Intracranial pressure

Intracranial pressure
Severely high ICP can cause herniation.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Intracranial pressure, (ICP), is the pressure exerted by three structures inside the cranium; brain parenchyma, CSF and blood. The norma ICP is 10-15 mmHg and is usually maintained by equilibrium of the intracranial contents. Intracranial hypertension ( IH), is elevation of the pressure in the cranium. It typically occurs when the ICP is >20 mmHg.

Historical Perspective[edit | edit source]

• [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
• In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
• In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].

Classification[edit | edit source]

• Elevated intracranial pressure or Intracranial hypertension may be classified into two subtypes/groups:

• Acute
• Chronic

• Intracranial hypertension may also be classified as various stages:
  • Stage 1: Minimal increases in ICP due to compensatory mechanisms
  • Stage 2:
    • Any change in volume greater than 100–120 mL
    • Exhaustion of compensatory mechanisms
    • Compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increase MAP and CP
  • Stage 3:

Increased ICP

One of the most damaging aspects of brain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure. ICP is very likely to cause severe harm if it rises beyond 40 mmHg in an adult. Even intracranial pressures between 25 and 30 mm Hg are usually fatal if prolonged, except in children, who can tolerate higher pressures for longer periods. An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause the brain to herniate, and restrict blood supply to the brain, leading to an ischemic cascade.

Intracranial Hypertension

Minimal increases in ICP due to compensatory mechanisms is known as stage 1 of intracranial hypertension. When the lesion volume continues to increase beyond the point of compensation, the ICP has no other resource, but to increase. Any change in volume greater than 100–120 mL would mean a drastic increase in ICP. This is stage 2 of intracranial hypertension. Characteristics of stage 2 of intracranial hypertension include compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increase MAP and CPP. Stage 3 intracranial hypertension is characterised by a sustained increased ICP, with dramatic changes in ICP with small changes in volume. In stage 3, as the ICP approaches the MAP, it becomes more and more difficult to squeeze blood into the intracranial space. The body’s response to a decrease in CPP is to raise blood pressure and dilate blood vessels in the brain. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Neurologic changes seen in increased ICP are mostly due to hypoxia and hypercapnea and are as follows: decreased LOC, Cheyne-Stokes respirations, hyperventilation, sluggish dilated pupils and widened pulse pressure.

Pathophysiology

Several pathophysiologic mechanisms are thought to be involved in the pathogenesis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH). These mechanisms are as follows:

• • Mass effect
    • It can occur secondary to brain tumor, contusions, subdural or epidural hematoma, or abscess
  • Cerebral edema or Generalized brain swelling
    • It can occur secondary to ischemic-anoxia states, hypertensive encephalopathy, pseudotumor cerebri, hypercarbia, and hepatocerebral syndrome.
    • These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
  • Increase in venous pressure
    • Secondary to venous sinus thrombosis, heart failure, neck surgery or obstruction of superior mediastinal or jugular veins.
  • Obstruction to CSF flow
    • Secondary to hydrocephalus, extensive meningeal disease (e.g., infectious, carcinomatous, granulomatous, or hemorrhagic), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
  • Increased CSF production
    • Meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
  • Increased cerebral blood flow (CBF)
    • Increased CBF is generally seen in conditions associated with hypercapnia and hypoxia
  • Drugs
    • Albendazole, Ciprofloxacin
  • Idiopathic
    • Pseudotumor cerebri

The Monro-Kellie Hypothesis:

• The Monro-Kellie hypothesis explains the relationship between the contents of the cranium and intracranial pressure. It explains the underlying pathophysiology of elevated intracranial pressure or intracranial hypertension
• In normal physiological state, intracranial contents (the brain tissue, the blood, and the cerebrospinal fluid) maintain an equilibrium state and keep the ICP within normal range by acting as compensatory mechanisms for small volume changes
• Compensatory mechanisms are being exhausted by large volume changes, eventually causing significantly elevated intracranial pressures and potential herniation

Intracranial components and their proportions:

• Brain parenchyma volume: 1400 ml (80%)
• CSF volume: 10 ml (10%)
• Blood volume: 10 ml (10%)

Causes

Common Causes

• Aneurysm 
• Arnold-chiari malformation
• Behçet's disease
• Brain tumor
• Cerebral edema
• Cerebral venous sinus thrombosis
• Choroid plexus tumor
• Chronic kidney disease
• Colloid cyst of third ventricle
• Contusions
• Crouzon craniofacial dysostosis
• Cushing's syndrome
• Dural arteriovenous fistula
• Encephalitis
• Epidural haemorrhage
• Epidural hematoma
• Erdheim-chester disease
• Excess cerebrospinal fluid
• Head trauma
• Hydrocephalus
• Hypertensive brain hemorrhage
• Hypertensive encephalopathy
• Idiopathic intracranial hypertension
• Insulin like growth factor 1
• Intracranial granuloma
• Intracranial haemorrhage
• Intraventricular hemorrhage
• Meningioma
• Meningitis
• Meningoencephalitis
• Multiple hamartoma syndrome
• Obstruction of superior mediastinal veins
• Obstruction of jugular veins
• Status epilepticus
• Stroke
• Subarachnoid haemorrhage
• Subdural haemorrhage
• Subdural hematoma
• Vasculitis
• Venous sinus thrombosis

Differential Diagnosis of Increased Intracranial Pressure (ICP)

• [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:

• [Differential dx1]
• [Differential dx2]
• [Differential dx3]
  

Epidemiology and Demographics

• The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
• In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].

Age

• Patients of all age groups may develop [disease name].

• [Disease name] is more commonly observed among patients aged [age range] years old.
• [Disease name] is more commonly observed among [elderly patients/young patients/children].

Gender

• [Disease name] affects men and women equally.

• [Gender 1] are more commonly affected with [disease name] than [gender 2].
• The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.

Race

• There is no racial predilection for [disease name].

• [Disease name] usually affects individuals of the [race 1] race.
• [Race 2] individuals are less likely to develop [disease name].

Risk Factors

• Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

Natural History, Complications and Prognosis

• The majority of patients with [disease name] remain asymptomatic for [duration/years].
• Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
• If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
• Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
• Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].

Diagnosis

Diagnostic Criteria

• The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:

• [criterion 1]
• [criterion 2]
• [criterion 3]
• [criterion 4]

History and Symptoms

• Symptoms of elevated intracranial pressure may include the following:

• Headache
• Nausea
• Vomiting
• Hyperventilation (due to injury to brain stem or tegmentum is damaged.
• Changes in your behavior
• Weakness or problems with moving or talking
• Lack of energy or sleepiness
• Seizure

Physical Examination

• Physical examination may be remarkable for

• Ocular palsies (abducens (CrN VI) palsies)
• Altered level of consciousness
• Papilledema
• Pupillary dilatation
• Cushing's triad ( Elevated systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern.
• Cheyne-Stokes respiration
• Bulging of fontanels in infants

Laboratory Findings

• There are no specific laboratory findings associated with [disease name].

• A [positive/negative] [test name] is diagnostic of [disease name].
• An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
• Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

Electrocardiogram

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

X-ray

There are no x-ray findings associated with [disease name].

OR

An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Echocardiography or Ultrasound

There are no echocardiography/ultrasound findings associated with [disease name].

OR

Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

CT scan

There are no CT scan findings associated with [disease name].

OR

[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

MRI

There are no MRI findings associated with [disease name].

OR

[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

There are no other diagnostic studies associated with [disease name].

OR

[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

• There is no treatment for [disease name]; the mainstay of therapy is supportive care.

• The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
• [Medical therapy 1] acts by [mechanism of action 1].
• Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery

• Surgery is the mainstay of therapy for [disease name].
• [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
• [Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention

• There are no primary preventive measures available for [disease name].

• Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].

• Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].

Additional Resources

• Monroe A. Observations on the structure and function of the nervous system, Edinburgh: Creech & Johnson; 1783.
• Kelly G. An account of the appearances observed in the dikssection of two of three individuals presumed to have perished in the storm of the 3rd, and whose bodies were deiscovered in the vicinity of the Leith on the morning of the 4th of November 1821, with some reflections on the pathology of the brain, Trans Med Chir Sci Edinb 1824;1:84–169.

External links

• Gruen P. 2002. "Monro-Kellie Model" Neurosurgery Infonet. USC Neurosurgery. Accessed January 4, 2007.
• National Guideline Clearinghouse. 2005. Guidelines for the management of severe traumatic brain injury. Firstgov. Accessed January 4, 2007.

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