Intracranial pressure (ICP) is the pressure of cerebrospinal fluid (CSF) within the cerebral ventricles. ICP is the product of the rate of cerebrospinal fluid (CSF) formation (Iformation), resistance to CSF drainage (Rout), and pressure in the dural venous sinuses (Pd), a formula proposed by Davson (ICP = Rout × Iformation + Pd).1 Thus, ICP is regulated by venous pressure, cerebral blood flow, and CSF circulation.
Normal values for CSF production, sagittal sinus pressure, and resistance to CSF outflow are 0.2 to 0.7 mL/min, 5 to 8 mmHg, and 6 to 10 mm Hg/mL/min, respectively.
ICP increases with age.
In the newborn, the normal value for ICP is approximately 82 mm H2O, or 6 mmHg.2
Normal CSF pressure in healthy children obtained during lumbar puncture is a mean of 19.6 cm H2O (10th to 90th percentile, 11.5 to 28.0 cm H2O).
Sedation may increase opening CSF pressure by up to 3.5 cm H2O.
Volume status, blood pressure, and end-tidal CO2 may also affect ICP and must be considered when deciding on interventions to treat intracranial hypertension.
An opening pressure above 28 H2O may not be “abnormal” if signs of increased ICP (papilledema, abducens nerve palsy, hydrocephalus, subdural fluid, other intracranial pathology) are absent.3
Monro-Kellie doctrine
The skull is a rigid cavity containing brain (1200–1600 mL), arterial and venous blood (100–150 mL), and CSF or other extracellular fluid (100–150 mL)
Expansion of one compartment is offset by a decrease in volume of the others. The pressure–volume relationship is expressed by the formula C ∼ dV/dp, where C represents compliance and dV represents the change in volume that accompanies a change in pressure (dp) (Figure 40-1).
As ICP increases, compliance decreases. In cases of intracranial pathology, such as traumatic brain injury (TBI) or space-occupying lesions (tumors, arachnoid cysts, hemorrhage), compliance is decreased and small increases in the volume of one compartment result in large increases in ICP. Cranial causes of decreased compliance can include hyperostosis, craniosynostosis, and traumatic skull injury without brain injury such as a depressed skull fracture.
Intracranial pressure, cerebral perfusion, and autoregulation
Under normal conditions, cerebral blood flow (CBF) is a constant of approximately 50 mL/100 gm brain/min.
CBF is determined by the vascular gradient across the cerebral beds and is a product of cerebral perfusion pressure (CPP) and cerebrovascular resistance (CVR), according to the formula CBF = CPP/CVR.4
The relationship between CPP and ICP is expressed by the formula CPP = MAP – ICP.
Autoregulation is the mechanism by which CBF is kept constant despite changes in CPP.
When autoregulation is intact, increases in blood pressure lead to a decrease in cerebral artery caliber to maintain a constant CBF by increasing CVR.
When CPP falls below the lower limit of autoregulation (40–50 mmHg in the mature brain), CBF is dependent on MAP.
This is a “pressure-passive” circulation in which decreases in MAP result in corresponding decreases in cerebral perfusion and risk for ischemic injury.
Cumulative data from pediatric traumatic brain injury studies suggest ICP >20 mmHg or CPP <40 mmHg are associated with poor outcome.
Diagnosis of intracranial hypertension requires a high index of clinical suspicion and cannot be excluded based on a normal computerized tomography (CT) or magnetic resonance imaging (MRI) scan. Imaging signs of intracranial hypertension include decrease in size or loss of cisterns, uncal and other herniation, midline shift, and loss of grey-white differentiation. Clinical signs range from subtle changes in mental status to cranial neuropathies, focal weakness, posturing, stupor, and coma.
