Evaluation and Management of Elevated Intracranial Pressure in Adults

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  Clear Find Previous Topic New Search Evaluation and management of elevatedintracranial pressure in adults ContributorsDisclosuresDate INTRODUCTION — Elevated intracranial pressure (ICP) is a potentiallydevastating complication of neurologic injury. Elevated ICP maycomplicate trauma, central nervous system (CNS) tumors,hydrocephalus, hepatic encephalopathy, and impaired CNS venousoutflow (table 1) [1]. Successful management of patients with elevated ICP requires prompt recognition, the judicious use of invasivemonitoring, and therapy directed at both reducing ICP and reversing itsunderlying cause.The evaluation and management of adult patients with elevated ICP willbe reviewed here. Elevated intracranial pressure in children and specificcauses and complications of elevated ICP (eg, ischemic stroke,intracerebral hemorrhage, traumatic brain injury) are discussedseparately. (See Elevated intracranial pressure (ICP) in children  and Management of acute severe traumatic brain injury , section on'Intracranial pressure' and Initial assessment and management of acutestroke  and Spontaneous intracerebral hemorrhage: Treatment andprognosis  and Treatment of aneurysmal subarachnoid hemorrhage ,section on 'Management of complications'.)PHYSIOLOGY — Intracranial pressure is normally ≤15 mmHg in adults,and pathologic intracranial hypertension (ICH) is present at pressures≥20 mmHg. ICP is normally lower in children than adults, and may besubatmospheric in newborns [2]. Homeostatic mechanisms stabilize ICP,with occasional transient elevations associated with physiologic events,including sneezing, coughing, or Valsalva maneuvers.  Intracranial components — In adults, the intracranial compartment isprotected by the skull, a rigid structure with a fixed internal volume of 1400 to 1700 mL. Under physiologic conditions, the intracranialcontents include (by volume) [3]:Brain parenchyma — 80 percentCerebrospinal fluid — 10 percentBlood — 10 percentPathologic structures, including mass lesions, abscesses, andhematomas also may be present within the intracranial compartment.Since the overall volume of the cranial vault cannot change, an increasein the volume of one component, or the presence of pathologiccomponents, necessitates the displacement of other structures, anincrease in ICP, or both. Thus, ICP is a function of the volume andcompliance of each component of the intracranial compartment, aninterrelationship known as the Monro-Kellie doctrine [4,5].The volume of brain parenchyma is relatively constant in adults, althoughit can be altered by mass lesions or in the setting of cerebral edema(figure 1). The volumes of CSF and blood in the intracranial space vary toa greater degree. Abnormal increases in the volume of any componentmay lead to elevations in ICP.CSF is produced by the choroid plexus and elsewhere in the centralnervous system (CNS) at a rate of approximately 20 mL/h (500 mL/day)[6]. CSF is normally resorbed via the arachnoid granulations into thevenous system. Problems with CSF regulation generally result fromimpaired outflow caused by ventricular obstruction or venouscongestion; the latter can occur in patients with sagittal (or other)venous sinus thrombosis. Much less frequently, CSF production canbecome pathologically increased; this may be seen in the setting of choroid plexus papilloma. (See Cerebrospinal fluid: Physiology andutility of an examination in disease states .)Cerebral blood flow (CBF) determines the volume of blood in theintracranial space. CBF increases with hypercapnia and hypoxia. Otherdeterminants of CBF are discussed below. Autoregulation of CBF may beimpaired in the setting of neurologic injury, and may result in rapid andsevere brain swelling, especially in children [7-9].In summary, the major causes of increased intracranial pressure include:Intracranial mass lesions (eg, tumor, hematoma)Cerebral edema (such as in acute hypoxic ischemicencephalopathy, large cerebral infarction, severe traumatic braininjury)  Increased cerebrospinal fluid (CSF) production, eg, choroid plexuspapillomaDecreased CSF absorption, eg, arachnoid granulation adhesionsafter bacterial meningitisObstructive hydrocephalusObstruction of venous outflow, eg, venous sinus thrombosis, jugularvein compression, neck surgeryIdiopathic intracranial hypertension (pseudotumor cerebri)Intracranial compliance — The interrelationship between changes in thevolume of intracranial contents and changes in ICP defines thecompliance characteristics of the intracranial compartment. Intracranialcompliance can be modeled mathematically (as in other physiologic andmechanical systems) as the change in volume over the change inpressure (dV/dP).The compliance relationship is nonlinear, and compliance decreases asthe combined volume of the intracranial contents increases. Initially,compensatory mechanisms allow volume to increase with minimalelevation in ICP. These mechanisms include:Displacement of CSF into the thecal sacDecrease in the volume of the cerebral venous blood viavenoconstriction and extracranial drainageHowever, when these compensatory mechanisms have been exhausted,significant increases in pressure develop with small increases in volume,leading to abnormally elevated ICP (figure 2).Thus, the magnitude of the change in volume of an individual structuredetermines its effect on ICP. In addition, the rate of change in the volumeof the intracranial contents influences ICP. Changes that occur slowlyproduce less of an effect than those that are rapid. This can berecognized clinically in some patients who present with largemeningiomas and minimally elevated or normal ICP. Conversely, otherpatients may experience symptomatic elevations in ICP from smallhematomas that develop acutely.Cerebral blood flow — Following a significant increase in ICP, brain injurycan result from brainstem compression and/or a reduction in cerebralblood flow (CBF). CBF is a function of the pressure drop across thecerebral circulation divided by the cerebrovascular resistance, aspredicted by Ohm's law [10]: CBF = (CAP - JVP) ÷ CVRwhere CAP is carotid arterial pressure, JVP is jugular venous pressure,  and CVR is cerebrovascular resistance.Cerebral perfusion pressure (CPP) is a clinical surrogate for theadequacy of cerebral perfusion. CPP is defined as mean arterial pressure(MAP) minus ICP. CPP = MAP - ICPAutoregulation — CBF is normally maintained at a relatively constantlevel by cerebrovascular autoregulation of CVR over a wide range of CPP(50 to 100 mmHg) (figure 3) [11,12]. However, autoregulation of CVR can become dysfunctional in certain pathologic states, most notablystroke or trauma. In this setting, the brain becomes exquisitely sensitiveto even minor changes in CPP [11-13].Another important consideration is that the set-point of autoregulation isalso changed in patients with chronic hypertension. With mild tomoderate elevations in blood pressure, the initial response is arterial andarteriolar vasoconstriction. This autoregulatory process both maintainstissue perfusion at a relatively constant level and prevents the increase inpressure from being transmitted to the smaller, more distal vessels [11].As a result, acute reductions in blood pressure, even if the final valueremains within the normal range, can produce ischemic symptoms inpatients with chronic hypertension (figure 3) [11]. Cerebral perfusion pressure — Conditions associated with elevated ICP,including mass lesions and hydrocephalus, can be associated with areduction in CPP. This can result in devastating focal or global ischemia.On the other hand, excessive elevation of CPP can lead to hypertensiveencephalopathy and cerebral edema due to the eventual breakdown of autoregulation, particularly if the CPP is >120 mmHg [11,14,15]. Ahigher level of CPP is tolerated in patients with chronic hypertensionbecause the autoregulatory curve has shifted to the right (figure 3)[11,15]. (See Moderate to severe hypertensive retinopathy and hypertensive encephalopathy in adults , section on 'Mechanisms of vascular injury'.)Ultimately, global or local reductions in CBF are responsible for theclinical manifestations of elevated ICP. These manifestations can befurther divided into generalized responses to elevated ICP and herniationsyndromes.CLINICAL MANIFESTATIONS — Global symptoms of elevated ICP includeheadache, which is probably mediated via the pain fibers of cranial nerve(CN) V in the dura and blood vessels, depressed global consciousnessdue to either the local effect of mass lesions or pressure on the midbrainreticular formation, and vomiting.
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