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.
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.
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]
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:
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:
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
Differentiating Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) from Other Diseases on the Basis of Seizure, Visual disturbance, and Constitutional Symptoms[edit | edit source]
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.
Natural History, Complications and Prognosis[edit | edit source]
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.
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.
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 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.
Noninvasive devices still need further large randomized trials to prove their clinical efficacy. They are not used in clinical practice but are still under investigation and include:[75][76]
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:[edit | edit source]
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]
CSF is usually drained at a rate of 1 to 2 mL/minute for 2 to 3 minutes. The procedure is repeated after every 2 to 3 minutes, until ICP is less than 20mmHg
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.
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