1、Feb,2017Xie Zongyi(谢宗义谢宗义),MD&PhD,Associate Prof.Email:Wechat:873061410Department of NeurosurgeryChapter 1.Increased Intracranial Pressure and Brain HerniationPart 1.Increased Intracranial PressurePart 2.Acute Brain Herniation SyllabusPart 1To master the Definition,Consequences and Clinical manifest
2、ation of increased ICP;To be familiar with Cause,common diseases,Diagnosis and Management principles of increased ICP;To know Regulation of ICP and Pathophysiology of increased ICPPurpose and RequirementsPart 2To master the Definition and Clinical manifestation of brain herniation;To be familiar wit
3、h Anatomy and Management principles of brain herniationHeadache,vomiting,conscious at 2 hr post-TBI Coma at 3hr post-TBI,WHY?Representative CasePart 1.Increased Intracranial PressureoutlineDefinition of increased ICP Clinical manifestation Diagnosis of increased ICP Regulation of ICPCause of increas
4、ed ICP PathophysiologyTreatments of increased ICP Increased Intracranial Pressure(ICP)is characterized by a sustained increase in ICP(greater than 2.0 kPa),associated with clinical syndromeNote:1.Definition of increased ICP Increased ICP is a major clinical syndrome,not a disease,resulted from many
5、neurological illnesses.It is the most important neurological condition requiring prompt diagnosis and urgent treatment.4.disturbance of consciousness and changes in vital signs5.relative neurological signs:6th nerve paralysis-diplopia 1.Headache2.projectile vomiting3.Papilloedema“triad”2.Clinical ma
6、nifestation of increased ICPThe clinical manifestation will be determined in large part by the cause of the increased ICP.However,some of the clinical symptoms and signs will be the same,no matter what the cause of the increased ICP.The major features are:Headache WHEN:The headache is usually worse
7、on waking in the morning,and is relieved by vomiting.The headache is worse at night sometimes,because ICP increases during sleep,probably from vascular dilatation due to carbon dioxide retention.WHERE:is located usually at the frontal part,temporal part,occipital and neck region.WHAT:continuous swel
8、ling painWHY:The cause of the headache is probably traction on the pain-sensitive blood vessels and compression of the pain-sensitive dura at the base of the cranium.Projectile vomitingThe vomiting is usually worse in the morning.Papilloedema Papilloedema is the objective and definitive sign of incr
9、eased ICP.WHY:Papilloedema is due to transmission of the raised pressure along the subarachnoid sheath of the optic nerve.WHAT:Under fundoscopic examination,there is failure of the normal pulsations of the retinal veins and venous congestion.As the pressure rises,the optic nerve head becomes more sw
10、ollen,and the disc margins will become blurred.Flame-shaped haemorrhages develop,particularly around the disc margins and alongside the vessels.Long-standing papilloedema from prolonged increased ICP will subsequently develop into secondary optic atrophy.NormalPathologicalDisturbance of consciousnes
11、s Drowsiness.Drowsiness is the most important clinical feature of increased ICP.It is the portent of rapid neurological deterioration and must never be brushed aside as simply sleepiness,or disaster will almost certainly occur.ComaChanges in vital signs-Cushing response(also referred to as Cushing r
12、eflex,vasopressor response)is classically defined as an increase in systolic and pulse pressure(hypertension),reduction of the heart rate(bradycardia),irregular respiration(bradypnoea,apnea),and increased temperature.arises only from acute prolonged increase in ICP.Whenever a Cushing response occurs
13、,there is a high probability that death will occur in the near future(seconds to minutes).immediate intervention is needed!Harvey Cushing(1869-1939),Father of Neurosurgery1.Clinical history:headache and projectile vomiting2.Neurological examination:Papilloedema is a definitive sign of raised ICP 3.H
14、ow to diagnose increased ICP3.Radiological examinations:CT/MRI:CT or MRI can help determine the location and property of lesion.Midline structure shift and compression of ventricles suggest a raised ICP.CT scan is the first choice.However,MRI scan is the optimum selection.4.Lumbar puncture:How much
15、is the ICP?What property of CSF?is very dangerous if ICP raised,WHY?5.ICP MonitoringTo guide treatment modality,evaluate prognosisIntracranial Pressure(ICP)is the pressure inside the cranial vault，created by the total volume of the intracranial contents and exerted on cranial wall.Normal ValueAdult：
16、0.7-2.0kPa(70-200mmH2O);Children：0.5-1.0kPa(50-100mmH2O)4.1 Definition of ICPthree contents:Brain tissue(80-85%),CSF(10%),and cerebral blood(5-10%)total volume of intracranial cavity:14001500ml4.Regulation of ICP4.2 Regulation of ICPIn 1783 Alexander Monro deduced that the cranium was a rigid box fi
17、lled with a nearly incompressible brain and that its total volume tends to remain constant.The doctrine states that any increase in the volume of the cranial contents(e.g.brain,blood or cerebrospinal fluid),will elevate intracranial pressure.Further,if one of these three elements increase in volume,
18、it must occur at the expense of volume of the other two elements.In 1824 George Kellie confirmed many of Monros early observations.Monro-Kellie doctrineVintracranial vault(constant)=Vbrain+Vblood+VcsfWhat does this mean?Therefore,the change in intracranial CSF volume plays major role in physiologica
19、l regulation of ICP.Under physiological condition,brain tissue is incompressible and has little capacity to store oxygen and glucose,and depends on a steady supply of oxygen and nutrients provided by a continuous flow of blood matched to its metabolic demand.It shows that brain tissue and cerebral b
20、lood volume compromise little room to reduce ICP.ICP 0.7 kPa:increase in absorption and reduction in secretion of CSF;when ICP rising,displacement of intracranial CSF into spinal subarachnoid spacePhysiological regulation of ICP by change in CSF volume is effective and limited(lower than 5%of total
21、volume)-Volume BufferingCirculation of CSF?However,in the acute pathological condition,volume buffering is lower than 3%of total volume.Increased volume of normal intracranial contents Mass lesionDecreased capacity of cranial cavity 123 intracranial hematoma brain tumor brain abscess 5.Cause of incr
22、eased ICPbrain edema hydrocephalus Increased volume of cerebral bloodFig 1Fig 2large depressed skull fracture craniostenosis 5.2 Common diseases Traumatic brain injuryBrain tumor intracranial hemorrhagebrain abscess brain hypoxia A.ageB.Progression rate of intracranial disorders C.Location of intrac
23、ranial disordersD.Degree of cerebral edemaE.General systemic disease6.1 Factors affecting the increased ICP6.Pathophysiology of increased ICP A.ageinfant elder sutureB.Progression rate of intracranial disorders Volume-pressure Responseclinical significance However,as soon as volume buffering capacit
24、y is exhausted(decompensation),any small additions of volumes from the mass lesion or normal intracranial contents(eg.brain edema,severe cough)result in immediate elevation of ICP leading prompt deterioration of neurological conditions.This curve provides an explanation for clinical process of intra
25、cranial pathology.During the period of compensation,the state of patient with intracranial disorder keeps stable.C.Location of intracranial disorders lesion within the ventricles or around the midline lesion located in venous sinusD.Degree of cerebral edemabrain abscess cerebral parasitic diseaseast
26、rocytomasE.General systemic disease Hepatic coma;pulmonary infection;High Fever;Uremia;acid-base imbalance 1.Decreased CBF2.brain herniation3.brain edema4.Cushing response5.hemorrhage of digestive tract6.neurogenic pulmonary edema 6.2 Consequences of increased ICP1.Decreased CBF(cerebral blood flow)
27、,cerebral ischemia，brain deathCBFCPP=MAP-ICPCVRNomal CPP:70 90mmHgCBF depends on cerebral perfusion pressure(CPP)and cerebral vascular resistance(CVR),and is directly related to CPP and inversely related to CVR ICP(200mmH2OICP480mmH2O)CPP40mmHg autoregulation is exhausted CBF falls rapidly Cerebral
28、ischaemia；When ICP equals the MAP,CPP is zero,and blood flow ceases.4.Cushing response1st stage:ICP rises rapidly decreased CPP activate general sympathetic nervous system vasomotor center increases systolic BP in an effort to increase CPP;2nd stage:Baroreceptors in the aortic arch,which detect the
29、increase in SBP,trigger a parasympathetic response via the Vagus nerve induces bradycardia,or slowed heart rate.Final stage:Raised ICP,or some other endogenous stimulus result in distortion and/or increased pressure on the brainstem(respiratory center)results in irregular respiratory pattern and/or
30、apneaMechanism1.General treatmentTreatments of increased ICP7.3.Surgical therapy2.Medical therapy1.General treatment1).close observation of changes in consciousness,pupil and vital signs;2).elevation of the head of the bed,can help cerebral venous flow to reduce ICP;3).keeping upper airway patency t
31、o avoid hypoxia induced brain edema and increased ICP;4).controlled fluid infusion:The amount of fluid to maintain the balance of fluid input and output 2.Medical therapy1)hypertonic dehydration:20%Mannitol is widely used in clinical practice.Glycerin Fructose Furosemide2)hormone therapy:to improve
32、function of BBB and lower permeability of capillary.Desamethasone Methylprednisolone Controversy!3)Subhypothermia therapy:Lower cerebral metabolism,Reduce cerebral oxygen consumption,Prevent development of hydrocephalus.4)Accessory hyperventilation5)anti-infection therapy 1.3.Surgical therapyinludin
33、g lesion resection、hematoma evacuation;is a fundamental principle of treatment of increased ICP.1)Etiological treatmentPre-Post-intracranial hemorrhagePre-Post-Glioma1.8.Management of increased ICP2)external decompression or decompressive craniectomywhen brain tissue externally bulges to the bone wi
34、ndow,it is necessary to remove the bone flap in order to expand the cranial volume.1.3)internal decompression 8.Management of increased ICPResection of part of brain tissue(the non-dominant hemisphere frontal,temporal pole)to reduce the volume of the cranial contents4)bypass operation of CSF:includi
35、ng external ventriculardrainage,ventriculoperitoneal shuntexternal ventricular drainagewhen obstruction of circulation pathway of CSF induced hydrocephalus.ventriculoperitoneal shuntPre-5D Post-thalamic hemorrhagePart 1.Increased Intracranial PressurePart 2.Acute Brain Herniation Part 2.Acute Brain
36、Herniation Anatomy relative to brain herniationDefinition of brain herniationClassificationTranstentorial herniationTransforamen magna herniationoutlinetentorium cerebelli falx cerebri tentorial notch 1.Anatomy relative to brain herniation is the displacement of part of brain tissue from its origina
37、l location into anatomic defects/incisures caused by pressure gradients that develop between craniospinal mon diseases:Traumatic brain injury,Brain tumor,intracranial hemorrhage,Brain abscess,etc.#2.Definition of brain herniation#3.Classification of brain herniationTranstentorial herniation or tempo
38、ral uncal herniationForamen magnum herniation or cerebellar tonsillar herniationsubfalcine herniation or gyri callousus herniation Based on location of herniation and dispalced brain tissue#4.Transtentorial herniation or temporal uncal herniationmedial aspect of temporal lobe through tentoriumPathop
39、hysiology midbrain compressed and distorted compressed aqueduct impairs CSF flow(obstructive hydrocephalus)haemorrhage in pons and midbrainrisk to-ipsilateral 3rd nerve-posterior cerebral artery-ipsilateral cerebral peduncleMidbrain haemorrhage and necrosis following tentorial herniation#Clinical ma
40、nifestationa.Symptom of increased ICPc.contralateral hemiplegia decerebrate rigidityd.deterioration of conscious statee.Disorder of vital signs:Cushing response,respiratory failure b.pupillary changes pupil dilatation:initially on ipsilateral side,finally bilateral sidesTentorial herniation due to l
41、arge cerebral glioblastoma Emergent Treatments keeping upper airway patency to avoid hypoxia induced brain edema and increased ICP rapid intravenous injection of 20%Mannitol 250-500ml；removal lesions causing increased ICP;palliative operation if leision is unclear:resection of part of brain tissue;v
42、entricular puncture and external drainage external ventricular drainageVery effective emergent measure to brain herniation!#5.Transforamen magna herniation or Tonsillar herniationPathophysiology Foramen magnum herniationcerebellar tonsils move down-with medulla form cone shapeexit of 4th ventricle b
43、locked impairing CSF flow(obstructive hydrocephalus)compress breathing and cardiac center in medulla#Clinical manifestationacute medulla injuryb.disordered vital signs:abnormalities of respiratory rate and rhythm sudden stopped respiration,without pupillary changes.a.Severe symptom of increased ICP:
44、Severe headache,repeated vomitingThe 4th ventricle medulloblastomaSame to treatments of Transtentorial herniationEmergent TreatmentsLumbar punctureLumbar puncture is dangerous and should be avoided if ICP raised.Why?Is there any way you might check for raised ICP before doing an LP?疝出部位疝出部位疝出组织疝出组织受
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