Intracranial pressure

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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., Sabeeh Islam, MBBS[2]

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. Hans Queckenstedt's was the first person to use lumbar needle for ICP monitoring. Intracranial hypertension is generally categorized as acute or chronic. 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. Several pathophysiologic mechanisms are thought to be involved in the pathogenesis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH). All mechanisms eventually lead to brain injury from brain stem compression and decreased cerebral blood supply or ischemia. Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) must be differentiated from other diseases that cause headache, nausea, vomiting and neurologic deficits such as tumor, abscess or space occupying lesion, venous sinus thrombosis, neck surgery, Obstructive hydrocephalus, meningitis, subarachnoid hemorrhage, choroid plexus papilloma, and Malignant systemic hypertension. The diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) is made when ICP is >20 mmHg. CT scan or MRI may be considered initial diagnostic investigations.  Intracranial hypertension is considered to be emergency condition.  Treatment includes resuscitative measures and specific directed therapy.  Resuscitative measures include oxygen, blood pressure and ICP monitoring, osmotic diuresis, head elevation up to 30 degrees, therapeutic hypothermia and seizure prophylaxis.

Historical Perspective

  • In 1950s, therapeutic hypothermia (goal core temperature of 32-34C) was first introduced as a treatment for brain injury. [1]
  • In early 1800s, the Monro-Kellie hypothesis and the CSF physiology was first introduced by Alexander Monro and George Kellie.
  • Hans Queckenstedt's was the first person to use lumbar needle for ICP monitoring.

Classification

  • Elevated intracranial pressure or Intracranial hypertension may be classified into two subtypes/groups:
  • 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:
      • Sustained increased ICP
      • Dramatic changes in ICP with small changes in volume
      • The ICP approaches the MAP

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.

Pathophysiology

Intracranial components and their proportions:

  • Brain parenchyma volume: 1400 ml (80%)[2]
  • CSF volume: 10 ml (10%)
  • Blood volume: 10 ml (10%)

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.[3]
  • Compensatory mechanisms are being exhausted by large volume changes, eventually causing significantly elevated intracranial pressures and potential herniation.[4]

Intracranial compliance:

  • There is an inverse relationship between intracranial components and the compliance.
  • Generally the normal compliance is maintained by compensatory mechanisms such as
    • Increased CSF reabsorption via thecal sac
    • Increased venoconstriction to decrease cerebral venous flow
    • Decreased cerebral venous flow via increased extracranial drainage

Cerebral Blood Flow (Ohm's Law):

  • Cerebral blood flow is generally assessed by subtracting jugular venous pressure from carotid arterial pressure and dividing by cerebrovascular resistance, as follows:[5][6][7]
    • CBF = (CAP - JVP) ÷ CVR
    • Cerebral perfusion is assessed by cerebral perfusion pressure (CPP). CPP is calculated by subtracting ICP from mean arterial pressure, as follows:
    • CPP = MAP - ICP[8]
    • In normal physiological states, ICP and CPP is maintained by autoregulation.[4]

Several pathophysiologic mechanisms are thought to be involved in the pathogenesis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH). All mechanisms eventually lead to brain injury from brain stem compression and decreased cerebral blood supply or ischemia. These mechanisms are as follows:

    • Mass effect
    • Cerebral edema or Generalized brain swelling
    • 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
    • Idiopathic


Causes

Common Causes

Differential Diagnosis of Increased Intracranial Pressure (ICP)

Differentiating Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) from Other Diseases on the Basis of Seizure, Visual disturbance, and Constitutional Symptoms

On the basis of seizure, visual disturbance, and constitutional symptoms, meningioma must be differentiated from oligodendroglioma, astrocytoma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Diseases Clinical manifestations Para-clinical findings Gold
standard 		Additional findings
Symptoms Physical examination
Lab Findings MRI Immunohistopathology
Head-
ache 		Seizure Visual disturbance Constitutional Focal neurological deficit
Adult primary brain tumors
Meningioma
[10][11][12] 		+ +/− +/− − + −
  • Well circumscribed
  • Extra-axial mass
  • Whorled spindle cell pattern
  • May be associated with NF-2
Glioblastoma multiforme
[13][14][15] 		+ +/− +/− − + −
  • Pseudopalisading appearance
Oligodendroglioma
[16][17][18] 		+ + +/− − + −
  • Chicken wire capillary pattern
  • Fried egg cell appearance
Hemangioblastoma
[19][20][21][22] 		+ +/− +/− − + −
Pituitary adenoma
[23][24][15] 		− − + Bitemporal hemianopia − −
  • It is associated with MEN1 disease.
Schwannoma
[25][26][27][28] 		− − − − + −
  • Split-fat sign
  • Fascicular sign
  • Often have areas of hemosiderin
  • S100+
Primary CNS lymphoma
[29][30] 		+ +/− +/− − + −
  • Single mass with ring enhancement
Childhood primary brain tumors
Pilocytic astrocytoma
[31][32][33] 		+ +/− +/− − + −
Medulloblastoma
[34][35][36] 		+ +/− +/− − + −
  • Homer wright rosettes
Ependymoma
[37][15] 		+ +/− +/− − + −
  • Hydrocephalus
  • Causes an unusually persistent, continuous headache in children.
Craniopharyngioma
[38][39][40][15] 		+ +/− + Bitemporal hemianopia − +
Pinealoma
[41][42][43] 		+ +/− +/− − + vertical gaze palsy
  • May cause prinaud syndrome (vertical gaze palsy, pupillary light-near dissociation, lid retraction and convergence-retraction nystagmus
Vascular
AV malformation
[44][45][15] 		+ + +/− − +/− −
Brain aneurysm
[46][47][48][49][50] 		+ +/− +/− − +/− −
  • MRA and CTA
Infectious
Bacterial brain abscess
[51][52] 		+ +/− +/− + +
  • Central hypodense signal and surrounding ring-enhancement in T1
  • Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding edema in T2
  • History/ imaging
Tuberculosis
[53][15][54] 		+ +/− +/− + +
  • Lab data/ Imaging
Toxoplasmosis
[55][56] 		+ +/− +/− − +
  • History/ imaging
Hydatid cyst
[57][15] 		+ +/− +/− +/− +
  • Imaging
CNS cryptococcosis
[58] 		+ +/− +/− + +
  • We may see numerous acutely branching septate hyphae
  • Lab data/ Imaging
CNS aspergillosis
[59] 		+ +/− +/− + +
  • Multiple abscesses
  • Ring enhancement
  • Peripheral low signal intensity on T2
  • We may see numerous acutely branching septate hyphae
  • Lab data/ Imaging
Other
Brain metastasis
[60][15] 		+ +/− +/− + + −
  • Based on the primary cancer type we may have different immunohistopathology findings.
  • History/ imaging

ABBREVIATIONS

CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli, MRA=Magnetic resonance angiography, CTA=CT angiography

Epidemiology and Demographics

  • The prevalence of intracranial hypertension is approximately 1.0 per 100,000 individuals worldwide.

Gender

  • Idiopathic ICH is more prevalent among women of childbearing age.

Risk Factors

  • Common risk factors in the development of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include underlying pathologies such as; mass lesions, abscesses, and hematomas.
  • Other risk factors include

Natural History, Complications and Prognosis

  • Early clinical features include nausea, vomiting, and confusion.
  • If left untreated, patients may progress to have severe neurologic consequences such as brain herniation, brain death, respiratory depression, brain infections, coma and death.
  • Common complications of intracranial hypertension include brain herniation and neurologic deficits.

Diagnosis

Diagnostic Criteria

  • The diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) is made when ICP is >20 mmHg.

History and Symptoms

  • Symptoms of elevated intracranial pressure may include the following:

Physical Examination

  • Physical examination may be remarkable for

Laboratory Findings

  • There are no specific laboratory findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).

Electrocardiogram

  • There are no ECG findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).

X-ray

  • There are no x-ray findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).

CT scan

  • CT scan may be helpful in the diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).
  • Findings on CT scan suggestive of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include presence of mass lesions, midline shift or hemorrhage.
  • CT scan is particularly helpful for people with acute rise in ICP.

MRI

  • MR venography (MRV) is preferred over MRI for the diagnosis of cerebral venous thrombosis
  • MRI has a greater sensitivity to detect subtle intracranial masses (eg, gliomatosis cerebri) and meningeal-based pathologies and should be done if no contraindications (eg, pacemakers, metallic clips in head, metallic foreign bodies) present

Other Diagnostic Studies

Other diagnostic studies for Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include invasive and non-invasive ICP monitoring, particularly preferred in patients with no CT or MRI findings, at risk of developing increased ICP, and comatosed.

Treatment

Medical Therapy

  • The management of intracranial hypertension is generally directed towards treating the cause/etiology of the raised intracranial pressure.
  • Intracranial hypertension is considered a medical emergency and the management includes emergent resuscitative as well as specific treatment.

Resuscitation:

General principles for resuscitation include:[83][84][85][86][87][88][89]

  • Maintain oxygen
  • Head elevation
  • Hyperventilation to achieve a PaCO2 of 26-30 mmHg
  • Osmotic diuresis with intravenous mannitol and Lasix
  • Appropriate sedation, if patient requires intubation. Propofol is considered to be the preferred agent.
  • Therapeutic hypothermia to achieve a low metabolic state
  • Appropriate choice of fluids to achieve euvolemic state. Avoid hypotonic agents
  • Allow permissive hypertension. Treat hypertension only when CPP >120 mmHg and ICP >20 mmHg
  • Seizure prophylaxis with anticonvulsant therapy.[90]


Other therapies for intracranial hypertension:

  • Osmotic diuresis can be achieved by hypertonic saline bolus or mannitol. Hypertonic saline is usually considered to be more effective compared to mannitol for acute ICP reduction. Mannitol can be given as a bolus of 1 g/kg when prepared as 20% solution. The dose is usually repeated every 6-8 hours. It should be used cautiously in patients with renal insufficiency. Intravenous Lasix (0.5 to 1 mg/kg) is usually given with mannitol.[91][92]
  • Glucocorticoids are usually preferred when the underlying etiologies brain tumor are underlying CNS infection. Their use is contraindicated in head injury, cerebral infarction and intracranial hemorrhage.[93]
  • Phenobarbital is considered to have a neuroprotective effect by decreasing brain metabolism. It is given as a loading dose of 5 to 20 mg/kg, followed by 1 to 4 mg/kg per hour. EEG monitoring is used to guide therapy. A burst suppression seen on EEG indicates maximal dosing.[94]

Surgery

Surgical options for persistent intracranial hypertension include

Prevention

  • Effective measures for the primary prevention of intracranial hypertension include early detection of underlying intracranial etiology such as tumor or congenital deformities.
  • Once diagnosed and successfully treated, patients with intracranial hypertension are followed up every 6 months to 1 year with a head CT scan to prevent secondary complications.

References

  1. ↑ Welch K (May 1980). "The intracranial pressure in infants". J. Neurosurg. 52 (5): 693–9. doi:10.3171/jns.1980.52.5.0693. PMID 7373397.
  2. ↑ Whedon JM, Glassey D (2009). "Cerebrospinal fluid stasis and its clinical significance". Altern Ther Health Med. 15 (3): 54–60. PMC 2842089. PMID 19472865.
  3. ↑ Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B (February 1981). "Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema"". J. Neurosurg. 54 (2): 170–8. doi:10.3171/jns.1981.54.2.0170. PMID 7452330.
  4. ↑ 4.0 4.1 Aldrich EF, Eisenberg HM, Saydjari C, Luerssen TG, Foulkes MA, Jane JA, Marshall LF, Marmarou A, Young HF (March 1992). "Diffuse brain swelling in severely head-injured children. A report from the NIH Traumatic Coma Data Bank". J. Neurosurg. 76 (3): 450–4. doi:10.3171/jns.1992.76.3.0450. PMID 1738026.
  5. ↑ Strandgaard S, Paulson OB (June 1989). "Cerebral blood flow and its pathophysiology in hypertension". Am. J. Hypertens. 2 (6 Pt 1): 486–92. doi:10.1093/ajh/2.6.486. PMID 2757806.
  6. ↑ Strandgaard S, Andersen GS, Ahlgreen P, Nielsen PE (1984). "Visual disturbances and occipital brain infarct following acute, transient hypotension in hypertensive patients". Acta Med Scand. 216 (4): 417–22. PMID 6516910.
  7. ↑ Enevoldsen EM, Jensen FT (May 1978). "Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury". J. Neurosurg. 48 (5): 689–703. doi:10.3171/jns.1978.48.5.0689. PMID 641549.
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  32. ↑ Pedersen CL, Romner B (January 2013). "Current treatment of low grade astrocytoma: a review". Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
  33. ↑ Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
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  36. ↑ Burger, P. C.; Grahmann, F. C.; Bliestle, A.; Kleihues, P. (1987). "Differentiation in the medulloblastoma". Acta Neuropathologica. 73 (2): 115–123. doi:10.1007/BF00693776. ISSN 0001-6322.
  37. ↑ Yuh, E. L.; Barkovich, A. J.; Gupta, N. (2009). "Imaging of ependymomas: MRI and CT". Child's Nervous System. 25 (10): 1203–1213. doi:10.1007/s00381-009-0878-7. ISSN 0256-7040.
  38. ↑ Brunel H, Raybaud C, Peretti-Viton P, Lena G, Girard N, Paz-Paredes A, Levrier O, Farnarier P, Manera L, Choux M (September 2002). "[Craniopharyngioma in children: MRI study of 43 cases]". Neurochirurgie (in French). 48 (4): 309–18. PMID 12407316.
  39. ↑ Prabhu, Vikram C.; Brown, Henry G. (2005). "The pathogenesis of craniopharyngiomas". Child's Nervous System. 21 (8–9): 622–627. doi:10.1007/s00381-005-1190-9. ISSN 0256-7040.
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  42. ↑ Sano, Keiji (1976). "Pinealoma in Children". Pediatric Neurosurgery. 2 (1): 67–72. doi:10.1159/000119602. ISSN 1016-2291.
  43. ↑ Baggenstoss, Archie H. (1939). "PINEALOMAS". Archives of Neurology And Psychiatry. 41 (6): 1187. doi:10.1001/archneurpsyc.1939.02270180115011. ISSN 0096-6754.
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  45. ↑ Fleetwood, Ian G; Steinberg, Gary K (2002). "Arteriovenous malformations". The Lancet. 359 (9309): 863–873. doi:10.1016/S0140-6736(02)07946-1. ISSN 0140-6736.
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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.

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