinical trials, or to patients with intracranial
hypertension refractory to other therapies.

58. Removal of CSF
 When hydrocephalus is identified, a ventriculostomy
should be inserted.
 CSF should be removed at a rate of approximately 1
to 2 mL/minute, for two to three minutes at a time,
with intervals of two to three minutes in between until
a satisfactory ICP has been achieved (ICP <20 mmHg)
or until CSF is no longer easily obtained.
 A lumbar drain is generally contraindicated in the
setting of high ICP due to the risk of transtentorial
herniation.

59. Decompressive
craniectomy
 Decompressive craniectomy removes the rigid
confines of the bony skull, increasing the potential
volume of the intracranial contents and circumventing
the Monroe-Kellie doctrine.
 Importantly, it has been demonstrated that in
patients with elevated ICP, craniectomy alone lowered
ICP 15 percent, but opening the dura in addition to
the bony skull resulted in an average decrease in ICP
of 70 percent
TI
[Evaluation of the clinical benefit of decompression hemicraniectomy in intracranial hypertension not controlled by medical treatment].
AU
Jourdan C, Convert J, Mottolese C, Bachour E, Gharbi S, Artru F
SO
Neurochirurgie. 1993;39(5):304.

60. “
”
“Nobody works
better under
pressure. They just
work faster.”
― Brian Tracy