Increased Intracranial Pressure-STAT Pearls
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Pinto, V., Tadi, P., & Adeyinka, A. (2022). Increased
intracranial pressure.
National Institutes of Health-
StatPearls. NCBI Bookshelf.
https://www.ncbi.nlm.nih.gov/books/NBK482119/
Affiliations
1
Baylor College of Medicine
2
Asram Medical College, Eluru, India
3
The Brooklyn Hospital Center
Last Update: August 1, 2022.
Continuing Education Activity
The pressure in the cranial vault is measured in millimeters of mercury (mm
Hg) and is normally less than 20 mm Hg. The cranium is a rigid structure
that contains 3 main components: brain, cerebrospinal fluid, and blood. Any
increase in the volume of its contents will increase the pressure within the
cranial vault. An increase in the volume of one component will result in a
decrease in volume in one or two of the other components. The clinical
implication of the change in volume of the component is a decrease in
cerebral blood flow or herniation of the brain. This activity reviews the
cause, pathophysiology, and presentation of increased intracranial pressure
and highlights the role of the interprofessional team in its management.
Objectives:
Describe the causes of increased intracranial pressure.
Review the clinical presentation of a patient with increased
intracranial pressure.
Summarize the treatment of increased intracranial pressure.
Explain modalities to improve care coordination among
interprofessional team members in order to improve outcomes for
patients affected by increased intracranial pressure.
Access free multiple choice questions on this topic.
Introduction
Intracranial hypertension (IH) is a clinical condition that is associated with
an elevation of the pressures within the cranium. The pressure in the
cranial vault is measured in millimeters of mercury (mm Hg) and is
normally less than 20 mm Hg.
The cranium is a rigid structure that contains three main components:
brain, cerebrospinal fluid, and blood. Any increase in the volume of its
contents will increase the pressure within the cranial vault. The Monroe-
Kellie Doctrine states that the contents of the cranium are in a state of
constant volume.[1]
That is, the total volumes of the brain tissues,
cerebrospinal fluid (CSF), and intracranial blood are fixed. An increase in
the volume of one component will result in a decrease in volume in one or
two of the other components. The clinical implication of the change in
volume of the component is a decrease in cerebral blood flow or herniation
of the brain.
CSF is a clear fluid found in the subarachnoid spaces and ventricles that
cushions the brain and spinal cord. It is secreted by the choroid plexus in
the lateral ventricles, travels to the third ventricle via the foramen of
Monroe. From the third ventricle, CSF reaches the fourth ventricle through
the aqueduct of Sylvius. From here, it flows into the subarachnoid space via
the foramina of Magendie and Luschka and is eventually reabsorbed into
the dural venous sinuses by arachnoid granulation.
Etiology
The causes of increased intracranial pressure (ICP) can be divided based on
the intracerebral components causing elevated pressures:
Increase in brain volume
Generalized swelling of the brain or cerebral edema from a variety of
causes such as trauma, ischemia, hyperammonemia, uremic
encephalopathy, and hyponatremia
Mass Effect
Hematoma
Tumor
Abscess
Infarct
Increase in Cerebrospinal Fluid
Increased production of CSF
Choroid plexus tumor
Decreased Reabsorption of CSF
Obstructive hydrocephalus
Meningeal inflammation or granulomas
Increase in Blood Volume
Increased cerebral blood flow during hypercarbia, aneurysms
Venous stasis from
Venous sinus thromboses,
Elevated central venous pressures, e.g., heart failure
Other Causes
Idiopathic or benign intracranial hypertension
Skull deformities such as craniosynostosis
Hypervitaminosis A, tetracycline use
Epidemiology
The true incidence of intracranial hypertension is unknown. The Centers for
Disease Control and Prevention (CDC) estimates that in 2010, 2.5 million
people sustained a traumatic brain injury (TBI). TBI is associated with
increased ICP. ICP monitoring is recommended for all patients with severe
TBI. Studies of American-based populations have estimated that the
incidence of idiopathic intracranial hypertension (IIH) ranges from 0.9 to
1.0 per 100,000 in the general population, increasing in women that are
overweight.[2]
Pathophysiology
The harmful effects of intracranial hypertension are primarily due to brain
injury caused by cerebral ischemia. Cerebral ischemia is the result of
decreased brain perfusion secondary to increased ICP. Cerebral perfusion
pressure (CPP) is the pressure gradient between mean arterial pressure
(MAP) and intracranial pressure (CPP = MAP - ICP).[3]
CPP = MAP - CVP if
central venous pressure is higher than intracranial pressure. CPP target for
adults following severe traumatic brain injury is recommended at greater
than 60 to 70 mm Hg, and a minimum CPP greater than 40 mm Hg is
recommended for infants, with very limited data on normal CPP targets for
children in between.
Cerebral autoregulation is the process by which cerebral blood flow varies
to maintain adequate cerebral perfusion. When the MAP is elevated,
vasoconstriction occurs to limit blood flow and maintain cerebral perfusion.
However, if a patient is hypotensive, cerebral vasculature can dilate to
increase blood flow and maintain CPP.
History and Physical
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Clinical suspicion for intracranial hypertension should be raised if a patient
presents with the following signs and symptoms: headaches, vomiting, and
altered mental status varying from drowsiness to coma. Visual changes can
range from blurred vision, double vision from cranial nerve defects,
photophobia to optic disc edema, and eventually optic atrophy. Infants in
whom the anterior fontanelle is still open may have a bulge overlying the
area.
Cushing triad is a clinical syndrome consisting of hypertension,
bradycardia, and irregular respiration and is a sign of impending brain
herniation. This occurs when the ICP is too high the elevation of blood
pressure is a reflex mechanism to maintain CPP. High blood pressure causes
reflex bradycardia and brain stem compromise affecting respiration.
Ultimately the contents of the cranium are displaced downwards due to the
high ICP, causing a phenomenon known as herniation which can be
potentially fatal.[4]
Evaluation
The evaluation of increased ICP should include detailed history taking,
physical examination, and ancillary studies.
It is extremely important to identify increased ICP as early as possible to
prevent herniation and death. For example malignant middle cerebral artery
stroke presenting with increased ICP. Malignant middle cerebral artery
stroke is seen more commonly in the younger population. Usually, these
patients are admitted to the ICU setting. Following the neurological exam
closely is very important. Usually, there is an altered mental status and
development of a fixed and dilated pupil. Patients presenting with findings
suggestive of cerebral insult should undergo computed tomography (CT)
scan of the brain; this can show the edema, which is visible as areas of low
density and loss of gray/white matter differentiation, on an unenhanced
image. There can also be an obliteration of the cisterns and sulcal spaces. A
CT scan can also reveal the cause in some cases. If flattened gyri or
narrowed sulci, or compression of the ventricles, is seen, this suggests
increased ICP. Serial CT scans are used to monitor the progression or
improvement of the edema.[5]
A funduscopic exam can reveal papilledema which is a tell-tale sign of
raised ICP as the cerebrospinal fluid is in continuity with the fluid around
the optic nerve.
Imaging- a computed tomography (CT) of the head or magnetic resonance
imaging (MRI) can reveal signs of raised ICP such as enlarged ventricles,
herniation, or mass effect from causes such as tumors, abscesses, and
hematomas, among others.
Measurement of Opening Pressure with a Lumbar Puncture
In this procedure, a needle is introduced in the subarachnoid space. This
can be connected to a manometer to give the pressure of the CSF prior to
drainage. A measurement greater than 20 mm Hg is suggestive of raised
ICP. Brain imaging should precede an LP because LP can cause a sudden
and rapid decrease in ICP and the sudden change in volume can lead to
herniation.
ICP Monitoring
[6]
Several devices can be used for ICP monitoring.
The procedure involves the placement of a fiber optic catheter into the
brain parenchyma to measure the pressure transmitted to the brain tissue.
External Ventricular Drain (EVD)
A drain placed directly into the lateral ventricles can be connected to a
manometer to give a reading for the pressure in the ventricles.
Optic Nerve Sheath Diameter (ONSD)
[7]
The use of ultrasound to measure the diameter of the optic nerve sheath has
been recently identified as a method to indicate raised ICP. This is
usually measured 3 mm behind the globe with 2–3 measurements taken in
each eye. The threshold for denoting elevated ICP usually ranges from 0.48
cm to 0.63 cm.
Treatment / Management
Assessment and management of the airway, specifically breathing and
circulation should always be the priority.[8]
Management principles should be targeted toward:
Maintenance of cerebral perfusion pressure by raising MAP
Treatment of the underlying cause.
Lowering of ICP.[9]
Measures to lower ICP include:[10]
Elevation of the head of the bed to greater than 30 degrees.
Keep the neck midline to facilitate venous drainage from the head.
Hypercarbia lowers serum pH and can increase cerebral blood flow
contributing to rising ICP, hence hyperventilation to lower pCO2 to
around 30 mm Hg can be transiently used.
Osmotic agents can be used to create an osmotic gradient across
blood thereby drawing fluid intravascularly and decreasing cerebral
edema. Mannitol was the primary agent used at doses of 0.25 to 1
g/kg body weight and is thought to exert its greatest benefit by
decreasing blood viscosity and to a lesser extent by decreasing blood
volume. Side effects of mannitol use are eventual osmotic diuresis and
dehydration as well as renal injury if serum osmolality exceeds 320
mOsm.[11]
Steroids are indicated to reduce ICP in intracranial
neoplastic tumors, but not in traumatic brain injury.
Three percent hypertonic saline is also commonly used to decrease
cerebral edema and can be administered as a 5 ml/kg bolus or a
continuous infusion, monitoring serum sodium levels closely. It is
considered relatively safe while serum sodium is < than 160mEq/dl or
serum osmolality is less than 340 mOsm.[12]
Drugs of the carbonic anhydrase inhibitor class, such as
acetazolamide, can be used to decrease the production of CSF and is
used to treat idiopathic intracranial hypertension.
Lumbar punctures, besides being diagnostic, can be used to drain
CSF thus reducing the ICP. The limitation to this is raised ICP
secondary to mass effect with a possible risk of herniation if the CSF
pressure drops too low.
Similar to a lumbar puncture, an EVD can also be used to not only
monitor ICP but also to drain CSF.
Optic nerve fenestrations can be performed for patients with chronic
idiopathic hypertension at a risk of blindness. Neurosurgical shunts
such as ventriculoperitoneal or lumbar-peritoneal shunts can divert
CSF to another part of the body from where it can be reabsorbed.[13]
Intravenous (IV) glyburide is being investigated in the prevention of
hemispheric stroke edema. It acts by inhibiting SUR1 receptors.[14]
Barbiturates can be considered in cases where sedation and usual
methods of treatment are not successful in reducing the ICP.[15]
Therapeutic hypothermia to 32-35 degrees Celcius can be used in a
refractory rise in ICP not responding to hyperosmolar therapy and
barbiturate coma. But its use has been questioned in recent days.
A decompressive craniectomy is a neurosurgical procedure wherein a
part of the skull is removed, and dura lifted, allowing the brain to
swell without causing compression.[16]
It is usually considered as a
last resort when all other ICP lowering measures have failed.
Differential Diagnosis
Acute nerve injury
Blood dyscrasias and stroke
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Hydrocephalus
Intracranial hemorrhage
Intracranial epidural abscess
Lyme disease
Meningioma
Migraine variants
Subarachnoid hemorrhage
Prognosis
Prognosis depends on the underlying etiology and severity of the
presentation. Benign intracranial hypertension does not increase the risk of
death rate by itself; rather, the death rate is increased by morbid obesity
which is a common association with benign intracranial hypertension. Visual
loss is significant morbidity in IIH.
Deterrence and Patient Education
Any patient likely to develop increased intracranial pressure should be
educated regarding the warning symptoms of the same including persistent
headaches and vomiting.
Pearls and Other Issues
A patient who presents with a headache, vomiting, and blurred vision
should be evaluated for neurologic deficits and receive head imaging to rule
out the causes of intracranial hypertension.
All patients with severe TBI (Glasgow coma scale of 3 to 8 on initial
presentation) should follow the latest guidelines on the management of
severe TBI that includes monitoring of ICP, maintenance of CPP greater
than 60 to 70 mm Hg for adults, and treatment of ICP greater than 22 mm
Hg.
Enhancing Healthcare Team Outcomes
The clinical presentation of increased intracranial pressure can easily be
mistaken for other issues, such as intoxication, stroke, infection, or post-
ictal state. It requires a high index of suspicion, particularly in milder cases.
In more severe cases, close neurological monitoring and consultation with
neurology and neurosurgery are important. Communication regarding
indications/risks/contraindications for ICP monitoring or craniotomy needs
to be ongoing, particularly with respect to goals of care. Nursing care must
pay close attention to changes in neurologic status, any change in vitals
such as an increasingly erratic heart rate, development of bradycardia,
accurate and equal intake and output when having diuresis, and
maintenance of proper blood pressure. As the patient recovers, physical
therapy, occupational therapy, and speech-language pathology can help the
patient maximize function after the brain injury and evaluate patient safety
both before and after discharge.
Patient education regarding avoidance of future complications should come
from all team members, with social work involvement to ensure home safety
after discharge, and the patient's primary care provider should be updated,
to ensure appropriate follow-up. In cases of vasogenic edema due to brain
tumor, both oncology, radiation oncology, and neurosurgery should be
consulted to co-manage the evaluation and management of the neoplasm,
determine the best treatment for the tumor (resection/radiation/palliation)
based on the tumor type/stage, and follow up with the patient after
discharge. And, finally, the patient and the patient's family and care
providers should be educated about what to watch for that may suggest the
need for re-evaluation because of recurrence, or complications from any of
the interventions.
Review Questions
Access free multiple choice questions on this topic.
Comment on this article.
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Disclosure:
Venessa Pinto declares no relevant financial relationships
with ineligible companies.
Disclosure:
Prasanna Tadi declares no relevant financial
relationships with ineligible companies.
Disclosure:
Adebayo Adeyinka declares no relevant financial
relationships with ineligible companies.
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Bookshelf ID: NBK482119PMID: 29489250